Evidence‐based (S3) guideline for the treatment of androgenetic

© 2011 The Authors • JDDG © Blackwell Verlag GmbH, Berlin 9 (Suppl. 6): S1–S57 JDDG | Supplement 6˙2011 (Band 9)

Evidence-based (S3) guideline

Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in menAnja Blumeyer1, Antonella Tosti2, Andrew Messenger3, Pascal Reygagne4, Veronique del Marmol5, Phyllis I. Spuls6, Myrto Trakatelli7, Andreas Finner8, Franklin Kiesewetter9, Ralph Trüeb10, Berthold Rzany11,Ulrike Blume-Peytavi1

(1) Department of Dermatology and Allergy, Clinical Research Center for Hair and Skin Science, Charité –Universitätsmedizin, Berlin, Germany

(2) Department of Dermatology, University of Bolognia, Italy and Department of Dermatology and Cutaneous Surgery,Miller School of Medicine, University of Miami, FL, USA

(3) Department of Dermatology, University of Sheffield, UK(4) Centre Sabouraud, Hôpital St. Louis, Paris, France(5) Private Practice and Dermatology Department, Hopital Erasme, Université Libre de Bruxelles, Bruxelles, Belgium(6) Department of Dermatology, Academic Medical Center, Amsterdam, The Netherlands(7) Department of Dermatology and Venerology, Papageorgiou Hospital, Aristotle University, Thessaloniki, Greece(8) Private Practices, Berlin, Leipzig, Germany(9) Department of Dermatology, Venerology and Allergology, University of Erlangen, Germany(10) Department of Dermatology, University Hospital Zürich and Private Practice, Wallisellen, Switzerland(11) Department of Dermatology and Allergy, Division of Evidence based Medicine, Charité – Universitätsmedizin,

Berlin, Germany

SummaryAndrogenetic alopecia is the most common hair loss disorder, affecting bothmen and women. Initial signs of androgenetic alopecia usually develop duringteenage years leading to progressive hair loss with a pattern distribution.Moreover, its frequency increases with age and affects up to 80 % Caucasianmen and 42 % of women.Patients diagnosed with androgenetic alopecia may undergo significant im-pairment of quality of life. Despite the high prevalence and the variety of thera-peutic options available, there have been no national or international evidence-based guidelines for the treatment of androgenetic alopecia in men andwomen so far. Therefore, the European Dermatology Forum (EDF) initiated aproject to develop an evidence-based S3 guideline for the treatment of andro-genetic alopecia. Based on a systematic literature research the efficacy of thecurrently available therapeutic options was assessed and therapeutic recom-mendations were passed in a consensus conference.The purpose of the guideline is to provide dermatologists as well as generalpractitioners with an evidence-based tool for choosing an efficacious and safetherapy for patients with androgenetic alopecia.

Keywords• alopecia• androgenetic• Therapy• Guideline• hair loss

I Introduction to the guideline1.1 Needs/problems and issues inpatient careAndrogenetic alopecia (AGA) is a com-mon chronic dermatologic disease, af-fecting both men and women. It is cha-racterized by progressive hair loss usuallyoccurring in a pattern distribution. Thefrequency increases with age. In Caucasi-

ans, at the age of 70 or beyond 80 % ofmen and up to 42 % of women havesigns of androgenetic alopecia. Thoughthe prevalence is high in elderly patients,androgenetic alopecia often already startsat puberty.

Independent of age and gender, pati-ents diagnosed with androgenetic

alopecia undergo significant impair-ment in their quality of life. Hair is an important feature of image. Hair lossaffects self-esteem, personal attractiven-ess and may lead to depression and othernegative effects of life [1]. Androgeneticalopecia is clearly a burden for both sexes, but it is substantially more distres-sing for women [2].

DOI: 10.1111/j.1610-0379.2011.07802.x Evidence-based (S3) guidline S1

S2 Introduction to the guideline

JDDG | Supplement 6˙2011 (Band 9) © 2011 The Authors • JDDG © Blackwell Verlag GmbH, Berlin 9 (Suppl. 6): S1–S57

Patient’s therapeutic experiences. Alt-hough there is a significant impairmentin quality of life in many of the patients,Alfonso et al. revealed that three out offour men with androgenetic alopecia hadnever pursued therapy for hair loss [1].On the other hand, lots of patients trieddifferent therapies promising hair regro-wth in vain and are dissatisfied with current therapeutic approaches whenthey first come to see a specialist. Conse-quently, their compliance is often poor.Men who had their hair loss successfullytreated reported psychosocial benefitswith improvements for self-esteem andpersonal attractiveness [1].

Patient’s compliance. There are discre-pancies between the interest for effectivehair regrowth and willingness to performa long-term therapeutic regimen. Limi-ted efficacy, poor tolerance, fear and lackof information on treatment durationand possible adverse events lead to disap-pointment again.

Therapeutic concepts. The individualtherapeutic concepts are still mainly ba-sed on physicians’ personal experienceswithout taking into account the currentevidence-based knowledge regarding theefficacy of the therapies.

1.2 Purpose of the guidelineThe purpose of the guideline is to providedermatologists with an evidence-basedtool for choosing an efficacious and safetherapy for patients with androgeneticalopecia. The current guideline aims toprevent progressive hair loss and associa-ted dermatological and psychosociallong-term complications by improvingthe individual therapeutic concept.

Improved patient care. The use of theseevidence-based recommendations in cli-nical routine will lead to an improvedpatient care, as the physicians’ personalexperiences and traditional therapeuticconcepts will be added and, if necessary,replaced by evidence-based assessmentsof the efficacy of the different therapeu-tic options.

Insure optimal usage of therapeuticregimen. In addition to the efficacy as-sessment the guideline provides detailson administration and safety aspects ofsystemic, topical or surgical therapy.These instructions for use should

decrease reservations of physicians andpatients and assure that the therapy isprovided in an optimal way. Initiation ofthe right therapy at the right time canprevent or at least slow down severe pro-gression.

Improvement of patient’s knowledgeand compliance. Patients’ compliance is most important in the individual res-ponse on a therapeutic concept. Goodcompliance is not only related with a balance of benefits, costs and adverse effects, but also requires the patient to beinformed. By increasing the level of thepatients’ knowledge about the optimaluse of each therapy and its possible complications, patients’ compliance, res-ponse rates and satisfaction will increase.Information on administration and ad-verse reactions should serve to eliminateor reduce these and therefore will addi-tionally improve compliance.

1.3 Directions for use of the GuidelineThe current guideline is meant for der-matologists, general practitioners in cli-nics as well as in private practice andother specialists who are involved in thetreatment of androgenetic alopecia. Itshould provide support in the develop-ment of individual therapeutic concepts.Each chapter summarizes the efficacy re-sulting from the evidence-based evalua-tion separately for men and women.Moreover, the experts provide informa-tion on practical aspects important forthe different therapeutic regimens. Theusers of the guideline should be aware,that the listed aspects are not intended to be exhaustive. General obligations,which are part of every individual thera-peutic decision, such as known allergies,potential intolerance reactions or contra-indications are not conclusively indivi-dually listed.Consequently, the users of the guidelinehave to consider additionally the manu-facturer’s product information and checkthe recommendations concerning com-pleteness and up-to-datedness of dosages,contraindications or drug-interactions. Although the authors took care that theguideline corresponds to the currentstate of the art at the time of completion,authors and publishers cannot take res-ponsibility for dosages and therapeuticchoices, as there may be changes and up-dates in between the actualisation cyclesof the guideline. Therefore, the usage of

the recommendations is at the reader’sown responsibility and users are reque-sted to keep informed about new know-ledge regularly published parallel to theguidelines. The authors and publishersof the guideline would be pleased, if readers could inform them on potentialinaccuracies.

1.4 MethodologyLiterature research. A detailed descrip-tion of methodology reflecting the pro-cess of developing the guidelines can befound in the method report of the guide-lines. The methodology was defined asfirst step in development of the guide-line. It was orientated on the standards ofthe AGREE instrument and on the me-thodology of the European S3 guidelinefor the treatment of psoriasis vulgaris.To assess the efficacy of the individualtherapeutic processes, a systematic searchof literature in the databases Medline,Embase and Cochrane Library was conducted at 25th January 2007 and up-dated at 07th August 2008. Overall, 1 245articles were found. Additional 51 articleswere added by hand search. 125 articleswere found by updating the literature research. Overall, after checking fordoublets and relevance 396 articles wereevaluated using the literature evaluationform (LEF) (see Appendix 1). 85 articlesfulfilled the inclusion criteria of the gui-deline and built consequently the basis ofthe guideline. Figure 1 summarizes theprocess of literature research.The evidence-based evaluations of theseguidelines are restricted on the efficacy ofthe particular therapeutic options. Allother issues outlined in the guideline,e.g. instructions for use, adverse eventsand contraindications, are based on opi-nions and personal experiences of themembers of the guideline group.

Evidence assessment. The methodolo-gical quality of each study, which wasincluded in the evidence-based analy-sis, was defined by the grade of evidence. We assessed the grade of evidence according to the followingscheme:A1 Meta-analysis, which includes at

least one randomized clinical trial ofgrade A2 evidence with consistent results of the different studies.

A2 Randomized, double-blind, compa-rative clinical studies of high-quality(e.g. sample size calculation, flow

Introduction to the guideline/Introduction to androgentic alopecia S3

chart of patient inclusion, ITT-analysis,sufficient size).

B Randomized, clinical studies of lesserquality or other comparable studies(not-randomized, cohort- or case-control-studies).

C Non-comparable studies.D Expert opinion.The grade of evidence was determinedwithin the LEF form by the particularexpert group and the staff member. Thescheme for grading the evidence wasused for assessment of monotherapies aswell as combination therapies.

Level of evidence. After determining thegrades of evidence of the individual stu-dies, the grades of all studies belongingto a particular therapeutic regimen weresummarized in a level of evidence. Thelevel of evidence takes into account themethodological quality of the trials(grade of evidence) and the intertrialconsistence of the results.1 Studies grade A1 evidence or studies

with mainly consistent results gradeA2 evidence.

2 Studies grade A2 evidence or studieswith mainly consistent results grade Bevidence.

3 Studies grade B evidence or studieswith mainly consistent results grade Cevidence.

4 Little to missing systematic evidence.

Therapeutic recommendation. Gradesand levels of evidence were considered inthe formal consensus process. The guide-line group defined particularly relevantsections requiring consensus. These pas-sages were discussed and approved at theconsensus conferences. The resulting evi-dence-based therapeutic recommendati-ons aim to optimize the therapeutic pro-cess and to support the practitioner inthe individual decision on a suitabletherapy. Nevertheless, the decision pro-cess on a particular therapy remainscomplex and limited on the individualcase. It is not possible to define a strictclinical algorithm.

Strength of recommendation.This guide-line summarizes the characteristics of theavailable drugs and their evidence-basedtherapeutic efficacies. The consented therapeutic recommendations were addi-tionally weighted by the strength of recommendation. The strength of recom-mendation considers efficacy, evidence level, safety and practicability and wasconsented in a formal consensus process.The expert group agreed on a 5-pointscale. This scale is illustrated by arrows: �� We recommend� We suggest � Can be considered� We do not suggest �� We do not recommend

II Introduction to androgeneticalopeciaAndrogenetic alopecia is the most frequent form of alopecia in men andwomen. Today, in our societies, strongand dense hair is associated with youth,beauty, healthiness, attractiveness andsuccess. Consequently, in patients presenting with androgenetic alopeciaprogressive thinning of hair often causesa psychological distress. Patients are looking for effective hair loss treatmentsin order to stop and prevent further thinning and to optimally stimulateregrowth. Knowledge on the efficacy ofthe different therapeutic options is essen-tial for treating doctors and interestgroups in the management of the diseaseand will lead to enhanced patient satis-faction.

2.1 Epidemiology Androgenetic alopecia in men and wo-men is present in populations of diffe-rent ethnicities. Typically, frequency andseverity increase with age. The highestprevalence is reported in the Caucasianpopulation. At the age of 70 and beyondaround 80 % of men and up to 42 % of women suffer from androgeneticalopecia [3, 4]. Usually, initial signs ofthe disease already develop in men at teenage [3–6]. Female pattern hair lossshows peaks of incidence at teenage andin postmenopause.In the Asian population the frequency ofandrogenetic alopecia in male and female patients is lower compared to theEuropeans. There is no information onthe prevalence of the disease in Africanmen and women.

2.2 AetiologyAndrogenetic alopecia is characterized bya non-scarring progressive miniaturiza-tion of the hair follicle in predisposedmen and women, usually in a specificpattern distribution. Its aetiology is mul-tifactorial and polygenetic [3].In men androgenetic alopecia is an and-rogen-dependent trait. The terminal hairfollicle becomes susceptible againstdihydrotestosteron, which leads to ashortened anagen phase and miniaturiza-tion of terminal to vellus hair. The deve-lopment of male androgenetic alopecia ispredominantly hereditary. In men, fa-mily analyses showed strong concor-dance rates in twins and increased riskfor sons with bald fathers [7]. Moreover,


Figure 1: Schematic presentation of the process of systematic literature research.

S4 Introduction to androgentic alopecia


variant regions on the androgen receptorgene and at chromosome 20p11 are asso-ciated with the development of androge-netic alopecia in men [8, 9].In female patients, little is known aboutthe aetiology of androgenetic alopecia.Regarding inheritance, incidence of54 % respectively 21 % are reported forwomen with male respectively femalefirst degree relatives suffering from and-rogenetic alopecia [10, 11]. Possibly,early and late onset female androgeneticalopecia have different genetic traits. Theandrogen dependence is likewise uncer-tain in women, that is to say, other fac-tors seem to be involved.Nevertheless, it is important to considerthat there is a subset of women with and-rogenetic alopecia and associated hormo-nal dysregulation. Detailed informationon the steps in diagnostic procedure canbe found in the S1 guideline for diagno-stic evaluation in androgenetic alopeciain men, women and adolescents [3].

2.3 Clinical featuresClinically, androgenetic alopecia is characterized by a drift from terminal tovellus hairs and progressive thinning,usually in a pattern distribution. The different patterns can occur in men aswell as in women, though the frequen-cies are gender-specific. Moreover, it is not rare to observe a diffuse thinningof the parietal and occipital areas in addition [3].

Male pattern, Hamilton-NorwoodThe most frequent clinical pattern inmen with androgenetic alopecia, onlyoccasionally observed in women presentswith a recession of the frontal hair line,mainly in a triangular pattern, later follo-wed by a vertex thinning (Figure 2).

Female pattern, Ludwig The so-called female pattern is characte-rized by a diffuse thinning of the centro-parietal region with preserving the fron-tal hair line (Figure 3). It is the mostcommon type in women, occasionallyalso observed in men.

Christmas tree patternSimilarly to the Ludwig pattern, theChristmas tree pattern shows diffusecentro-parietal thinning, but additio-nally, the frontal hair line is breached (Figure 4). The Christmas tree pattern isanother common pattern in women.

2.4 DiagnosisAndrogenetic alopecia is usually diagno-sed clinically by examination of hair andscalp showing a non-scarring alopecia inthe typical pattern distribution [3]. The clinical examination should also in-clude a pull test and an examination offacial and body hair as well as nails to

exclude differential diagnoses; diffusetelogen effluvium, alopecia areata and ci-catrical alopecia in particular [3]. Due to the high prevalence of androge-netic alopecia its coincident appearanceto other hair diseases should be takeninto account. If a differential diagnosiscannot be excluded clinically, further

Figure 3: Ludwig classification, female pattern (Olsen EA. Female pattern hair loss. J Am Acad Der-matol 2001; 45(Suppl.): S70–80.

Figure 2: Hamilton-Norwood classification, male pattern (Norwood OT. Male pattern baldness: classification and incidence). South Med J 1975: 68(11); 1359–65.

Introduction to androgentic alopecia/Therapeutic options and therapy assessment S5

diagnostics such as evaluations of hairroots, laboratory or histology can behelpful.

2.5 Hair growth assessmenttechniquesTo document the extent of androgeneticalopecia in clinical practice, the differentclassifications of the pattern distributionare subdivided (Hamilton-Norwood I–VII, Ludwig I–III, Christmas tree pat-tern I–III). However, a generally applica-ble definition for the extent ofandrogenetic alopecia does not exist.Moreover, the documentation of the de-gree of the pattern distribution is oftenunsuitable to reflect the course of andro-genetic alopecia. As androgenetic alopecia is a naturallyprogressive disease, therapy can havetwo required outcomes: cessation of hairloss and induction of hair regrowth. Inclinical practice, the evaluation and follow-up of hair growth is generally restricted to individual assessment of patient and physician. In clinical studies,the subjective hair growth assessment bypatient and investigator are substantiatedby objective hair count/density methodsand assessment of standardized globalphotographs.The global photographic assessmentis a semi-objective tool in hair growthevaluation. Global photographs are as-sessed by experts blinded to treatmentand time. Automatic digitalized photographicsystems are able to quantify hair density,hair thickness, anagen/telogen hair ratio,terminal/vellus hair ratio within an inve-stigational area. A dot tattoo guarantiesthe analysis of the same area to ensure re-producibility in studies. The technique is

limited by the size of the measured area.In clinical trials comparison to baselineand to placebo resp. another treatment isnecessary for efficacy assessment of a the-rapeutic option.Within the development of the S3 guide-line the experts voted on a ranking ofthe different investigative methods andoutcome parameters. The global photo-graphic assessment was voted to be themost effective method in hair growthevaluation, as the whole scalp hair is eva-luated in a standardized way. Patient’sand investigator’s perception can beexcluded. According to the experts, glo-bal photographs should also be used inroutine clinical practice for long-termfollow-up.

2.6 Risk/benefit considerationsIn routine clinical practice the individualdecision for a particular treatment ofandrogenetic alopecia does not only de-pend on the efficacy, but also on prac-ticability, risks and costs. The assessmentof cost effectiveness has to be made bybalancing the costs with the benefit attained. Consequently, expensive thera-peutic options can also be cost-effective,if they are highly effective. As the patient usually has to bear the fullcosts of the treatment, consideration ofpatient-relevant benefit is essential.The benefit attained in the therapy ofandrogenetic alopecia is not only stabi-lization, prevention of progression andinduction of hair growth, but also an im-proved quality of life. The guideline offers evidence-based ana-lyses of the existing therapeutic optionsthat help to make suitable cost-benefitdecisions in the assessment of the specificcase.

III Therapeutic options and therapy assessmentThe following chapters summarize theevidence-based efficacy assessment of thedifferent therapeutic options in the treat-ment of androgenetic alopecia in menand women. Efficacy was evaluated sepa-rately for men and women.

Result tables. All studies that fulfilledthe inclusion criteria of the guideline arelisted in result tables (see Appendix 2).The evidence-based results of the trialsare outlined in the particular chapter,but can be read in detail in the result tables, if required. Based on the result tables the expert group passed therapeuticrecommendations for the different regi-mens by formal consensus process.

Overview of common therapeutic options. Table 1 shows a summary of evidence level, efficacy to prevent pro-gression and/or improve androgeneticalopecia, safety aspects and practicabilityfor the most common therapeutic inter-ventions. Its intention is to provide a firstrough orientation. Its exclusive use is notsufficient for individual therapeutic choi-ces. Deeper observation of the individualfactors of a given patient and its impacton the different therapeutic regimens arenecessary.

3.1 Minoxidil3.1.1 IntroductionMinoxidil was originally developed as anoral drug (trade name Loniten®) to treathigh blood pressure. Its possible use inandrogenetic alopecia was discoveredwhen its side effect of increasing hairgrowth was observed.Chemically, minoxidil is a pyrimidinederivate. It was the first product to be approved for the treatment of AGA inboth men and women. The 2 % topicalsolution was first approved by the U.S.Food and Drug Administration (FDA)in1988 for the treatment of androgene-tic alopecia in men and in 1991 in wo-men. The 5 % solution was approved in1997 for the treatment of androgeneticalopecia in men followed by approvalof the 5 % foam in 2006 also for thetreatment of androgenetic alopecia inmen.

3.1.2 Mechanism of actionTo exert its effect minoxidil needs to betransformed to its active metabolite,


Figure 4: Christmas tree pattern (Olsen EA. Current and novel methods for assessing efficacy of hairgrowth promoters in pattern hair loss. J Am Acad Dermatol 2003; 48(2): 253–62).

Table 1: Summary of evidence level, efficacy, safety aspects and practica-bility for the most common therapeutic interventions.

