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Editorial – referring to the article published on pp 595–604 of this issue The Metabolic Syndrome and Erectile Dysfunction: Multiple Vascular Risk Factors and Hypogonadism Graham Jackson Cardiothoracic Centre, St Thomas’ Hospital, London SE1 7EH, UK In this issue Corona and colleagues conclude that erectile dysfunction (ED) is more severe in patients with the metabolic syndrome and associated with an increased incidence of hypogonadism [1]. The findings have important lifestyle, prevention, and therapeutic implications. Unfortunately, the definition of the metabolic syndrome is not as precise as the name implies [2]. It is an umbrella term for a cluster of cardiovascular risk factors including type 2 diabetes, hyperlipidae- mia, abdominal obesity, and hypertension second- ary to ‘‘insulin resistance’’ and as a consequence, hyperinsulinaemia. Umbrellas protect us from the elements and there is a danger that in using a unifying label we may not address each element of risk optimally. The definition itself has been challenged by the American Diabetes Association and the European Association for the Study of Diabetes [2]. In a joint statement they conclude that ‘‘too much critically important information is miss- ing to warrant its designation as a ‘syndrome’.’’ They encourage the treatment of all cardiovascular risk factors irrespective of whether the ‘‘metabolic syndrome’’ has been diagnosed. Although the National Cholesterol Education Program’s Adult Treatment Panel (ATP III), World Health Organiza- tion (WHO), and International Diabetes Federation (IDF) offer different definitions, there are similarities we can extract for day-to-day practical use [3–5]. The first is central obesity with a waist-to-hip ratio >0.90 in men and >0.85 in women, which translates to a waist circumference in European men of 94 cm and 80 cm in women. In addition there should be any two of the following: raised triglyceride level >1.7 mmol/l, reduced high-density lipoprotein (HDL) cholesterol of <1.0 mmol/l in men and <1.3 mmol/l in women, blood pressure >130/ 85 mm Hg or treated blood pressure or raised fasting glucose 6.1 mmol/l (and possibly 5.6 mmol/l). Including diabetics and those with clinical cardio- vascular disease seems pointless because their risk status is known so that they add little to the understanding of risk for those otherwise having features of the ‘‘metabolic syndrome.’’ Therefore, however we view these varying definitions, what we are talking about is increased vascular risk and, in turn, reducing it. The best philosophy is never to view a single vascular risk factor in isolation. The patients in the study by Corona et al. had multiple risk factors with considerable central obesity. The questionnaire component reflecting the presence of organic ED showed a progressive increase as the number of metabolic syndrome components increased. In addition, there was a 3- fold increase in the prevalence of hypogonadism and as the number of criteria for the metabolic syndrome increased so did the incidence of hypo- gonadism. The major determinants of hypogonad- ism were abdominal obesity and hyperglycaemia, both of which have been previously connected [6,7]. Makhsida et al., reviewing the literature from 1988 to 2004, reported a strong association between hypo- gonadism and ‘‘metabolic syndrome’’ [8]. They speculated that testosterone therapy might have a european urology 50 (2006) 426–427 available at www.sciencedirect.com journal homepage: www.europeanurology.com DOI of original article: 10.1016/j.eururo.2006.02.053 E-mail address: [email protected]. 0302-2838/$ – see back matter # 2006 G. Jackson. Published by Elsevier B.V. on behalf of European Association of Urology. All rights reserved. doi:10.1016/j.eururo.2006.03.035

The Metabolic Syndrome and Erectile Dysfunction: Multiple Vascular Risk Factors and Hypogonadism

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Editorial – referring to the article published on pp 595–604 of this issue

The Metabolic Syndrome and Erectile Dysfunction: MultipleVascular Risk Factors and Hypogonadism

Graham Jackson

Cardiothoracic Centre, St Thomas’ Hospital, London SE1 7EH, UK

e u r o p e a n u r o l o g y 5 0 ( 2 0 0 6 ) 4 2 6 – 4 2 7

avai lable at www.sc iencedi rect .com

journal homepage: www.europeanurology.com

In this issue Corona and colleagues conclude thaterectile dysfunction (ED) is more severe in patientswith the metabolic syndrome and associated withan increased incidence of hypogonadism [1]. Thefindings have important lifestyle, prevention, andtherapeutic implications.

Unfortunately, the definition of the metabolicsyndrome is not as precise as the name implies [2]. Itis an umbrella term for a cluster of cardiovascularrisk factors including type 2 diabetes, hyperlipidae-mia, abdominal obesity, and hypertension second-ary to ‘‘insulin resistance’’ and as a consequence,hyperinsulinaemia. Umbrellas protect us from theelements and there is a danger that in using aunifying label we may not address each element ofrisk optimally. The definition itself has beenchallenged by the American Diabetes Associationand the European Association for the Study ofDiabetes [2]. In a joint statement they conclude that‘‘too much critically important information is miss-ing to warrant its designation as a ‘syndrome’.’’They encourage the treatment of all cardiovascularrisk factors irrespective of whether the ‘‘metabolicsyndrome’’ has been diagnosed. Although theNational Cholesterol Education Program’s AdultTreatment Panel (ATP III), World Health Organiza-tion (WHO), and International Diabetes Federation(IDF) offer different definitions, there are similaritieswe can extract for day-to-day practical use [3–5]. Thefirst is central obesity with a waist-to-hip ratio>0.90in men and >0.85 in women, which translates to awaist circumference in European men of �94 cm

DOI of original article: 10.1016/j.eururo.2006.02.053E-mail address: [email protected].

