Peptic ulcer disease in cystic fibrosis: an unusual occurrence in black adolescents.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J A Perman.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The objective of this study was to determine the influence of frequent and long-term consumption of legume seeds on colonic function. Two groups of subjects were studied--one group habitually consumed legume seeds as part of their normal diet, a second group only infrequently consumed legumes. No differences between these groups could be detected for fecal output and frequency, intestinal transit time, VFA excretion or fecal pH during 23-day study periods in which subjects consumed either their usual diet or 100 g red kidney beans, daily. However, the addition of beans to the diets of both groups provided significantly more dietary fiber, and produced greater fecal output and a higher concentration of VFA in feces. Fecal output appeared to be determined by two independent parameters--dietary fiber intake and VFA excretion. Beans provided a physiologically useful source of dietary fiber and favorably influenced colonic function.
Measurement of hydrogen (H2) in expired air by interval sampling after oral administration of carbohydrate detects sugar malabsorption. Standard breath H2 tests require comparison of H2 concentrations in expired air samples obtained immediately before and after delivery of a test substrate. Comparison of interval samples assumes that minute ventilation (VE) remains constant unless H2 is independent of VE. Because healthy individuals have variable VE, we determined how H2 is influenced by changes in VE. H2 concentration was studied at different ventilatory rates in eight healthy adults. It varied inversely with VE in all subjects. We also compared the effect of changes in VE on the relationship between H2 and carbon dioxide (CO2) concentrations in expired air samples. At constant VE, the relationship between H2 and CO2 was linear (r = 0.95, P less than 0.001). As VE changed, the relationship between H2 and CO2 became nonlinear. Changes in VE altered methane concentrations in expired air samples from two subjects in a manner comparable to the effect on H2. These results demonstrate that breath H2 concentrations vary with ventilatory rate. Under conditions where frequent changes in VE are likely, independent measures for ensuring constant VE over sampling times are necessary. Use of CO2 as an internal standard to normalize H2 values to an alveolar concentration is appropriate only under conditions of constant VE.
Excretion of hydrogen in breath commonly persists despite an overnight fast. Although elevation of hydrogen concentration above the fasting value after administration of a test sugar is evidence of malabsorption, the significance of the fasting value itself is unknown. We determined the normal limits of fasting breath hydrogen in healthy children and adults, and in patients with chronic diarrhea or recurrent abdominal pain. Fasting breath hydrogen in 221 healthy children and 9 healthy adults averaged 7.1 +/- 5.0 parts per million (mean +/- SD), exceeding 30 parts per million in less than 1%. No value exceed 42 parts per million. In 73 patients with recurrent abdominal pain and 76 patients with chronic diarrhea, fasting breath hydrogen was less than 42 parts per million in 97% and 83%, respectively. History and laboratory data were reviewed in the 15 patients where fasting breath hydrogen exceeded 42 parts per million. Seven had documented small bowel bacterial overgrowth and an additional 3 patients had radiographic evidence of intestinal stasis. Using test dinner meals, we prospectively evaluated the effect of previously ingested foods containing complex carbohydrates on fasting breath hydrogen. Dinner meals consisting of rice, wheat, or beans influenced fasting breath hydrogen values, but did not result in elevated fasting breath hydrogen in healthy individuals. Rice bread resulted in uniformly low fasting breath hydrogen values in healthy subjects (2.0 +/- 2.5 parts per million), but fasting breath hydrogen remained elevated in patients with bacterial overgrowth. Our studies indicate that conditions for measurement of the fasting breath hydrogen value may be standardized to improve discrimination between normal and abnormal values.
In two unrelated boys, 5.3 and 3.8 years of age with hereditary fructose intolerance, apparently isolated growth retardation (-2.71 S.D. and -2.40 S.D.) occurred after infancy, even though acute symptomatic fructose intoxication was prevented by restriction of dietary fructose. When more stringent restriction of dietary fructose was instituted (approximately 40 mg per kilogram of body weight per day), growth velocity increased from the 25th to the 97th percentile in one child and from well below the 3d to above the 75th percentile in the other. When restriction of dietary fructose was experimentally relaxed (from 10 to 250 mg per kilogram per day), neither boy had symptoms, hypoglycemia, or evidence of hepatic or renal dysfunction, but both had sustained hyperuricemia and hyperuricosuria and increases in the plasma concentration and urinary excretion of magnesium. We conclude that in patients with hereditary fructose intolerance, clinically important chronic fructose intoxication can occur after infancy without causing symptoms of acute fructose intoxication and can be expressed as an apparently isolated, reversible retardation of somatic growth with a continuing disorder of adenine nucleotide metabolism, characterized in part by recurrently increased rates of degradation of adenine nucleotides.
Explore the source record for details and available documents.
