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TOPIC HIGHLIGHT

Small intestinal bacterial overgrowth syndrome

Jan Bures, Jiri Cyrany, Darina Kohoutova, Miroslav Frstl, Stanislav Rejchrt, Jaroslav Kvetina, Viktor Vorisek,

Marcela Kopacova

Jan Bures, Jiri Cyrany, Darina Kohoutova, Stanislav Rejchrt,Marcela Kopacova,2nd Department of Medicine, Charles Uni-versity in Praha, Faculty of Medicine at Hradec Kralove, Univer-

sity Teaching Hospital, Sokolska 581, 500 05 Hradec Kralove,

Czech Republic

Miroslav Frstl,Institute of Clinical Microbiology, CharlesUniversity in Praha, Faculty of Medicine at Hradec Kralove,

University Teaching Hospital, Sokolska 581, 500 05 Hradec

Kralove, Czech Republic

Jaroslav Kvetina, Institute of Experimental Biopharmaceu-tics, Joint Research Centre of Czech Academy of Sciences and

PRO.MED.CS Praha a.s., Heyrovskeho 1207, 500 03 Hradec

Kralove, Czech RepublicViktor Vorisek, Institute of Clinical Biochemistry and Diagnos-tics, Charles University in Praha, Faculty of Medicine at Hradec

Kralove, University Teaching Hospital, Sokolska 581, 500 05

Hradec Kralove, Czech Republic

Author contributions:Bures J, Cyrany J, Kohoutova D, FrstlM, Rejchrt S, Kvetina J, Vorisek V and Kopacova M contributed

equally to this work.

Supported byThe Research Project MZO 00179906 from theMinistry of Health, Czech Republic, and by Research Grant

GACR 305/08/0535, Czech Republic

Correspondence to: Jan Bures, Professor, MD, PhD, 2ndDepartment of Medicine, Charles University in Praha, Faculty of

Medicine at Hradec Kralove, University Teaching Hospital, So-

kolska 581, 500 05 Hradec Kralove,Czech Republic. [email protected]

Telephone:+420-495-834240 Fax:+420-495-834785Received:January 13, 2010 Revised:February 19, 2010

Accepted:February 26, 2010Published online:June 28, 2010

Abstract

Human intestinal microbiota create a complex polymi-

crobial ecology. This is characterised by its high popula-tion density, wide diversity and complexity of interaction.

Any dysbalance of this complex intestinal microbiome,both qualitative and quantitative, might have serioushealth consequence for a macro-organism, includingsmall intestinal bacterial overgrowth syndrome (SIBO).

SIBO is dened as an increase in the number and/or

alteration in the type of bacteria in the upper gastro-

intestinal tract. There are several endogenous defence

mechanisms for preventing bacterial overgrowth: gastric

acid secretion, intestinal motility, intact ileo-caecal valve,

immunoglobulins within intestinal secretion and bacte-riostatic properties of pancreatic and biliary secretion.

Aetiology of SIBO is usually complex, associated with

disorders of protective antibacterial mechanisms (e.g.

achlorhydria, pancreatic exocrine insufciency, immuno-

deficiency syndromes), anatomical abnormalities (e.g.

small intestinal obstruction, diverticula, stulae, surgicalblind loop, previous ileo-caecal resections) and/or motil-

ity disorders (e.g. scleroderma, autonomic neuropathyin diabetes mellitus, post-radiation enteropathy, small

intestinal pseudo-obstruction). In some patients more

than one factor may be involved. Symptoms related to

SIBO are bloating, diarrhoea, malabsorption, weight

loss and malnutrition. The gold standard for diagnosing

SIBO is still microbial investigation of jejunal aspirates.

Non-invasive hydrogen and methane breath tests are

most commonly used for the diagnosis of SIBO using

glucose or lactulose. Therapy for SIBO must be com-plex, addressing all causes, symptoms and complica-

tions, and fully individualised. It should include treat-ment of the underlying disease, nutritional support and

cyclical gastro-intestinal selective antibiotics. Prognosis

is usually serious, determined mostly by the underlying

disease that led to SIBO.

