[Sonographic detection of kidney infarctions using ultrasound contrast media]. / Sonographischer Nachweis des embolischen Niereninfarktes mit Echokontrastmittel.

UNLABELLED: Contrast-enhanced CT is currently the gold standard for the diagnosis of kidney infarction. Particularly in patients with renal insufficiency, however, the use of iodine contrast media is limited. Sonographic examination using ultrasound contrast media may be an alternative for these patients. CASE REPORTS: We examined three patients with suspected ischaemic kidney infarction with ultrasound contrast media. Scanning was performed with low mechanical index, and SonoVue was used as by contrast-enhancing agent. In all three patients, kidney infarctions were clearly shown. In two patients, the lesions were confirmed by contrast-enhanced CT, in one no CT was performed because of impaired renal function. CONCLUSION: Kidney infarctions can reliably be detected by contrast-enhanced ultrasound using SonoVue as contrast agent. This is particularly valuable in patients with renal impaired renal function and other contraindications against iodine contrast media.

[Pancreatic tail tumor as an unusual first manifestation of Wegener's disease]. / Pankreasschwanztumor als ungewöhnliche Erstmanifestation eines M. Wegener.

A fifty-year-old, previously healthy woman presented with abdominal pain and weight loss. Diagnostic work-up revealed a mass in the tail of the pancreas with the appearance of a pancreatic carcinoma. Partial pancreatectomy was performed. Postoperatively, the patient's kidney function deteriorated. Pathohistological examination of the resected tissue showed a granulomatous vasculitis but no maligant tumor. Renal biopsy revealed a rapid progressive glomerulonephritis. Positive C-ANCA screening confirmed the diagnosis of Wegener's disease and an immunosuppressive therapy was established. This case demonstrates the difficult management of a potentially benign pancreatic mass, as reliable discrimination from pancreatic adenocarcinoma is not always possible.

Better acceptance of Fecal Occult Blood Test (FOBT) for colorectal cancer screening during hospitalization.

INTRODUCTION: Colorectal cancer (CRC) is a leading cause of illness and death in the Western world. Screening with fecal occult blood test (FOBT) significantly reduces the death rate and the incidence from CRC but these tests are not widely accepted. We investigated the possible contribution of hospitalization to a better acceptance of CRC screening. PATIENTS AND METHODS: From October 1998 through September 2000, 721 consecutive patients between 45 and 75 years of age admitted for various reasons were asked for participation in the study. They were asked to participate in FOBT-screening. In case of refusal of FOBT they were asked a second time after detailed information. In patients who accepted 3 consecutive FOBT's were performed. In case of positive FOBT results colonoscopy and gastroscopy were performed. RESULTS: 149 (82 male/67 female) patients were included. 94 (63.5%) of them agreed to undergo FOBT primarily and 10 (6.8%) secondarily after detailed information. The total acceptance rate of the FOBT was 69.8% (m/w : 69.1%/71.6%). In one of 5 cases with a positive FOBT result colorectal cancer (CRC) was diagnosed. Information on repetition of FOBT after one year could be obtained from 82 patients (55%). 37 patients (45%) had undergone repeated FOBT. None of the 37 patients was motivated by the FOBT screening during hospitalization. CONCLUSIONS: Staying in a hospital offers a good chance to achieve a higher acceptance of the FOBT. Therefore, hospitalization may contribute to a better colorectal cancer prevention. However, motivation to regularly repeat screening does not last in all patients. Therefore, public campaigns as well as medical counseling need to continuously stress the necessity of CRC screening procedures.

Interrelation between ABH blood group 0, Lewis(B) blood group antigen, Helicobacter pylori infection, and occurrence of peptic ulcer.

