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Biomedical subjects

S Ghazvinian

Publications and source records attributed to S Ghazvinian.

7 recordsLinked to original sources
PubMed1983

Clinical pharmacology of bupropion and imipramine in elderly depressives.

The clinical efficacy and adverse reaction profile of bupropion, an atypical antidepressant, was compared with the tricyclic imipramine in 63 elderly depressives. Patients were randomly assigned to treatment with 150 or 450 mg/day of bupropion, 150 mg/day of imipramine, or placebo for 35 days. Both doses of bupropion were equivalent to imipramine in antidepressant efficacy. The higher dose of bupropion had a more rapid onset of effect than the low dose and significantly greater anxiolytic activity than either imipramine or the lower dose. Both doses of bupropion had adverse reaction profiles strikingly similar to placebo and, in marked contrast to imipramine, did not produce sedation or anticholinergic side effects. Cognition improved equally in all groups. It was concluded that bupropion has therapeutic advantages over the tricyclics in the treatment of elderly depressives.

Age Factors↗
PubMed1982

Treating the depressed elderly patient: the comparative behavioral pharmacology of mianserin and amitriptyline.

MIA is an effective antidepressant, comparable in therapeutic efficacy to the TCAs. Further, because of its weak antimuscarinic effects. Further, because of its weak antimuscarinic effects, MIA produces no significant cognitive impairment, alteration of cardiovascular function of anticholinergic side effects compared to the TCA's. While drowsiness is the most frequently reported adverse reaction with MIA, an h.s. dosing schedule can provide relief of insomnia and improve the quality of sleep (47,61). Therefore, because of MIA's advantageous pharmacodynamic profile, it offers an improvement in therapeutic index over the TCAs in the treatment of depression in the elderly.

Aged↗
PubMed1976

Tumor hypoglycemia: deficient splanchnic glucose output and deficient glucagon secretion.

Fasting hypoglycemia occurred in a patient with a histologically benign mesothelioma; the serum insulin was low (2-4 muU./ml.), as was the glucose utilization rate. Splanchnic glucose output was markedly decreased on direct measurement (21 mg./min.; normal: 108-180 mg./min.). Splanchnic uptake of gluconeogenic substrates plasma glucagon was low normal during hypoglycemia and responded poorly to oral and intravenous alanine. The nonsuppressible insulin-like (NSILA-s) and somatomedin-like activities of the serum were not elevated, and the tumor did not release insulin-like activity on incubation nor did it contain somatostatin. The marked decrease in splanchnic glucose output was the principal cause of hypoglycemia, was associated with an apparent decrease in glycogenolysis, and was at least partly due to deficient glucagon secretion. The relationship of the tumor to these defects is unclear. The tumor may have secreted an unknown insulin-like material affecting primarily the liver and/or pancreatic alpha cell. The approach used here may serve as a paradigm for the analysis of hypoglycemia not caused by excessive insulin.

Glucagon↗