2010 Baishideng. All rights reserved.

Key words:Bacterial overgrowth; Breath test; Hydrogen;

Methane; Small intestine

Peer reviewers:Antonio Gasbarrini, MD, Professor, Depart-ment of Internal Medicine, Gemelli Hospital, Catholic University

of Rome, Largo A. Gemelli 8, 00168 Rome, Italy; Anthony PMoran, BSc, PhD, DSc, FRSC, MRIA, Professor, Department of

Microbiology, National University of Ireland Galway, University

Road, Galway, Ireland

2978 June 28, 2010|Volume 16|Issue 24|WJG|www.wjgnet.com

World J Gastroenterol 2010 June 28; 16(24): 2978-2990ISSN 1007-9327 (print)

2010 Baishideng. All rights reserved.

Online Submissions: http://www.wjgnet.com/[email protected]

doi:10.3748/wjg.v16.i24.2978

Marcela Kopacova, Associate Professor, MD, PhD,

Series Editor

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Bures J et al. Small intestinal bacterial overgrowth syndrome

Bures J, Cyrany J, Kohoutova D, Frstl M, Rejchrt S, Kvetina J,

Vorisek V, Kopacova M. Small intestinal bacterial overgrowth syn-

drome. World J Gastroenterol2010; 16(24): 2978-2990 Available

from: URL: http://www.wjgnet.com/1007-9327/full/v16/i24/2978.

htm DOI: http://dx.doi.org/10.3748/wjg.v16.i24.2978

INTRODUCTION

Human intestinal microbiota create a complex polymi-crobial ecology. This is characterised by its high popula-tion density, wide diversity and complexity of interaction.The duodenum and proximal jejunum normally containsmall numbers of bacteria, usually lactobacilli and en-terococci, gram-positive aerobes or facultative anaerobes(< 104organisms per mL). Coliforms may be transientlypresent (< 103bacteria per mL) and anaerobic Bacteroidesare not found in the jejunum in healthy people. Up toone third of jejunal aspirates might be sterile in healthyvolunteers. The distal ileum is a transition zone betweensparse populations of aerobic bacteria of the proximalsmall intestine and very dense populations of anaerobicmicro-organisms in the large bowel[1-3]. The epithelialsurface of the small intestine in a healthy human is notcolonised. Occasional groups of bacteria can be foundin low concentrations within the lumen. Bacteria do notform clusters and spatial structures, and the luminal con-tents are separated from the mucosa by a mucus layer[4].

Any dysbalance of this complex intestinal microbi-

ome, both qualitative and quantitative, might have serioushealth consequences for a macro-organism, includingsmall intestinal bacterial overgrowth syndrome (SIBO).

DEFINITION

SIBO is a very heterogeneous syndrome characterised byan increased number and/or abnormal type of bacteriain the small bowel. Most authors consider diagnostic ofSIBO to be the finding of 10

5bacteria [i.e. colony-forming units (CFU)] per mL of proximal jejunal aspira-tion. The normal value is10

4CFU/mL[3, 5-7].

PREVALENCE

The overall prevalence of SIBO in the general publicis unknown. In general, SIBO is substantially underdi-agnosed. There are several reasons for this fact. Somepatients may not seek healthcare or SIBO may not beproperly diagnosed by medical investigations. SIBOmight be asymptomatic or with non-specic symptomsonly, and last but not least, all symptoms might be in-correctly ascribed to the underlying disease (leading toSIBO). Of course, diagnostic yield also depends on themethods used for investigation. According to different

studies with the investigation of small sets of clinicallyhealthy people as a control, findings consistent withSIBO were found in 2.5% to 22%[8-17].

In particular diseases and disorders, literature data on

prevalence differ substantially. For instance, the prevalenceof SIBO in patients fullling diagnostic criteria for irri-table bowel syndrome was 30%-85%[9-11,16,18,19]. The preva-lence of SIBO in coeliac disease non-responding to agluten-free diet was up to 50%[20]. In liver cirrhosis, SIBO

was diagnosed in more than 50% of cases

[21,22]

. In a smallgroup of elderly people (70 to 94 years old) with lactosemalabsorption, SIBO was documented in 90%[23]. An in-teresting study was performed on asymptomatic morbidlyobese subjects and SIBO was found in 17% (compared to2.5% in non-obese persons)[15].