BACKGROUND: Helicobacter pylori is a human pathogen that causes chronic gastritis and peptic ulcers. Epidemiological studies demonstrated that individuals who are blood group 0 positive or represent non-secretors of their blood group antigens are more likely to develop peptic ulcers. The Lewis(b) blood group antigen has been reported to mediate the attachment of H. pylori to human gastric mucosa. The aim of this study was to examine the interrelation between Le(a-b+) phenotype, blood group 0, H. pylori infection, and peptic ulcer occurrence. PATIENTS AND METHODS: The study population consisted of 330 consecutive patients (185 men, 145 women) referred to endoscopy of the upper gastrointestinal tract for various reasons. AB0(H) blood groups and Lewis(a,b) phenotype were carried out by standard haemagglutination assays. Antibodies (IgG) against H. pylori were determined by a quantitative enzyme-linked immunosorbent assay (ELISA). RESULTS: 49 of the 330 patients (14.8 %) showed duodenal or gastric ulcers with a H. pylori seroprevalence of 87.8 %. The IgG immune response to H. pylori was not dependent on ABH blood group phenotype. There was also no significant association between the secretor status and the presence of H. pylori infection. Secretors, 35/238 (14.7 %), were no more likely to have gastroduodenal ulcer compared with non-secretors, 9/65 (13.8 %). CONCLUSION: Our data show no association between secretor status or specific ABH blood group on the one hand, and H. pylori infection or occurrence of gastroduodenal ulcers on the other. Determination of ABH blood groups or secretor status is, therefore, not a useful tool to characterize the individual risk for gastroduodenal ulcer or to guide any diagnostic procedures.

[Fatty liver in adult celiac disease]. / Fettleber bei adulter Sprue.

HISTORY AND ADMISSION FINDINGS: A 31-year-old woman was admitted because of heptomegaly and abnormal liver functions. For years she had suffered from diarrhoea but its cause had never been elucidated. She was underweight and had mild ankle edema. The liver margin was palpable at 20 cm below the midcostal margin, but the abdominal examination was otherwise unremarkable. INVESTIGATIONS: Sonography revealed a very large fatty liver. Biopsy showed fatty infiltration of nearly all the hepatocytes, without significant inflammation and fibrosis. Small-intestinal biopsy showed the typical histology of coeliac disease. Laboratory tests indicated abnormal liver function with increased transaminases, alkaline phosphatase, GPT and LDH, but no sign of inflammatory aetiology. These findings suggested that the liver changes were due to the coeliac disease. TREATMENT AND COURSE: After the patient had been put on a gluten-free diet the diarrhoea stopped and she started to gain weight. The liver function tests briefly became worse, but over the following 6 weeks normalized completely. The patient gained 5 kg in the subsequent 18 months and the liver became sonographically normal. The small-intestinal biopsy now showed merely discrete villar atrophy. CONCLUSION: Coeliac disease should be considered in any case of fatty liver of unknown cause. Strict gluten-free dietary treatment of the underlying cause can quickly lead to complete regression of the hepatic changes.

Effects of sodium selenite on deoxycholic acid-induced hyperproliferation of human colonic mucosa in short-term culture.

It has been shown that in vitro incubation of human colonic biopsies with the secondary bile acid deoxycholic acid (DCA) leads to the hyperproliferation of colonic crypt cells with an expansion of the proliferative zone, which is regarded as a biomarker of increased cancer risk. Sodium selenite (SSE), on the other hand, has been implicated as a protective agent in experimental studies, but toxic effects were reported as well, depending on the dose of SSE. To elucidate the effects of SSE on human colonic mucosa, biopsies from endoscopically normal sigmoid colon tissue of 30 subjects were incubated with 5 microM DCA or a combination of 5 microM DCA and SSE in concentrations of 5, 10, 20, 50, 80, and 100 microM, respectively. Equimolar NaCl incubations served as a control. Proliferating cells were labeled by bromodeoxyuridine immunohistochemistry, and the labeling index (LI) was computed. In the experiments using 5, 10, and 20 microM SSE, the whole crypt LI was significantly lower after DCA + SSE incubation (0.136, 0.118, and 0.110, respectively) compared to that after incubation with DCA alone (0.172, 0.157, and 0.165, respectively; P < 0.01). The corresponding LIs during DCA + SSE incubation were comparable to the LIs obtained after NaCl incubation (average LI = 0.14). Contrary to this finding, severe cell damage was observed in the biopsies that were incubated with the higher SSE concentrations of 50 microM and above. The antiproliferative effects of SSE may indicate a possible protective effect in the prevention of human colon cancer development. However, the observed toxic effects of higher SSE concentrations strongly suggest the need for additional studies before general recommendations for the use of SSE in colon cancer prevention can be made.

Effects of resistant starch on the colon in healthy volunteers: possible implications for cancer prevention.

