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Biomedical subjects

H J Binder

Publications and source records attributed to H J Binder.

At least 145 records · Page 8Linked to original sources
PubMed1976

Serum lysozyme in inflammatory bowel disease.

Serum lysozyme activity was measured in 18 patients with ulcerative colitis and 40 patients with Crohn's disease by both the turbidimetric and lysoplate method. Only one patient with ulcerative colitis and eight patients with Crohn's disease had increased serum lysozyme activity by either or both methods. Both methods appeared equally sensitive in detecting increased serum lysozyme activity. In Crohn's disease, the percent with elevated values increased with increase in disease activity.

Colitis, Ulcerative↗
PubMed1976

Effect of bile salts and fatty acids on the colonic absorption of oxalate.

These studies were designed to evaluate the effect of bile salts and fatty acids on colonic oxalate absorption. Five millimolar deoxycholate significantly increased oxalate absorption from 34.2 +/- 9.4 nmoles per min per g dry weight to 330.4 +/- 47.3 (P less than 0.001) and changed water absorption to water secretion. Deoxycholate also increased the absorption of urea, decreased the electrical potential difference, and increased colonic clearance of oxalate, observations which are consistent with an increase in colonic mucosal permeability. In contrast, taurocholate did not increase oxalate absorption. Ricinoleic acid also significantly increased the absorption. These results suggest that bile salts and fatty acids increase colonic absorption of oxalate. Oleic acid had similar effects on oxalate absorption but was less effective than ricinoleic acid. Octanoic acid, a medium chain fatty acid, did not alter oxalate absorption of oxalate by a nonspecific alteration of mucosal permeability. These observations may further explain many of the clinical phenomena associated with enteric hyperoxaluria.

Animals↗
PubMed1975

Bile salt alteration of ion transport across jejunal mucosa.

The effect of conjugated dihydroxy and trihydroxy bile salts on electrolyte transport across isolated rabbit jejunal mucosa was studied. Both taurochenodeoxycholic acid and taurocholic acid increased the short-circuit current (Isc) in bicarbonate-Ringer solution but not in a bicarbonate-free, chloride-free solution. Taurochenodeoxycholic acid was significantly more effective than taurocholic acid in increasing Isc. The presence of theophylline prevented the taurochenodeoxycholic acid- and taurocholic acid-induced increase in Isc. Transmural ion fluxes across jejunal mucosa demonstrated that 2 mM taurochenodeoxycholic acid decreased net Na+ absorption, increased net Cl- secretion and increased the residual flux (which probably represents HCO3- secretion). These studies support the hypothesis that cyclic AMP may be a mediator of intestinal electrolyte secretion.

Animals↗
PubMed1975

Jejunal fluid and electrolyte secretion in carcinoid syndrome.

To evaluate the pathogenesis of the diarrhea of carcinoid syndrome, triple-lumen jejunal-perfusion studies were performed in three patients with carcinoid syndrome and diarrhea and eleven control subjects. In contrast to the net absorption observed in the control subjects during perfusion with an isotonic mannitol-saline solution, net secretion occurred in two of the three carcinoid-syndrome patients. Glucose absorption and glucose-stimulated fluid absorption were normal in the carcinoid-syndrome patients. Methysergide controlled the diarrhea and in one patient net absorption was observed during methysergide therapy. These studies suggest that intestinal secretion may be one of the pathogenetic factors responsible for the diarrhea of carcinoid syndrome and provide additional evidence of the importance of intestinal electrolyte secretion in the genesis of many diarrheal states.

Aged↗
PubMed1975

Glucagon secretion in acute and chronic pancreatitis.

Plasma pancreatic glucagon concentrations were determined in the basal state and after the infusion of alanine in 10 patients with acute pancreatitis (5 in an initial episode of pancreatitis), in 10 patients with chronic pancreatic insufficiency, and in 21 healthy controls. In acute pancreatitis, basal glucagon levels were nine times normal but were higher during the initial attack than with a history of previous attacks. The glucagon response to alanine was also increased threefold to fourfold in initial attacks. In contrast, after recovery from the initial attack of acute pancreatitis, during acute episodes of pancreatitis in patients with a history of previous attacks, and in patients with pancreatic insufficiency, alanine failed to elicit a consistent rise in plasma glucagon. The data suggest that hyperglucagonemia may contribute to the hyperglycemia of acute pancreatitis, particularly during the initial episode. Loss of alpha cell responsiveness to alanine provides a sensitive index of previous pancreatitis.

Acute Disease↗
PubMed1975

A controlled trial of azathioprine in the management of chronic ulcerative colitis.