AETIOLOGY

There are several endogenous defence mechanisms forpreventing bacterial overgrowth: gastric acid secretion, in-testinal motility, intact ileo-caecal valve, immunoglobulinswithin intestinal secretion and bacteriostatic properties of

pancreatic and biliary secretion[24].The aetiology of SIBO is usually complex, associated

with disorders of protective antibacterial mechanisms(e.g. achlorhydria, pancreatic exocrine insufciency, immu-nodeficiency syndromes), anatomical abnormalities (e.g.small intestinal obstruction, diverticula, fistulae, surgicalblind loop, previous ileo-caecal resections) and/or motil-ity disorders (e.g. scleroderma, autonomic neuropathy indiabetes mellitus, post-radiation enteropathy, small intesti-nal pseudo-obstruction). In some patients more than onefactor may be involved. Aetiological and predisposingfactors cannot be separated in some patients. SIBO may

occur in elderly people without any evident underlyingsmall intestinal pathology.In some cases, a vicious circle arises: an underlying

disease is complicated by SIBO and then SIBO directly(as a morphological impact) or vicariously (by malab-sorption or nutrient deciency) causes further deteriora-tion of the underlying disease.

Out of all diseases and disorders associated with SIBO(listed below in detail), 90% of cases comprise small intes-tinal motility disorders (of various aetiology) and chronicpancreatitis[2].

Achlorhydria

Achlorhydria (due to chronic atrophic gastritis) and long-term administration of proton pump inhibitors may causebacterial overgrowth in the stomach and duodenum. Pro-ton pump inhibitors not only increase duodenal bacterialcolonisation but also accelerate intestinal transit

[24].

Exocrine pancreatic insufciencyChronic pancreatitis is complicated by SIBO in 30%-40%of cases[7,25]. Multiple factors can be involved: exocrinepancreatic insufciency (with absence of anti-bacterial ef-fect of proteolytic enzymes), abnormal chyme in the smallintestinal lumen, motility disorders, administration of

painkillers and ongoing alcohol consumption in some ofpatients. Cystic brosis is also associated with increasedrisk of SIBO. Fridgeet al

[26] diagnosed SIBO in 14/25 (56%)patients with cystic brosis. SIBO may be a causative fac -


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tor of diarrhoea in advanced pancreatic cancer[27] apartfrom pancreatic exocrine insufciency, chemotherapy orprevious surgery.

Immunodeciency syndromes

Various immunodeciency syndromes, such as IgA de-ciency, common variable immunodeciency, AIDS andothers, are complicated by miscellaneous infection com-plications, including SIBO[28,29].

Small intestinal obstruction and stagnationAll anatomical pathology associated with small intesti-nal obstruction and stagnation could be associated withSIBO, e.g. strictures, adhesions, tumours of the smallbowel. Large and/or multiple duodenal and jejunal di-verticula are often complicated by SIBO. Sequelae ofprevious abdominal surgery (afferent loop syndrome

after Billroth-

gastric resection, Roux-en-Y stasis syn-drome, bariatric bypass surgery) may also lead to SIBO(with metabolic and nutritional disarrangement) [7,30-32].

Small intestinal pseudo-obstruction and some neurologi-cal diseases (e.g. myotonic dystrophy, Parkinson disease,Chagasic enteropathy) can be complicated by SIBO thatis responsible for malabsorption and weight loss[33-36]. Spi-nucci et al

[37]described an interesting case of endogenous

ethanol production in a patient with chronic intestinalpseudo-obstruction and SIBO.

Tursi et al[38] investigated bacterial overgrowth in the

small bowel in patients with acute diverticulitis of thecolon. Small intestinal overgrowth was found in 53/90

(59%) subjects. The authors assumed that the primarymechanism is a slow large bowel transit with stasis offaeces in the colon. This results in dysmicrobia in thelarge bowel with metabolic changes and induction ofinflammation. Subsequent reverse peristalsis facilitatescolonisation of the small intestine by bacteria comingfrom the large bowel. SIBO deteriorates symptoms ofacute colonic diverticulitis, protracts the course of thedisease and thus could be an independent risk factor forfuture relapses of acute diverticulitis of the large bowel.Rifaximin was effective in the treatment of both acutecolonic diverticulitis and SIBO in these patients[38].