Recent evidence suggests that resistant starch (RS) is the single most important substrate for bacterial carbohydrate fermentation in the human colon. During two 4-wk periods. 12 healthy volunteers consumed a controlled basal diet enriched with either amylomaize starch (55.2 +/- 3.5 g RS/d; high-RS diet) or available cornstarch (7.7 +/- 0.3 g RS/d; low-RS diet). Approximately 90% of the RS consumed disappeared during intestinal passage; increased fermentation was verified by elevated breath-hydrogen excretion. During the high-RS diet, fecal wet and dry weight increased 49% and 56%, respectively (P < or = 0.005), whereas stool water content did not change significantly. Fecal concentrations and daily excretion of short-chain fatty acids were not different in the two study periods. During the high-RS diet, bacterial beta-glucosidase activity decreased by 26% (P < or = 0.05). Fecal concentrations of total and secondary bile acids were significantly lower during the high-RS than during the low-RS period [a decrease of 30% (P < or = 0.05) and 32% (P < or = 0.01), respectively, in total and secondary bile acids] whereas concentrations of primary bile acids were unaffected by RS consumption. During the high-RS diet, fecal concentrations of total neutral sterols decreased by 30% (P < or = 0.005) and fecal concentrations of 4-cholesten-3-one decreased by 36% (P < or = 0.05). These data suggest that RS has potentially important effects on bacterial metabolism in the human colon that may be relevant for cancer prevention.

In vitro fermentation of high-amylose cornstarch by a mixed population of colonic bacteria.

BACKGROUND: Malabsorbed starch is probably the most important substrate for bacterial fermentation in the human large intestine. Fermentability of starch may depend on the composition of the colonic flora and its adaptation to the substrate supply. METHODS: Ten healthy volunteers were fed a controlled diet containing either 7.0 to 8.3 or 50.7 to 59.7 g/d of resistant starch (Hylon VII) for 4 weeks. At the end of each diet period, fecal starch concentrations were measured. Fecal samples were incubated in 48-hour batch cultures containing 10 g/L Hylon VII or digestible Lintner's starch. Bacterial breakdown of starch and short-chain fatty acid concentrations were measured at 0, 3, 6, 12, 24, and 48 hours. RESULTS: Fecal starch concentrations were higher during the Hylon VII period (35.7 +/- 16 vs 8.9 +/- 3.3 mg/g). Starch was fermented rapidly and completely in vitro in all but two subjects. Fermentability of resistant starch was comparable to that of digestible starch. No differences were found between the dietary periods. Fermentation of resistant starch produced higher rates of n-butyrate. Two subjects had substantially higher fecal starch concentrations. In vitro starch breakdown in these subjects was slow and incomplete. CONCLUSIONS: Fermentation of resistant starch by the colonic microflora was rapid and complete in 8 of 10 subjects. No adaptation of the fermentation capacity was observed after 4 weeks of dietary resistant starch supplementation. Fermentation of resistant starch increased the proportion of n-butyrate in vitro. In two subjects, fecal starch concentrations were substantially higher than in the other subjects and in vitro starch fermentation was slow and incomplete.

Histological changes in the colonic mucosa following irrigation with short-chain fatty acids.

OBJECTIVES: Short-chain fatty acids (SCFAs) derived from bacterial fermentation of complex carbohydrates are preferred luminal nutrients of the colonic mucosa. Starvation of colonocytes through lack or impaired metabolism of luminal SCFAs may be a cofactor in the pathogenesis of ulcerative colitis. DESIGN: A detailed histological evaluation of colonic biopsy specimens was performed in patients with active distal ulcerative colitis who were treated with rectal enemas containing a mixture of SCFAs, n-butyrate alone or saline placebo. Together with light microscopic parameters of mucosal inflammation, the pattern of crypt cell proliferation (proliferating cell nuclear antigen) and the mucosal activity of factor XIII were assessed. RESULTS: Butyrate reduced the density of polymorphonuclear leucocytes in the lamina propria (4 weeks: P = 0.063; 8 weeks: P = 0.091); other inflammatory parameters remained unchanged. Both butyrate and the SCFA mixture reduced significantly the number of proliferating cells in the upper 40% of crypts. Tissue factor XIII activity in active ulcerative colitis was significantly lower than in mucosa from normal colons; however, it was not affected by SCFA or butyrate irrigation. CONCLUSION: SCFAs and butyrate have a more marked effect on crypt cell proliferation than on parameters of inflammation in patients with active ulcerative colitis.

