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A Stesin

Publications and source records attributed to A Stesin.

2 recordsLinked to original sources
PubMed1993

Alcohol-induced bone disease: relationship to age and parathyroid hormone levels.

Alcohol abuse leads to osteopenia and fractures. Epidemiological evidence suggests that older alcoholics are at substantially greater risk of fractures than younger alcoholics. To examine the interaction of age and alcohol abuse on bone mineral homeostasis, we studied 27 subjects with a history of 10 more years of alcohol abuse ranging in age from 26-68 years. They were evaluated for disordered bone mineral homeostasis by assessing bone density (by quantitative computed tomography of the lumbar spine), histomorphometry of a transcortical biopsy from the iliac crest, serum levels of vitamin D metabolites and parathyroid hormone, and serum and urine levels of bone minerals. Seventeen of the subjects were found to have spinal compression fractures by routine radiologic procedures. The older the subject the more likely the subject was to have such a fracture. Bone densitometry indicated a marked reduction in spinal bone density with 15 subjects below 2 SD of normal aged-matched controls. Bone density fell sharply with the age of the subject. Histomorphometry of iliac crest bone biopsies revealed no evidence of osteomalacia, but total resorption surfaces were increased. Consistent with the lack of osteomalacia were the normal levels of the vitamin D metabolites. The increased total resorption surfaces were correlated with high normal or elevated levels of parathyroid hormone as indicated both by radioimmunoassay and by urinary cAMP levels. Bone formation and active bone resorption (resorption surfaces containing osteoclasts) did not correlate with parathyroid hormone levels, however, but correlated negatively with age.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Cocaine increases natural killer cell activity.

The administration of epinephrine to humans increases natural killer (NK) cell activity and numbers. If endogenous catecholamines regulate NK cells, then their activity should be increased by cocaine, an agent that potentiates endogenous catecholamines. We investigated the in vivo effect of cocaine on NK cell activity and on the distribution of lymphocyte subsets, including NK cells. Intravenous cocaine (0.6 mg/kg) produced a three- to fourfold increase in NK cell activity in peripheral blood. The increase was accompanied by a marked and selective increase in circulating NK cells, as identified by the Fc receptor (Leu-11). Normal saline and benzoylecgonine, a major metabolite of cocaine, had little effect on NK cell activity or on levels of Leu-11+ cells. Other lymphocyte subpopulations were not increased by cocaine. The time course of the alterations in NK cell numbers and activity paralleled plasma levels of cocaine. In vitro cocaine did not increase NK cell activity. Our results indicate that cocaine selectively alters the activity and distribution of the NK lymphocyte subset. Because cocaine increases the activity of endogenous catecholamines, these findings suggest that human NK cells are selectively regulated by the sympathetic nervous system.

Adult↗