Therapy

Level of evidence

Efficacy to prevent

progression

Efficacy to im

prove

Safety

Practicability (patient)

Practicability(physician)

Male patients

Finasteride 1 +++ ++ +++ ++++ +++ / ++++

Minoxidil 5% 1 +++ ++ ++++ + / ++ +++

Surgery 4 - +++ ++

+ intervention

+++ long-term

+

Female patients

Minoxidil 2% 1 +++ ++ ++++ + +++

Hormones oral Hyperandrogenismnormal hormones

3+

+ / -+

+ / -+ +

+++ +++

++ ++

Surgery 4 - ++ ++

+ intervention

+++ long-term

+

S6 Therapeutic options and therapy assessment


minoxidil sulphate by the enzyme sul-photranspherase, which is present in theouter root sheath of anagen follicles. Theexact mechanism by which minoxidilpromotes hair growth is still unclear. Itsactive metabolite, minoxidil sulphateopens ATP-sensitive potassium channelsin cell membranes, which conveys vaso-dilatory effect. Vasodilatation, however,does not appear to be responsible for mi-noxidil-induced hair growth. Studies on skin blood flow after topical minoxi-dil application produced inconsistent results.Other possible effects of minoxidil onthe hair follicles include:a) increased expression of vascular endo-

thelial growth factor (VEGF) mRNAin the dermal papilla. This indicatesthat the drug induces angiogenesis inthe dermal papilla.

b) activation of cytoprotective prostag-landin synthase-1, a cytoprotectiveenzyme that stimulates hair growth.

c) increased expression of hepatocytegrowth factor (HGF) m-RNA; HGFis an hair growth promoter.

3.1.3 Efficacy – males34 studies assessing the efficacy of mino-xidil in male patients with androgeneticalopecia met the inclusion criteria for theguideline [12–45]. 3 out of them treatedmale and female patients. 25 studieswere placebo controlled. The majority ofstudies obtained grade A2 and B evi-dence (A2 = 17, B = 13, C = 3) resultingin evidence level 1.In general most of the trials assessed theefficacy of minoxidil solution 2 % res-pectively 3 %, applied twice daily. In alltrials that examined the effect of minoxi-dil 2 % solution, regular topical applica-tion resulted in hair regrowth.

OutcomesThe mean change from baseline totalhair count ranged between 5.4 hairs/cm2

and 29.9 hairs/cm2 (11.0–54.8 %) at 4to 6 months and between 15.5 hairs/cm2

and 83.3 hairs/cm2 (14.8–248.5 %) at12 months [12, 13, 17, 19, 22, 23, 26,27, 29, 30, 35, 38–40, 42, 43]. At 4 to 6 months the mean total haircount changes in the majority of studies

were statistically significant compared toplacebo (p between 0.074 and < 0.0001).At 12 months most of the older trialsswitched the placebo group also to minoxidil treatment. Comparable to the results in total haircount the mean changes in nonvellus haircounts were also significantly different toplacebo (p between < 0.05 and 0.001).There was a mean change in nonvellushair counts between 4.7 hairs/cm2 to37.3 hairs/cm2 (17.2–59.4 %) at6 months, between 9.4 hairs/cm2 to41.8 hairs/cm2 (8.8–443.8 %) at12 months [12, 13, 17–22, 24, 26, 27,29, 30, 33, 35, 43, 45].The increases from total and nonvellushair counts at 6 and 12 months did sig-nificantly differ from baseline haircounts (p between 0.01 > p < 0.0001).It must be noted that the reported pla-cebo rate in most of the minoxidil stu-dies is very high. The mean increase frombaseline total hair count of the placebogroup ranged between 6.1 hairs/cm2 and22.4 hairs/cm2 (9.3 and 48.8 %) at 4 to6 months.

DosageConcentration. Minoxidil dosages below2 % showed significant reduced meanchanges from baseline total hair count in comparison to minoxidil 2 % at6 months [30, 45]. The mean changesfrom nonvellus hair counts were not significantly different for minoxidil0.1 %, 1 %, 2 % at 6 months.Minoxidil 3 % solution, applied twicedaily was not significantly different fromminoxidil 2 %, twice daily (mean changefrom total hair count/nonvellus haircount at 4 respectively 12 months) [21,25, 26, 29, 31, 32, 39, 40, 43]. OnlyKatz et al. reported a significance ofp = 0.0464 at 4 months in mean changeof nonvellus hair counts [24].2 studies comparing minoxidil 2 % solu-tion, twice daily and minoxidil 5 % solu-tion, twice daily were included in the evi-dence-based analysis [33, 37]. In bothstudies the outcome of the minoxidil5 % group was superior to minoxidil2 % (mean change from baseline nonvel-lus hair count 18.6 hairs/cm2 (12.3 %)vs. 12.7 hairs/cm2 (8.8 %) at 12 months,p = 0.025, mean % change from baselinetotal hair count 30 % vs. 25 % at24 months, p = 0.455).Application frequency. Olsen et al. showed,that minoxidil 3 % applied twice daily was

Therapeutic options and therapy assessment S7

superior to application once daily (meanchange from baseline total hair count64.4 hairs/cm2 vs. 44.1 hairs/cm2 at33 months, p = 0.015, mean changefrom baseline nonvellus hair count4.4 hairs/cm2 vs. –13.4 hairs/cm2 at36 months) [32].

FormulationThe standard formulation of minoxidil isa solution containing propylenglycol.Olsen et al. studied a foam formulationcontaining 5 % minoxidil [34]. The meanchange from baseline nonvellus haircount was highly significant differentfrom placebo at 16 weeks (20.9 hairs/cm2

[13.4 %] vs. 4.7 hairs/cm2 [3.4 %],p < 0.0001).Piepkorn et al. examined minoxidil 2 % in a gel formulation and as solution[36]. Whereas placebo gel and solutionreached comparable percentage improve-ment in subject’s assessment (33 vs.36 %), minoxidil 2 % gel, twice dailyhad 26 % improvement, minoxidil 2 % solution, twice daily 48 % impro-vement after 6 months in subject eva-luation.

Minoxidil vs. finasterideIn comparison to finasteride 1 mg dailyArca et al. reported an 80 % improve-ment in global photographic assessmentfor minoxidil 5 %, twice daily and 52 %for finasteride at 12 months [14]. On theother hand, a study by Saraswat et al. reported superiority of minoxidil 2 %solution, applied twice daily, in compari-son to finasteride 1 mg/d (mean changefrom baseline total hair count36.1 hairs/cm2 [29.1 %] vs. 19.6 [14.8 %]at 12 months, p = 0.003) [42].

3.1.4 Efficacy – females11 studies that investigated the efficacyof topical minoxidil in female patientssuffering from androgenetic alopeciacould be included in the evidence-basedevaluation [15, 39, 40, 46–53]. 3 studiestreated male and female patients. 7 stu-dies obtained grade B evidence, 4 studiesgrade A2 evidence, resulting in an evi-dence level 1.

OutcomesMinoxidil 1 % solution, applied twicedaily led to mean changes from baselinetotal hair count at 6 months from15.2 hairs/cm2 (8.0 %) [54]. Minoxidil2 % solution showed mean changes

from baseline nonvellus hair count at6 months between 21.0 hairs/cm2 and50.1 hairs/cm2 (12.4–31.3 %) [39, 47–51, 53].Except the study by Whiting et al. allstudies showed significant differentmean changes from baseline hair countsin comparison to placebo (p between0.02 and < 0.001).

DosageConcentration. The mean changes innonvellus hair counts between minoxidil5 % and 2 % in female patients were notstatistically significant (p = 0.129). At12 months the mean change from non-vellus hair count was 20.7 hairs/cm2

(13.8 %) for minoxidil 2 %, twice daily,24.5 hairs/cm2 (17.3 %) for minoxidil5 %, twice daily and 9.4 hairs/cm2

(6.8 %) for placebo, twice daily(p < 0.001 vs. placebo).

Minoxidil vs. AlfatradiolIn comparison to topical alfatradiol0.025 %, once daily, minoxidil 2 % solution, twice daily, led to increased hair counts after 6 months [46]. The mean change from baseline totalhair count was –7.8 hairs/cm2 (–4.3 %)for alfatradiol and 15.3 hairs/cm2

(8.7 %) for minoxidil 2 % (p < 0.0005).

3.1.5 Instructions for use / PracticabilityTreatment with minoxidil converts parti-ally miniaturized (intermediate) hairs toterminal hairs and produces at least apartial normalization of the hair folliclemorphology.Minoxidil should be applied as 1 ml ofsolution with a pipette or half a cap offoam to dry hair and scalp once in themorning and again in the evening andleft in place for at least four hours. Whenusing spray applicator it has to be spreadevenly over the affected areas. Handsshould be washed with warm water afterapplication.Treatment efficacy should be assessed atleast 6 months after initiation of therapyand treatment should be maintained aslong as the patient is interested to main-tain the efficacy.Some patients may experience increasedhair shedding during the first months ofthe treatment. This is transitory and onlyindicates that the drug is stimulatingtelogen follicles to re-enter anagen. It isimportant to inform the patient about apossible telogen shedding, before the tre-

atment is started. If shedding occurs,therapy should be maintained. Usually,increased effluvium due to telogen shedding normalizes within a few weeksto months. Good patient-practitioner-relationship and detailed patient informa-tion are essential for good compliance.Stopping topical minoxidil application isfollowed by increased shedding, usually 3 months after discontinuing the treatment.The main reported side effect of topicalminoxidil is hypertrichosis, which is morecommon with the 5 % concentration,but can also be due to incorrect applica-tion. To avoid contamination of the pil-low with subsequent contact with facepatients should be advised to apply thedrug at least 2 hours before going to bed. Irritant and allergic contact dermatitismay also occur. Irritation is more com-mon with the 5 % solution due to itshigher propylene glycole content.Contact dermatitis should be excludedby patch testing. If it is due to propyleneglycole, an alternative vehicle can beused, whereas if irritation and contactdermatitis are due to minoxidil itself,drug interruption is unavoidable.Minoxidil is contraindicated duringpregnancy and lactation.

3.1.6 Combination therapiesA study by Berger et al. failed to show, thatcombination of minoxidil 5 % solutionand pyrithione zinc shampoo is superior tominoxidil monotherapy [16]. Minoxidil5 % solution, twice daily combined withpyrithione zinc shampoo 1 x/d vs. minoxi-dil 5 % solution twice daily and placeboshampoo showed mean change from base-line total hair count of 6.2 hairs/cm2 and12.3 hairs/cm2 respectively.Bazzano et al. compared in a study ofmale and female patients minoxidil0.5 % solution, 2 x/d, tretinoin 0.025 %solution, 2 x/d, placebo and the combi-nation of minoxidil 0.5 % with tretinoin0.025 % [15]. At 12 months, 58 % ofthe patients of the tretinoin group and66 % of the patients with the combinedtreatment had at least 20 % or more in-crease from baseline total hair count.Shin et al. failed to prove significancebetween minoxidil 5 % solution, twicedaily and a combination of minoxidil5 % and tretinoin 0.01 %, once daily[44]. The mean change from baseline total hair count at 18 weeks was15.9 hairs/cm2 (12.8 %) vs. 18.2 hairs/cm2

(14.7 %) (p not significant).


be metabolized by this cytochrome, suchas warfarin, theophylline, digoxine andpropanolol.

3.2.3 Efficacy – malesFinasteride18 studies looking at the efficacy of fina-steride in male patients with androgene-tic alopecia met the inclusion criteria ofthe guideline [14, 42, 56–71]. 16 ofthem assessed the efficacy of finasteridemonotherapy in male patients with and-rogenetic alopecia. 12 studies obtainedgrade A2 evidence, 5 grade B and 1 gradeC. 12 studies were placebo controlled.Summarizing these results an evidencelevel 1 can be attributed for finasteride.

OutcomesIn all of the included trials, the intake offinasteride 1 mg daily led to a significantincrease in total hair counts compared toplacebo. The mean change from baselinetotal hair count was 7.0 hairs/cm2

(3.3 %) in the frontal/centroparietal re-gion (p < 0.0001 vs. placebo) [60] and13.5 hairs/cm2 (7.3 %) in the vertex(p < 0.0001 vs. placebo) [64] at6 months. The mean increase from baseline total hair counts at 12 months was between 7.2 hairs/cm2 (3.6 %) and36.1 hairs/cm2 (29.1 %) for the vertex (pbetween < 0.05 and 0.001 vs. placebo)[57, 60, 64, 65, 67, 68] and9.3 hairs/cm2 (4.9 %) and 9.6 hairs/cm2

(4.6 %) in the frontal/centroparietal re-gion (p between < 0.01 and 0.001 vs.placebo) [62, 72]. The placebo groupshowed at the same time mean changesfrom baseline total hair count between2.4 hairs/cm2 (1.4 %) and –10.1 hairs/cm2 (–5.2 %).At global expert panel assessment between37 % and 54 % of the patients were ra-ted as improved at 12 months (p < 0.001vs. placebo) [57, 58, 60, 64, 65, 71]. Inaddition, subjective assessments by inve-stigator and patients yielded significantimprovements in the finasteride group[57, 58, 60, 64, 65, 69].Long-term results were available for 24,36, 48 and 60 months. The mean chan-ges from baseline total hair counts were13.0 hairs/cm2 (6.2 %) at 24 months[60], 8.5 % at 36 months [63], 7.2 % at48 months [63] and 7.5 hairs/cm2

(4.3 %) at 60 months [71] respectively.The changes were statistically significantin comparison to placebo.

3.2 5-alpha-reductase-inhibitors3.2.1 IntroductionAndrogenetic alopecia occurs after pu-berty in men with an inhered sensitivityto the effects of androgens on androgene-tic sensitive scalp hair follicles. AGA doesnot develop in men without testosterone,and we know since 1974 that AGA doesnot occur in men with a genetic defi-ciency of the enzyme 5-alpha-reductasetype II which converts testosterone todihydrotestosterone (DHT) [55]. Twotypes of 5-alpha-reductase-inhibitorsexist in humans. Type I predominates inliver, skin and scalp. Type II predomina-tes in prostate and genitourinary tract,but also in the human hair follicle.Initially, pharmaceutical 5-alpha-reductase-inhibitors were developed forthe treatment of benign prostatic hyper-plasia. Two drugs inhibiting the 5-alpha-reductase are available on the market: fi-nasteride registered in Europe in 1992,and dutasteride registered in 2003. Fina-steride is a type II 5-alpha-reductase-inhibitor which decreases DHT of about65 % in serum, prostate and scalp. Duta-steride inhibits both type I and type II 5-alpha-reductase resulting in a decrease ofthe serum DHT level of about 90 %.Two years after the registration of fina-steride for the treatment of benignprostatic hyperplasia, first publicationsappeared concerning the efficacy of fina-steride in androgenetic alopecia in malepatients. At the same time, the drug wasregistered in the US (1993) and Europe(1994) for therapy of mild to moderateandrogenetic alopecia in men.First report on the use of dutasteride as atreatment for androgenetic alopecia waspublished in 2006, but up to now it isstill only registered for treatment of be-nign prostatic hyperplasia.

3.2.2 Mechanism of actionA single oral administration of finaste-ride 1 mg decreases serum DHT as wellas scalp DHT up to 70 % compared tobaseline. Tachyphylaxis is not observedwith long-term administration.Finasteride is quickly absorbed after oralintake with peak plasma level occurring1 to 2 hours after drug intake. The serumhalf-life of the drug is about 6 hours.90 % of the drug is bound to plasmaproteins. Finasteride is metabolised inthe liver by hydroxylation and oxidationusing P 450 3A4 pathway but withoutinteraction with other drugs known to

Topical minoxidil 2 % solution, 2 x/d incombination with an oral hormonal con-traceptive led to a mean change from ba-seline total hair count of 16.1 hairs/cm2

(8.6 %) at 6 months, 16.9 hairs/cm2

(9.1 %) at 12 months, whereas cypro-terone acetate 50 mg in combinationwith oral hormonal contraceptive led to decreased values (–2.8 hairs/cm2

[–1.4 %] at 6 months, –7.8 hairs/cm2

[–3.9 %] at 12 months [p < 0.001]) [52].

3.1.7 SummaryMinoxidil 2 % solution is effective toprevent progression and improve andro-genetic alopecia in male and female pati-ents (evidence level 1). Minoxidil 5 %solution is more effective than the 2 %solution in male patients (evidence level2). Patients should be informed on telo-gen shedding within the first 8 weeks oftherapy. Further studies are required tocompare efficacy of minoxidil solutionand foam formulation.

3.1.8 Therapeutic recommendation – Male

3.1.9 Therapeutic recommendation – Female

Topical minoxidil 2 % solution1 ml twice daily is recommen-ded to improve or to preventprogression of AGA in femalepatients above 18 years withAGA.There is not enough data to recommend the 5 % minoxidilsolution instead of the 2 % solution.The response to treatment shouldbe assessed at 6 months. If succes-sful, treatment needs to be conti-nued to maintain efficacy.

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Topical minoxidil 2 to 5 % solu-tion 1 ml twice daily is recom-mended to improve or to pre-vent progression of AGA inmale patients above 18 yearswith mild to moderate AGA(Hamilton-Norwood IIv–V). We suggest using 5 % solutionfor greater efficacy.There is not enough data to recommend the 5 % minoxidilfoam instead of the 5 % solution. The response to treatment shouldbe assessed at 6 months. If succes-sful, treatment needs to be conti-nued to maintain efficacy.

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Finasteride is not indicated in womenand is contraindicated in pregnant wo-men, because of the risk of feminisationof a male foetus. Finasteride-treated menmust avoid donating blood.The level of finasteride in the semen oftreated man is very low even with regularintake of finasteride 5 mg/day, and thereis no risk in case of sexual relation withpregnant women. Use of a condom is notnecessary for this reason.The recommended dosage is 1 mg a day,but in a study with a lower dosage of0.2 mg/day significant improvementcompared to placebo was observed. If apatient forgets a pill, taking the doubledosage the next day is therefore not re-commended. In case of adverse events adosage of 0.2 mg/ daily or a dosage of 0.5to 1 mg every other day can be discussed,although no clinical studies are available.Minimal period of use prior to assessingthe efficacy is 6 months for reducing hairloss and 12 months for regrowth of hair.If a patient intends to switch from mino-xidil to finasteride we recommend acombination therapy for at least 3 butpreferably 6 months before disconti-nuing minoxidil in order to avoid signifi-cant hair loss while finasteride action cantake over.Finasteride reduces PSA level. If treat-ment is started after the age of 45 years,monitoring of PSA level should be consi-dered. The PSA levels should be doubleto compensate the reduction due to fina-steride, resulting in an interpretation ofthe test remaining accurate.Additional research is required on higherdosages of finasteride and different sub-groups of female patients with patternhair loss including females of childbea-ring potential and postmenopausal wo-men as well as females with or withoutclinical signs of hyperandrogenism. Ne-vertheless, use of finasteride in females ofchildbearing potential can be consideredonly in combination with a safe contra-ceptive method due to the risk of malfor-mation of genitals in male fetus (femi-nization). Overall, women undersystemic finasteride should avoid dona-ting blood.

3.2.6 Combination therapiesLeavitt et al. observed 79 male patientsundergoing hair transplantation and re-ported that the combination with fina-steride 1 mg daily led to increased haircounts after 12 months, whereas hair

evidence were included in the evidence-based evaluation, resulting in a level ofevidence 2 [61, 73].

OutcomesStough et al. reported a significant meanincrease from baseline total hair count of 6.8 hairs/cm2 at 6 months and16.5 hairs/cm2 at 12 months for dutaste-ride 0.5 mg daily [73]. Olsen et al. sho-wed in a study with 416 patients a significant increase from baseline totalhair count for the different tested dutasteride dosages (dutasteride 0.1 mg15.4 hairs/cm2 (8.7 %), dutasteride0.5 mg 18.6 hairs/cm2 [10.2 %], dutaste-ride 2.5 mg 21.5 hairs/cm2 [11.3 %]) at24 weeks) [61]. Dutasteride 2.5 mg dailyshowed the best increase in hair count.The mean change from total hair countof finasteride 5 mg was significantly diffe-rent to dutasteride 2.5 mg (14.8 hairs/cm2

[8.4 %] vs. 21.5 hairs/cm2 [11.3 %],p = 0.009). All dutasteride arms and fina-steride 5 mg showed a significant diffe-rence of p < 0.001 vs. placebo.Assessing the dutasteride results it is ne-cessary to remark, that the most effectivedosage of dutasteride 2.5 mg is 5 timeshigher than the standard dosage in thetreatment of benign prostatic hyperplasia(dutasteride 0.5 mg corresponds to fina-steride 5 mg). Trials comparing dutaste-ride to the standard dosage of finasteride1 mg daily are required.

3.2.4 Efficacy – females2 studies assessing the efficacy of finaste-ride 1 mg daily in female patients were in-cluded in the evidence-based evaluation[68, 74]. The grades of evidence were A2and B, resulting in an evidence level 2.

OutcomesBoth studies showed a further progressionof hair loss. The mean change from base-line hair count at 12 months was –14.6hairs/cm2 (–5.9 %) and –8.7 hairs/cm2

(–5.8 %). Moreover, the mean decreasefrom baseline hair count in the finasteridegroup outvalued the placebo group(0 hairs/cm2 [0 %] resp. –6.6 hairs/cm2

[–4.0 %]). Trials with higher finasteridedosages or subgroup analyses in female pa-tients of childbearing age were not available.

3.2.5 Instructions for use / PracticabilityFinasteride can be taken with or withoutfood and there is no known interactionwith other drugs.

Price et al. reported increase in hairweight at 12 to 48 months (20.4 % at12 months, 21.5 % at 24 months,19.5 % at 36 months and 21.6 % at48 months vs. –5.2 %, –14.2 %, –14.8 % or –24.5 % in the placebogroup, p < 0.001) [62, 63].