Bile acid metabolism by colonic bacteria in continuous culture: effects of starch and pH.

Secondary bile acids (BA) have been shown to be involved as a promoting agent in the adenoma-carcinoma sequence of colorectal cancer. In previous studies, fermentation of starch has been shown to inhibit the degradation of primary to secondary BA by the colonic microflora. This study was designed to investigate BA metabolism in continuous cultures of mixed fecal bacteria to get further insights into the mechanisms of this inhibition. Fermentation vessels were fed with media containing cholic (0.6 g/l) and chenodeoxycholic acid (0.4 g/l). Cultures were either starch-free or enriched with starch (10 g/l). pH was controlled and adjusted to 7.0 or 6.0. Total culture duration was 28 days and concentrations of BA, short-chain fatty acids (SCFA), and starch were measured periodically. At pH 6, significantly more primary BA remained in the media and less secondary BA were produced. Total BA concentrations were lower at pH7. SCFA concentrations were higher in the vessels supplemented with starch. Starch was completely fermented and not present in significant amounts in any fermentation vial after the first week. These data indicate that bacterial breakdown of primary to secondary BA is inhibited when starch is simultaneously fermented. This effect can be explained by the reduction of pH resulting from SCFA production. Considering these findings, resistant starch which escapes assimilation in the small bowel may be a protective factor against colorectal cancer.

Metabolic consequences of total colectomy.

Colectomy is performed for inflammatory bowel disease, familial polyposis syndrome and colorectal carcinoma. Surgical procedures are ileostomy with or without pouch, ileorectal anastomosis or ileal pouch-anal anastomosis. One of the major functions of the intact large intestine is to absorb water and electrolytes. After colectomy, as much as 400-1000 ml of nearly isotonic ileostomy fluid may be excreted, resulting in a chronic salt and water depletion. This is compensated for by an activation of the renin-angiotensin-aldosterone system. Reduced urine volumes may cause kidney stones. Both dehydration and renal sodium retention are probably less frequent in patients with ileal pouch-anal anastomosis. Absorption of nutrients in general is not impaired by colectomy. The large intestine salvages energy from malabsorbed organic matter through absorption of the short-chain fatty acids produced in bacterial fermentation. In ileostomy patients, fermentation is negligible, which leads to a significant loss of energy in the ileostomy fluid. Pouches are colonized by a bacterial flora similar to colonic bacteria. In these patients conservation of energy from malabsorbed substrate may be similar to healthy subjects. Resection of ileum and bacterial colonization may lead to malabsorption of vitamin B12 and bile acids. The latter may cause increased incidence of biliary cholesterol stones. Pouchitis is a frequent problem which may be caused by a deficiency of short-chain fatty acids and glutamine in the pouch contents. It is concluded that although the colon is not essential as a digestive organ in man, colectomy results in a number of metabolic changes. The ileal pouch-anal anastomosis may in part substitute for the functions of the large intestine.

Effects of short-chain fatty acids on the inflamed colonic mucosa.

Selected inflammatory conditions of the distal alimentary tract may respond to topical SCFA treatment. The rationale for using SCFA enemas is based on Roediger's (1980) observation that butyrate is the preferred fuel of colonocytes and that SCFA deficiency could lead, in the short term, to mucosal hypoplasia and, in the long term, to colitis. The absence of luminal nutrients is especially evident in the excluded rectum after complete diversion of the faecal stream. Harig et al. (1989) were the first to treat successfully diversion colitis with SCFA irrigation (acetate 60 mM, propionate 30 mM, n-butyrate 40 mM). However, subsequent studies could not reproduce the initial positive data. In distal ulcerative colitis an impaired mucosal oxidation of SCFAs has been described despite their luminal abundance. Pilot studies using either the SCFA mixture or butyrate monotherapy have yielded promising results. However, extended confirmatory studies with a larger sample size have not yet been performed. Preliminary data are also available for the use of SCFA in pouchitis and radiation proctitis. In summary, SCFA topical therapy seems to be a promising option in distinct forms of inflammatory bowel disease; however, the routine use of SCFAs cannot be recommended until their efficacy has been confirmed in larger trials.

Antagonistic effects of sulfide and butyrate on proliferation of colonic mucosa: a potential role for these agents in the pathogenesis of ulcerative colitis.