Irritable bowel syndromeThe aetio-pathogenesis of irritable bowel syndrome hasnot yet been satisfactorily claried. Symptoms of SIBOand irritable bowel syndrome overlap to a large degree.As mentioned earlier, SIBO is frequently found in per-sons fullling criteria of irritable bowel syndrome (30%-85%)[9-11,16,18,19]. According to authors of the bacterial hy-pothesis, SIBO is the primary event and irritable bowelis secondary to SIBO. In some patients, the onset of ir-ritable bowel is preceded by infective gastroenteritis (so-called post-dysenteric bowel disturbance)[39]. Analysis ofthe microbial genome found different faecal microbiota in

healthy people and patients with irritable bowel (e.g. phy-lotypes Coprococcus, Collinsella, Coprobacillus)[40-42]. Believ-ers in an opposite hypothesis stated that irritable bowelis a primary factor (with motor disturbance, visceral

afferent hypersensitivity, psycho-social dysfunction) inwhich motility disorders enable secondary bacterialovergrowth[40,43]. A third group of authors recommendstrict distinction between irritable bowel syndrome (thehydrogen breath test with lactulose must be negative)

and SIBO (in such a case, it is not irritable bowel despitethe diagnostic criteria having been met) in patients withidentical symptoms

[44]. The last authors stated an opin-

ion that SIBO does not play any signicant role in thepathogenesis of irritable bowel[45].

Pimentel et al[12]

found abnormal lactulose breath testresults in 93/111 (84%) patients with irritable bowel syn-drome. Successful treatment of SIBO using neomycin(in 35% of patients) was associated with relief of subjec-tive symptoms. There was another interesting nding inthis study: a subgroup of persons with a methanogenicphenotype was associated with constipation in 100%(constipation-predominant irritable bowel syndrome)[12].

Another study found that methanogenic status was neverassociated in irritable bowel syndrome with diarrhoea andCrohns disease or ulcerative colitis with diarrhoea[13]. Theassociation of methanogenic phenotype and constipationwas also revealed by other authors[8].

Coeliac diseaseA wide range of 9% to 55% of patients have been dia-gnosed with SIBO as a complication of coeliac dis-ease[20,46-48]. The prevalence of SIBO is high, especially inpatients who do not respond to a gluten-free diet and/orhave lactose intolerance[20,46,47].

Crohns diseaseSIBO is frequently found in Crohns disease (in about25%). Loss of the ileo-caecal valve (due to previous ileo-caecal resection) and/or large entero-enteric and entero-colic stulae are important predisposing factors[49-55]. Cas-tiglione et al[56]found bacterial overgrowth more frequentlyin those who underwent surgery (30%) compared to non-operated patients (18%). Furthermore, SIBO may mimican acute flare of Crohns disease (including increasedbowel movements and lower body weight)[57]. Smokersmay exhibit increased H2 production which could lead tofalse positive test results. However, in the study by Klauset al[57]there was no difference in the proportion of smok-ers and their respective daily consumption of cigarettesbetween patients with Crohns disease with and withoutSIBO.

Short bowel syndromeThe problem of short bowel syndrome is not limited onlyto the reduced absorptive surface area. The loss of the ileo-caecal valve and the loss of the ileal break from resectionof the distal small bowel would accelerate the transit ofchyme throughout the entire gastrointestinal tract. Undi-gested food becomes a substrate for bacterial fermenta-

tion. Large intestinal bacterial ora colonise proximallyinto the small intestine to result in SIBO. Because digestionand absorption cannot be completed without adequatetime, these patients face chronic postprandial diarrhoea.



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These problems may be exacerbated by SIBO that furtheraccelerates transit and worsens digestion, absorption andmalnutrition[58].

SIBO is an independent negative factor deterioratingadaptation of the small intestine in children after exces-

sive bowel resections. SIBO lengthens the dependence ofthese patients on total parenteral nutrition and deterioratesmalabsorption and hepatopathy associated with shortbowel syndrome[59,60]. SIBO may lead to intestinal failurein these patients

[61].

Non-alcoholic steatohepatitisWigg et al

[17] found a higher prevalence of SIBO (11/22,50%) in non-alcoholic steatohepatitis (NASH) comparedto healthy control subjects (5/23, 22%). Higher valuesfor the xylose-lactulose test in patients with NASH cor-related with higher serum levels of tumor necrosis factor-(TNF-). However, they were not associated with increasedintestinal permeability or increased serum endotoxin[17]. Inanother study of NASH[62], SIBO was diagnosed in halfof the patients (6/12) but only in one subject (1/11, 9%)in the healthy control group. Treatment with ciprooxacin

suppressed bacterial overgrowth, increased serum insulinand decreased endogenous ethanol production but did notinuence serum acetylated ghrelin (half values compared to

controls). Changes in fasting insulin and ethanol followingciprofloxacin suggest that these parameters may be influ-enced by small intestinal bacterial activity

[62]. In an experi-

mental model of NASH in rats, there was a slower transittime and higher quantity of coliform bacteria (Escherichia

coli). Treatment with gentamicin (cidomycin) acceleratedthe transit time, decreased TNF- levels and alleviated se-

verity of liver involvement in experimental animals. ThusSIBO might play an important role in the pathogenesis ofNASH[63].

