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Biomedical subjects

S E Silvis

Publications and source records attributed to S E Silvis.

At least 37 records · Page 2Linked to original sources
PubMed1985

Final report on the United States Multicenter Trial comparing ranitidine to cimetidine as maintenance therapy following healing of duodenal ulcer.

Patients with recently healed duodenal ulcers were enrolled at 14 participating centers in a 12-month study comparing the effectiveness of ranitidine and cimetidine, two H2-receptor blockers, for maintenance therapy. Patients were randomly assigned to take bedtime doses of 150 mg of ranitidine (n = 60) or 400 mg of cimetidine (n = 66). Endoscopic examinations were scheduled at baseline and after 4, 8, and 12 months of therapy, or when symptoms compatible with active ulcer disease developed. Life-table analysis indicated a relapse rate of 16% for the ranitidine subjects and 43% for the cimetidine subjects during the 12-month period (p = 0.01). Therapy was discontinued in one ranitidine subject and two cimetidine subjects for adverse events considered drug-related. There were no drug-related laboratory abnormalities in either treatment group. No significant drug-related adverse effects were seen with either drug during this 1-year trial. At the doses prescribed, ranitidine was superior to cimetidine as maintenance therapy in duodenal ulcer disease.

Cimetidine↗
PubMed1985

Sodium morrhuate stimulates granulocytes and damages erythrocytes and endothelial cells: probable mechanism of an adverse reaction during sclerotherapy.

Stimulated by a patient with dyspnea, thrombocytopenia, and leukopenia after sodium morrhuate sclerotherapy, we studied the effect of this agent on the plasma coagulation and complement systems, the formed elements of the blood, and cultured human endothelial cells. The addition of sodium morrhuate to citrated plasma did not cause clotting or shorten the prothrombin time or partial thromboplastin time. Incubation of a 1:100 dilution of the clinical sodium morrhuate preparation in heparinized plasma led to a modest rise in [C3a]. The addition of the drug (dilutions 1:50 to 1:300) to granulocytes caused prompt aggregation (and, at the higher concentrations, granulocyte cytotoxicity [trypan blue exclusion; lactate dehydrogenase release]), but the same dilutions failed to aggregate platelets. However, 0.05% morrhuate added to washed red blood cells caused a prompt 84.0% (+/- 0.8% SEM) hemolysis, rendering the supernatant buffer a potent platelet aggregant. Not only was this sclerosing agent toxic to granulocytes and red cells, but a 1:1000 dilution of the drug also caused the destruction of 35.5% (+/- 6.6%) of cultured endothelial cells as measured by chromium 51 release. Three other agents in current use (ethanolamine oleate, sodium tetradecyl sulfate, and polidocanol) were studied and found to cause effects qualitatively similar to those of sodium morrhuate. We conclude that these drugs cause phlebosclerosis not primarily through induction of plasma coagulation, but by directly damaging endothelium and red cells, triggering platelets, and aggregating granulocytes at the venous wall endothelium. These effects likely derive from the surfactant properties of sodium morrhuate as well as its high arachidonate content.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Coagulation↗
PubMed1984

Results of the United States ranitidine maintenance trials.

In two long-term studies, efficacy and safety of maintenance therapy with ranitidine (150 mg at bedtime) versus a placebo or cimetidine (400 mg at bedtime) were assessed. Fourteen centers enrolled 125 patients in the ranitidine-cimetidine study, and 26 centers enrolled 277 patients in the ranitidine-placebo study. Both studies were conducted for 12 months. Using life-table analysis, 15 percent of the ranitidine-treated patients and 44 percent of the cimetidine patients relapsed by the 12th month of treatment (p less than 0.007). Ulcer recurrence rates were in 19, 24, and 35 percent for the ranitidine-treated patients and 44, 54, and 60 percent for patients taking placebo at four, eight, and 12 months, respectively (p less than 0.001). Possible reasons for the increased effectiveness of ranitidine over cimetidine are the increased potency of ranitidine and longer acid suppression during the middle and later periods of sleep. No significant changes were observed in multiple laboratory parameters, ophthalmoscopic examinations, electrocardiographic results, or vital signs. All therapies appeared to be safe during this 12-month trial.

Adult↗
PubMed1984

Demodulated low frequency currents from electrosurgical procedures.

