Serum gastrin in Zollinger-Ellison syndrome: I. Prospective study of fasting serum gastrin in 309 patients from the National Institutes of Health and comparison with 2229 cases from the literature.

Pepsinogens, Pepsins, and Pepsin Inhibitors

Gastric secretion in Zollinger-Ellison syndrome. Correlation with clinical expression, tumor extent and role in diagnosis--a prospective NIH study of 235 patients and a review of 984 cases in the literature.

Despite general awareness of Zollinger-Ellison syndrome (ZES) by most physicians and more than 3000 articles written about it since 1955, the diagnosis of ZES is still delayed for a mean of 5 years. Recent studies show it is being delayed even more with the widespread use of proton pump inhibitors. A number of tumor markers, in addition to assessing serum gastrin, such as chromogranin A, neuronspecific enolase, and subunits of chorionic gonadotropin, have been proposed for use in either the diagnosis of pancreatic endocrine tumors, such as gastrinomas, or for assessment of tumor extent and growth. In this article important recent insights into the diagnosis of ZES as well as the clinical usefulness of assessing tumor markers for diagnosis and determination of disease extent and growth are discussed. Approximately 25% of ZES cases are due to multiple endocrine neoplasia type 1 (MEN1). A number of important studies in this group of patients are also reviewed. Finally, almost every patient with ZES has marked gastric acid hypersecretion, and its current treatment as well as the longterm possible side effects are reviewed briefly.

Zollinger-Ellison syndrome revisited: diagnosis, biologic markers, associated inherited disorders, and acid hypersecretion.

Depression of metabolism by hypothyroidism decreases oxidant production and thus protects tIssues against oxidant damage. Moreover, it is well-known that abnormal gut motility is a common manifestation in hypo/hyperthyroidism. In this study, we aimed to investigate the putative beneficial effects of methimazole on oxidative injury and dysmotility in a rat colitis model. Methimazole (0.04%) was administered in drinking water starting 15 days prior to induction of colitis. Colitis was induced by intracolonic administration of trinitrobenzene sulfonic acid (30 mg/ml; 0.8 ml) in ethanol. Six days after the induction of colitis, the fecal output was measured and used as an index for colonic motility. All rats were decapitated on the seventh day. The distal colon was weighed and the mucosal lesions were scored. Colonic lipid peroxidation (LP) and glutathione (GSH) measurements were performed. The macroscopic score, the colonic wet weight and LP values of the euthyroid colitis group were found to be higher than those of the control group (P<0.05-0.001). All these parameters were reduced in the methimazole-treated colitis group (P<0.01-0.001). The decrease in colonic GSH levels in the colitis group was completely abolished in the methimazole-treated colitis rats (P<0.01). Induction of colitis increased the average fecal output compared with the control group (P<0.05) and methimazole in the colitis group exaggerated the fecal output (P<0.001). In conclusion, methimazole reduces colonic oxidative injury probably due to hypometabolism, which is associated with a decrease in the production of reactive oxygen intermediates and an increase in the response of antioxidant systems.

/pdf/methimazole-induced-hypothyroidism-in-rats-ameliorates-2fevyw8xfw.pdf

Methimazole-induced hypothyroidism in rats ameliorates oxidative injury in experimental colitis

Myoelectrical activity was studied in normothyroid and hypothyroid Labrador dogs in the resting state, following injection of pentagastrin, bethanechol chloride, and after feeding. Hypothyroidism was produced by total thyroidectomy and chronic treatment with thiouracil. Electrodes were surgically implanted over the serosa of the stomach, duodenum, jejunum, and ileum and used for repeated recording of myoelectrical activity of gastrointestinal muscles. A strain gauge was implanted over the gastric antrum and served to record mechanical activity of the stomach. As compared with control dogs, hypothyroid animals showed (a) decreased frequency of electrical control activity of the stomach and jejunum, (b) decreased occurrence of electrical response activity (spike potentials) following stimulation, and (c) decreased mechanical response to the same stimulants, ie, pentagastrin, bethanechol chloride, and food.

Myoelectrical and Mechanical Activity of Stomach and Intestine in Hypothyroid Dogs

1. Adult male rats with permanent gastric fistulas were infused intravenously for 24 hr. with histamine dihydrochloride in normal saline. The infusion rate was 100 ml./kg./24 hr.; doses of histamine tested in this study were 5, 10, 25, 50, 75, 100, 125, 250, 500, 1000, 1500, and 2000 mg./kg./24 hr.

Determination of histamine dose causing maximal gastric secretion. Study in rats with gastric fistulas.

Adult male rats with permanent gastric fistulas, in some of whom the cardia and pylorus had been ligated, were infused intravenously for 24 hr with histamine dihydrochloride. The output of HCl, pepsin, and hexosamine in 24-hr secretion was studied. Prior to infusion, rats' stomachs were washed with either normal saline or 2M NaCl; hypertonic NaCl is known to induce reduction of gastric mucus. In animals with reduced gastric mucus, glandular peptic ulcers were found at the end of histamine infusion. No gastric lesions were detected in stomachs washed with normal saline. The occurrence of peptic ulcers in rats correlated satisfactorily with the alteration of the gastric “mucus barrier” but was not dependent upon the acidity or pepsin content of gastric juice.

Experimental deficiency of gastric “mucus barrier”

An anticholinergic, propantheline bromide, was given in a dosage of 5 mg./ kg. body weight twice daily to rats. Gastric function was studied after 3, 6, 9, and 12 months of this treatment. Gastric content was collected after (1) pyloric and cardia ligation; (2) pyloric ligation only; and (3) during a 24-hr, intravenous infusion of histamine. Under the experimental conditions described, a significant reduction of gastric secretion was found in rats after long-term administration of propantheline bromide. This is considered due to the impairment of gastric secretory function induced by repeated inhibition of gastric secretion over a prolonged period.

Effect of long-term treatment with an anticholinergic drug on gastric secretion in rats.

Totally isolated canine stomach, included into a perfusion system containing a living “supporting” dog, serving as an oxygenator, is able to secrete juice rich in H+ for several hours. Blood circulating in this system is homologous blood and the stomach may be stimulated by intraarterial continuous infusion of a secretion stimulant. The ex vivo preparation was used for the study of secretion stimulated by histamine and/or bethanechol chloride, a stable cholinergic drug. All combinations of histamine plus bethanechol chloride used in this study gave higher outputs of HCl and pepsin than could be accounted for on the basis of summation of stimulatory effects. Outputs of HCl and pepsin were higher when two agents were given together than the maximal output of either HCl or pepsin during stimulation by one agent. Potentiation with regard to acid and pepsin secretion was evident when a cholinergic drug, in various doses, was superimposed on histamine stimulation.

Influence of cholinergic stimulation on gastric secretory response to histamine in ex vivo isolated canine stomach

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