Hydrogen Excretion Research Articles

Passage of carbohydrate into the colon

Abstract To quantify passage of unabsorbed dietary starch into the colon, 7 healthy volunteers had a multilumen tube positioned close to the ileocecal junction. Marker solution was perfused slowly, 20–40 cm above an aspiration site, to estimate, by marker dilution, flow through the ileum. On consecutive days, subjects ate liquidized meals containing 20 or 60 g starch; ileal aspirates were analyzed for starch and glucose for 5–6 h fasting and 4–7 h postprandially. Volume and carbohydrate concentrations were used to derive total carbohydrate traversing the ileum. In different subjects, unabsorbed carbohydrate was 453–4023 mg (2.3%–20.1%, mean 9.3%) for the smaller meal and 1332–6352 mg (2.2%–10.4%, mean 6.0%) for the larger. In 4 volunteers, hydrogen breath tests were performed on separate occasions after sucrose (50 g), lactulose (26 g), and the 20-g meal. Lactulose increased hydrogen excretion; sucrose and the test meal did not. We conclude that 2%–20% of dietary starch escapes absorption in the small bowel, confirming others' results using breath tests alone. Breath tests, though more convenient than intubation studies, may be a less sensitive index of starch malabsorption.

Fecal Reducing Substances and Breath Hydrogen Excretion as Indicators of Carbohydrate Malabsorption

Summary:Data from serial determinations of fecal volume, characteristics, pH, and reducing substances, and postprandial breath hydrogen (H2) concentrations in severely malnourished children receiving milk‐based recovery diets were used to evaluate the quality of the correspondence among diagnostic indices for carbohydrate malabsorption, with specific emphasis on the comparison of breath H2 excretion and fecal reducing substances. Only postprandial breath H2 results for subjects with a proven capacity to mount an H2 response to the nonabsorbable disaccharide, lactulose, were included. There was a poor correlation between the diagnostic indication provided by the breath test and fecal reducing sugars. Biological considerations about the metabolism of unabsorbed carbohydrates in relation to colonic transit time and fecal flora may explain the poor degree of correlation. The two indices should not be considered interchangeable, but should be used selectively in accordance with the clinical situation.

Fecal reducing substances and breath hydrogen excretion as indicators of carbohydrate malabsorption.

Data from serial determinations of fecal volume, characteristics, pH, and reducing substances, and postprandial breath hydrogen (H2) concentrations in severely malnourished children receiving milk-based recovery diets were used to evaluate the quality of the correspondence among diagnostic indices for carbohydrate malabsorption, with specific emphasis on the comparison of breath H2 excretion and fecal reducing substances. Only postprandial breath H2 results for subjects with a proven capacity to mount an H2 response to the nonabsorbable disaccharide, lactulose, were included. There was a poor correlation between the diagnostic indication provided by the breath test and fecal reducing sugars. Biological considerations about the metabolism of unabsorbed carbohydrates in relation to colonic transit time and fecal flora may explain the poor degree of correlation. The two indices should not be considered interchangeable, but should be used selectively in accordance with the clinical situation.

Breath hydrogen test and sucrase isomaltase deficiency.

Sucrose breath hydrogen tests were performed on 7 children with proved sucrase isomaltase deficiency. All children had raised breath hydrogen excretion. The amount of hydrogen produced and symptoms experienced increased with increasing sucrose loads. The sucrose breath hydrogen test appears to be a reliable indicator of sucrose malabsorption in sucrase isomaltase deficiency.

Respiratory excretion of hydrogen and methane in Italian subjects after ingestion of lactose and milk.

Lactose malabsorption, by the breath hydrogen test, and lactose intolerance (presence of symptoms) were studied in twenty healthy Italian subjects after intake of 12.5, 25 and 50 g lactose, whole milk and low-lactose milk. A rise in respiratory concentration of hydrogen (greater than 20 ppm) (malabsorption) was found in fifteen subjects after 50 g lactose, in thirteen after 25 g and in seven after 12.5 g. Symptoms generally occurred in subjects presenting a rise in respiratory hydrogen excretion, but such a rise was often observed without symptoms. Thirteen subjects presented symptoms after 50 g lactose, but only three after 25 g and one after 12.5 g. Whole milk (500 ml) gave a lower incidence of lactose malabsorption than 25 g lactose (7/20 versus 13/20, P less than 0.05) and more subjects developed symptoms (7/20 versus 3/20, NS). Low-lactose milk produced no malabsorbers and one intolerant. Breath methane was detected constantly in seven subjects and in three on some of the days of observation. Respiratory methane excretion generally appeared to be unrelated to lactose ingestion.