DosageConcentration. Two studies examiningdifferent finasteride dosages could be in-cluded in the evidence-based evaluation[58, 64]. Roberts et al. examined finaste-ride 0.01 mg, 0.2 mg, 1 mg and 5 mgversus placebo [64]. The mean changefrom baseline total hair counts under finasteride therapy (0.2 mg, 1 mg and5 mg) was significantly different to placebo at 6 and 12 months (p < 0.001),whereas dosage of 0.01 mg showed progressing hair loss (difference to placebo not statistically significant). Thedifferences in mean change from baselinetotal hair count between the finasteridegroups (0.2–5 mg) did not reach signifi-cance. Kawashima et al. reported 58 % respec-tively 54 % improvement in global expert panel assessments for finasteride1 mg respectively 0.2 mg [58]. The effi-cacies in both groups were comparableand significantly different compared toplacebo (p < 0.001).

Finasteride vs. MinoxidilOnly few data comparing finasteride1 mg daily and minoxidil solution is avai-lable. Two of the included studies exami-ned finasteride 1 mg against twice dailytopical application of minoxidil 2 % solution [42, 59]. Both studies showedsuperiority for finasteride. At 12 monthsthe mean change from baseline total haircount was 36.1 hairs/cm2 (29.1 %) for finasteride 1 mg and 19.6 hairs/cm2

(14.8 %) for minoxidil 2 %, twice dailyapplication (p = 0.003) [42]. 87 % of thepatients taking finasteride vs. 42 % of theminoxidil 2 % patients were rated as im-proved (p < 0.001) [59]. Arca et al. reported a better outcome forminoxidil 5 % solution applied twicedaily against finasteride 1 mg daily atglobal photographic assessment of thefrontal/parietal region at 12 months(80 % vs. 52 % improvement) [14].

Dutasteride2 studies investigating dutasteride inandrogenetic alopecia with grade A2


treatment. They fall into two broadgroups: antiandrogens and oestrogenic(or anti-oestrogenic) drugs, although evi-dence of efficacy for any of these treat-ments is limited or absent.

3.3.2 Mechanism of actionAntiandrogens act primarily throughblockade of the androgen receptor. Diffe-rent agents may have other relevant effectson endocrine biology including inhibi-tion of steroid synthesis and progestatio-nal activity. Antiandrogens have mainlybeen delivered systemically and used inwomen (they are contraindicated in mendue to their feminizing action).Topical oestrogens and anti-oestrogenshave been used in both men and women.The rationale for their use is less clearthan for antiandrogens as the effect, ifany, of oestrogens on human hair growthis unknown. Oestrogens inhibit hair growth in several other mammals len-ding some support for the potential ofantioestrogens to promote hair growth inhumans.

3.3.3 Efficacy – malesOral hormonal treatmentThere is no evidence to support the use of oral oestrogens or antiandrogensto improve or prevent progression ofandrogenetic alopecia in male patients(evidence level 4).

Topical hormonal treatmentThere are only two controlled trials oftopical hormonal treatment that haveemployed modern methods of asses-sment.

OutcomesSovak et al. [76] studied the change ofanagen hair count following daily topicalapplication of the antiandrogen fluridilversus placebo. At 12 months, the res-ponse to fluridil was not significantly dif-ferent from placebo. Thus, there is limi-ted evidence that topical fluridil isineffective in men [76]. Gassmueller et al. [77] compared topicalapplication of fulvestrant (70 mg/mltwice daily), an oestrogen receptor anta-gonist, to minoxidil 2 % and placebo. At16 weeks the mean change from baselinehair counts was not significantly diffe-rent from placebo in the fulvestrantgroup, whereas there was a significant in-crease in hair counts in subjects treatedwith minoxidil. Thus, there is evidence

contraceptive method is essential as fina-steride may lead to feminisation of themale foetus.

3.2.8 Therapeutic recommendation –Male

3.2.9 Therapeutic recommendation –Female

3.3 Hormones3.3.1 IntroductionThe role of androgens in the aetiology of androgenetic alopecia has led to thewidespread use of hormonal agents in its

Oral finasteride 1 mg daily isnot suggested in the treatmentof postmenopausal women withfemale pattern hair loss.

High quality controlled clinical trialswith finasteride at different dosageson female patients are required.

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DutasterideOral dutasteride 0.5 mg a daycan be considered to improve orto prevent progression of AGAin male patients above 18 yearswith mild to moderate AGA(Hamilton-Norwood IIv–V).

High quality controlled clinical trialscomparing dutasteride 0.5 mg to fina-steride 1 mg are needed.

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FinasterideOral finasteride 1 mg a day is re-commended to improve or toprevent progression of AGA inmale patients above 18 yearswith mild to moderate AGA(Hamilton-Norwood IIv–V).The response to treatmentshould be assessed at 6 months,although in some men it maynot become evident until 12months. If successful, treatmentneeds to be continued to main-tain efficacy.There is insufficient evidence tosupport the use of topical fina-steride. For greater efficacy the combi-nation of oral finasteride 1 mg,1 x/d and topical minoxidil 2 %to 5 % solution, 2 x/d can beconsidered.

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transplantation alone resulted in decrea-sed hair count in the frontal area (meanchange from total baseline hair count18.5 hairs/cm2 [2.6 %] vs. –13.5 hairs/cm2

[–8.9 %], p = 0.019) [70].Khandpur et al. compared the combi -nation of finasteride 1 mg daily with minoxidil 2 % solution twice daily respectively ketoconazole 2 % shampoo,3 x weekly to finasteride 1 mg daily andminoxidil 2 % solution twice daily asmonotherapies [59]. At 12 months,100 % of the patients of each combinedtherapy, 87 % for finasteride and 42 %for minoxidil 2 % solution were rated asimproved by the investigator. The combi-nation of minoxidil 2 % and finasteride1 mg was statistically significant superiorto finasteride or minoxidil monothera-pies. Furthermore, Diani et al. showed anadditive effect of finasteride and minoxi-dil in stumptail macaque [75]. Working mechanisms of minoxidil andfinasteride are different. Thus, associa-tion of both drugs is possible and can beconsidered in motivated patients.

3.2.7 SummaryFinasteride 1 mg daily is effective in prevention of hair loss progression andinduction of hair regrowth in androgene-tic alopecia in male patients (evidence level 1).Evaluation of the efficacy should be as-sessed 6 months after treatment initia-tion. Patients should be aware of the reductionof prostate-specific antigen, which is im-portant in prostate cancer screening inmen older than 45 years.Further studies comparing the efficacy offinasteride 1 mg vs. minoxidil 5 % areneeded. If therapeutic approach is insuf-ficient the combination of finasteride1 mg and minoxidil 2 % or 5 % can beconsidered.There is no reason to use dutasteride0.5 mg instead of finasteride 1 mg, ashigher dosages are needed to reach com-parable efficacy and comparison studiesvs. finasteride 1 mg daily are missing.In postmenopausal female patients finasteride 1 mg failed to show efficacy(evidence level 2). Additional research isrequired at higher dosages and in diffe-rent subgroups of female patients withandrogenetic alopecia. If finasteride isused in women its use is off-label and at own responsibility; in particular inwomen of childbearing age, a safe




Side effects of cyproterone acetate in-clude depressive mood changes and livertoxicity. There is an increased risk of ve-nous thromboembolism in patients ta-king oestrogen-containing oral contra-ceptives, which may be greater in thosetaking cyproterone acetate than otheroral contraceptives. Spironolactone 100–200 mg per day is ta-ken continuously. Concurrent contra-ception is required in fertile women. Sideeffects include menstrual disturbanceand hyperpotassemia.

3.3.6 Combination therapiesThere are no instructive studies of com-bination therapy (e.g. minoxidil + anti-androgen).

3.3.7 SummaryThere is little evidence to support the useof oral or topical hormonal treatment inmen and women in androgenetic alope-cia (evidence level 4) and limited evi-dence that oral cyproterone acetate maybe helpful in women with AGA and hy-perandrogenism.

3.3.8 Therapeutic recommendation –Male

3.3.9 Therapeutic recommendation –Female

There is no or insufficient evi-dence to support the use of oralantiandrogens (chlormadinoneacetate, cyproterone acetate(CPA), drosperinone, spirono-lactone, flutamide) to improveor prevent progression of AGAin female patients.

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The use of oral oestrogens orandrogen-receptor-antagonistsis inappropriate to improve orprevent progression of AGA inmale patients.There is insufficient evidence tosupport the use of topical al-fatradiol to improve or preventprogression of AGA in male pa-tients.We suggest that topical fluridilshould not be used in male pati-ents with AGA.We suggest that topical fulve-strant should not be used inmale patients with AGA.

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Topical hormonal treatmentOutcomesBlume-Peytavi et al. [46] reported a decreased total hair count after 6 monthstherapy with alfatradiol 0.025 % solutiononce daily (mean change from baseline –7.8 hairs/cm2, –4.3 %, p < 0,0005). Sub-jects treated with minoxidil 2 % solutiontwice daily showed increased total haircounts at 6 months (15.3 hairs/cm2;8,7 %). Non-vellus hair counts and cumu-lative hair thickness also showed a decrease in the alfatradiol group and an increase inthe minoxidil group at 6 months (–6.0 hairs/cm² vs. 14.0 hairs/cm², p < 0,001; –0.5 mm/cm² vs. 1.8 mm/cm2, p < 0.0001).There are 3 earlier studies [78, 80, 81]on the efficacy of the topical oestrogen alfatradiol in women and one of topicaloestrogen combined with corticosteroid[79]. All assessed response using a tricho-gram. Two studies did not analyse maleand female subjects separately and arenot considered further [79, 80]. Orfanosand Vogels reported a mean decrease intelogen rate of 24.4 % for patients trea-ted with alfatradiol 0,025 % solutiononce daily at 30 weeks [78].In a study by Georgala et al. the meanchange from baseline anagen/telogen ra-tios at 12 and 24 weeks of treatmentwith alfatradiol solution once daily was38.7 % and 44.6 % respectively [82].The change in anagen/telogen ratio differed significantly from placebo treat-ment (–3.9 % at 24 weeks; p < 0.01). As there are contrary results on the effi-cacy of topical alfatradiol, the evidence isinsufficient to support its use in femalepatients with androgenetic alopecia. Fur-ther studies are needed to clarify the effi-cacy of alfatradiol. Gassmueller et al. [77] compared fulve-strant (70 mg/ml twice daily) to minoxidil2 % and placebo. The mean change in to-tal hair count did not differ from placebo(14.7 hairs/cm², 6.9 % vs. 15.3 hairs/cm²,7.9 %). Therefore, we suggest that topicalfulvestrant is not effective in women withandrogenetic alopecia. There is no evidence supporting the useof topical natural oestrogens, progesto-gens or antiandrogens in female andro-genetic alopecia.

3.3.5 Instructions for use / PracticabilityOral antiandrogen therapy in women. Cyproterone acetate (25–50 mg per day,days 1–10) is generally prescribed togetherwith an oral contraceptive e.g. Dianette®.

that topical fulvestrant is ineffective inmen.There are three earlier studies on the effi-cacy of the topical oestrogen alfatradiol(= 17 alpha-oestradiol) in men. Unfortu-nately they either had no control group[78, 79] and/or the results were not re-ported separately for each sex [79, 80].In one study, topical corticosteroid wasincluded [79].

3.3.4 Efficacy – femalesOral hormonal treatmentTwo studies met the inclusion criteria(grade of evidence B, level of evidence 3).

OutcomesPeereboom-Wynia et al. compared agroup of women treated for one yearwith Diane® (50 µg estradiol + 2 mg cyproterone acetate) + 20 mg cypro-terone acetate days 1–14 with an untrea-ted control group [81]. Trichogram datashowed a mean change in anagen percentage from 49.7 at baseline to 74.4after one year in the treated group compared to a fall from 60.4 to 48.8 in the controls. Subjects appeared not to be randomized to treatment or control groups and hair counts were notperformed [81].Vexiau et al. reported a mean change intotal hair count of –2.8 hairs/cm²(–1,4)at 6 months and –7,8 % hairs/cm² (–3;9 %) at 12 months in subjects recei-ving oral contraceptive + 50 mg cypro-terone acetate [52] whereas subjectstreated with a combination of minoxidil2 % solution twice daily and oral contra-ceptive showed a mean increase in haircount of 16.1 hairs/cm2 (8.6 %) at6 months and 16.9 hairs/cm² (9.1 %) at12 months. The differences in total haircount at 12 months were statistically sig-nificant between groups (p < 0.0001). In subgroup analysis, patients under tre-atment with cyproterone acetate with cli-nical signs of hyperandrogenism tendedto show increased hair counts at12 months compared to those withouthyperandrogenism, although the resultswere not statistically significant. Conse-quently, there is insufficient evidencethat oral hormonal treatment preventsprogression or improves androgeneticalopecia in female patients. Nevertheless,subgroup analysis suggests that oral cyproterone acetate may improve andro-genetic alopecia in female patients withhyperandrogenism.


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Oral CPA can be considered inwomen with clinical or bioche-mical evidence of hyperandro-genism.There is insufficient evidence tosupport the use of topical al-fatradiol to improve or preventprogression of AGA in femalepatients.There is no evidence to supportthe use of topical natural oestro-gens or progesterones to im-prove or prevent progression ofAGA in female patients.There is no evidence to supportthe use of topical fluridil to im-prove or prevent progression ofAGA in female patients.We suggest that topical fulve-strant should not be used in fe-male patients with AGA.

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On frontal-superior global photography,67 % of patients improved and 30 % didnot improve after hair transplantationalone, versus 94 % and 6 % after combi-nation therapy, respectively. This is a considerably higher efficacythan previously reported in other studieswith finasteride alone.The differing results of hair counts andfrontal-superior global photography inhair transplantation alone may partly bedue to replacement and compensation ofminiaturizing hairs by thicker perma-nent hair from the occipital area. Magni-fication should be used when making re-cipient sites in-between pre-existing hairs.

3.4.4 Efficacy – femalesOnly few of the 77 assessed publicationsconcerning hair surgery studied efficacyin female patients. None of them fulfil-led the inclusion criteria, resulting in anevidence level 4. This may be due tomany reasons, such as high variation intechniques, multiple steps in the surgicalprocess, problems in measuring hair gro-wth, lack of funding and difficult patientrecruitment.

3.4.5 Instructions for use / PracticabilityWhile scalp reduction and flap surgery incombination with extenders is only suc-cessfully performed by a few skilled sur-geons, hair transplantation is extensivelyconducted worldwide with further refi-ned micro-techniques and larger graftnumbers.Hair transplantation in suitable candida-tes with a good donor hair supply, per-formed by a skilled team of a surgeonand several assistants, can permanentlyimprove androgenetic alopecia by up to3 stages on the Norwood-Hamiltonscale. In women, hair transplantation can beconsidered in the male pattern and thefrontal accentuation subtypes and Ludwigstage II of stabilized androgenetic alope-cia. This only applies if sufficient perma-nent donor hair is available and no overly-ing diffuse telogen effluvium is present.In most cases, more than one surgical ses-sion is required and often only criticalareas can be improved. Magnificationshould be used to cautiously insert thegrafts in between pre-existing hair follicles. The best long-term results can be achie-ved in medically controlled or sponta-neously stabilized androgenetic alopecia.In patients with progressive alopecia,

The technical success of this multi-stepprocedure is determined by the ability ofthe surgical team to successfully harvest,prepare and insert the grafts without im-pairing their viability. Another aspect is aminimal trauma to the recipient and do-nor areas.The cosmetic effect greatly depends onthe aesthetic skills of the surgeon, as wellas patient selection, planning of the pro-cedure considering an optimum life-longresult, the creation of an authentic hair-line design, the distribution of graftswith different numbers of hair and thenatural creation of recipient sites withappropriate size, density and direction.

3.4.3 Efficacy – malesAlthough there are a lot of publicationsdealing with hair surgery, only 3 studiesout of 77 analyzed publications fulfilledthe inclusion criteria, resulting in an evi-dence level 4. This may be due to manyreasons, such as high variation in techni-ques, multiple steps in the surgical pro-cess, problems in measuring hair growth,lack of financial support and difficult pa-tient recruitment.

OutcomesBernstein et al. compared different pre-paration techniques for follicular unittransplantation [83]. The resulting meanharvested hairs were 17 % higher for pre-paration by dissecting microscope com-pared to preparation by magnifyingloupe with transillumination (9.6 %more follicular units and 2.28 vs. 2.14mean hairs per follicular unit). Uebel et al. [84] showed that treatmentof follicular units (FU) with plateletplasma growth factor before implanta-tion could reduce the number of non-surviving FU grafts after follicular unittransplantation compared to follicularunit transplantation alone (mean changefrom baseline FU graft number: –25 (–17.6 %) vs. –40 (–28.2 %), p < 0.001).In a study by Leavitt et al. [70], the com-bination of FU transplantation and fina-steride 1 mg daily in patients with parti-ally still existing hair in the recipient arearesulted in an increase of hair density12 months after transplantation, whereasthe patients treated with FU transplanta-tion alone had decreased hair counts.The mean change from baseline total haircount at 12 months was 18.5 hairs/cm2

(12.6 %) and –13.5 hairs/cm2 (–8.9 %)respectively (p = 0.019).

3.4 Surgery3.4.1 IntroductionHair restoration surgery involves hairtransplantation, scalp reduction surgeryor a combination of both.Compared to scalp reduction surgeryhair transplantation is less invasive. Inandrogenetic alopecia, hairless areas canbe permanently covered again cosmeti-cally, albeit with a decreased density. Inareas with decreased hair density, thedensity can be at least temporarily im-proved. Over the last decades, hair transplanta-tion has evolved into a microsurgicalprocedure. Follicular units of 1 to 4 hairsare transplanted in large numbers andhigh densities.

3.4.2 Mechanism of actionThe efficacy of hair transplantation is ba-sed on donor dominance, i.e. non-and-rogen-sensitive hair follicles keep theirproperties even when transplanted intoscalp areas affected by androgeneticalopecia. Follicles that are not affected by miniatu-rization are re-distributed over the scalpunder local anaesthesia.The outcome of hair transplantation re-sult objectively depends on the numberof transplanted hairs in relation to thearea to be covered or densified, on thequality of hairs such as colour and cali-ber, and on the characteristics of the reci-pient area.




3.4.9 Therapeutic recommendation – Female

3.5 Miscellaneous3.5.1 IntroductionBesides the pharmacologic therapeuticoptions minoxidil, 5-alpha-reductase-inhibitors, hormonal preparations andhair surgery, which were already assessedin the previous chapters, the patient dia-gnosed with androgenetic alopecia facesa confusing array of products claiming tobe efficient in androgenetic alopecia.The range of products is wide and rea-ches from topical to systemic modalities;it includes cosmetic to pharmaceuticalproducts, natural products, functionalfood and even electrostatic/-magnetic orlaser treatment.Though scientific investigations are rarein the majority of cases, the patient is at-tracted by hair growth promoting claimsof advertisement or distribution of my-ths, rumours and assumptions providedin different internet fora.Within the consultation the practitionerwill be confronted with questions con-cerning the efficacy of some of the follo-wing products. It is therefore importantfor the development of a stable patient-physician-relationship to be informed onthese products, to know their propertiesand their potentials as well as limits.

3.5.2 Mechanism of actionThe assumed mechanisms of action inandrogenetic alopecia are as various asthe number of products. Though it re-mains unclear how these products me-diate their effects, most of them claim atleast one of the following mechanisms: a) Promotion of hair regrowth by activa-

tion of the dermal papillae and conse-quently induction of anagen hair re-growth.

b) Comparable to minoxidil promotinghair regrowth by improving the peri-follicular vascularisation.

c) Hormonal effects, mainly inhibition of5-alpha-reductase and reducing the ac-tivity of dihydrotestosterone (DHT).

d Anti-inflammatory activity.e) Improvement of hair follicle nutrition.In Table 2 we aimed to group the diffe-rent therapeutic options based on theirassumed main mechanism of action.

Surgery, especially follicular unittransplantation (FUT) can beconsidered in female patientswith sufficient donor hair.

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alopecia, a combination of medical andsurgical therapy seems to be superior tosurgery alone. Leavitt et al. [70] reported a better clini-cal outcome for male patients treatedwith combination of finasteride 1 mgdaily and hair surgery versus male pati-ents treated with hair surgery alone 12month after follicular unit transplanta-tion (see section efficacy males).In female patients there is lack of evi-dence concerning combination therapies.We suggest that combination therapymay reduce further post-operative pro-gression of androgenetic alopecia.

3.4.7 Summary3 studies concerning hair surgery fulfil-led the inclusion criteria of the S3 guide-line (evidence level 4). Hair transplanta-tion can be considered to improveandrogenetic alopecia in suitable patientswith sufficient donor hair supply andmedically controlled or spontaneouslystabilized androgenetic alopecia, especi-ally for the fronto-parietal area. As hairsurgery does not influence progression ofandrogenetic alopecia, long-term resultsin early stages depend on spontaneousrespectively medical stabilization. Theresult greatly depends on the skills of thesurgical team and the adjustment of thesurgical plan to individual patient cha-racteristics. Preparation of follicularunits using dissecting microscopes andpre-treatment of FU’s with platelet gro-wth factor lead to higher graft survivalrates.While follicular unit transplantation(FUT) can be considered a standard, es-pecially when stereo-microscopic dissec-tion is used by a skilled team, other com-ponents of the surgical technique requirefurther evaluation.Combination of finasteride 1 mg andfollicular unit transplantation may re-duce post-operative progression of and-rogenetic alopecia.