Low frequency currents produced incidental to electrosurgical procedures are usually only a minor threat unless they are coupled directly into the heart through a catheter or a thoracic surgical procedure. However, should the low frequency blocking capacitors in the electrosurgical generator fail in the conducting state, extremely dangerous low frequency currents of many milliamperes may flow into the patient. Even with properly functioning capacitors, low frequencies up to several milliamperes may be produced by some generators. The results of this study show that the coagulation mode of operation produces greater amounts of low frequency currents than the "pure cutting" mode at the same power setting. These results also demonstrate that the higher the generator power output, the higher the magnitude of the low frequency currents.

Animals↗
PubMed1983

Abnormal zinc metabolism in type II diabetes mellitus.

Zinc metabolism in 20 patients with stable type II diabetes mellitus was investigated. Twenty-five percent of these patients had depressed serum zinc concentrations, and all demonstrated hyperzincuria. Urinary zinc loss was greater when proteinuria was present and correlated with the mean serum glucose concentration. Studies of gastrointestinal zinc absorption suggested zinc malabsorption in patients with type II diabetes mellitus. Glucose infusion in normal dogs produced hyperzincuria without a diminution in serum zinc. It is concluded that hyperzincuria, resulting from a glucose-mediated process that is not osmotic, interacts with impaired zinc absorption to produce zinc deficiency in patients with type II diabetes mellitus.

Adult↗
PubMed1983

Effect of exorphins on gastrointestinal function, hormonal release, and appetite.

Peptic digestion of gluten results in the production of substances having opiatelike activity in bio- and receptor assays. These substances have been termed exorphins. In this study, we determined the effect of gluten, hydrolyzed gluten, and hydrolyzed gluten plus the opiate blocker naloxone on a variety of hormonal parameters, gastrointestinal transit time, small bowel mucosal integrity, and satiety. Hydrolyzed gluten prolonged intestinal transit time, and this effect was reversed by concomitant administration of naloxone. Hydrolyzed gluten also produced a naloxone-reversible increase in plasma somatostatinlike activity, which may have been responsible for the delayed transit time. No effects of the "exorphins" could be demonstrated on serum gastrin, cortisol, carbohydrate metabolism, or small bowel mucosal integrity. Although a number of studies have suggested a role for endogenous opiates in appetite regulation, we could not demonstrate any effect of "exorphins" on the amount of calories ingested nor on the perception of satiety. This study defines a potential role for small opiatelike peptides in foodstuffs in the regulation of intestinal function.

Adult↗
PubMed1982

Endogenous opiates and stress ulceration.

Parenteral administration of the opiate antagonist, naltrexone, had a cytoprotective effect against stress-induced ulceration. This effect appears to be due to blockade of peripheral rather than central endogenous opiates and is not related to the central inhibitory effect of opiates on gastric acid secretion. Opiates have complex effects on gastric mucosal blood flow which may explain their role in stress ulceration.

Animals↗
PubMed1982

Central regulation of gastric acid secretion: the role of neuropeptides.

A variety of stimuli can act through the central nervous system to alter gastric acid secretion. Lesioning and stimulation experiments have established roles for the lateral and ventromedial hypothalamus and the limbic system in the central regulation of gastric acid secretion. Recently a number of neuropeptides have been demonstrated to alter gastric acid secretion after central administration. Thyrotropin-releasing hormone (TRH) and gastrin both increase gastric acid secretion, whereas bombesin, calcitonin, the endogenous opioid peptides and neurotensin decrease gastric acid secretion. With the exception of bombesin, all the other neuropeptides appear to produce their effects through a vagally mediated mechanism. In addition, a number of these neuropeptides, when centrally administered, have been demonstrated to exert a potent cytoprotective effect against stress ulcer development. This review develops a peptidergic hypothesis of gastric acid secretion, suggesting that the final integration of the cephalic phase of gastric acid secretion is brought about by maintaining a delicate balance in the concentration of a number of interacting peptides and monoamines.

Animals↗
PubMed1982

Effect of cimetidine on the absorption of vitamin B12.

The effect of cimetidine on the absorption of orally administered crystalline or food (egg yolk-bound) vitamin B12 (B12) was studied in 13 patients. Absorption or crystalline B12 was normal and not significantly changed by cimetidine. In contrast, the uptake of food-bound B12 decreased in all patients, from a mean of 5.3% without the drug to 2.5% after it, a fall of 53% (p less than 0.0001). This impairment of B12 absorption raises the possibility that long-term, full-dose therapy with cimetidine may produce B12 deficiency similar to that seen in other hypochlorhydric states. Our data indicate that cimetidine-induced B12 malabsorption would not be detected by the standard Schilling test.

Absorption↗