Pulmonary hydrogen and methane and plasma ammonia after the administration of lactulose or sorbitol.

The gut microfloral metabolism of sorbitol and lactulose was investigated in 10 healthy control subjects and 10 patients with cirrhosis of the liver, by measuring the pulmonary excretion of the fermentational gases hydrogen and methane during 3 h. A possible acute effect on venous plasma ammonia after a single dose of sorbitol or lactulose was also investigated. No significant difference in fermentation gas excretion was found after ingestion of sorbitol compared with lactulose in healthy controls or cirrhotic patients (p greater than 0.05). Neither sorbitol nor lactulose had significant effect on plasma ammonia concentrations during the first 3 h after ingestion. These findings indicate that both sorbitol and lactulose are extensively fermented by the colonic flora and that the possibility of replacing lactulose with the much cheaper sorbitol in the treatment of portal-systemic encephalopathy ought to be investigated. The suggested acute gut-ammonia trapping effect of lactulose caused by acidification of the gut lumen from fermentative end-products was not supported by the present findings.

Small-bowel bacterial overgrowth in the postgastrectomy syndrome.

Jejunal flora, bile acid deconjugation, and breath hydrogen (H2) and methane (CH4) excretion were studied in 22 Billroth II (BII)-operated patients with chronic postprandial symptoms, dumping (9), vomiting (7), pain (10), and diarrhoea (14). Sixteen were below 90% of desirable weight. Two control groups were included, one comprising 5 symptom-free, BII-operated volunteers and another comprising 12 healthy, unoperated volunteers. The numbers of bacteria recovered from jejunal secretions in the postgastrectomy patients did not differ significantly from those recovered in the symptom-free BII-operated controls but were significantly lower in the unoperated controls. Production of fermentation gas in anaerobic media supplemented with carbohydrates occurred in 17 of 22 postgastrectomy patients and in 4 of 5 BII-operated controls but in none of the unoperated controls. Bacterial bile acid deconjugating activity did not differ significantly between the postgastrectomy patients and the BII-operated controls but was significantly lower in the unoperated controls. Breath H2 excretion after glucose ingestion was significantly higher in the postgastrectomy patients than in both the BII-operated and the unoperated controls. The addition of pectin or guar gum to the glucose meal largely prevented postprandial symptoms and breath hydrogen excretion. Six out of 12 postgastrectomy patients treated with metronidazole recorded symptomatic effects, mainly on diarrhoea. Our findings indicate that jejunal bacterial overgrowth may be a major cause of the symptoms in some postgastrectomy patients. The tests available for demonstration of small-bowel bacterial overgrowth, perhaps with the exception of the glucose H2 breath test, did not differentiate satisfactorily between symptom-producing and non-symptom-producing abnormal jejunal flora. Thus these tests may seem to have a limited practical diagnostic value in such patients.

Bacterial overgrowth in jejunal and ileal disease.

The number of bacteria recovered in anaerobic cultures of jejunal secretions was significantly higher in a group of 10 patients with jejunal disease and stagnation of gut content in the proximal small bowel than in a group of 10 patients with similar conditions in the distal ileum. Some overlap in bacterial numbers occurred between patients with jejunal disease, ileal disease, and healthy controls, whereas production of fermentation gas in anaerobic media supplemented with glucose occurred only in cultures from the patients with jejunal disease. The 14C-glycocholic acid test showed increased output of breath 14CO2 in both patient groups, whereas faecal 14C was significantly increased only in patients with ileal disease. Increased breath hydrogen excretion after glucose ingestion was recorded in 8 of 10 patients with jejunal disease only. Breath methane excretion, previously found in 44% of healthy subjects, was absent in all of 28 patients with Crohn's disease of the small, indicating that these patients have a gut flora that is different from that of the healthy population.