3.4.8 Therapeutic recommendation – Male

Surgery, especially follicular unittransplantation (FUT) can beconsidered in male patients withsufficient donor hair.We suggest follicular unit trans-plantation (FUT) to be combi-ned with finasteride 1 mg dailyto achieve a better clinical out-come.

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hair transplantation should only be per-formed if additional surgery is possiblein terms of donor hair reserve.Patients should be extensively counselledregarding the possible outcome and theprogressive nature of androgenetic alope-cia which may require subsequent sur-gery and/or medical therapy.Body dysmorphic disorder or unrealisticexpectations are contraindications forthis aesthetic surgery.If hair transplantation is performed inearly progressive AGA, a sufficient re-serve of donor hair should be availablefor additional surgery, grafts should alsobe transplanted in-between miniaturi-zing hairs and the vertex area should notbe transplanted initially.Follicular unit transplantation (FUT)has become the standard technique inhair transplantation. Physiologic follicu-lar units are smaller with less interfollicu-lar tissue and can thus be placed denserinto finer, less traumatic recipient sites.Larger grafts with multiple FU’s shouldonly be used in combination with FUTand in patients with a very good donorhair supply.The harvesting of FU grafts from the do-nor area is usually performed by carefulexcision of a hair-bearing strip. Severaltechniques are used to minimize follicletranssection and scar formation duringthis step. The use of stereo-microscopesthen allows for exact and fast dissectionof large numbers of FU’s with minimaltrauma. Individual extraction of FU’s from thedonor area is also possible but associatedwith a potentially higher risk of follicleinjury and impairment of graft viability.Recipient sites are prepared with diffe-rent instruments. The creation of slitsusing micro-blades adapted to graft sizeenables achieving high densities. In the frontal area, a transition zone of 1-hair-FU’s is created with micro- andmacro-irregularities for a more naturalappearance.Patients should be informed, that tem-porary post-operative telogen effluviummay appear if pre-existing hair is present.This may be minimized by making smal-ler incisions using magnification. The final result can be evaluated at 9–12 months.

3.4.6 Combination therapiesAs hair surgery has no efficacy to preventfurther progression of androgenetic




3.5.3 Efficacy – males and femalesContrary to the previous chapters the efficacy of the miscellaneous therapies issummarized together for males and fe-males, as evidence proving the efficacy ofthe particular therapies in androgeneticalopecia is mainly not available.For almost 50 % of the therapeuticagents no literature fulfilling the inclu-sion criteria of the guideline was found.Furthermore, the evaluation is limited,as most of the tested products containmultiple different substances, e.g. foodsupplements with aminoacids and trace

elements or different herbal preparati-ons. Only 11 of the 20 trials that wereincluded into the guideline examined asingle therapeutic agent. The available evidence is therefore insuf-ficient resulting in evidence level 4 forthe different therapeutic options. Hereafter, a short overview on the diffe-rent therapeutic agents is provided. Aminoacids, especially cysteine is sup-posed to lead to increased growth factorsinvolved in hair growth. Morganti et al.report a significant mean change in totalhair count in male and female patients

after a 50-week-treatment with an oralsupplement containing cysteine, histi-dine, copper and zinc taken 4 times daily(29 % vs. 11 % placebo, p < 0.005) [85].A combination of cysteine, calcium pan-tothenate and millet seed twice a day for6 months in 40 female patients showedincreased anagen rate that was signifi-cantly different to placebo (p = 0.0225)[86].Trace elements like copper and zinc aresuggested to improve hair nutrition,though studies examining the link bet-ween serum and hair follicle concentra-tion of trace elements, vitamins etc. failto show correlation. As zinc and copperwere only studied in combination withother agents, evidence is missing.Different opinions exist concerning thesupplementation of iron in absence ofiron deficiency in androgenetic alopeciapatients. Various observational studiesdiscussed the relationship between hairloss and decreased serum ferritin levelswith controversial results [87]. There isinsufficient evidence for iron supple-mentation in absence of iron deficiencyin patients with androgenetic alopecia.Vitamins, especially biotin and niacin,are also claimed to have hair growth pro-moting properties and have positive in-fluence on hair nutrition. Draelos et al.studied the effect of topically appliedniacin derivates once daily in 60 femalepatients. After 6 months 69 % were ratedas improved in global photographic assessment (p = 0.04 vs. placebo) [88].Prager et al. reported 60 % improvementrated by investigator in 26 male patientsafter 18–24 weeks treatment with an oral combination containing biotin andniacin, but also ß-sitosterol and saw palmetto [89]. Proanthocyanidines like procyanidineB belongs to the group of flavonoids,which are antioxidants. Their mecha-nism of action may be inhibition oftransforming growth factor TGF-ß andconversion of telogen follicles to anagenhair follicles. Kamimura et al. showed,that the topical application of procya-nidine B 1 % twice daily leads to signifi-cant mean changes from total hair countin male patients after 6 months(p < 0.0005 vs. placebo) [90]. Millet seed is a natural product that con-tains silicic acid, aminoacids, vitaminesand minerals. An oral supplement com-posed of millet seed extract, cysteine andcalcium pantothenate (Priorin®) taken

Table 2: Overview on the assumed main mechanism of action of miscel-laneous treatments.

Promotion of hair regrowth

• Aminoacids• Iron supplements in absence of iron deficiency• Vitamines (biotin, niacin derivates)• Proanthocyanidines• Millet seed (silic acid, aminoacids, vitamines, minerals)• Marine extract and silicea component• Chinese herbals• Ginkgo biloboa• Aloe vera• Ginseng• Bergamot• Hibiscus• Sorphora• Caffeine• Melatonin• Retinoids• Ciclosporine• Electromagnetic/-static field• Low level laser

Improved perifollicular vascularisation

• Prostaglandines (viprostol, latanoprost)• Aminexil• Glyceroloxyesters and silicium • Minerals• Niacin derivates• Mesotherapy

DHT-inhibitory activity

• Saw palmetto• ß-sitosterol• Polysorbate 60• Green tea• Cimicifuga racemosa

Anti-inflammatory activity

• Ketoconazol• Zinc pyrithione• Corticosteroids

Improved hair nutrition

• Vitamines (biotin, niacin derivates)• Trace elements (zinc, copper)

Others • Botulinum toxin


twice daily for 6 months led to increasedanagen rates female patients (p = 0.0225vs. placebo) [86]. Viviscal® is a similaroral supplement composed of marine extracts and a silicea component. Lassuset al. studied this supplement in compa-rison to fish extract and in combinationwith topical and oral use [91, 92]. Dueto lack of placebo respectively standardfor comparison the results are deficient.Two trials examining the efficacy of topi-cal applied herbal preparations fulfilledthe inclusion criteria of the guideline[93, 94]. As the ingredients of the parti-cular herbal preparations significantlydiffer, they have to be evaluated separa-tely. Kessels et al. reported modest in-crease in hair regrowth in 396 male pati-ents, who applied a Chinese herbalpreparation twice daily for 6 months.The mean change in nonvellus haircounts was 26.6 hairs/cm2 vs.21.8 hairs/cm2, p = 0.02 vs. placebo)[94]. Greenberg et al. reported a meanchange from baseline total hair count of77.4 % in 24 men after 40 weeks usageof herbal extract containing fennel, poly-gonum, menthe, chamomile, thuja, hi-biscus) (p = 0.003) [93].No trials were found concerning the na-tural products gingko biloboa, aloevera, ginseng, bergamot, hibiscus orsorphora. Animal models and resp. or invitro studies suggest hair growth promo-ting properties. The agents are used incosmetic hair care products. There are different hair care productswith caffeine claiming to be effective inthe treatment of androgenetic alopecia inmen and women. In vitro studies withcaffeine showed higher transfollicular pe-netration rates [95]. Caffeine is sugge-sted to prevent progression and inducehair regrowth in androgenetic alopecia.Studies investigating this hypothesis aremissing/not available.Topical application of melatonin leadsto the induction of anagen hair in animalmodels. A small trial, which did not ful-fil the inclusion criteria of the guideline,reported significantly increased anagenhair rates in trichogram in women withandrogenetic alopecia or diffuse efflu-vium after topical use of melatonin0.1 % for 6 months [96].Retinoids modulate proliferation, diffe-rentiation of keratinocytes and the T-cellimmune response. Moreover, its usage aspharmaceutical excipient to improve mi-noxidil resorption is discussed. Two trials

fulfilled the inclusion criteria of the gui-deline [15, 44]. Bazzano et al. reportedin 58 % of the male and female patients,who treated their scalp twice daily withtretinoin 0.025 % solution, at least 20 %increase from baseline hair count at12 months [15]. It is conspicuous thatthe placebo and the minoxidil 0.5 %group reached no improvement at all.The trial was not blinded or randomized.Shin et al. failed to show superiority ofminoxidil 5 % solution combined withtretinoin 0.01 % once daily vs. minoxidil5 % solution applied twice daily in 31male patients [44]. The mean changesfrom baseline total hair count did notdiffer significantly at 18 weeks, thoughthe combination of minoxidil and treti-noin led to slightly elevated values(15.9 hairs/cm2 vs. 18.2 hairs/cm2). The induction of hypertrichosis is wellknown as adverse event in systemic treat-ment with ciclosporin. Experimentalmodels could demonstrate this effect fortopical application of ciclosporin, too. Ina small study by Gilhar et al. 2 patientsout of 8 responded to topical applicationof ciclosporin for 12 months [97].Besides cosmetic and pharmaceuticagents physical treatments such as pul-sed electromagnetic/-static field and lowlevel laser therapy are also suggested to beefficient in androgenetic alopecia. Four trials for pulsed electrostatic fieldcould be included into the evidence-ba-sed evaluation of the guideline [98–101].Though the trials showed modest in-crease in total, anagen or nonvellus haircounts, the use in clinical routine isdoubtful due to unfavourable cost-bene-fit ratio.Satino et al. examined the effects of a lowlevel laser comb in androgenetic alopecia[102]. They reported a mean changefrom baseline total hair count of14.1 hairs/cm2. A control group forcomparison was missing.Cimicifuga racemosa is a natural productwith positive influence on the oestrogeniclevel. It is mainly used for perimenopausalcomplaints. No evidence was found for itsefficacy in androgenetic alopecia, thoughit is likely that elevation of oestrogen levelsin menopause can improve androgeneticalopecia in female patients.Other therapeutic agents may act by in-hibition of the activity of dihydrotesto-sterone (DHT), namely saw palmetto,ß-sitosterol, green tea or polysorbate60.

The application of a lotion containingsaw palmetto extract twice a day showedstatistically significant improvement inmean change from baseline total haircount at 50 weeks (p < 0.005 vs. placebo)[85]. A combination of saw palmetto, ß-sitosterol, nicacin and biotin in an oralsoftgel taken twice daily also led to animprovement significantly differentcompared to placebo treatment (investi-gator assessment 60 % improved vs.11 %) [89].A trial by Groveman et al. failed to proveefficacy of the non-ionic detergent poly-sorbate 60 applied twice daily topicallyin 174 male patients [103]. After 16weeks global photographic assessmentfor the polysorbate group was below theplacebo group.Whereas the previous agents claim tohave mechanism of action comparable to5-alpha-reductase-inhibitors, others mayimprove perifollicular vascularization si-milar to minoxidil. Aminexil is a vasodi-latator chemically similar to minoxidil.Studies providing evidence for its effi-cacy are missing.Another promising group of substanceswere the prostaglandine analogues suchas viprostol or latanoprost. They me-diate vasodilatatory effects and latano-prost leads in topical use as eye drops toinduction of prolonged eyelashes. Unfor-tunately, the topical application of vipro-stol for 24 weeks in male patients did notshow significant difference compared toplacebo or vehicle treatment [104].Minerals and niacin derivates shouldhave positive effects on perifollicular vas-cularisation in addition to their hair gro-wth promoting properties. Reygagne etal. assessed the efficacy of a topical com-bination of glycerol oxyesters and sili-cium (Maxilene®) [38]. In comparisonto standard minoxidil treatment Maxi-lene® led to statistically significant hairloss.Another therapeutic regimen that claimsto improve androgenetic alopecia by im-provement of vascularization and hairnutrition is the mesotherapy. Differentagents, e.g. vitamins are intracutaneouslyinjected. There was no evidence of effi-cacy found.The injection of botulinum toxin is alsosuggested to improve androgeneticalopecia. A traction component by ten-sion of the musculus occipitofrontalis isdiscussed, but studies are missing/notavailable.


Furthermore, we would like to thankProfessor Dr. med Berthold Rzany andProfessor Dr Phyllis Spuls for their sup-port in the methodological developmentof the Guideline; especially Professor Rzanyfor moderating the consensus process.The authors thank R. Erdmann, S.Lönnfors, I. Orsin, S. Rosumek, and H.Thomas, Department of Dermatologyand Allergy, Charité-UniversitätsmedizinBerlin for valuable continuous support.Without the help of everybody it wouldnot have been possible to create this S3-Guideline.

Prof. Dr. med. U. Blume-Peytavi, Dr. med. A. Blumeyer

Correspondence toProf. Dr. med. Ulrike Blume-PeytaviDepartment of Dermatology and AllergyClinical Research Center for Hair andSkin ScienceCharité – Universitätsmedizin BerlinCharitéplatz 1D-10117 Berlin, GermanyPhone: +49-30-45051-8229Fax: +49-30-45051-8952E-Mail: [email protected]

References1 Alfonso M, Richter Appelt H, Tosti

A, Viera MS, Garcia M. The psycho-social impact of hair loss among men:A multinational European study.Curr Med Res Opin 2005; 21(11):1829–36.

2 Cash TF, Price VH, Savin RC. Psy-chological effects of androgeneticalopecia on women: comparisonswith balding men and with femalecontrol subjects. J Am Acad Dermatol1993; 29(4): 568–75.

3 Blume-Peytavi U, Blumeyer A, TostiA, Finner A, Marmol V, Trakatelli M,Reygagne P, Messenger A; EuropeanConsensus Group. S1 guideline fordiagnostic evaluation in androgeneticalopecia in men, women and adoles-cents. Br J Dermatol 2011; 164(1):5–15.

4 Messenger A. Androgenetic alopeciain men. In: Blume-Peytavi U, Tosti A,Whiting DA, Trüeb R: Hair growthand disorders. Berlin Heidelberg:Springer Verlag, 2008: 159–70.

5 Kim BJ, Kim JY, Eun HC, Kwon OS,Kim MN, Ro BI. Androgeneticalopecia in adolescents: a report of 43

as speaker from Procter & Gamble. Participated as employee of Charité inclinical and research trials from the com-panies mentioned above and L’Oréal,Galderma and Innéov. Received unre-stricted research grant from J & J.del Marmol V: Has given lectures for andreceived honorarium as speaker forMEDA, Merck and Medipress.Finner A: Received honorarium as spea-ker for Merz Pharmaceutics GmbH.Kiesewetter F: No conflict of interestdeclared.Messenger A: Has acted in the past as aconsultant for Johnson & Jonhnson (actually Pfizer) and MSD (Merck,Sharp & Dohme). Currently investigatorin a Johnson & Johnson sponsored clini-cal trial.Reygagne P: Has given lectures for Bailleul-Biorga, Galderma, Innéov, JanssenCilag, MSD and Pierre Fabre Dermato-logie. Is a member of the advisory boardto Galderma. Is or has been investigatorfor Ducray, Galderma, Innéov, John-son & Johnson and L’Oréal recherché.Rzany B: No conflict of interest declared.Spuls PI: No conflict of interest declared.Tosti A: Has given lectures and receivedhonorarium as speaker for MSD (Merck,Sharp&Dohme), received honorariumfor advisory board from Procter&Gamble,participated in clinical trials for Inneov.Trakatelli M: Has given lectures for theEuropean Skin College sponsored byMEDA.Trüeb R: Has given lectures and receivedhonorarium as speaker for Merz Pharma-ceutics GmbH and Spirig AG. Is or hasbeen member of the advisory board/con-sultant to the following companies:ASATONA, Lexington.

AcknowledgmentsWe would like to thank the EuropeanDermatology Forum (EDF) representedby Professor Dr. med. Wolfram Sterry,Chairman of the EDF guidelines com-mittee for the financial support thatmade this S3-Guideline for the treatmentof androgenetic alopecia possible.We are especially grateful to all the authors and co-authors who invested anincredible amount of time, energy anddiscipline in evaluating the literature andcombining the acquired evidence-basedknowledge with their renowned expertiseand long-standing practical experience inthe field into the Therapeutic Recom-mendations.

A further therapeutic approach is to acton the inflammatory component of and-rogenetic alopecia. Ketoconazole or zincpyrithione are antimicrobial and are ef-fective agents in the treatment of seborr-hoic dermatitis. As concomitant seborr-hoeic dermatitis is common inandrogenetic alopecia and may aggravatehair loss, impact on androgenetic alope-cia is difficult to evaluate. Berger et al.showed significant improvement for 1 %pyrithione zinc shampoo, minoxidil 5 %solution or the combination of bothcompared to placebo treatment at 26weeks [16]. The mean change from base-line hair count for the 1 % pyrithionezinc shampoo group was significantly be-low the standard therapy with minoxidil.Combination of minoxidil and pyrit-hione zinc was inferior to minoxidil mo-notherapy.

3.5.4 Instructions for use / PracticabilityFor instructions for use the reader is as-ked to consult the product informationof the particular product.

3.5.5 Combination therapiesPatients often ask for one of the particu-lar miscellaneous therapies in combina-tion with another treatment. As evidenceis insufficient to missing for the therapiesmentioned above, they cannot be recom-mended in combination. Additional usedepends on the individual case and deci-sion of the patient and the physician.

3.5.6 SummaryPlenty of oral and topical miscellaneoustherapies are claimed to be effective inthe treatment of androgenetic alopecia inmen and women. There is insufficient tomissing evidence for this assumption(evidence level 4).

3.5.7 Therapeutic recommendation –Male and Female

Conflicts of InterestBlumeyer A: No conflict of interest declared. Blume-Peytavi U: Advisor to Johnson& Johnson (J & J), Almirall, Follica andDr. Hans Karrer. Received honorarium

There is no or insufficient evi-dence that the molecules sum-marized in Table 2, substancesand interventions improve orprevent progression of AGA inmale and female patients.

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S16 Therapeutic options and therapy assessment/References


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7 Smith MA, Wells RS. Male-typealopecia, alopecia areata, and normalhair in women; family histories. ArchDermatol 1964; 89: 95–8.

8 Hillmer AM, Brockschmidt FF, Hanneken S, Eigelshoven S, SteffensM, Flaquer A, Herms S, Becker T,Kortüm AK, Nyholt DR, Zhao ZZ,Montgomery GW, Martin NG,Mühleisen TW, Alblas MA, MoebusS, Jöckel KH, Bröcker-Preuss M, Erbel R, Reinartz R, Betz RC, CichonS, Propping P, Baur MP, Wienker TF,Kruse R, Nöthen MM. Susceptibilityvariants for male-pattern baldness onchromosome 20p11. Nat Genet2008; 40(11): 1279–81.

9 Richards JB, Yuan X, Geller F, Waterworth D, Bataille V, Glass D,Song K, Waeber G, Vollenweider P,Aben KK, Kiemeney LA, Walters B,Soranzo N,Thorsteinsdottir U, Kong A, Rafnar T, Deloukas P, SulemP, Stefansson H, Stefansson K, Spec-tor TD, Mooser V. Male-patternbaldness susceptibility locus at20p11. Nat Genet 2008; 40(11):1282–4.

10 Birch MP, Messenger JF, MessengerAG. Hair density, hair diameter andthe prevalence of female pattern hairloss. Br J Dermatol 2001; 144(2):297–304.

11 Norwood OT. Incidence of femaleandrogenetic alopecia (female patternalopecia). Dermatol Surg 2001;27(1): 53–4.

12 Alanis A, Barbara F, Meurehg C, DeOca FL, Ramirez L. Double-blindcomparison of 2 % topical minoxidiland placebo in early male patternbaldness. Curr Ther Res Clin Exp1991; 49(5): 723–30.

13 Anderson CD, Hansted B, AbdallahMA, Oumeish OY, Rushaidat Q,Moerk C, Juhlin L; Scandinavian andMiddle-Eastern topical minoxidilstudy group. Topical minoxidil inandrogenetic alopecia. Scandinavianand Middle East experience. Int JDermatol 1988; 27(6 Suppl.): 447–51.

14 Arca E, Acikgoz G, Tastan HB, KöseO, Kurumlu Z. An open, randomi-zed, comparative study of oral finaste-

References S17

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55 Imperato-McGinley J, Guerrero L,Gautier T, Peterson RE. Steroid 5alpha-reductase deficiency in man: an inherited form of male pseu-dohermaphroditism. Science 1974;186(4170): 1213–5.