0302-2838/$ – see back matter # 2006 G. Jackson. Published by Elsevier B.V. on behalf of Eu

and �80 cm in women. In addition there should beany two of the following: raised triglyceride level>1.7 mmol/l, reduced high-density lipoprotein(HDL) cholesterol of <1.0 mmol/l in men and<1.3 mmol/l in women, blood pressure >130/85 mm Hg or treated blood pressure or raised fastingglucose �6.1 mmol/l (and possibly 5.6 mmol/l).Including diabetics and those with clinical cardio-vascular disease seems pointless because their riskstatus is known so that they add little to theunderstanding of risk for those otherwise havingfeatures of the ‘‘metabolic syndrome.’’ Therefore,however we view these varying definitions, what weare talking about is increased vascular risk and, inturn, reducing it. The best philosophy is never toview a single vascular risk factor in isolation.

The patients in the study by Corona et al. hadmultiple risk factors with considerable centralobesity. The questionnaire component reflectingthe presence of organic ED showed a progressiveincrease as the number of metabolic syndromecomponents increased. In addition, there was a 3-fold increase in the prevalence of hypogonadismand as the number of criteria for the metabolicsyndrome increased so did the incidence of hypo-gonadism. The major determinants of hypogonad-ism were abdominal obesity and hyperglycaemia,both of which have been previously connected [6,7].Makhsida et al., reviewing the literature from 1988 to2004, reported a strong association between hypo-gonadism and ‘‘metabolic syndrome’’ [8]. Theyspeculated that testosterone therapy might have a

ropean Association of Urology. All rights reserved. doi:10.1016/j.eururo.2006.03.035

e u r o p e a n u r o l o g y 5 0 ( 2 0 0 6 ) 4 2 6 – 4 2 7 427

role as a treatment option for the metabolicsyndrome though no studies have been done tosupport this idea. I think we need to walk before werun, but the idea is attractive and worthy of study.

In Corona’s study, the impact of ED is reflected inincreased somatised anxiety—a process whereby anemotion is expressed or experienced as a physicalsymptom leading to a symptom being falselyconsidered to originate in a physical illness. Essen-tially, the individual has little or no insight into theproblem, going from doctor to doctor seeking aphysical diagnosis or explanation. In other words,ED is distressing and a cause of much unhappiness.

So what can be our practical take home messages:

� A

ll vascular risk factors need to be measured in allpatients with ED. They need to be addressedaggressively to reduce cardiovascular morbidityand mortality and perhaps benefit ED [9].

� A

ccumulative risk factors compatible with the‘‘metabolic syndrome’’ increase the incidence ofED, but the diagnostic label should not lead tocomplacency about overall risk reduction.

� L

ifestyle changes are essential as a form ofprevention and management.

� H

ypogonadism is associated with coronary arterydisease and increased vascular risk as part of themetabolic syndrome. Testosterone should bemeasured routinely. Defining hypogonadism asa total testosterone level of<8 mmol/l assumes anabsolute rather than relative diagnosis and thismay need to be revisited as part of individualisedmanagement (some men may need to be morethan just normal).

It is to be hoped Corona and colleagues willreport back to us on the impact of testosterone

replacement therapy on their patients with ED andhypogonadism and any changes in vascular riskparameters observed in their study.

References

[1] Corona G, Mannucci E, Schulman C, et al. Psychobiologic

correlates of the metabolic syndrome and associated

sexual dysfunction. Eur Urol 2006;50:595–604.

[2] Khan R, Buse J, Ferrannini E, Stern M. The metabolic

syndrome: time for a critical appraisal. Diabetes Care

2005;28:2289–304.

[3] Grundy SM, Brewer Jr HB, Cleeman JI, Smith Jr SC, Lenfant

C, National Heart, Lung and Blood Institute, American

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[4] World Health Organization: Definition, diagnosis and clas-

sification of diabetes mellitus and its complications: report

of a WHO consultation. Geneva, Switzerland: World Health

Organization; 1999.

[5] International Diabetes Federation. The IDF Consensus

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www.idf.org/webdata/docs/Metac_syndrome_def.pdf.

Accessed 06/03/06.

[6] Fedman HA, Goldstein I, Hatzichristou DG, et al. Impotence

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54–61.

[7] Esposito K, Giughano D. Obesity, the metabolic syndrome

and sexual dysfunction. Int J Impot Res 2005;17:391–8.

[8] Makhsida N, Shah J, Yan G, et al. Hypogonadism and

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[9] Kostis JB, Jackson G, Rosen R, et al. Sexual dysfunction and

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