It has been shown that feces of patients with ulcerative colitis uniformly contain sulfate reducing bacteria. Sulfide produced by these bacteria interferes with butyrate-dependent energy metabolism of cultured colonocytes and may be involved in the pathogenesis of ulcerative colitis. Mucosal biopsies from the sigmoid rectum of 10 patients (no caner, polyps, inflammatory bowel disease) were incubated with either NaCl, sodium hydrogen sulfide (1 mmol/L), a combination of both sodium hydrogen sulfide and butyrate (10 mmol/L), or butyrate. Mucosal proliferation was assessed by bromodeoxyuridine labeling of cells in S-phase. Compared to NaCl, sulfide increased the labeling of the entire crypt significantly, by 19% (p < 0.05). This effect was due to an expansion of the proliferative zone to the upper crypt (compartments 3-5), where the increase in proliferation was 54%. Sulfide-induced hyperproliferation was reversed when samples were coincubated with sulfide and butyrate. The study shows that sodium hydrogen sulfide induces mucosal hyperproliferation. Our data support a possible role of sulfide in the pathogenesis of UC and confirm the role of butyrate in the regulation of colonic proliferation and in the treatment of UC.

Effect of L-glutamine and n-butyrate on the restitution of rat colonic mucosa after acid induced injury.

BACKGROUND: L-glutamine and n-butyrate are important nutrients for colonocytes affecting both their structure and function. The effect of these epithelial substrates on resealing of rat distal colon after acid induced injury was studied. METHODS: Isolated colonic mucosa of 32 rats was mounted in Ussing chambers and exposed to Krebs-Ringer solution for four hours. Epithelial injury was induced by short-term exposure to luminal hydrochloric acid and resealing was studied with or without added glutamine or butyrate. RESULTS: Glutamine (luminal and serosal) reduced tissue conductance, mannitol and lactulose permeability, and permeation of enteropathogenic Escherichia coli. Glutamine (serosal) diminished conductance and mannitol permeability. Both interventions stimulated bromodeoxyuridine incorporation in nuclei of colonocytes. Luminal butyrate had no measurable effect on these parameters. CONCLUSIONS: These data suggest that L-glutamine stimulates repair mechanisms of rat colonic mucosa after acid injury. This effect on the gut barrier is associated with a stimulation of crypt cell proliferation. The addition of glutamine to parenteral solutions may be beneficial for patients under intensive care whose intestinal barrier is weakened in the course of sepsis and trauma.

[Pneumatosis cystoides intestinalis]. / Pneumatosis cystoides intestinalis.

HISTORY AND CLINICAL FINDINGS: A 56-year-old man was admitted to hospital for investigation of meteorism and severe flatulence for 10 months and irregular stools. He had no previous illness. On examination his abdomen was quite distended, with very active but low-pitched peristalsis. INVESTIGATION: Plain x-ray of the abdomen showed multiple round translucencies along the wall of the left hemicolon. Coloscopy revealed multiple firm-walled cysts in the descending and sigmoid colon which contained H2 in high concentration. Histologically there was slight inflammatory infiltration of the submucosa as well as some slit-like hollow spaces, pointing to the diagnosis of pneumatosis cystoides intestinalis. The H2 breath test, done to confirm the diagnosis, indicated increased H2-concentration, both on fasting and after lactulose. TREATMENT AND COURSE: A diet low in flatulence-producing carbohydrates satisfactorily controlled the symptoms, but the local findings remained unchanged over 4 years. CONCLUSION: Pneumatosis cystoides intestinalis should be included in the differential diagnosis of meteorism and flatulence. Diet can satisfactorily control the symptoms of this rare disease.

[Hydrogen metabolism in the large intestine--physiology and clinical implications]. / Wasserstoffmetabolismus im Dickdarm--Physiologie und klinische Bedeutung.

During the anaerobic metabolism of the colonic bacterial flora short chain fatty acids and the gases hydrogen (H2) and carbon dioxyde (CO2) are produced. In about 50% of a European and North-American population and in 90% of rural black Africans, methane is generated from H2 and CO2. In methane-negative individuals, sulfate reducing bacteria utilize H2 to reduce sulfate to sulfide. Methanogenesis and sulfate reduction are usually mutually exclusive. A competition exists for the common substrate hydrogen which is potentially regulated by the availability of sulfate in the colonic lumen. Other bacteria can use H2 to reduce CO2 to acetate (homoacetogenesis). Methane is an inert gas and has probably no direct effect in man. The metabolites of sulfate reduction (mercaptides, hydrogen sulfide) are toxic and hydrogen sulfide is supposed to play a role in the pathogenesis of ulcerative colitis. All H2-utilizing metabolisms reduce the gaseous volume in the colon and thus prevent flatulence. In patients with pneumatosis cystoides intestinalis methanogenesis is absent and sulfate reduction is insignificant. This deficiency provides an explanation for the massive H2-excretion in those patients and their symptoms.