Three substrates labeled with nonradioactive 13C have been employed to establish a trilogy of noninvasive breath tests to detect fat malabsorption in children and then to differentiate the etiology of the steatorrhea. Administration of 17 mg/kg of (13C)triolein Lipomul (The Upjohn Co., Kalamazoo, Mich.) resulted in a peak excretion rate of 13CO2 greater than 2.7% dose/h in 10 normal subjects (mean value 4.96 +/- 2.2% dose/h) whereas all 17 subjects with fat malabsorption were below this value (mean value, 0.75% +/- 0.63% dose/h); p less than 0.001). For the detection of fat malabsorption, the discriminative value of (13C)triolein was superior, 100% sensitive, and 89% specific, while the use of (13C)palmitic acid (17 mg/kg) or (13C)trioctanoin (7.5 mg/kg) alone yielded both false-positive and false-negative results. In 6 out of 6 cases, pancreatic insufficiency could be differentiated from mucosal disease (7 patients) or bile salt deficiency (4 patients) by the presence of abnormal triolein or trioctanoin breath tests, or both but normal palmitic acid breath tests. However, further differentiation of mucosal disorders from bile salt disorders could not be achieved using either a single- or a multiple-substrate breath test. The use of the single triolein breath test in children offers an attractive, sensitive alternative to conventional fecal fat measurements to establish the presence of steatorrhea, and when using 12C-lipid with multiple substrates, the tests are capable of providing additional insight into the mechanism of fat malabsorption.
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.
Hydrogen produced by colonic bacteria and excreted in breath is a useful index of carbohydrate malabsorption. Since colonic contents are often acidic in individuals with carbohydrate malabsorption and in normal newborns, we determined the effect of colonic acidification on H2 production. Acidification of colonic contents by dietary means significantly reduced excess breath H2 excretion from 55.4 +/- 11.1 (SEM) to 12.2 +/- 3.1 ml/4 h (P less than 0.05) after administration of 0.3 g/kg of the nonabsorbable sugar lactulose to five normal adult subjects. Similarly, the breath H2 response to lactose was reduced or eliminated in two proven lactose malabsorbers after acidification. The correlation between pH and H2 production from carbohydrate was further investigated in adults and neonates, using an in vitro fecal incubation system. Glucose disappearance and H2 production were pH dependent and highly correlated (r = 0.94) in the pH range 5.5-7.6. Maximal production of H2 from glucose by fecal incubates occurred at pH 7.0-7.45. Inhibition of H2 production from carbohydrate occurred at acid pH. H2 per hour from glucose at pH 6.2 and 5.5 averaged 60.2% and 24.2%, respectively, of that produced at neutral pH. Rapid reversal of pH-induced inhibition by neutralization indicated a metabolic, rather than a bactericidal process. The observations indicate that the breath H2 response to malabsorbed carbohydrate is affected by colonic pH. It appears that the efficiency of bacterial carbohydrate metabolism in the colon is pH dependent.
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.
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.
Explore the source record for details and available documents.
The accuracy of the serum ceruloplasmin level in distinguishing chronic active hepatitis from Wilson disease was compared to the 24-hour urinary copper excretion and hepatic copper content in 20 untreated patients with chronic active hepatitis and 25 with Wilson disease. Serum ceruloplasmin levels were decreased in five patients (25%) with chronic active hepatitis and were normal in seven patients (28%) with Wilson disease at the time of diagnosis. The 24-hour urinary copper excretion failed to provide accurate discrimination between the two groups, being elevated in all patients with Wilson disease and in five of eight patients with chronic active hepatitis studied. All patients with Wilson disease had hepatic copper levels greater than 400 microgram/gm dry weight, whereas patients with chronic active hepatitis had levels less than 300 microgram/gm dry weight. The discriminatory value of hepatic copper concentration makes this the most reliable test for differentiating chronic active hepatitis and Wilson disease in children and adolescents. The serum ceruloplasmin level may not be significantly accurate for definitive diagnosis in this age group.
To assess whether malabsorption of specific sugars is easily detected in a pediatric population by interval measurement of breath hydrogen excretion, hydrogen concentration was determined following administration of oral sucrose to six sucrose-intolerant children with congenital sucrase-isomaltase deficiency and in 16 sucrose-tolerant control subjects. Breath samples were collected by means of a newly devised nasal prong technique not requiring active patient cooperation and suitable for use in all age groups. Breath hydrogen concentrations obtained by samples collected by this method correlated highly (r = 0.94) with the previously validated modified Haldane-Priestley tube method for sampling alveolar air. Identification of sucrose-intolerant individuals was achieved on the basis of hydrogen excretion: peak values, expressed as parts per million above baseline (deltappm), equalled 114 +/- 63 (mean +/- SD) versus 2.4 +/- 3.6 deltappm in control subjects (P = 0.007). Best discrimination between the groups occurred at 90 minutes postingestion. The findings validate this simple method for collection of expired air and demonstrate that breath hydrogen determination permits the noninvasive detection of sucrose malabsorption in children.
Discrimination between hepatitis A and B is becoming easier as the serologic and clinical characteristics of each type become better known. Hepatitis A is generally a benign pediatric illness with few sequelae. In contrast, hepatitis B is more often associated with complications and may progress to chronic liver disease in as many as 10% of cases. Chronic persistent hepatitis appears to be a benign disorder not requiring therapy. Occasionally related etiologically to virus B, chronic active hepatitis is often associated with severe clinical illness. However, it generally responds to steroid therapy, at least initially, and may be arrested or cured.
Explore the source record for details and available documents.