56 Brenner S, Matz H. Improvement in androgenetic alopecia in 53–76-year-old men using oral finaste-ride. Int J Dermatol 1999; 38(12):928–30.

57 Kaufman KD, Olsen EA, Whiting D,Savin R, DeVillez R, Bergfeld W,Price VH, Van Neste D, Roberts JL,Hordinsky M, Shapiro J, BinkowitzB, Gormley GJ. Finasteride in the tre-atment of men with androgeneticalopecia. Finasteride Male PatternHair Loss Study Group. J Am AcadDermatol 1998; 39(4 Pt 1): 578–89.

58 Kawashima M, Hayashi N, IgarashiA, Kitahara H, Maeguchi M, MizunoA, Murata Y, Nogita T, Toda K,Tsuboi R, Ueki R, Yamada M, Yama-zaki M, Matsuda T, Natsumeda Y,Takahashi K, Harada S. Finasteride inthe treatment of Japanese men withmale pattern hair loss. Eur J Dermatol2004; 14(4): 247–54.

59 Khandpur S, Suman M, Reddy BS.Comparative efficacy of various treat-ment regimens for androgeneticalopecia in men. J Dermatol 2002;29(8): 489–98.

60 Leyden J, Dunlap F, Miller B, Winters P, Lebwohl M, Hecker D,Kraus S, Baldwin H, Shalita A, Draelos Z, Markou M, Thiboutot D,Rapaport M, Kang S, Kelly T, Pariser D, Webster G, Hordinsky M, Rietschel R, Katz HI, Terranella L,Best S, Round E, Waldstreicher J. Finasteride in the treatment of menwith frontal male pattern hair loss. JAm Acad Dermatol 1999; 40(6 Pt 1):930–7.

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46 Blume-Peytavi U, Kunte C, Krisp A,Garcia Bartels N, Ellwanger U, Hoff-mann R. Comparison of the efficacyand safety of topical minoxidil andtopical alfatradiol in the treatment ofandrogenetic alopecia in women. JDtsch Dermatol Ges 2007; 5(5):391–5.

47 DeVillez RL, Jacobs JP, Szpunar CA,Warner ML. Androgenetic alopecia inthe female. Treatment with 2 % topi-cal minoxidil solution. Arch Derma-tol 1994; 130(3): 303–7.

48 Jacobs JP, Szpunar CA, Warner ML.Use of topical minoxidil therapy forandrogenetic alopecia in women. IntJ Dermatol 1993; 32(10): 758–62.

49 Lucky AW, Piacquadio DJ, DitreCM, Dunlap F, Kantor I, Pandya AG,Savin RC, Tharp MD. A randomized,placebo-controlled trial of 5 % and 2% topical minoxidil solutions in thetreatment of female pattern hair loss.J Am Acad Dermatol 2004; 50(4):541–53.

50 Olsen EA. Topical minoxidil in thetreatment of androgenetic alopecia inwomen. Cutis 1991; 48(3): 243–8.

51 Tsuboi R, Yamazaki M, Matsuda Y,Uchida K, Ueki R, Ogawa H. Antisense oligonucleotide targetingfibroblast growth factor receptor(FGFR)-1 stimulates cellular activityof hair follicles in an in vitro organculture system. Int J Dermatol 2007;46(3): 259–63.

52 Vexiau P, Chaspoux C, Boudou P, FietJ, Jouanique C, Hardy N, Reygagne P.Effects of minoxidil 2 % vs. cypro-terone acetate treatment on femaleandrogenetic alopecia: a controlled,12-month randomized trial. Br J Der-matol 2002; 146(6): 992–9.

53 Whiting DA, Jacobson C. Treatmentof female androgenetic alopecia withminoxidil 2 %. Int J Dermatol 1992;31(11): 800–4.

54 Tsuboi R, Tanaka T, Nishikawa T,Ueki R, Yamada H, Katsuoka K,

randomized, placebo-controlled,double-blind clinical trial of a novelformulation of 5 % minoxidil topicalfoam versus placebo in the treatmentof androgenetic alopecia in men. JAm Acad Dermatol 2007; 57(5):767–74.

35 Petzoldt D, Borelli S, Braun-Falco O,Holzmann H, Laux B, Metz J, Pet-zoldt D, Wolff HH. The Germandouble-blind placebo-controlled eva-luation of topical minoxidil solutionin the treatment of early male patternbaldness. Int J Dermatol 1988; 27(6Suppl.): 430–4.

36 Piepkorn MW, Weidner M. Compa-rable efficacy of 2 % minoxidil geland solution formulations in the tre-atment of male pattern alopecia. J AmAcad Dermatol 1988; 18(5 Pt 1):1059–62.

37 Price VH, Menefee E, Strauss PC.Changes in hair weight and haircount in men with androgeneticalopecia, after application of 5 % and2 % topical minoxidil, placebo, or notreatment. J Am Acad Dermatol1999; 41(5 Pt 1): 717–21.

38 Reygagne P, Assouly P, Catoni I, Jouanique C, Maffi-Berthier N,Moisson YF, Mounier P, Pfister P, Ribrioux A, Smadja J, Coudert AC,Dubertret L. Male androgenic alopecia. Randomized trial versus 2 %minoxidil. Nouv Dermatol 1997;16(2): 59–63.

39 Rietschel RL, Duncan SH. Safety andefficacy of topical minoxidil in themanagement of androgenetic alope-cia. J Am Acad Dermatol 1987; 16(3Pt 2): 677–85.

40 Roberts JL. Androgenetic alopecia:treatment results with topical minoxi-dil. J Am Acad Dermatol 1987; 16(3Pt 2): 705–10.

41 Roenigk HH, Pepper E, Kuruvilla S.Topical minoxidil therapy for here-ditary male pattern alopecia. Cutis1987; 39(4): 337–42.

42 Saraswat A, Kumar B. Minoxidil vs.finasteride in the treatment of menwith androgenetic alopecia. ArchDermatol 2003; 139(9): 1219–21.

43 Savin RC. Use of topical minoxidil inthe treatment of male patternbaldness. J Am Acad Dermatol 1987;16(3 Pt 2): 696–704.

44 Shin HS, Won CH, Lee SH, KwonOS, Kim KH, Eun HC. Efficacy of 5 % minoxidil versus combined 5 %


S18 References


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79 Wüstner H, Orfanos CE. Alopeciaandrogenetica and its local treatmentwith estrogen- and corticosteroid externa. Z Hautkr 1974; 49(20):879–88.

80 Wozel G, Narayanan S, Jackel A, LutzGA. Alfatradiol (0.025 %) – An effec-tive and safe therapy for the treatmentof androgenetic alopecia in womenand men. Aktuel Dermatol 2005;31(12): 553–60.

81 Peereboom-Wynia JD, van der Willigen AH, van Joost T, Stolz E.The effect of cyproterone acetate onhair roots and hair shaft diameter inandrogenetic alopecia in females.Acta Derm Venereol 1989; 69(5):395–8.

82 Georgala S, Katoulis AC, Georgala C,Moussatou V, Bozi E, StavrianeasNG. Topical estrogen therapy forandrogenetic alopecia in menopausalfemales. Dermatology 2004; 208(2):178–9.

83 Bernstein RM, Rassman WR. Dissec-ting microscope versus magnifyingloupes with transillumination in thepreparation of follicular unit grafts. Abilateral controlled study. DermatolSurg 1998; 24(8): 875–80.

84 Uebel CO, da Silva JB, Cantarelli D,Martins P. The role of platelet plasmagrowth factors in male patternbaldness surgery. Plast Reconstr Surg2006; 118(6): 1458–66.

85 Morganti P, Fabrizi G, James B,Bruno C. Effect of gelatin-cystine andserenoa repens extract on free radicalslevel and hair growth. J Appl Cosme-tol 1998; 16(3): 57–64.

86 Gehring W, Gloor M. Use of the phototrichogram to assess the stimu-lation of hair growth – An in vitrostudy of women with androgeneticalopecia. Z Hautkr 2000; 75(7–8):419–23.

87 Trost LB, Bergfeld WF, Calogeras E.The diagnosis and treatment of irondeficiency and its potential relations-hip to hair loss. J Am Acad Dermatol2006; 54(5): 824–44.

88 Draelos ZD, Jacobson EL, Kim H,Kim M, Jacobson MK. A pilot studyevaluating the efficacy of topically ap-plied niacin derivatives for treatmentof female pattern alopecia. J CosmetDermatol 2005; 4(4): 258–61.

69 Whiting DA, Olsen EA, Savin R,Halper L, Rodgers A, Wang L, HustadC, Palmisano J; Male Pattern HairLoss Study Group.Efficacy and tole-rability of finasteride 1 mg in menaged 41 to 60 years with male patternhair loss. Eur J Dermatol 2003;13(2): 150–60.

70 Leavitt M, Perez-Meza D, Rao NA,Barusco M, Kaufman KD, Ziering C.Effects of finasteride (1 mg) on hairtransplant. Dermatol Surg 2003;31(10): 1268–76.

71 Finasteride Male Pattern Hair LossStudy Group. Long-term (5-year)multinational experience with fina-steride 1 mg in the treatment of menwith androgenetic alopecia. Eur JDermatol 2002; 12(1): 38–49.

72 Brenner S, Tamir A. Treatment of and-rogenic alopecia with topical minoxi-dil. Harefuah 1991; 121(9): 297–302.

73 Stough D. Dutasteride improves malepattern hair loss in a randomizedstudy in identical twins. J CosmetDermatol 2007; 6(1): 9–13.

74 Price VH, Roberts JL, Hordinsky M,Olsen EA, Savin R, Bergfeld W, Fiedler V, Lucky A, Whiting DA,Pappas F, Culbertson J, Kotey P, Meehan A, Waldstreicher J. Lack ofefficacy of finasteride in postme-nopausal women with androgeneticalopecia. J Am Acad Dermatol 2000;43(5 Pt 1): 768–76.

75 Diani AR, Mulholland MJ, Shull KL,Kubicek MF, Johnson GA, SchostarezHJ, Brunden MN, Buhl AE. Hairgrowth effects of oral administrationof finasteride, a steroid 5 alpha-reductase inhibitor, alone and incombination with topical minoxidilin the balding stumptail macaque. JClin Endocrinol Metab 1992; 74(2):345–50.

76 Sovak M, Seligson AL, Kucerova R,Bienova M, Hajduch M, Bucek M.Fluridil, a rationally designed topicalagent for androgenetic alopecia: firstclinical experience. Dermatol Surg2002; 28(8): 678–85.

77 Gassmueller J, Hoffmann R, WebsterA. Topical fulvestrant solution has noeffect on male and postmenopausalfemale androgenetic alopecia: resultsfrom two randomized, proof-of-concept studies. Br J Dermatol 2008;158(1): 109–15.

78 Orfanos CE, Vogels L. Local therapyof androgenetic alopecia with 17 al-

finasteride. J Am Acad Dermatol2006; 55(6): 1014–23.

62 Price VH, Menefee E, Sanchez M,Ruane P, Kaufman KD. Changes inhair weight and hair count in menwith androgenetic alopecia after treat-ment with finasteride, 1 mg, daily. JAm Acad Dermatol 2002; 46(4):517–23.

63 Price VH, Menefee E, Sanchez M,Kaufman KD. Changes in hairweight in men with androgeneticalopecia after treatment with finaste-ride (1 mg daily): three- and 4-yearresults. J Am Acad Dermatol 2006;55(1): 71–4.

64 Roberts JL, Fiedler V, Imperato-McGinley J, Whiting D, Olsen E,Shupack J, Stough D, DeVillez R,Rietschel R, Savin R, Bergfeld W,Swinehart J, Funicella T, HordinskyM, Lowe N, Katz I, Lucky A, DrakeL, Price VH, Weiss D, Whitmore E,Millikan L, Muller S, Gencheff C,Carrington P, Binkowitz B, Kotey P,He W, Bruno K, Jacobsen C, Terranella L, Gormley GJ, KaufmanKD. Clinical dose ranging studieswith finasteride, a type 2 5alpha-reductase inhibitor, in men with malepattern hair loss. J Am Acad Derma-tol 1999; 41(4): 555–63.

65 Stough DB, Rao NA, Kaufman KD,Mitchell C. Finasteride improvesmale pattern hair loss in a randomi-zed study in identical twins. Eur JDermatol 2002; 12(1): 32–7.

66 Trüeb RM, Itin P. Photographic do-cumentation of the effectiveness of 1mg oral finasteride in treatment ofandrogenic alopecia in the man inroutine general practice in Switzer-land. Praxis 2001; 90(48): 2087–93.

67 Van-Neste D, Fuh V, Sanchez-Pedreno P, Lopez-Bran E, Wolff H,Whiting D, Roberts J, Kopera D, SteneJJ, Calvieri S, Tosti A, Prens E, Guar-rera M, Kanojia P, He W, KaufmanKD. Finasteride increases anagen hairin men with androgenetic alopecia. Br JDermatol 2000; 143(4): 804–10.

68 Whiting DA, Waldstreicher J,Sanchez M, Kaufman KD. Measuringreversal of hair miniaturization inandrogenetic alopecia by follicularcounts in horizontal sections of serialscalp biopsies: results of finasteride 1mg treatment of men and postme-nopausal women. J Invest DermatolSymp Proc 1999; 4(3): 282–284.

References S19

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89 Prager N, Bickett K, French N, Marcovici G. A randomized, double-blind, placebo-controlled trial to determine the effectiveness of botanically derived inhibitors of 5-alpha-reductase in the treatment ofandrogenetic alopecia. J Altern Com-plement Med 2002; 8(2): 143–52.

90 Kamimura A, Takahashi T, WatanabeY. Investigation of topical applicationof procyanidin B-2 from apple toidentify its potential use as a hair gro-wing agent. Phytomedicine 2000;7(6): 529–36.

91 Lassus A, Eskelinen E. A comparativestudy of a new food supplement, Vi-viScal, with fish extract for the treat-ment of hereditary androgenic alope-cia in young males. J Int Med Res1992; 20(6): 445–53.

92 Lassus A, Santalahti J, Sellmann M.Combined topical external and oral ad-ministration of marine polysaccharidederivatives in the treatment of here-ditary androgenetic alopecia in adults.Nouv Dermatol 1994; 13(5): 254–5.

93 Greenberg JH, Katz M. Treatment ofandrogenetic alopecia with a 7.5 %herbal preparation. J Dermatol Treat1996; 7(3): 159–62.

94 Kessels AG, Cardynaals RL, BorgerRL, Go MJ, Lambers JC, KnottnerusJA, Knipschild PG. The effectivenessof the hair-restorer “Dabao” in maleswith alopecia androgenetica. A clini-cal experiment. J Clin Epidemiol1991; 44(4–5): 439–47.

95 Otberg N, Patzelt A, Rasulev U, Hagemeister T, Linscheid M, Sinkgraven R, Sterry W, Lademann J.The role of hair follicles in the percutaneous absorption of caffeine.Br J Clin Pharmacol 2008; 65(4):488–92.

96 Fischer TW, Burmeister G, SchmidtHW, Elsner P. Melatonin increasesanagen hair rate in women with and-rogenetic alopecia or diffuse alopecia:results of a pilot randomized control-led trial. Br J Dermatol 2004; 150(2):341–5.

97 Gilhar A, Pillar T, Etzioni A. Topicalcyclosporine in male pattern alopecia.J Am Acad Dermatol 1990; 22(2 Pt1): 251–3.

98 Bureau JP, Ginouves P, Guilbaud J,Roux ME. Essential oils and low-in-tensity electromagnetic pulses in thetreatment of androgen-dependentalopecia. Adv Ther 2003; 20(4): 220–9.

99 Maddin WS, Bell PW, James JH. Thebiological effects of a pulsed elec-trostatic field with specific referenceto hair. Electrotrichogenesis. Int JDermatol 1990; 29(6): 446–50.

100 Maddin WS, Amara I, Sollecito WA.Electrotrichogenesis: further evidenceof efficacy and safety on extended use.Int J Dermatol 1992; 31(12): 878–80.

101 Policarpi F, Giorgini S, Farella V,Melli MC, Campolmi P, Panconesi E.Effects of application of a pulsed elec-trostatic field in male and female and-rogenic alopecia. Ann Ital DermatolClin Sper 1993; 47(3): 227–32.

102 Satino JL, Markou M. Hair regrowthand increased hair tensile strengthusing the HairMax LaserComb forlow-level laser therapy. Int J CosmetSurg Aesthet Dermatol 2003; 5(2):113–7.

103 Groveman HD, Ganiats T, KlauberMR. Lack of efficacy of polysorbate60 in the treatment of male patternbaldness. Arch Intern Med 1985;145(8): 1454–8.

104 Olsen EA, DeLong E. Transdermalviprostol in the treatment of malepattern baldness. J Am Acad Derma-tol 1990; 23(3 Pt 1): 470–2.

Appendix 1 S21


Appendix 1: Guideline’s Inclusion Criteria

Excerpt from the Literature Evaluation Form (LEF)

A. Inclusion/Exclusion of an article:This serves as a prescreening. If the article is not included, neither the quality nor the results will be assessed. (tick a grey box = exclusionof the article)

1. Author + Year: ………………………………………………………………………………………………………………………………

2. Language:………………………………………………………………………………………………………………………………

3. Type of the study: prospective study? Yes No

4. Number of patients �20? Yes No Exception in identical twin studies no minimal patient number required.

5. Age: Adults (�18 years)

Adolescents (�12 years) (Studies of adolescents will be evaluated separately)

Children / n.d

6. Confirmed diagnosis of androgenetic alopecia male versus female pattern, respectively (diagnosis either clinically or by further diagnostic evaluations e.g. trichogram, TrichoScan, biopsy)?

Yes No/n.d.

7. Type of therapy?

monotherapy or combination therapy distinct classification not possible

8. Objective outcome measure of efficacy described? Yes No

For drug therapy:Mean change from baseline hair count in target area OR Measurement of hair growth/loss in target area by global photography

For surgical therapy:Mean change from baseline hair count in target area OR Measurement of hair growth/loss in target area by global photography ORGraft survival and global photography

9. Exception:

Category of the article: Review Safety study Other

Article should be quoted: Yes No

S22 Appendix 2


Ap

pen

dix

2:

Lite

ratu

re R

esu

lts

Tab

les.

Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method

mean change from baseline hair count

(total) hairs/cm2 (%)


(nonvellus) hairs/cm2 (%)


(anagen, telogen, anagen/telogen ratio)

mean change from baseline hair weight / thickness

global expert panel assessment

investigator assessment

patient assessment

Investigational area

Degree of evidence

Min

oxid

il

41

Roenigk

1987

777

mal

e6m

Arm

1:

min

oxid

il 2.

8%,

2x/d

, top

ical

46.6

%C

28

Montagnani

1990

33m

ale

24w

Arm

1:

Min

oxid

il 2%

so

luti

on, 2

x/d,

topi

cal

37.5

%C

23

Karam

1993

195

mal

e48

w

Arm

1:

min

oxid

il 2%

so

luti

on, 2

x/d,

topi

cal

manual hair count

44.7

(82

.1%

)p

< 0.

001

vs.

Bas

elin

e

47.8

(11

9.7%

)p

< 0.

0001

vs.

Bas

elin

eve

rtex

C

Min

oxid

il vs

. Pla

cebo

Mal

e

34

Olsen

2007

352

mal

e16

w

Arm

1: m

inox

idil

5% fo

am, 2

x/d,

topi

cal

Phototrichogram

20.9

(13

.4%

)p

< 0.

0001

vs.

Bas

elin

e

impr

oved

:38

.3%

un

chan

ged:

52.2

%p

< 0.

0001

vs. P

lace

bove

rtex

A2

Arm

2:

plac

ebo

foam

,2x

/d, t

opic

al4.

7 (3

.4%

)5.

2%un

chan

ged:

77.9

%

Con

tinu

ed

Appendix 2

Appendix 2 S23


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method







mean change from baseline hair weight / thickness



patient assessment


Degree of evidence

17

Califano

1991

132

mal

e24

w

Arm

1: m

inox

idil

2% s

olut

ion,

2x/d

, top

ical

manual hair count

18.8

(47

.6%

)17

.3 (

59.4

%)

vert

exA

2A

rm2:

pla

cebo

solu

tion

, 2x/

d,to

pica

l17

.9 (

48.8

%)

12.3

(46

.2%

)

13

Anderson

1988

154

mal

e24

w

Arm

1: m

inox

idil

2% s

olut

ion,

2x/d

, top

ical

manual hair count

25.4

(40

.0%

)p

= 0.

0001

vs.

Plac

ebo

25.4

(69

.9%

)p

= 0.

002

vs.

Plac

ebo

vert

exA

2

Arm

2: p

lace

bo,

2x/d

, top

ical

10

.3 (

15.5

%)

12.1

(31

.8%

)

22

Dutree-Meulenberg

1988

151

mal

e24

w

Arm

1: m

inox

idil

2% s

olut

ion,

2x/d

, top

ical

manual hair count

29.9

(35

.3%

)p

= 0.

02 v

s.Pl

aceb

o

17.5

(38

.0%

)p

= 0.

0003

vs.