Liver cirrhosisPortal hypertension in liver cirrhosis substantially changesthe intraluminal milieu of the gut. Liver cirrhosis is anindependent risk factor for SIBO. Small intestinal motilitydisorder, especially slow transit in advanced liver disease(Child-Pugh C) may partake in SIBO[64,65]. SIBO was di-

agnosed in 50%-60% of patients with liver cirrhosis[66,67]

.SIBO is a risk factor for the development of spontaneousbacterial peritonitis[22,68], however, its role in the patho-genesis has not yet been fully claried

[22]. Prevalence of

SIBO was higher in those patients with liver cirrhosis whohad spontaneous bacterial peritonitis (14/20, 70%) com-pared to those without it (4/20, 20%)[64]. However, thisnding was not conrmed in other studies[66]. SIBO mightcorrelate with systemic endotoxaemia[69]. It is necessary toremind ourselves that glucose hydrogen breath test in livercirrhosis correlates only to a small degree with microbio-logical analysis of jejunal aspirates (sensitivity 27%-52%,specicity 36%-80%)[70].

SclerodermaScleroderma (systemic sclerosis) is a chronic connectivetissue disease that affects the gastrointestinal tract in more

than 80% of patients[71]. Severe small bowel involvementby scleroderma can present as chronic intestinal pseudo-obstruction and SIBO. The reported prevalence of SIBOin scleroderma was 43% to 56%[72,73]. In our series, SIBOwas proved in 4/15 (27%) patients with systemic sclero-

sis by means of glucose hydrogen and methane breathtests. Half the cases of SIBO had neither diarrhoea norother signs of malassimilation at the time of examination.There was a tendency towards a higher dose of systemicglucocorticosteroids in persons with positive hydrogenand methane breath tests[74].

Autonomic neuropathy in diabetes mellitusGastrointestinal symptoms are present in 50%-70% of pa-tients with diabetes mellitus. Delayed gastric emptying (oreven diabetic gastroparesis) and intestinal motility disordersare the most important ndings (with an unfavourable im-pact on glycaemic control). Impaired intestinal motility is

often followed by SIBO[75-77]. In diabetes mellitus, rst andforemost all results must be interpreted according to the di-agnostic method that was used. Cuoco et al

[78] performed thelactulose hydrogen breath test and found that 21/74 (28%)of subjects were affected by SIBO and delayed oro-caecaltransit time. After treatment with rifaximin, three patientsstill showed SIBO, ve persistent delayed transit time with-out SIBO and 13 persons (62%) experienced a signicantimprovement in their oro-caecal time (without SIBO)[78].Reddymasu et al

[79]used hydrogen and methane breath testsafter glucose challenge. Thirty out of fty (60%) patientshad a positive breath test result for SIBO on the basis of

hydrogen (63%), methane (27%) or both criteria (10%).SIBO was more likely in diabetic patients with gastropareticsymptoms of longer duration[79].

In about one third of patients with diabetes, SIBO wasassociated with cardiovascular autonomic neuropathy[77].SIBO in diabetes may rarely manifest itself as protein-losing enteropathy

[80].

Radiation enteropathySIBO and lactose intolerance may occur during and/orafter pelvic (or abdominal) radiotherapy[81-83].

FibromyalgiaPimentel et al[14]found that 42/42 (100%) patients with

bromyalgia had an abnormal lactulose hydrogen breathtest. This was a signicantly higher rate compared to pa-tients with irritable bowel syndrome (93/111, 84%) andclinically healthy persons used as a control (3/15, 20%).Patients with bromyalgia also had a higher hydrogenicprole that correlated with somatic pain

[14].

Other disorders and diseases associated with SIBOVarious diseases and disorders have been described to beassociated with or complicated by SIBO, such as lympho-proliferative diseases (lymphoma, chronic lymphocytic

leukaemia), benign lymphoid hyperplasia of the ileum,metabolic bone disease, acromegaly, hypothyreosis, alco-holism and rosacea

[7,84-87]. The prevalence of SIBO rises

with age (about 50% in persons > 75 years old)[88].