FOOD INTOLERANCE: A MAJOR FACTOR IN THE PATHOGENESIS OF IRRITABLE BOWEL SYNDROME

Specific foods were found to provoke symptoms of irritable bowel syndrome (IBS) in 14 of 21 patients. In 6 patients who were challenged double blind the food intolerance was confirmed. No difference was detected in changes in plasma glucose, histamine, immune complexes, haematocrit, eosinophil count, or breath hydrogen excretion produced after challenge or control foods. Rectal prostaglandin E 2 (PGE 2), however, increased significantly, and in a further 5 patients rectal PGE 2 correlated with wet faecal weight. Food intolerance associated with prostaglandin production is an important factor in the pathogenesis of IBS.

Glycoproteins as Substrates for Production of Hydrogen and Methane by Colonic Bacterial Flora

Hydrogen and methane in human breath derive entirely from bacterial fermentation in the intestinal lumen. The sources of substrates utilized for these reactions have not been completely determined. Basal excretion of both gases occurs in the fasted state, while malabsorbed carbohydrate commonly results in increased hydrogen but not methane production. Using an in vitro fecal incubation system, we have studied hydrogen and methane production from glycoproteins of endogenous as well as dietary origin. All glycoproteins tested yielded hydrogen when incubated with fecal homogenates. Mean hydrogen production from substrates containing less than 3% sugar (human serum albumin, bovine serum albumin, and alpha-casein) averaged 2.2 +/- 0.9% of hydrogen production from equivalent amounts of glucose, while carbohydrate-rich mucin yielded 46.0 +/- 6.7% of hydrogen production from glucose. Glycoproteins of intermediate carbohydrate content, including transferrin and egg white, yielded intermediate values. Methane production from glycoproteins was optimal from carbohydrate-poor protein substrates in fecal homogenates which accumulated hydrogen and became rapidly acidic when incubated with pure carbohydrate. In contrast, methane production was comparable for essentially sugar-free proteins, glycoproteins, and glucose when hydrogen did not accumulate and neutral pH was maintained. We conclude that glycoproteins are substrates for hydrogen and methane production by colonic bacteria from healthy adults. In individuals with bacterial overgrowth syndromes and in protein-losing enteropathy, bacterial catabolism of endogenous glycoproteins may cause increased basal hydrogen and methane excretion. These findings also raise the possibility that measurement of hydrogen or methane after oral administration of dietary glycoproteins may be useful in detection of protein malabsorption.

Excretion of Breath and Flatus Gases by Humans Consuming High-Fiber Diets

The abilities of dietary fibers to promote the excretion of intestinal fermentation gases were evaluated in five healthy men. Flatus and breath gases were collected and analyzed during 3 days of each 9-day metabolic period. Responses to feeding xylan, pectin, cellulose and corn bran were compared to a fiber-free formula diet. Generally, hydrogen production increased throughout the day, whereas methane production remained more constant. Methane excretion was greater while consuming the xylan and pectin diets than while consuming the other diets. These two purified fibers also caused higher flatus volume, hydrogen and carbon dioxide excretion. Cellulose and corn bran generally resulted in breath and flatus gas excretion at levels equivalent to the fiber-free diets. Considerable variation was noted in the response of subjects to an individual diet. However, in most cases 2–5 days of frequent and daily consumption of the diets was necessary to establish a relatively constant level of gas excretion. This time may represent the period of microbial and enzymatic adaptation to the new dietary constituents.flatus humans gases pectin xylan cellulose corn bran fermentation fiber

Lactose Breath Hydrogen Test

The recent article by Barr et al, "Mucosal Function and Breath Hydrogen Excretion: Comparative Studies in the Clinical Evaluation of Children with Nonspecific Abdominal Complaints" (Pediatrics 68:526, 1981), provided some useful data on the utility of the lactose breath hydrogen test (LBHT) for the diagnosis of lactase deficiency in children with nonspecific abdominal complaints. However, two comments are in order. 1. Because new diagnostic tests must be compared to a "gold standard" test for evaluative purposes, the meat of this article resides in table 3, in which a LBHT is compared with lactase activity demonstrated on biopsy material.