Influence of starch fermentation on bile acid metabolism by colonic bacteria.

Secondary bile acids (BA) may be involved in the pathogenesis of colorectal cancer. In vivo, starch malabsorption has been shown to reduce fecal excretion of secondary BA. The present in vitro study was performed to investigate the effect of starch fermentation on BA metabolism by colonic bacteria. Fecal samples of healthy volunteers were incubated in anaerobic batch cultures for 48 hours with the primary bile acids cholic (0.6 g/l) and chenodeoxycholic acid (0.4 g/l). Media were starch free or enriched with starch (10 g/l). The pH was controlled and held at 6 or 7. In the starch-free incubations, secondary BA were rapidly formed, and degradation of primary to secondary BA was complete within 24 hours. The formation of secondary BA was partially inhibited by the addition of starch to the media. This effect was stronger at pH 6 than at pH 7. Starch was rapidly and completely fermented. In conclusion, this study showed that formation of secondary BA by fecal bacteria is inhibited when starch is simultaneously fermented, an effect that is mainly, but not completely, explained by reduction of pH.

Effect of free glutamine and alanyl-glutamine dipeptide on mucosal proliferation of the human ileum and colon.

BACKGROUND/AIMS: Glutamine (Gln) is considered a trophic factor for small intestinal epithelia, which is important during severe illness. Its use in parenteral nutrition is precluded by its instability, a problem that may be overcome by use of the stable dipeptide L-alanyl-L-glutamine (Ala-Gln). The hypothesis was tested that Gln or Ala-Gln may stimulate cell proliferation not only in the ileum but also in the proximal and distal colon and, thus, may contribute to the gut barrier function. METHODS: Biopsy samples from the normal human ileum, proximal colon, and rectosigmoid were incubated for 4 hours with Gln (2 mmol/L), Ala-Gln (2 mmol/L), and saline (control). Cells in S phase were labeled with bromodeoxyuridine. In longitudinal crypt sections labeled and quiescent cells were counted. RESULTS: Gln as well as Ala-Gln stimulated crypt cell proliferation in the ileum, proximal colon, and rectosigmoid colon. In ileal specimens, labeling was greater in the entire crypt, whereas in both colonic regions, the trophic effect was confined to the basal crypt compartments. CONCLUSIONS: Gln and Ala-Gln have trophic effects not only in the ileum, but also in the proximal and distal colon. This could be important during parenteral nutrition when mucosal atrophy may weaken the gut barrier.

Impaired hydrogen metabolism in pneumatosis cystoides intestinalis.

BACKGROUND: Pneumatosis cystoides intestinalis (PCI) is characterized by high levels of breath hydrogen. Clinical features of PCI may be due to abnormal H2 metabolism. METHODS: Breath levels of H2 and CH4 were measured in 3 patients and total gas in 2 patients with PCI on a polysaccharide-free (basal) diet and after administration of 15 g of lactulose. Metabolic activities and counts of methanogenic (MB) and sulfate-reducing (SRB) bacteria were measured in feces. Ten volunteers were also studied. RESULTS: Total H2 levels in patients were 383-420 mL/day on the basal diet and 1430-1730 mL/day after lactulose administration compared with 35 +/- 6 mL/day and 262 +/- 65 mL/day, respectively, in controls. Basal breath H2 levels in controls were 27 +/- 6 vs. 214 +/- 27 mL/day in patients and after lactulose ingestion, 115 +/- 18 vs. 370 +/- 72 mL/day. Four controls were methanogenic and had high fecal MB counts. The other controls had high SRB counts and sulfate reduction rates. All patients were nonmethanogenic and had low sulfate reduction rates. CONCLUSIONS: Patients with PCI excrete more H2 than controls. In normal subjects, H2 is consumed by MB or SRB; the activity of these bacteria is virtually absent in PCI. This may explain the gas accumulation in these patients.