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non-specific symptoms (bloating, flatulence, abdominaldiscomfort, diarrhoea, abdominal pain). In more severecases, there are signs of malabsorption (weight loss, ste-atorrhoea, malnutrition), liver lesion, skin manifestation(rosacea), arthralgias and deciency syndromes (anaemia,

tetany in hypocalcaemia induced by vitamin D deciency,metabolic bone disease, polyneuropathy due to vitaminB12deciency, impaired barrier function of the gut, etc.).Anaemia is usually macrocytic (megaloblastic) due tovitamin B12deciency. It could also be microcytic iron de-ciency (due to occult gastrointestinal blood loss) or nor-mocytic (as anaemia of chronic disease)[3,5-7]. Serum folateand vitamin K levels are usually normal. Serum vitamin Kcan even be increased owing to its bacterial overproduc-tion. Moreover, there are some concerns as to whetherendogenous intestinal production of vitamin K by bacte-ria might interfere with warfarin treatment in SIBO[98-100].In the case of oedema of lower extremities, the aetiologyis usually more complex (anaemia, malnutrition, hypopro-teinaemia, vitamin B12deciency).

D-lactic acidosis is a severe complication of patientswith short bowel syndrome (with intact large bowel). It iscaused by an excessive overgrowth of lactobacilli. Non-absorbed saccharides pass from the small intestine to thelarge bowel and they are fermented down to the D-isomer

of lactic acid. There is no human pathway to metaboliseD-lactic acid. D-lactic acid is absorbed from the large

bowel; its serum concentration is regularly increased inthese patients. Nevertheless, most patients remain asymp-tomatic. In clinically expressed cases, leading symptoms

comprise characteristic neurologic abnormalities includingconfusion, cerebellar ataxia, slurred speech, and loss ofmemory. Patients exhibit some degree of altered mentalstatus. They may complain of or appear to be drunk in theabsence of ethanol intake. In the treatment, it is necessaryto compensate metabolic acidosis and administer peroralantibiotics (metronidazole, rifaximin). To prevent this seri-ous complication, it is important to reduce peroral intakeof simple sugars, polysaccharides given in smaller amountstogether with a higher intake of fat[101].

DIAGNOSTICS

It is mandatory to consider SIBO in all cases of complexnon-specic dyspeptic complaints (bloating, abdominaldiscomfort, diarrhoea, abdominal pain), in motility disor-ders, anatomical abnormalities of the small bowel and inall malassimilation syndromes (malabsorption, maldiges-tion)[3,5-7].

Physical investigation usually provides non-specificfindings and could be modified by a primary underly-ing disease. The abdomen may be distended and a smallintestinal succussion splash might be identied. Physicalinvestigation can further reveal latent tetany, polyneuro-pathy and skin manifestation (rosacea).

Laboratory tests usually nd anaemia, low serum vita-min B12levels and laboratory signs of malnutrition (lym-phopenia, low serum prealbumin and transferrin).

The gold standard for diagnosing SIBO is still micro-

bial investigation of jejunal aspirates. Such a sample can beobtained by a special sonde or by means of enteroscopy.Nowadays, there are commercially available special aspira-tion catheters (with a spiral pattern of holes at the distaltip) for contaminate-free collection of fluids. Microbial

investigation places high demands on the quality of labo-ratory work (determination of quantitative proportion ofanaerobes) and has several difculties (low reproducibilityand identifying cultivation-resistant bacteria). Distributionof bacterial overgrowth might be irregular and that is whya single investigation might not detect it. Bacterial over-growth may be restricted to a particular, difcult-to-accessarea for aspiration (e.g. a blind loop)[7].

Hydrogen and methane breath tests are currently themost important diagnostic methods. The principles andmethods of hydrogen and methane breath tests were de-scribed in detail elsewhere[102-105]. In humans, hydrogen andmethane are exclusively produced by intestinal bacteria,namely in the large bowel in healthy people and also in thesmall intestine in the case of SIBO. About 80% of hydro-gen and methane is expelled by atus, 20% is exhaled bylungs and can be measured in breath[106]. Hydrogen andmethane breath tests to diagnose SIBO are performedafter peroral glucose or lactulose challenge. Most authors(including our Department) use gas chromatography forbreath analysis. A parallel measurement of CO2and cor-rection of hydrogen values to CO2concentration makethe measurement more precise[7,74,103,104]. Low humidity (

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