Effect of acetylsalicylic acid on symptoms and hydrogen excretion in the disaccharide tolerance test with lactose or lactulose

Prostaglandins play a role in the pathogenesis of symptoms of food intolerance. An alleviation of lactose intolerance by premedication with the prostaglandin-synthesis inhibitor acetylsalicylic acid (ASA) has been reported. We studied the effect of 900 mg of ASA and of a glucose placebo on disaccharide intolerance symptoms and on breath hydrogen (H2) excretion in 16 healthy adult males 12 of whom were lactose malabsorbers and received 50 g of lactose 30 to 40 min after ASA; the remaining four were lactose absorbers and received 30 g of lactulose. Premedication with ASA had no significant effect on the severity and duration of intolerance symptoms and on the timing of H2excretion. In contrast, the maximal breath H2concentration and the total H2excretion were significantly increased after ASA administration. We conclude that prostaglandins are of minor importance in causing the usually moderate symptoms of disaccharide intolerance. Prostaglandin-synthesis inhibition by ASA may reduce the motility of the colon thereby permitting more colonic gas (derived from unabsorbed carbohydrates) to be absorbed and excreted.

A sensitive analytical apparatus for measuring hydrogen production rates. I. Application to studies in small animals. Evidence of the effects of an α-glucosidehydrolase inhibitor in the rat

A gas analysis and sampling methodology is described for determining total hydrogen excretion rates in Wistar rats. Hydrogen concentrations are evaluated by gas chromatography, using a molecular sieve column connected to a reduction gas detector. Resolution of the analysis is 0.015 ppm hydrogen in a 2.5-ml sample which is 50–100 times more sensitive than previous techniques. Gas samples are obtained by a single-pass (as opposed to rebreathing) method in which hydrogen-free air is passed through glass cylinders containing the experimental animals. Mixing of the animal's excreted hydrogen with the chamber flow results in increased hydrogen concentrations at the chamber outlet, from which each animal's endogenous production rate can be determined. The method is completely automated and enables multiple studies to be performed simultaneously. As an assessment of the capability of the system to detecting variations in hydrogen production due to carbodydrate malabsorption, 5 male Wistar rats received feeding of both sucrose alone and sucrose plus a known α-glucosidehydrolase inhibitor. In this manner, each animal served as its own control in evaluating the effect of the inhibitor. Administration of sucrose alone resulted in a mean increase in hydrogen production rate of 39% over a 7-h time period, following the initial rise in hydrogen concentration from baseline levels. Administration of sucrose plus inhibitor caused corresponding increases of 95%. Because of the sensitivity and simplicity of the method, it is expected to be a valuable aid in continuing studies of carbohydrate malabsorption of various etiologies.

Effect of psyllium hydrophilic mucilloid on oral glucose tolerance and breath hydrogen in postgastrectomy patients.

Twenty postgastrectomy patients ingested glucose solutions with or without psyllium hydrophilic mucilloid to determine its effects on their blood glucose and breath hydrogen excretion. On the basis of the breath hydrogen tests following glucose alone, 15 had various degrees of glucose malabsorption which the addition of psyllium markedly reduced. In all 20 patients, psyllium significantly lowered peak blood glucose and prolonged its rate of fall. However, areas under the glucose concentration time curves were similar with and without psyllium, suggesting that total glucose absorption was unaltered by psyllium. In vitro, centrifuged psyllium-water-glucose slurries released glucose over 3 hr into water. Although the mechanisms of the psyllium alteration of the blood glucose and breath hydrogen responses are probably multifactorial, our studies suggest that release from the psyllium-glucose slurry results in a slower and more complete glucose absorption.

Interval breath hydrogen test in glucose-galactose malabsorption.

A simple test is described for the diagnosis of monosaccharide malabsorption in infancy caused by a congenital defect of glucose and galactose transport. Increased hydrogen (H2) excretion in expired air after ingestion of sugar was used to diagnose this condition in an infant with severe diarrhoea after breast feeding. Abnormal amounts of H2 were excreted after oral administration of glucose and galactose, but not after fructose. A carbohydrate free diet supplemented with fructose resulted in rapid weight gain and disappearance of diarrhoea. The diagnosis of glucose-galactose malabsorption was confirmed by 14C-glucose transport studies on a jejunal mucosal biopsy specimen. These findings indicate that interval breath H2 estimation in mixed expired air is a non-invasive, reliable procedure for detection of monosaccharide malabsorption in infancy.