Plac

ebo

vert

exA

2

Arm

2: p

lace

bo,

2x/d

, top

ical

18

.4 (

20.4

%)

5.9

(10.

7%)

35

Petzold

1988

201

mal

e24

w

Arm

1: M

inox

idil

2% s

olut

ion,

2x/d

, top

ical

manual hair count

16.1

(39

.2 %

)p

= 0.

0076

vs.

Plac

ebo

10.8

(33

.1%

)p

= 0.

0104

vs.

Plac

ebo

vert

exA

2A

rm2:

pl

aceb

o, 2

x/d,

to

pica

l 6.

1 (1

4.9%

)2.

5 (7

.3%

)

Con

tinu

ed

S24 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method







mean change from baseline hair

weight / thickness


investigatorassessment

patient assessment


Degree of evidence

30

Olsen

1986

100

mal

e6m

Arm

1: m

inox

idil

0.01

% s

olut

ion,

2x/d

, top

ical

manual hair count

16.5

(15

.3%

)9.

4 (1

4.2%

)

vert

exA

2

Arm

2: m

inox

idil

0.1%

sol

utio

n,2x

/d, t

opic

al18

.0 (

18.9

%)

15.9

(27

.1%

)

Arm

3: m

inox

idil

1% s

olut

ion,

2x/d

, top

ical

29.2

(27

.8%

)35

.3 (

53.3

%)

Arm

4: m

inox

idil

2% s

olut

ion,

2x/d

, top

ical

34.3

(33

.1%

)si

gnifi

cant

vs.

Arm

1-3,

537

.3 (

52.1

%)

Arm

5: p

lace

bo,

2x/d

, top

ical

17

.6 (

17.1

%)

15.9

(23

.1%

)

45

Shupack

1987

58m

ale

6m

Arm

1: p

lace

bo,

2x/d

, top

ical

phototrichogram

2.9

(14.

4%)

vert

exB

Arm

2: m

inox

idil

0.01

% s

olut

ion,

2x/d

, top

ical

0.3

(1.2

%)

p >

0.2

vs.

Plac

ebo

Arm

3: m

inox

idil

0.1%

sol

utio

n,2x

/d, t

opic

al

5.1

(16.

3%)

p <

0.01

vs.

Plac

ebo,

p >

0.1

vs. A

rm4/

5

Arm

4: m

inox

idil

1% s

olut

ion,

2x/d

, top

ical

7.8

(39.

6%)

p <

0.01

vs.

Plac

ebo,

p >

0.1

vs. A

rm3/

5

Arm

5: m

inox

idil

2% s

olut

ion,

2x/d

, top

ical

10.6

(58

.2%

)p

< 0.

01 v

s. Pl

aceb

o,p

> 0.

1 vs

. Arm

3/4

Con

tinu

ed

Appendix 2 S25


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

33

Olsen

2002

393

mal

e48

w

Arm

1: m

inox

idil

5% s

olut

ion,

2x/d

, top

ical

phototrichogram

18.6

(12

.3%

)p

< 0.

001

vs. P

lace

bo,

p =

0.02

5 vs

. Arm

2

impr

oved

:57

.9%

un

chan

ged:

30.3

%

vert

exA

2A

rm2:

min

oxid

il2%

sol

utio

n,2x

/d, t

opic

al

12.7

(8.

8%)

p <

0.01

3 vs

.Pl

aceb

o

impr

oved

:40

.8%

un

chan

ged:

48.6

%

Arm

3: p

lace

bo,

2x/d

, top

ical

3.

9 (2

.6%

)

impr

oved

:23

.2%

un

chan

ged:

60.6

%

18

Civatte

1987

247

mal

e24

w,

48w

Arm

1: m

inox

idil

2% s

olut

ion,

2x/d

, top

ical

manual hair count

24w

: 13.

3 (4

7.2%

)p

< 0.

01 v

s. B

asel

ine

48w

: 32.

0 (7

8.2%

)p

= 0.

02 v

s. B

asel

ine

vert

exA

2A

rm2:

24w

pl

aceb

o, 2

x/d,

to

pica

l, 25

-48w

min

oxid

il 2%

so

luti

on, 2

x/d,

topi

cal

24w

: 13.

3 (4

2.0%

)p

< 0.

01 v

s. B

asel

ine

48w

: 31.

4 (9

9.0%

)

Con

tinu

ed

S26 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

27

Lopez-Bran

1990

114

mal

e24

w,

48w

Arm

1: m

inox

idil

2% s

olut

ion,

2x/d

, top

ical

manual hair count

24w

: 5.4

(12

.1%

)48

w: 1

5.5

(34.

6%)

24w

: 4.7

(17

.2%

)48

w: 1

4.2

(52.

4%)

vert

exA

2A

rm2:

24w

pl

aceb

o, 2

x/d,

to

pica

l, 25

-48w

min

oxid

il 2%

so

luti

on, 2

x/d,

topi

cal

24w

: 4.7

(10

.4%

)48

w: 1

2.2

(27.

1%)

24w

: 2.9

(10

.8%

)48

w: 1

0.5

(39.

4%)

19

Civatte

1988

428

mal

e24

w,

48w

Arm

1: m

inox

idil

2% s

olut

ion,

2x/d

, top

ical

manual hair count

24w

: 23.

8 (5

4.8%

)p

= 0.

0611

vs.

Arm

248

w: 3

6.1

(83.

0%)

24w

: 13.

3 (4

8.6%

)p

= 0.

0187

vs.

Arm

248

w: 2

5.0

(91.

3%)

vert

exA

2A

rm2:

24w

pl

aceb

o, 2

x/d,

to

pica

l, 25

-48w

min

oxid

il 2%

,2x

/d, t

opic

al

24w

: 19.

9 (4

7.5%

)48

w: 3

4.6

(82.

7%)

24w

: 9.7

(39

.6%

)48

w: 2

2.6

(91.

8%)

12

Alanis

1991

240

mal

e24

w,

48w

Arm

1: m

inox

idil

2% s

olut

ion,

2x/d

, top

ical

manual hair count

24w

: 13.

7 (2

5.6%

)48

w: 2

5.5

(47.

8%)

p =

0.00

0 (2

4w, 4

8w)

vs.

Bas

elin

eve

rtex

A2

Arm

2: 2

4w

plac

ebo,

2x/

d,

topi

cal,

25-4

8wm

inox

idil

2%

solu

tion

, 2x/

d,to

pica

l

24w

: 5.1

(9.

3%)

48w

: 16.

9 (3

1.0%

)p

= 0.

000

(24w

, 48w

) vs

. B

asel

ine

Con

tinu

ed

Appendix 2 S27


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

36

Piepkorn

1988

72m

ale

6m

Arm

1: m

inox

idil

2% g

el, 2

x/d,

to

pica

l

manual hair count

26%

p <

0.05

vs.

Arm

2

vert

exB

Arm

2: p

lace

boge

l, 2x

/d, t

opic

al

33%

Arm

3: m

inox

idil

2% s

olut

ion,

2x/d

, top

ical

48%

p <

0.05

vs.

Arm

4

Arm

4: p

lace

boso

luti

on, 2

x/d,

topi

cal

36%

29

Olsen

1985

153

mal

e4m

,12

m

Arm

1: m

inox

idil

2% s

olut

ion,

2x/d

, top

ical

manual hair count

4m: 2

9.6

(53.

6%)

12m

: 63.

5 (1

14.9

%)

n.s.

vs.

Arm

3 (4

m),

n.s.

vs.

Arm

2 (4

m, 1

2m)

4m:

24.7

(10

0.0%

)12

m:

42.8

(17

3.0%

)

vert

exA

2

Arm

2: m

inox

idil

3% s

olut

ion,

2x/d

, top

ical

4m: 3

2.6

(52.

0%)

p =

0.04

vs.

Arm

312

m:

66.3

(10

6.0%

)

4m:

27.5

(95

.2%

)12

m:

53.5

(18

5.7%

)

Arm

3: 4

mpl

aceb

o, 2

x/d,

to

pica

l, 5-

12m

min

oxid

il 3%

so

luti

on, 2

x/d,

topi

cal

4m: 2

2.4

(39.

3%)

12m

: 61.

4 (1

08.0

%)

4m:

11.6

(44

.7%

)12

m:

42.9

(16

5.9%

)

Con

tinu

ed

S28 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

43

Savin

1987

96m

ale

4m,

12m

Arm

1: m

inox

idil

2% s

olut

ion,

2x/d

, top

ical

manual hair count

4m: 1

4.9

p =

0.00

76 v

s.

Bas

elin

e p

= 0.

013

vs. A

rm3

12m

: 16.

4p

< 0.

001

vs. B

asel

ine

4m: 1

1.4

12m

: 22.

0

vert

exA

2A

rm2:

min

oxid

il3%

sol

utio

n,2x

/d, t

opic

al

4m: 1

1.9

12m

: 28.

3p

< 0.

001

vs. B

asel

ine

4m: 9

.6

12m

: 30.

9

Arm

3: 4

mpl

aceb

o, 2

x/d,

to

pica

l, 5-

12m

min

oxid

il 3%

so

luti

on, 2

x/d,

topi

cal

4m: 9

.3

12m

: 24.

7p

<0.

001

vs. B

asel

ine

4m: 0

.8

12m

: 33.

2

24

Katz

1987

153

mal

e4m

,12

m

Arm

1: m

inox

idil

2% s

olut

ion,

2x/d

, top

ical

manual hair count

4m: 2

0.4

(216

.7%

)p

= 0.

0002

vs.

Arm

3, p

= 0

.046

4vs

. Arm

2 12

m: 4

1.8

(443

.8%

)

vert

exA

2

Arm

2: m

inox

idil

3% s

olut

ion,

2x/d

, top

ical

4m: 1

4.5

(168

.2%

)p

= 0.

0833

vs.

Arm

312

m: 3

9.6

(459

.1%

)

Arm

3: 4

mpl

aceb

o, 2

x/d,

to

pica

l, 5-

24m

min

oxid

il 3%

so

luti

on, 2

x/d,

topi

cal

4m: 9

.8 (

116.

3%)

12m

: 33.

1 (3

93.0

%)

Con

tinu

ed

Appendix 2 S29


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

21

De Villez

1987

64m

ale

4m,

12m

Arm

1: m

inox

idil

3% s

olut

ion,

2x/d

, top

ical

phototrichogram

4m: 1

.2p

< 0.

05 v

s. A

rm3,

n.s.

vs.

Arm

2 12

m: 9

.4

vert

exB

Arm

2: m

inox

idil

2% s

olut

ion,

2x/d

, top

ical

4m: 1

.2p

< 0.

05 v

s. A

rm3

12m

: 8.6

Arm

3: 4

m p

lace

bo,

2x/d

, top

ical

, 5-1

2mm

inox

idil

3% so

lutio

n,2x

/d, t

opic

al

4m: -

0.2

12m

: 4.9

31

Olsen

1987

127

mal

e13

2w

Arm

1: m

inox

idol

3% s

olut

ion,

2x/

d,to

pica

l

phototrichogram

64,4

65

.7

vert

exB

Arm

2:

24m

min

oxid

ol 3

%so

luti

on, 2

x/d,

to

pica

l, 25

33m

m

inox

idil

3%

solu

tion,

1x/

d, to

pica

l

44,1

46

.1

12

Alanis

1991

240

mal

e24

w,

48w

Arm

1: m

inox

idil

2%so

lutio

n, 2

x/d,

topi

cal

manual hair count

24w

: 9.9

(27

.7%

)48

w: 1

8.2

(50.

9%)

vert

exB

Arm

2: 2

4w p

lace

bo,

2x/d

, top

ical

, 25

-48w

min

oxid

il2%

sol

utio

n, 2

x/d,

topi

cal

24w

: 4.8

(12

.6%

)48

w: 1

2.3

(32.

4%)

Con

tinu

ed

S30 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

25

Koperski

1987

72m

ale

12m

,30

m

Arm

1: m

inox

idil

2% s

olut

ion,

2x/

d,

topi

cal

manual hair count

12m

: 46.

9 (1

91.7

%)

30m

: 22.

5 (9

1.7%

)p

< 0.

001

(4m

, 12m

)vs

. Bas

elin

en.

s. v

s. A

rm2

vert

exA

2A

rm2:

min

oxid

il 3%

sol

utio

n, 2

x/d,

topi

cal

12m

: 36.

7 (1

63.6

%)

30m

: 26.

5 (1

18.2

%)

p <

0.00

1 (4

m, 1

2m)

vs. B

asel

ine

Arm

3: 4

m p

lace

bo,

2x/d

, top

ical

, 5m

-30m

min

oxid

il3%

sol

utio

n, 2

x/d,

topi

cal

12m

: 44.

9 (2

00.0

%)

30m

: 36.

7 (1

63.6

%)

p <

0.01

(4m

),

p <

0.00

1 (1

2m)

vs.

Bas

elin

e

32

Olsen

1990

31m

ale

3y

Arm

1: m

inox

idil

3% s

olut

ion,

2x/d

, top

ical

phototrichogram

4.4

p =

0.01

5 vs

.A

rm2

vert

exB

Arm

2: 1

sty

min

oxid

il 3%

solu

tion,

2x/

d, to

pica

l,2nd

-3rd

y, 1

x/d,

4th-5

thy

2x/d

-13.

4

Con

tinu

ed

Appendix 2 S31


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

26

Kreindler

1987

150

mal

e4m

,12

m

Arm

1: m

inox

idil

2% s

olut

ion,

2x/

d,to

pica

l

manual hair count

4m: 1

5.9

(47.

4%)

12m

: 83.

3 (2

48.5

%)

p <

0.00

01 v

s.B

asel

ine

4m: 1

2.6

(91.

4%)

p =

0.00

18 v

s.Pl

aceb

o12

m: 4

0.4

(294

.3%

)

bald

area

A2

Arm

2: m

inox

idil

3% s

olut

ion,

2x/

d,to

pica

l

4m: 1

6.1

(50.

9%)

12m

: 72.

9 (2

31.1

%)

p <

0.00

01 v

s.B

asel

ine

4m: 1

0.2

(85.

3%)

p =

0.01

67 v

s.Pl

aceb

o 12

m: 3

4.9

(291

.8%

)

Arm

3: 4

m p

lace

bo2x

/d, t

opic

al,

5-12

m m

inox

idil

3% s

olut

ion,

2x/

d,to

pica

l

4m: 1

1.0

(37.

1 %

)12

m: 8

0.4

(271

.5%

)p

< 0.

0001

vs.

Bas

elin

e

4m: 3

.1 (

23.2

%)

12m

: 33.

1 (2

44.9

%)

20

Connors

1990

169

mal

e24

w,

48w

Arm

1: m

inox

idil

2% s

olut

ion,

2x/

d,to

pica

l

manual hair count

24w

: 7.7

(30

.6%

)p

< 0.

05 v

s. Pl

aceb

o48

w: 3

.3 (

13.1

%)

p =

0.07

(24

-48w

)ba

ldar

eaA

2A

rm2:

24w

plac

ebo,

2x/

d,

topi

cal,

25-4

8wm

inox

idil

2% s

olu-

tion

, 2x/

d, to

pica

l

24w

: 0.4

(1.

6%)

48w

: 7.8

(34

.1%

)p

< 0.

01 (

24-4

8w)

Con

tinu

ed

S32 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

37

Price

1999

36m

ale

96w

Arm

1: m

inox

idil

2%so

luti

on, 2

x/d,

topi

cal

manual hair count

25%

p =

0.07

4 vs

. Pla

cebo

,p

= 0.

455

vs. A

rm2

hair

wei

ght 1

5%p

< 0.

005

vs.

Plac

ebo,

p

= 0.

437

vs.

Arm

2

fron

tal/

parie

tal

BA

rm2:

min

oxid

il 5%

solu

tion

, 2x/

d, to

pica

l

30%

p

= 0.

010

vs.

Plac

ebo

22%

p =

0.00

0 vs

.Pl

aceb

o

Arm

3: p

lace

bo, 2

x/d,

topi

cal

9%

-15%

Arm

4: n

o tr

eatm

ent

10%

-1

0%

Mal

e an

d Fe

mal

e

39

Rietschel

1997

149

fem

ale

and

mal

e

4m,

12m

Arm

1: 1

sty

min

oxid

il2%

sol

utio

n, 2

x/d,

to

pica

l, 2n

dy m

inox

idil

3% s

olut

ion,

2x/

d,

topi

cal

manual hair count

4m: 4

.8 (

38.7

%)

n.s.

vs.

Bas

elin

e12

m: 2

3.0

(184

.4%

)p

< 0.

001

vs. B

asel

ine,

n.s.

vs.

Arm

2+3

4m:

1.5

(16.

8%)

12m

: 16

.0 (

175.

9%)

vert

exB

Arm

2: m

inox

idil

3%so

luti

on, 2

x/d,

topi

cal

4m: 5

.9 (

49.3

%)

n.s.

vs.

Bas

elin

e12

m: 2

3.3

(194

.9%

)p

< 0.

001

vs. B

asel

ine,

n.s.

vs.

Arm

3

4m:

1.7

(19.

5%)

12m

: 16

.9 (

195.

2%)

Arm

3: 4

m p

lace

bo,

2x/d

, top

ical

, 5m

-24m

min

oxid

i 3%

sol

utio

n2x

/d, t

opic

al

4m: 4

.7 (

36.5

%)

n.s.

vs.

Bas

elin

e12

m: 2

4.7

(194

.0%

)p

< 0.

001

vs. B

asel

ine

4m:

1.3

(13.

9%)

12m

: 17

.7 (

193.

4%)

Con

tinu

ed

Appendix 2 S33


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

40

Roberts

1987

60fe

mal

ean

dm

ale

4m,

12m

Arm

1: m

inox

idil

2%so

luti

on, 2

x/d,

topi

cal

manual hair count

4m: 2

2.0

(70.

8%)

n.s.

vs.

Arm

2+3

12m

: 50.

5 (1

62.7

%)

p =

0.00

01 v

s.

Bas

elin

e

vert

exB

Arm

2: m

inox

idil

3%so

luti

on, 2

x/d,

topi

cal

4m: 2

5.6

(83.

3%)

n.s.

vs.

Arm

312

m: 5

7.2

(186

.4%

)p

= 0.

0001

vs.

B

asel

ine

Arm

3: 4

m p

lace

bo,

2x/d

, top

ical

, 5-1

2mm

inox

idil

3%so

luti

on, 2

x/d,

topi

cal

4m: 1

6.5

(51.

8%)

12m

: 60.

5 (1

89.7

%)

p =

0.00

01 v

s.

Bas

elin

e

Fem

ale

51

Tsuboi

2007

280

fem

ale

24w

Arm

1: m

inox

idil

1%so

luti

on, 2

x/d,

topi

cal

phototrichogram

15.2

(8.

0%)

p <

0.00

1 vs

.Pl

aceb

o

8.2

(6.1

%)

p <

0.00

1 vs

.Pl

aceb

oba

ldar

eaA

2

Arm

2: p

lace

bo, 2

x/d,

topi

cal

2.9

(1.5

%)

2.0

(1.5

%)

48

Jacobs

1993

346

fem

ale

32w

Arm

1: m

inox

idil

2%so

luti

on, 2

x/d,

topi

cal

phototrichogram

33.1

(24

.2%

)p

= 0.

0148

vs.

Plac

ebo

bald

area

A2

Arm

2:

plac

ebo,

2x/

d, to

pica

l 19

.1 (

13.7

%)

Con

tinu

ed

S34 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

47

De Villez

1994

308

fem

ale

24w

,32

w

Arm

1: m

inox

idil

2%so

luti

on, 2

x/d,

topi

cal

phototrichogram

24w

: 21.

8 (1

5.5%

)32

w: 2

2.7

(16.

2%)

p =

0.02

vs.

Pla

cebo

bald

are

aA

2

Arm

2:

plac

ebo,

2x/

d, to

pica

l24

w: 9

.9 (

7.1%

)32

w: 1

0.1

(7.3

%)

53

Whiting

1992

33fe

mal

e24

w,

32w

Arm

1: m

inox

idil

2%so

luti

on, 2

x/d,

topi

cal

phototrichogram

21 (

12.4

%)

n.s.

vs.

Pla

cebo

bald

are

aB

Arm

2:

plac

ebo,

2x/

d, to

pica

l 17

(10

.6%

)

50

Olsen

1991

30fe

mal

e32

w

Arm

1: m

inox

idil

2%so

luti

on, 2

x/d,

topi

cal

phototrichogram

50.1

(31

.3%

)p

= 0.

006

vs. P

lace

bofr

onto

pa -

riet

alB

Arm

2:

plac

ebo,

2x/

d, to

pica

l 20

.6 (

13.4

%)

49

Lucky

2004

381

fem

ale

48w

Arm

1: m

inox

idil

5%so

luti

on, 2

x/d,

topi

cal

phototrichogram

24.5

(17

.3%

)p

< 0.

001

vs. P

lace

bo,

p =

0.12

9 vs

. Arm

2fr

onto

-/o

ccip

itop

a-ri

etal

A2

Arm

2: m

inox

idil

2%so

luti

on, 2

x/d,

topi

cal

20.7

(13

.8%

)p

< 0.

001

vs. P

lace

bo

Arm

3:

plac

ebo,

2x/

d, to

pica

l 9.