To determine the efficacy of azathioprine in the treatment of ulcerative colitis, a 6-month double blind trial was carried out. Thirty patients with chronic ulcerative colitis who required the equivalent of at least 10 mg of prednisone per day over the 3 months prior to entering the study were randomized into placebo and azathioprine (1.5 mg per kg) treatment groups. Reduction of steriods was a major objective of the trial. Age and sex distribution, number of bowel movements, sense of well being, steroid dosage, and findings on proctoscopy, rectal biopsy, and colon X-ray initially were similar in the two groups. No side effects were associated with azathioprine. Although steroid dose was lower (p less than 0.05) in the azathioprine group at the termination of the study, no difference between the two groups could be detected in the number of bowel movements, sense of well being, and findings on proctoscopy during the first 3 weeks compared with the last 3 and during the first 3 months compared with the last 3. Although azathioprine does not confer dramatic benefit upon patients with chronic ulcerative colitis who require steroids, it does permit reduction of steroid dosage without apparent worsening of the disease. Its major value in ulcerative colitis may be in facilitating significant decreases or complete discontinuance of steroids.

Adolescent↗
PubMed1975

A controlled evaluation of intravenous adrenocorticotropic hormone and hydrocortisone in the treatment of acute colitis.

This study compares the efficacy of intravenous adrenocorticotropic hormone (ACTH) with intravenous hydrocortisone in the treatment of patients with symptomatic inflammatory bowel disease. Drug doses were pharmacologically equivalent on the basis of achieved plasma cortisol levels and continuously monitored urinary corticoid excretion rates. Drug selection and patient evaluation were accomplished with a random double blind technique. Evaluation of 22 consecutive hospital patients indicates that ACTH and hydrocortisone, when administered intravenously in pharmacologically equivalent dosage, are therapeutically equivalent, that response to ACTH is rapid, with no therapeutic lag, and that differences in therapeutic responses cannont be corrrelated with differences in systemic steroid levels.

17-Hydroxycorticosteroids↗
PubMed1975

Effect of dioctyl sodium sulfosuccinate on colonic fluid and electrolyte movement.

These studies evaluated the effect of dioctyl sodium sulfosuccinate (DSS), a detergent and the active ingredient of some commercially available stool softeners, on intestinal fluid and electrolyte movement. DSS produced water, sodium and chloride secretion into the in vivo rat cecum. This secretion readily reverted to net absorption following replacement of DSS by isotonic saline. In in vitro studies, DSS increased the short circuit current and diminished sodium absorption. The increase in short circuit current was not observed either when HCO3 and chloride were absent from the incubation solution or when theophylline was present. DSS also significantly increased mucosal cyclic adenosine monophosphate levels. These results which are similar to previous studies of the effect of cholera enterotoxin on ileal mucosa and bile salts on colonic mucosa are consistent with the proposal that DSS stimulates fluid and electrolyte secretion which is mediated by increased mucosal cyclic adenosine 3':5' monophosphate.

Animals↗
PubMed1975

Effect of Shigella enterotoxin on electrolyte transport in rabbit ileum.

Shigella dysenteriae I is one of several bacteria which produces an enterotoxin capable of stimulating intestinal water and electrolyte secretion. Unlike cholera and Escherichia coli enterotoxins which have been shown to increase intracellular cyclic adenosine monophosphate levels in the small intestine, the mechanism by which shigella enterotoxin causes intestinal secretion is not known. To study shigella enterotoxin-stimulated intestinal secretion, rabbit ileal mucosa exposed in vivo to Shigella dysenteriae I enterotoxin was studied in vitro in a modified Ussing chamber. Fluid and electrolyte accumulation occurred in vivo and net sodium secretion was present in vitro in the enterotoxin-exposed tissue in contrast to net sodium absorption in control mucosa. Short-circuit current (Isc) was similar in shigella enterotoxin-exposed tissue compared with control tissue. The increase adenosine monophosphate was similar to enterotoxin-exposed and control mucosa. The addition of glucose resulted in a smaller increment of Isc in shigella enterotoxin-treated tissue. Mucosal cyclic adenosine monophosphate levels in enterotoxin-exposed mucosa did not differ from those of control. These results indicate that the characteristics of rabbit ileal mucosa exposed to shigella enterotoxin and cholera enterotoxin markedly differ, although both produce electrolyte secretion both in vivo and in vitro. These studies further suggest that, in contrast to its role in cholera enterotoxin-induced intestinal secretion, cyclic adenosine monophosphate may not be in the mediator of shigella enterotoxin stimulation of intestinal fluid and electrolyte secretion.

Animals↗
PubMed1973

Familial hypophosphatemic rickets: defective transport of inorganic phosphate by intestinal mucosa.

Uptake of inorganic phosphate is impared in intestinal mucosa from hemizygous males and heterozygous females with X-linked familial hypophosphatemic rickets. Considerable intrafamilial and interfamilial variation in uptake of inorganic phosphate is observed in affected patients. Uptake by normal mucosa is concentrative and energy-dependent, and is mediated by at least two systems with widely different affinities. These results lend direct support to the thesis that the primary metabolic disturbance in this disease results from impaired transport of inorganic phosphate in kidney and gut.

Biological Transport↗