Mucosal Function and Breath Hydrogen Excretion: Comparative Studies in the Clinical Evaluation of Children with Nonspecific Abdominal Complaints

To evaluate the role of the lactose breath hydrogen test for the detection of lactose malabsorption in children with chronic nonspecific abdominal complaints, breath hydrogen excretion was measured in 131 children with recurrent abdominal pain (n = 75) or chronic nonspecific diarrhea (n = 56) following a lactose load (2 gm/kg; maximum 50 gm). The data were compared to those obtained from lactose tolerance tests (n = 113) and symptom response following a lactose load (n = 109) performed simultaneously with the lactose breath hydrogen test, and with results from small bowel biopsies obtained in 31 children to determine dissacharidase activity and mucosal histology. The results indicate that an increase in breath hydrogen of greater than 10 ppm above base line values (delta ppm) by 120 minutes ("early increase" response) completely discriminates between biopsy-proven isolated lactase-insufficient and lactase-sufficient children. A similar increase after 120 minutes ("late increase" response) is consistent both with normal mucosal function and partial lactase insufficiency due to mucosal injury. Breath hydrogen responses predicted assayed lactase activity in all patients with isolated lactase insufficiency, but were "falsely negative" in four of ten children whose lactase insufficiency was secondary to mucosal injury. In both clinical groups, lactose malabsorbers report significantly more symptoms than absorbers (P less than .001), but neither symptom reports nor tolerance tests are accurate methods for distinguishing lactose malabsorbers from absorbers. Although the lactose breath hydrogen test provides objective documentation of lactose malabsorption, it is equally predictive of assayed lactase activity in all clinical groups.

Breath hydrogen reflects canine intestinal ischemia.

The relationship between breath hydrogen excretion and intestinal ischemia was investigated in nine mechanically ventilated dogs under pentobarbital anesthesia. An ileal segment was isolated in situ, ligated at each end, and insufflated with hydrogen. Expired air was collected at intervals. Blood volume was reduced 30% by three successive equivalent hemorrhages 10 min apart. Local bowel ischemia was produced by clamping the blood supply to the isolated segment for 10 min. Graded hemorrhage produced step-wise reductions in breath hydrogen concentration, to 77 +/- 13, 66 +/- 15, and 35 +/- 8% (mean +/- S.E.) of baseline after the first, second, and third hemorrhages, respectively. These reductions correlated highly (r = 0.84; P less than 0.01) with declines in mean aortic blood pressure. Occlusion of blood supply caused a significant (P less than 0.025) decrease in breath hydrogen concentration and excretion to 39 +/- 14% of baseline. Termination of occlusion was followed within 2 min by a 7-fold increase in breath H2 concentration above the original baseline, probably reflecting reactive hyperemia. Breath hydrogen measurements appear to reflect functional (hemorrhagic shock-induced) and mechanical (vascular occlusion induced) enteric ischemia in dogs.

Milk tolerance, gastric emptying, and breath hydrogen excretion

Milk tolerance, gastric emptying, and breath hydrogen excretion

Failure of the hydrogen breath test to detect pulmonary sugar malabsorption.

Five patients with sucrase-isomaltase deficiency, and one patient with primary glucose-galactose malabsorption had no increases in breath hydrogen excretion after oral sucrose or glucose. Anaerobic incubation with sugars of stool suspensions from 5 patients with primary sugar malabsorption produced by trace of hydrogen (17 microliter) in only one, while those from 13 or 14 controls produced a mean hydrogen volume of 640 microliter under similar conditions. Altered bacterial metabolism is a probable explanation. Breath hydrogen excretion did increase appreciably in 2 of these patients after oral lactulose showing that hydrogen excretion may vary according to the substrate. Therefore, observation of breath hydrogen excretion after lactulose is not recommended as a means of predicting false-negative breath tests with other sugars. The hydrogen breath test is not a reliable mean of diagnosing primary sugar malabsorption in children.