4 (6

.8%

)

Con

tinu

ed

Appendix 2 S35


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

and

Fin

aste

rid

e an

d O

ther

Th

erap

ies.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

14

Arca

2004

65m

ale

12m

(52w

)

Arm

1: m

inox

idil

5%

solu

tion

, 2x/

d, to

pica

l

7-point-ratingscale

80%

fron

tal/

parie

tal

BA

rm2:

fina

ster

ide

1mg,

1x/d

, ora

l52

%

42

Saraswat

2003

99m

ale

12m

Arm

1: fi

nast

erid

e 1

mg,

1x/d

, ora

l

manual hair count

36.1

(29

.1%

)p

= 0.

003

vs.

Min

oxid

il

62%

p =

0.19

vs. A

rm2

bald

are

aB

Arm

2: m

inox

idil

2%

solu

tion

, 2x/

d, to

pica

l19

.6 (

14.8

%)

56%

16

Berger

2003

200

mal

e26

w

Arm

1: m

inox

idil

5% s

o-lu

tion

, 2x/

d, to

pica

l +py

rith

ione

zin

c 1%

sham

poo,

1x/

d, to

pica

l

phototrichogram

6,2

vert

exA

2

Arm

2: m

inox

idil

5%

solu

tion

, 2x/

d, to

pica

l +pl

aceb

o sh

ampo

o, 1

x/d,

topi

cal

12,3

Arm

3: p

yrit

hion

e zi

nc1%

sha

mpo

o, 1

x/d,

to

pica

l5,

7

Arm

4: p

lace

bosh

ampo

o, 1

x/d,

topi

cal

-0.6

Con

tinu

ed

S36 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

and

Oth

er T

her

apie

s.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

38

Reygagne

1997

72m

ale

6m

Arm

1: m

inox

idil

2%

solu

tion

, 2x/

d, to

pica

l

phototrichogram

6.8

(11.

0%)

p <

0.00

1 vs

.A

rm2

anag

en:

4.5

(9.8

%)

p =

0.06

vs.

Arm

2

vert

exB

Arm

2: m

axile

ne lo

tion

(gly

cero

l oxy

este

rs a

ndor

gani

c si

liciu

m),

1x/

d,to

pica

l

-3.0

(-4

.8%

) -1

.8 (

-3.7

%)

44

Shin

2007

31m

ale

18w

Arm

1: m

inox

idil

5%

solu

tion

, 2x/

d, to

pica

l

phototrichogram

15.9

(12

.8%

)p

< 0.

05 v

s.

Bas

elin

e

14.0

(41

.9%

)p

< 0.

05 v

s.

Bas

elin

e

anag

en r

atio

-0

.014

(-2

.5%

)n.

s. v

s. B

asel

ine

hair

dia

met

er:

m2.

6 (7

.5%

)p

< 0.

05 v

s.B

asel

ine

tran

siti

o-na

l zon

eto

bald

ing

area

A2

Arm

2: m

inox

idil

5% +

tret

inoi

n 0.

01%

solu

tion

, 1x/

d, to

pica

l,m

orni

ng p

lace

bo

solu

tion

, 1x/

d, to

pica

l,ev

enin

g

18.2

(14

.7%

)p

< 0.

05 v

s.

Bas

elin

e,n.

s. v

s. A

rm1

6.1

(14.

3%)

p <

0.05

vs.

B

asel

ine,

n.s.

vs.

Arm

1

-0.0

33 (

-6.0

%)

n.s.

vs.

Bas

elin

e

1.9

(5.3

%)

n.s.

vs.

B

asel

ine

15

Bazzano

1996

56fe

mal

ean

dm

ale

12m

Arm

1:

plac

ebo,

2x/

d, to

pica

l

manual hair count

0%

bald

are

aB

Arm

2: m

inox

idil

0.5%

,2x

/d, t

opic

al0%

Arm

3: tr

etin

oin

0.02

5%so

luti

on 2

x/d,

topi

cal

58%

Arm

4: m

inox

idil

0.5%

+Tr

etin

oin

0.02

5%

solu

tion

, 2x/

d, to

pica

l66

%

Con

tinu

ed

Appendix 2 S37


Tab

le 3

:Li

tera

ture

Tab

le. M

inox

idil

and

Ho

rmo

nes

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

46

Blume-Peytavi

2007

103

fem

ale

6m,

12m

Arm

1: m

inox

idil

2%

solu

tion

, 2x/

d, to

pica

l

TrichoScan

6m: 1

5.3

(8.7

%)

p =

0.00

25 v

s.

Bas

elin

e,p

< 0.

0005

vs.

Arm

212

m: 1

7.3

(9.9

%)

n.s.

vs.

6m

hair

thi

ckne

ss(m

m/c

m2 )

6m: 1

.8p

< 0.

0001

vs.

Bas

elin

e12

m: 2

.1ce

ntro

-pa

riet

alB

Arm

2: 0

-6m

: alfa

trad

iol

0.02

5% s

olut

ion,

1x/

d,to

pica

l, 7-

12m

: min

oxi-

dil 2

% s

olut

ion,

2x/

d,to

pica

l

6m: -

7.8

(-4.

3%)

n.s.

vs.

Bas

elin

e12

m: 9

.8 (

5.4%

)p

< 0.

0001

vs.

6m

6m: -

0.5

n.s.

vs.

Bas

elin

e12

m: 0

.4

52

Vexiau

2002

66fe

mal

e6m

,12

m

Arm

1: m

inox

idil

2%

solu

tion

, 2x/

d, to

pica

l +or

al c

ontr

acep

tive

(eth

inyl

oes

trad

iol 3

0 µg

and

gest

oden

e 75

µg)

,1x

/d, 2

1 of

28

days

, ora

l

phototrichogram

6m: 1

6.1

(8.6

%)

12m

: 16.

9 (9

.1%

)p

< 0.

001

vs. B

ase-

line

and

Arm

2

6m: 1

4.0

p =

0.00

3 vs

.B

asel

ine,

p <

0.00

1 vs

.A

rm2

12m

: 14.

9

anag

en:

(hai

rs/c

m2 )

25p

< 0.

001

vs.

Arm

2

fron

to-

pari

etal

BA

rm2:

cyp

rote

rone

ac

etat

e 50

mg,

1x/

d,

20 o

f 28

days

, ora

l + o

ral

cont

race

ptiv

e (e

thin

yl e

stra

diol

35

µgan

d cy

prot

eron

e ac

etat

e2

mg)

, 1x/

d, 2

1 of

28

day

s, o

ral

6m: -

2.8

(-1.

4%)

12m

: -7.

8 (-

3.9%

)p

= 0.

85 v

s.

Bas

elin

e

6m: -

6.0

n.s.

vs.

Bas

elin

e12

m: 5

.9-5

.6

Con

tinu

ed

S38 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. F

inas

teri

de.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

Fina

ster

ide

66

Trüeb

2001

265

mal

e6m

Arm

1: fi

nast

erid

e 1

mg,

1x/

d, o

ral

n.a.

39.9

%C

Fina

ster

ide

vs. P

lace

bo

65

Stough

2002

18m

ale

1y

Arm

1: fi

nast

erid

e1m

g, 1

x/d,

ora

l

phototrichogram

16 (

9.8%

)p

< 0.

05 v

s.

plac

ebo

44%

p <

0.01

vs.

plac

ebo

vert

exA

2

Arm

2: p

lace

bo,

1x/d

, ora

l-4

(-2

.5%

) 11

%

67

van Neste

2000

212

mal

e48

w

Arm

1: fi

nast

erid

e 1

mg,

dai

ly, o

ral

phototrichogram

7.2

(3.6

%)

p <

0.00

1 vs

. pl

aceb

o

anag

en,

hair

s/cm

2(%

):18

(14

.5%

)p

< 0.

001

vs. p

lace

bove

rtex

A2

Arm

2: p

lace

bo,

daily

, ora

l -1

0.1

(-5.

2%)

anag

en,

hair

s/cm

2(%

):-9

.0 (

-7.6

%)

58

Kawashima

2004

414

mal

e48

w

Arm

1: fi

nast

erid

e 1

mg,

1x/

d, o

ral

impr

oved

: 58%

p <

0.00

1 vs

. pla

cebo

unch

ange

d: 4

0%

vert

exA

2A

rm2:

fina

ster

ide

0.2

mg,

1x/

d, o

ral

impr

oved

: 54%

p <

0.00

1 vs

. pla

cebo

unch

ange

d: 4

1%

Arm

3: p

lace

bo,

1x/d

, ora

l im

prov

ed: 6

%un

chan

ged:

72%

Con

tinu

ed

Appendix 2 S39


Tab

le 3

:Li

tera

ture

Tab

le. F

inas

teri

de

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

57

Kaufman

1998

1553

mal

e12

m

Arm

1:b

finas

teri

de

1 m

g, 1

x/d,

ora

l

phototrichogram

16.9

(11

.0%

)p

< 0.

001

vs. p

lace

bo

48%

(12

m)

66%

(24

m)

p <

0.00

1(1

2m)

vs. p

lace

bo

vert

exA

2

Arm

2: p

lace

bo 1

x/d,

oral

-4

.1 (

-2.7

%)

7% (

12m

)7%

(24

m)

Arm

3: 1

sty

finas

teri

de1m

g, 1

x/d,

ora

l,2nd

y pl

aceb

o, 1

x/d,

ora

l

Arm

4: 1

sty

plac

ebo,

1x/d

, ora

l, 2nd

y fin

aste

-ri

de 1

mg,

1x/

d, o

ral

64

Roberts

1999

693

mal

e6m

,12

m

Arm

1: fi

nast

erid

e 5m

g,1x

/d, o

ral

phototrichogram

6m: 1

2.9

(7.7

%)

12m

: 18.

2 (1

0.8%

)p

< 0.

001

(6,1

2m)

vs.

base

line

and

plac

ebo

51%

(6m

)48

% (

12m

)p

< 0.

001

vs. p

lace

bo

vert

exA

2

Arm

2: p

lace

bo, 1

x/d,

oral

6m: -

3.9

(-2.

1%)

12m

: -3.

9 (-

2.1)

10%

(6m

)3%

(12

m)

Arm

3: fi

nast

erid

e 1

mg,

1x/d

, ora

l

6m: 1

3.5

(7.3

%)

12m

: 16.

7 (9

.0%

)p

< 0.

001

(6,1

2m)

vs.

base

line

and

plac

ebo

52%

(6m

)54

% (

12m

)p

< 0.

001

vs. p

lace

bo

Arm

4: fi

nast

erid

e 0.

2m

g, 1

x/d,

ora

l

6m: 1

0.8

(6.1

%)

12m

: 12.

7 (7

.2%

)p

< 0.

001

(6,1

2m)

vs.

base

line

and

plac

ebo

38%

(6m

)38

% (

12m

)p

< 0.

001

vs. p

lace

bo

Arm

5: fi

nast

erid

e 0.

01m

g, 1

x/d,

ora

l6m

: -1.

8 (-

1.0%

)12

m: -

3.5

(-2.

0 %

)12

% (

6m)

10%

(12

m)

Con

tinu

ed

S40 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. F

inas

teri

de

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

69

Whiting

2003

424

mal

e2y

Arm

1: fi

nast

erid

e 1

mg,

1x/

d, o

ral

impr

oved

: 39%

p <

0.00

1 vs

. pla

cebo

unch

ange

d: 5

5%ve

rtex

A2

Arm

2: p

lace

bo, 1

x/d,

oral

impr

oved

: 4%

unch

ange

d: 7

3%

71

The Finasteride Male Pattern Hair Loss Study Group

2002

1553

mal

e24

m,

60m

Arm

1: fi

nast

erid

e1m

g, 1

x/d,

ora

l

phototrichogram

7.5

(4.3

%)

p <

0.00

1 vs

. ba

selin

e an

d pl

aceb

o

impr

oved

: 48%

p <

0.00

1 vs

. pla

cebo

unch

ange

d: 4

2%p

< 0.

001

vs. p

lace

bo

vert

exA

2

Arm

2: p

lace

bo, 1

x/d,

oral

-46.

9 (-

26.5

%)

p <

0.00

1 vs

. bas

elin

eim

prov

ed: 6

%un

chan

ged:

19%

Arm

3: 1

sty

finas

teri

de 1

mg,

1x/

d,or

al, 2

ndy

plac

ebo,

1x/d

, ora

l, 3rd

y-5th

yfin

aste

ride

1 m

g,1x

/d, o

ral

Arm

4: 1

sty

plac

ebo,

1x/d

ora

l, 2nd

y-5th

yfin

aste

ride

1 m

g,1x

/d,

oral

Con

tinu

ed

Appendix 2 S41


Tab

le 3

:Li

tera

ture

Tab

le. F

inas

teri

de

con

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

62

Price

2002

66m

ale

48w

,96

w

Arm

1: fi

nast

erid

e 1

mg,

1x/

d, o

ral

manual hair count

48w

: 12.

4%96

w: 9

.1%

p <

0.00

1 (4

8, 9

6w)

vs. b

asel

ine

p <

0.01

(48

w),

p <

0.00

1 (9

6w)

vs. p

lace

bo

hair

wei

ght:

48w

: 20.

4%96

w: 2

1.5%

p <

0.00

1(4

8w, 9

6w)

vs. p

lace

bofr

onto

-pa

riet

alA

2

Arm

2: p

lace

bo, 1

x/d,

oral

48w

: 3.2

%96

w: -

6.3%

p =

0.11

(48

w)

p <

0.05

(96

w)

hair

wei

ght:

48w

: -5.

2%96

w: -

14.2

%

60

Leyden

1999

326

mal

e6m

,12

m,

24m

Arm

1: fi

nast

erid

e 1

mg,

1x/

d, o

ral

phototrichogram

6m: 7

.0 (

3.3%

)12

m: 9

.6 (

4.6%

)24

m: 1

3.0

(6.2

%)

p <

0.00

1 vs

. pla

cebo

impr

oved

: 37%

p <

0.00

1 vs

. pl

aceb

oun

chan

ged:

62%

fron

tal/

cent

ro-

pari

etal

A2

Arm

2: p

lace

bo, 1

x/d,

oral

, 2nd

y fin

aste

ride

1 m

g, 1

x/d,

ora

l

6m: -

4.0

(-1.

8%)

12m

: -2.

0 (-

0.9%

)24

m: 8

.0 (

3.7%

)

impr

oved

: 7%

unch

ange

d: 8

6%

72

Brenner

1999

28m

ale

6m,

12m

,24

m

Arm

1: fi

nast

erid

e 5

mg,

1x/

d, o

ral

manual hair count

6m: 6

.4 1

2m: 1

6.7

24m

: 34.

6p

< 0.

05 (

6,12

,24m

)vs

. bas

elin

ep

< 0.

01 (

12,2

4m)

vs. p

lace

boba

ld a

rea

B

Arm

2: p

lace

bo, 1

x/d,

oral

6m: -

2.6

12m

: -1.

324

m: -

14.1

Con

tinu

ed

S42 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. F

inas

teri

de

and

Oth

er T

her

apie

s.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

63

Price

2006

28m

ale

36m

(144

w),

48m

(192

w)

Arm

1: fi

nast

erid

e 1

mg,

1x/d

, ora

l

manual hair count

36m

: 8.5

%48

m: 7

.2%

p =

0.11

9 (3

6m)

vs. p

lace

bop

< 0.

05 (

48m

) vs

. pla

cebo

wei

ght

(%)

36m

: 19.

5%48

m: 2

1.6%

p <

0.00

1(3

6m, 4

8m)

vs. p

lace

bo

fron

to-

pari

etal

A2

Arm

2: p

lace

bo, 1

x/d,

oral

36m

: -1.

6%48

m: -

13.0

%

wei

ght

(%)

36m

: -14

.8%

48m

: -24

.5%

Fina

ster

ide

vs. O

ther

The

rapi

es

14

Arca

2004

65m

ale

12m

(52w

)

Arm

1: m

inox

idil

5%

solu

tion

, 2x/

d, to

pica

l80

%

fron

tal/

parie

tal

B

Arm

2: fi

nast

erid

e 1m

g,1x

/d, o

ral

52%

42

Saraswat

2003

99m

ale

12m

Arm

1: fi

nast

erid

e 1

mg,

1x/d

, ora

l

manual hair count

36.1

(29

.1%

)p

= 0.

003

vs.

min

oxid

il

62%

p =

0.19

vs.

Arm

2ba

ld a

rea

B

Arm

2: m

inox

idil

2%

solu

tion

, 2x/

d, to

pica

l19

.6 (

14.8

%)

56%

Con

tinu

ed

Appendix 2 S43


Tab

le 3

:Li

tera

ture

Tab

le. F

inas

teri

de

and

Oth

er T

her

apie

s/C

om

bin

atio

n T

her

apie

s.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

59

Khandpur

2002

100

mal

e12

m

Arm

1: fi

nast

erid

e 1

mg,

1x/d

, ora

l

87%

p <

0.03

vs. A

rm2

p <

0.00

1vs

. Arm

3p

= 0.

3vs

. Arm

4

B

Arm

2: fi

nast

erid

e 1

mg,

1x/d

, ora

l + m

inox

idil

2% s

olut

ion,

2x/

d,

topi

cal

100%

p <

0.00

1vs

. Arm

3p

= 1

vs. A

rm4

Arm

3: m

inox

idil

2%

solu

tion

, 2x/

d, to

pica

l

42%

p <

0.00

14vs

. Arm

4

Arm

4: fi

nast

erid

e 1

mg,

1x/d

, ora

l +ke

toco

nazo

le 2

%

sham

poo,

3x/

w, t

opic

al

100%

Com

bina

tion

The

rapi

es

70

Leavitt

2005

79m

ale

12m

Arm

1: h

airt

rans

plan

ta-

tion

+ fi

nast

erid

e 1m

g,1x

/d, o

ral

macrophotograph

18.5

(12

.6%

)p

= 0.

019

(Arm

1 vs

. Arm

2)fr

onta

lA

2A

rm2:

ha

irtr

ansp

lant

atio

n +

plac

ebo,

1x/

d, o

ral

-13.

5 (-

8.9%

)

Con

tinu

ed

S44 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. F

inas

teri

de

in F

emal

e Pa

tien

ts.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

Fina

ster

ide

–Fe

mal

e Pa

tien

ts

68

Whiting

1999

163

fem

ale

and

mal

e12

m

Arm

1: fi

nast

erid

e 1m

g,1x

/d, o

ral,

mal

e

biopsy

17.7

(5.

5%)

41.5

(34.

8%)

vert

exm

en,

fron

tal/

pari

etal

wom

en

B

Arm

2: p

lace

bo, 1

x/d,

oral

, mal

e -0

.8 (

-0.3

%)

7.7

(5.8

%)

Arm

3: fi

nast

erid

e 1m

g,1x

/d, o

ral,

fem

ale

-14.

6 (-

5.9%

) 1.

5 (1

.0%

)

Arm

4: p

lace

bo, 1

x/d,

oral

, fem

ale

0.0

(0.0

%)

8.5

(5.3

%)

74

Price

2000

137

fem

ale

1y

Arm

1: fi

nast

erid

e 1

mg,

1x/d

, ora

l

phototrichogram

-8.7

(-5

.8%

)p

< 0.

01 v

s.

base

line

n.s.

vs.

pla

cebo

A/T

rat

io1.

8 (2

9.5%

)

impr

oved

:11

%un

chan

ged:

77%

fron

tal/

pari

etal

A2

Arm

2: p

lace

bo, 1

x/d,

oral

-6.6

(-4

.0%

)p

< 0.

05 v

s.

base

line

A/T

rat

io1.

7 (2

9.8%

)

impr

oved

:16

%un

chan

ged:

77%

Con

tinu

ed

Appendix 2 S45


Tab

le 3

:Li

tera

ture

Tab

le. D

uta

ster

ide

and

Fin

aste

rid

e.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

Dut

aste

ride

73

Stough

2007

34m

ale

6m,

12m

Arm

1: d

utas

teri

de

0.5

mg,

1x/

d, o

ral

phototrichogram

6m: 6

.812

m: 1

6.5

sign

ifica

nt (

6m)

vs. p

lace

bop

= 0.

14 (

12m

) vs

. pla

cebo

vert

exA

2

Arm

2: p

lace

bo, 1

x/d,

oral

6m: -

11.0

12m

: -3.

8

61

Olsen

2006

416

mal

e24

w

Arm

1: d

utas

teri

de 0

.1m

g, 1

x/d,

ora

l

phototrichogram

15.4

(8.

7%)

p <

0.00

1 vs

. pla

-ce

bo39

%

vert

exA

2

Arm

2: d

utas

teri

de

0.5

mg,

1x/

d, o

ral

18.6

(10

.2%

)p

< 0.

001

vs.

plac

ebo

63%

p =

0.02

6 vs

.A

rm 4

Arm

3: d

utas

teri

de

2.5

mg,

1x/

d, o

ral

21.5

(11

.3%

)p

< 0.

001

vs.

plac

ebo

78%

p <

0.00

1 vs

.A

rm4

Arm

4: fi

nast

erid

e 5

mg,

1x/

d, o

ral

14.8

(8.

