Our research group has conducted clinical trials of standard (imipramine, fluoxetine, and sertraline) and alternative antidepressants (dextroamphetamine and testosterone replacement therapy) in the treatment of clinical depression among patients with human immunodeficiency virus (HIV) illness. This report presents secondary analyses of data pooled from these trials with the purpose of comparing the antidepressant efficacy of these various agents. In all trials, a DSM-III-R depressive disorder was the primary criterion for study entry, and each treatment resulted in significant improvement after both 2 and 6 weeks of treatment according to the Hamilton Depression Rating Scale (HDRS). Response rates for standard antidepressants ranged from 70% to 74%, with similar, high response rates found in trials of dextroamphetamine (93%) and testosterone (81%). The response rate of each active drug treatment was superior to that of placebo (33%). Each treatment was well-tolerated in terms of side effects, and there was essentially no effect of any treatment on CD4 cell count. Differences in trial design, entrance criteria, and measurements require that caution be used in interpreting these results; nonetheless, each of the five treatments studied demonstrated strong efficacy and possessed relatively unique benefits, providing health care providers with valuable treatment options in addressing individual needs of patients.

1-Naphthylamine↗

PubMedDate not supplied

Growth factor insensitivity in renal failure.

Advanced chronic renal failure is associated with multiple endocrine and metabolic abnormalities that result from changes in the secretion and metabolism of hormones and growth factors and the target organ sensitivity to their physiological actions. As a consequence, growth retardation, bone disease, pertubations in lipid, carbohydrate and protein metabolism are commonly seen in patients with chronic renal failure. The recent availability of recombinant growth factors has provided new therapeutic opportunities for correcting these abnormalities. However because of the presence of end-organ resistance relatively high dose therapy is required and this carries an increased risk of side effects. One logical approach to this problem would be to prevent or treat the underlying resistance and thus restore sensitivity to endogenous GH or low doses of the recombinant molecule. To achieve this goal, a better understanding of the mechanism of growth factor resistance is required. In this lecture, in honor of the memory of Frank Carone. I review our current state of knowledge of the impact of advanced renal failure on the tissue sensitivity to insulin, growth hormone and insulin-like-growth factor I.

Animals↗