4%)

p <

0.00

1 vs

. pla

-ce

bop

= 0.

009

vs. A

rm3

57%

Arm

5: p

lace

bo, 1

x/d,

oral

-6

.3 (

-3.5

%)

2%

Con

tinu

ed

S46 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. H

orm

on

es O

ral.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

Hor

mon

es O

ral

81

Peereboom-Wynia

1989

30fe

mal

e12

m

Arm

1: e

thin

yl o

estr

adio

l50

m +

CPA

2 m

g 1x

/d,

oral

, day

5-2

7 of

men

-st

rual

cyc

le, C

PA 2

0 m

g,1x

/d, o

ral d

ay 5

-20

ofm

enst

rual

cyc

le

trichogram

anag

en /

te

loge

n ra

tio

2.8

(164

.7%

)ce

ntro

-pa

riet

alB

Arm

2:

no tr

eatm

ent

-1.2

(-

50%

)

52

Vexiau

2002

66fe

mal

e6m

,12

m

Arm

1: m

inox

idil

2%

solu

tion

, 2x/

d, to

pica

l +or

al c

ontr

acep

tive

(eth

inyl

oes

trad

iol 3

0 µg

and

gest

oden

e 75

µg)

,1x

/d, 2

1 of

28

days

, ora

l

phototrichogram

6m: 1

6.1

(8.6

%)

12m

: 16.

9 (9

.1%

)p

< 0.

001

(12m

) vs

.B

asel

ine

and

Arm

2

anag

en(h

airs

/cm

2 ) 25

p <

0.00

1 vs

.A

rm2

fron

to-

pari

etal

BA

rm2:

cy

prot

eron

e ac

etat

e 50

mg,

1x/

d, 2

0 of

28

day

s, o

ral +

ora

l co

ntra

cept

ive

(eth

inyl

estr

adio

l 35

µg a

nd

cypr

oter

one

acet

ate

2 m

g), 1

x/d,

21

of

28 d

ays,

ora

l

6m: -

2.8

(-1.

4%)

12m

: -7.

8 (-

3.9%

)p

0 0.

85 (

12m

) vs

.B

asel

ine

-5.6

Con

tinu

ed

Appendix 2 S47


Tab

le 3

:Li

tera

ture

Tab

le. H

orm

on

es T

op

ical

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

Hor

mon

es T

opic

al

77

Gassmueller

2008

172

mal

ean

dfe

mal

e16

w

Arm

1: F

ulve

stra

nt

70 m

g/m

l, 2x

/d,

topi

cal,

men

TrichoScan

8.2

(4.4

%)

p 0

0.81

5 vs

.Pl

aceb

op

< 0.

001

vs.

Min

oxid

il

hair

thi

ckne

ssm

m/c

m2

0.84

(5.

4%)

p =

0.96

8 vs

. Pla

cebo

p <

0.00

1 vs

. Min

oxid

il

vert

exA

2

Arm

2: p

lace

bo, 2

x/d,

to

pica

l, m

en

8.0

(4.4

%)

0.7

(4.4

%)

Arm

3: m

inox

idil

2%

solu

tion

, 2x/

d,

topi

cal,

men

25

.4 (

13.3

%)

2.9

(17.

3%)

Arm

4: fu

lves

tran

t 70

mg/

ml,

2x/d

, to

pica

l, w

omen

14.7

(6.

9%)

p 0

0.34

0 vs

. Pl

aceb

o

1.54

(7.

2%)

p =

0.22

7

Arm

5: p

lace

bo, 2

x/d,

to

pica

l, w

omen

15

.3 (

7.9%

) 1.

58 (

8.1%

)

46

Blume-Peytavi

2007

103

fem

ale

6m,

12m

Arm

1: m

inox

idil

2%

solu

tion

, 2x/

d, to

pica

l

TrichoScan

6m: 1

5.3

(8.

7%)

p =

0.00

25 v

s.

Bas

elin

ep

< 0.

0005

vs.

Arm

212

m: 1

7.3

(9.9

%)

6m: 1

4.0

p =

0.00

3 vs

.B

asel

ine

12m

: 14.

9p

< 0.

001

vs.

Arm

2

hair

thi

ckne

ssm

m/c

m2

6m: 1

.8p

< 0.

0001

vs. B

asel

ine

12m

: 2.1

cent

ro-

pari

etal

BA

rm 2

: 0-6

m: a

lfatr

a-di

ol 0

.025

% s

olut

ion,

1x/d

, top

ical

, 7-1

2m:

min

oxid

il 2%

sol

utio

n,2x

/d, t

opic

al

6m: -

7.8

(-4.

3%)

n.s.

vs.

Bas

elin

e12

m: 9

.8 (

5.4%

)p

< 0.

0001

vs.

6m

6m: -

6.0

n.s.

vs.

Bas

e-lin

e12

m: 5

.9

6m: -

0.5

n.s.

vs.

Bas

elin

e12

m: 0

.4

Con

tinu

ed

S48 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. H

orm

on

es T

op

ical

co

nti

nu

ed.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

82

Georgala

2004

75fe

mal

e12

-24

w

Arm

1: A

lfatr

adio

l lot

ion

0.03

%, 1

x/d,

topi

cal,

12w

trichogram

A/T

rat

io 0

.65

(38.

7%)

p <

0.01

vs.

Pl

aceb

o,n.

s. v

s. A

rm2

bald

are

aB

Arm

2: A

lfatr

adio

l lot

ion

0.03

%, 1

x/d,

topi

cal,

24w

0.7

(44.

6%)

p <

0.01

vs.

Pla

-ce

bo

Arm

3: p

lace

bo lo

tion

,1x

/d, t

opic

al, 2

4w-0

.06

(-3.

9%)

80

Wozel

2005

233

fem

ale

and

mal

e30

w

Arm

1: a

lfatr

adio

l0.

025%

sol

utio

n, 1

x/d,

topi

cal,

men

trichogram

telo

gen

rate

-6.7

(-2

1.1%

)

fron

tal

CA

rm2:

alfa

trad

iol

0.02

5% s

olut

ion,

1x/

d,to

pica

l, w

omen

-5.8

(-2

4.4%

)

78

Orfanos

1980

69fe

mal

ean

dm

ale

6m

Arm

1: A

lfatr

adio

l0.

025%

sol

utio

n, 1

x/d,

topi

cal

trichogram

%im

prov

emen

tfr

om b

asel

ine

telo

gen

rate

****

63%

tria

ngu-

lar

B

Arm

2: p

lace

bo, 1

x/d,

to

pica

l 37

%

Con

tinu

ed

Appendix 2 S49


Tab

le 3

:Li

tera

ture

Tab

le. H

orm

on

es T

op

ical

co

nti

nu

ed/S

urg

ery.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

79

Wüstner

1974

50fe

mal

ean

dm

ale

6mes

trog

en a

ndco

rtic

oid,

1x/d

, top

ical

trichogram

52%

%im

prov

emen

tfr

om b

asel

ine

telo

gen

rate

****

52%

trian

gular

/pa

riet

alC

76

Sovak

2002

43m

ale

3m,

9m

Arm

1: fl

urid

il, 1

x/d,

topi

cal

phototrichogram

anag

en h

airs

/cm

2

3m: 9

.3 (

13.5

%)

9m: 1

0.6

(15.

5%)

B

Arm

2: p

lace

bo, 1

x/d,

topi

cal

3m: 6

.5 (

10.1

%)

9m:1

3.1

(20.

5%)

Surg

ery

84

Uebel

2006

20m

ale

7m

Arm

1: fo

llicu

lar

unit

tran

spla

ntat

ion

manual hair count

folli

cula

r un

its

(%)

‘-40

(-2

8.2%

)p

< 0.

001

(Arm

1 vs

. Arm

2)

pari

etal

CA

rm2:

folli

cula

r un

ittr

ansp

lant

atio

n +

plat

elet

pla

sma

grow

thfa

ctor

add

ed b

efor

eim

plan

tati

on

folli

cula

r un

its

(%)

‘-25

(-1

7.6%

)

70

Leavitt

2005

79m

ale

12m

Arm

1: h

airt

rans

plan

-ta

tion

+ fi

nast

erid

e1m

g, 1

x/d,

ora

l

macrophotograph

18.5

(12

.6%

)p

= 0.

019

(Arm

1 vs

. Arm

2)

impr

oved

: 94%

unch

ange

d: 6

%

fron

tal

A2

Arm

2:

hair

tran

spla

ntat

ion

+pl

aceb

o, 1

x/d,

ora

l-1

3.5

(-8.

9%)

impr

oved

: 67%

unch

ange

d: 3

0%

Con

tinu

ed

S50 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. S

urg

ery/

Mis

cella

neo

us

Ora

l.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

83

Bernstein

1998

41m

ale

Arm

1: fo

llicu

lar

unit

tran

spla

ntat

ion,

pre

-pa

rati

on b

y di

ssec

ting

mic

rosc

ope

mea

n ha

irs/

folli

cula

r un

it

2,28

pari

etal

BA

rm2:

folli

cula

r un

ittr

ansp

lant

atio

n,

prep

arat

ion

bym

agni

fyin

g lo

upe

wit

htr

ansi

llum

inat

ion

mea

n ha

irs/

folli

cula

r un

it2,

14

Mis

cella

neou

s O

ral

89

Prager

2002

26m

ale

18–

24w

Arm

1: a

ctiv

e or

al

soft

gel s

uppl

emen

t (ß

-sit

oste

rol 5

0 m

g +

saw

pal

met

to e

xtra

ct20

0 m

g, le

cith

in

50 m

g, in

isot

ol 1

00m

g, p

hosp

hati

dyl

chol

ine

25 m

g, n

iaci

n15

mg,

bio

tin

100

g),

2x/d

, ora

l

7-point-rating scale

60%

B

Arm

2: s

oftg

el p

lace

bo,

2x/d

, ora

l11

%

91

Lassus

1992

40m

ale

6m

Arm

1: v

ivis

cal

(mar

ine

extr

acts

and

silic

ea c

ompo

nent

),2x

/d, o

ral

manual hair count

4.8

(38.

1 %

)p

< 0.

001

vs.

Arm

2ba

ld a

rea

A2

Arm

2: fi

sh e

xtra

ct,

2x/d

, ora

l 0.

3 (2

.1%

)

Con

tinu

ed

Appendix 2 S51


Tab

le 3

:Li

tera

ture

Tab

le. M

isce

llan

eou

s To

pic

al.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

Mis

cella

neou

s To

pica

l

90

Kamimura

2000

30m

ale

6m

Arm

1: p

rocy

anid

in1%

sol

utio

n, 2

x/d,

to-

pica

l

phototrichogram

26,7

p <

0.00

5 vs

. Pla

-ce

bo

8.0

p <

0.02

vs.

Plac

ebo

vert

exB

Arm

2: p

lace

bo, 2

x/d,

topi

cal

0,3

-3.3

88

Draelos

2005

60fe

mal

e6m

Arm

1:

Nia

cin

deri

vate

s (o

ctyl

nic

otin

ate

0.5%

and

myr

isty

lni

coti

nate

5.0

%),

1x/d

, top

ical

7-point-rating scale

69%

p =

0.04

vs.

Plac

ebo

vert

exA

2

Arm

2: p

lace

bo, 6

drop

s, 1

x/d,

topi

cal

33%

94

Kessels

1991

396

mal

e6m

Arm

1: h

erba

l pre

para

-ti

on, 2

x/d,

topi

cal

manual hair count

26,6

p =

0.02

vs.

Plac

ebo

bald

are

aA

2

Arm

2: p

lace

bo, 2

x/d,

topi

cal

21,8

Con

tinu

ed

S52 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. M

isce

llan

eou

s To

pic

al c

on

tin

ued

.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

Mis

cella

neou

s To

pica

l

93

Greenberg

1996

24m

ale

40w

Arm

1: h

erba

l ext

ract

crea

m (

7.5%

ext

ract

of fe

nnel

, pol

ygon

um,

men

tha,

cha

mom

ile,

thuj

a, h

ibis

cus)

, 1x/

d,to

pica

l

manual hair count

77,4

%p

= 0.

003

vs.

Plac

ebo

169.

4%p

= 0.

01 v

s.Pl

aceb

otr

iang

u-la

rB

Arm

2: p

lace

bo c

ream

1x/d

, top

ical

3%

33.9

%

104

Olsen

1990

72m

ale

6m

Arm

1:

vipr

osto

l sol

utio

n 12

0 µg

, 2x/

d,

topi

cal

phototrichogram

-3.9

(-4

.0%

)n.

s. v

s.A

rm2/

3

vert

exA

2A

rm2:

veh

icle

, 2x/

d,to

pica

l

-9.1

(-9

.5%

)n.

s. v

s.A

rm1/

3

Arm

3: p

lace

bo, 2

x/d,

topi

cal

-3.1

(-3

.3%

)

38

Reygagne

1997

72m

ale

6m

Arm

1: m

inox

idil

2%so

luti

on, 2

x/d,

topi

cal

phototrichogram

6.8

(11.

0%)

p <

0.00

1 vs

.A

rm2

anag

en (

hair

s/cm

2 )4.

5 (9

.8%

)p

= 0.

06 v

s. A

rm2

vert

exB

Arm

2: m

axile

ne lo

tion

(gly

cero

l oxy

este

rs a

ndor

gani

c si

liciu

m),

1x/d

, top

ical

-3.0

(-4

.8%

) -1

.8 (

-3.7

%)

Con

tinu

ed

Appendix 2 S53


Tab

le 3

:Li

tera

ture

Tab

le. M

isce

llan

eou

s To

pic

al c

on

tin

ued

/Co

mb

inat

ion

Th

erap

ies.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

103

Groveman

1985

174

mal

e 16

w

Arm

1:

poly

sorb

ate

60 2

5%lo

tion

, 2x/

d, to

pica

l2,

6%**

full

view

A2

Arm

2: p

lace

bo, 2

x/d,

topi

cal

4,7%

**

86

Gehring

2000

40fe

mal

e6m

Arm

1: m

illet

see

d ex

trac

t, L-

cyst

eine

and

calc

ium

pan

toth

enat

e,2x

/d, o

ral

phototrichogram

anag

en r

ate

12.1

(16

.0%

)p

= 0.

0225

vs.

Pl

aceb

oce

ntro

-pa

riet

alB

Arm

2: p

lace

bo, 2

x/d,

oral

8.

4 (1

1.3%

)

Com

bina

tion

The

rapi

es

92

Lassus

1994

30m

ale

8m

Arm

1: v

ivis

cal

(pol

ysac

char

ides

and

salt)

, 2x/

d 80

kg,

3x/

d>

80 k

g, o

ral +

viv

isca

lsh

ampo

o 2-

3x/w

93.3

%B

Con

tinu

ed

S54 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. M

isce

llan

eou

s To

pic

al/C

om

bin

atio

n T

her

apie

s.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

16

Berger

2003

200

mal

e 26

w

Arm

1: m

inox

idil

5% s

olut

ion,

2x/d

, top

ical

+ p

yrit

hion

e zi

nc 1

%sh

ampo

o, 1

x/d,

topi

cal

phototrichogram

6,2

vert

exA

2

Arm

2: m

inox

idil

5% s

olut

ion,

2x/d

, top

ical

+ p

lace

bo s

ham

poo,

1x/d

, top

ical

12,3

Arm

3: p

yrit

hion

e zi

nc 1

%

sham

poo,

1x/

d, to

pica

l5,

7

Arm

4: p

lace

bo s

ham

poo,

1x/

d,

topi

cal

-0.6

15

Bazzano

1986

56fe

mal

ean

dm

ale

12m

Arm

1: p

lace

bo, 2

x/d,

topi

cal

manual hair count

% >

20%

in

crea

se f

rom

base

line

0%

bald

are

aB

Arm

2: m

inox

idil

0.5%

, 2x/

d,

topi

cal

0%

Arm

3: tr

etin

oin

0.02

5% s

olut

ion

2x/d

, top

ical

58%

Arm

4: m

inox

idil

0.5%

+ T

reti

noin

0.02

5% s

olut

ion,

2x/

d, to

pica

l66

%

Con

tinu

ed

Appendix 2 S55


Tab

le 3

:Li

tera

ture

Tab

le. M

isce

llan

eou

s To

pic

al/C

om

bin

atio

n T

her

apie

s.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

85

Morganti

1998

60fe

mal

ean

dm

ale

50w

Arm

1:

loti

on c

onta

inin

g sa

wpa

lmet

to e

xtra

ct,

2x/d

, top

ical

manual hair count

27%

p <

0.00

5 vs

. B

asel

ine

hair

wei

ght

32%

fron

tal/

pari

etal

B

Arm

2:

plac

ebo

loti

on, 2

x/d,

topi

cal

13%

7%

Arm

3:

diet

sup

plem

ent

cont

aini

ng l-

cist

in,

lmet

hion

in, C

u, Z

n,4x

/d, o

ral

29%

p <

0.00

5 vs

. B

asel

ine

42%

Arm

4:

plac

ebo

supp

lem

ent,

4x/d

, ora

l11

%

-8%

Arm

5: lo

tion

con

tai-

ning

saw

pal

met

to e

x-tr

act,

2x/d

, top

ical

+di

et s

uppl

emen

t con

-ta

inin

g l-

cist

in, l

me-

thio

nin,

Cu,

Zn,

4x/

d,or

al

38%

p <

0.00

5 vs

.A

rm1/

360

%

Con

tinu

ed

S56 Appendix 2


Tab

le 3

:Li

tera

ture

Tab

le. M

isce

llan

eou

s To

pic

al/C

om

bin

atio

n T

her

apie

s.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

Pul

sed

Ele

ctro

mag

neti

c Fi

eld

101

Policarpi

1993

30fe

mal

ean

dm

ale

18w

,36

w

Arm

1: p

ulse

del

ectr

osta

tic

field

, 1-2

sess

ions

per

wee

k

phototrichogram

anag

en:

18w

: 4.5

%36

w: 6

.2%

bald

are

aB

Arm

2: p

lace

bo

sess

ions

, 1-2

x/w

eek

18w

: 0.9

%36

w: 1

.0%

99

Maddin

1990

73m

ale

36w

Arm

1: p

ulse

del

ectr

osta

tic

field

,1x

/w, w

eek

1, 1

7, 3

32x

/w

manual hair count

11.8

(66.

1%)

p =

0.02

98vs

. Arm

2ve

rtex

A2

Arm

2: s

ham

trea

tmen

t, 1x

/w, w

eek

1, 1

7, 3

3 2x

/w5.

6 (2

5.6%

)

100

Maddin

1992

34m

ale

12w

,34

w

Arm

1: p

ulse

del

ectr

osta

tic

field

,1x

/w, p

retr

eatm

ent

36w

pul

sed

elec

tros

ta-

tic

field

manual hair count

12w

: 5.

9 (2

0.0%

)34

w:

24.7

(84

.0%

)

vert

exB

16w

,30

w

Arm

2: p

ulse

del

ectr

osta

tic

field

,1x

/w, p

retr

eatm

ent

36w

sha

m e

lect

rost

atic

field

16w

: -0

.8 (

-2.5

%)

30w

: 17

.5 (

55.6

%)

Con

tinu

ed

Appendix 2 S57


Tab

le 3

:Li

tera

ture

Tab

le. M

isce

llan

eou

s To

pic

al/C

om

bin

atio

n T

her

apie

s.

ArtNumber

Author

Year

Number of patients

Gender

Time of evaluation

Dosage

Method








weight / thickness



patient assessment


Degree of evidence

98

Bureau

2003

93fe

mal

ean

dm

ale

6m

Arm

1: h

erba

l sol

utio

n(p

imen

ta r

acem

osa,

myr

tus

com

mun

is, c

e-dr

us a

tlant

ica,

laur

usno

bilis

, pog

oste

mon

patc

houl

i, ro

smar

inus

offic

inal

is, s

alvi

a sc

la-

rae,

thym

us s

atur

eioi

-de

s, c

anan

ga o

dora

ta),

3x/w

, top

ical

+ p

ulse

del

ectr

omag

neti

c fie

ld3x

/w, t

opic

al

phototrichogram

34 (

22.4

%)

p =

0.00

3 vs

. B

asel

ine,

p =

0.01

vs.

Arm

2ba

ld a

rea

A2

Arm

2: p

lace

bo, 3

x/w

,to

pica

l + p

ulse

d el

ec-

trom

agne

tic

field

3x/w

, top

ical

9 (5

.5%

)n.

s. v

s. B

asel

ine

102

Satino

2003

35fe

mal

ean

dm

ale

6m

Arm

1:H

airM

ax L

aser

Com

b(l

ow le

vel l

aser

ther

apy)

,co

mb

hair

1x/

d 5-

10m

inut

esm

anua

l hai

r co

unt

manual hair count

14.1

(76

.2%

)n.

s. v

s. B

asel

ine

12.3

(60.

0%)

vert

ex/

tem

pora

lC

* bl

indi

ng ti

ll 12

m, a

fter

war

ds o

pen

stud

y de

sign

** m

ean

of 3

rev

iew

ers

***

inve

stig

ator

= o

utco

me

asse

ssor

Documents

Evidence‐based (S3) guideline for the treatment of androgenetic