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Endocr Rev. 2003 Apr;24(2):183-217.

Androgens and coronary artery disease.

Wu FC, von Eckardstein A.

Source

Department of Endocrinology, Manchester Royal Infirmary, University of Manchester, Manchester M13 9WL, United Kingdom. [email protected]

Abstract

A significant and independent association between endogenous testosterone (T) levels and coronary events in men and women has not been confirmed in large prospective studies, although cross-sectional data have suggested coronary heart disease can be associated with low T in men. Hypoandrogenemia in men and hyperandrogenemia in women are associated with visceral obesity; insulin resistance; low high-density lipoprotein (HDL) cholesterol (HDL-C); and elevated triglycerides, low-density lipoprotein cholesterol, and plasminogen activator type 1. These gender differences and confounders render the precise role of endogenous T in atherosclerosis unclear. Observational studies do not support the hypothesis that dehydroepiandrosterone sulfate deficiency is a risk factor for coronary artery disease. The effects of exogenous T on cardiovascular mortality or morbidity have not been extensively investigated in prospective controlled studies; preliminary data suggest there may be short-term improvements in electrocardiographic changes in men with coronary artery disease. In the majority of animal experiments, exogenous T exerts either neutral or beneficial effects on the development of atherosclerosis. Exogenous androgens induce both apparently beneficial and deleterious effects on cardiovascular risk factors by decreasing serum levels of HDL-C, plasminogen activator type 1 (apparently deleterious), lipoprotein (a), fibrinogen, insulin, leptin, and visceral fat mass (apparently beneficial) in men as well as women. However, androgen-induced declines in circulating HDL-C should not automatically be assumed to be proatherogenic, because these declines may instead reflect accelerated reverse cholesterol transport. Supraphysiological concentrations of T stimulate vasorelaxation; but at physiological concentrations, beneficial, neutral, and detrimental effects on vascular reactivity have been observed. T exerts proatherogenic effects on macrophage function by facilitating the uptake of modified lipoproteins and an antiatherogenic effect by stimulating efflux of cellular cholesterol to HDL. In conclusion, the inconsistent data, which can only be partly explained by differences in dose and source of androgens, militate against a meaningful assessment of the net effect of T on atherosclerosis. Based on current evidence, the therapeutic use of T in men need not be restricted by concerns regarding cardiovascular side effects. Available data also do not justify the uncontrolled use of T or dehydroepiandrosterone for the prevention or treatment of coronary heart disease.

Reversibility of the effects on blood cells, lipids, liver function and hormones in former anabolic-androgenic steroid abusers.

Urhausen A, Torsten A, Wilfried K.

Source

Faculty of Clinical Medicine, Institute of Sports and Preventive Medicine, University of Saarland, Germany. [email protected]

Abstract

BACKGROUND:

In contrast to the acute effects of anabolic-androgenic steroid (AAS) abuse, the long-term risk profile of former long-term abusers (ExA) is less clear.

METHODS:

Blood parameters of 32 male bodybuilders and powerlifters were studied. Fifteen ExA had not been abusing AAS for at least 12-43 months on average (mean dosage 700 mg for 26 weeks per year over 9 years), 17 athletes (A) were still abusing AAS (750 mg for 33 weeks per 8 years).

FINDINGS:

Hemoglobin (+5%), leucocytes (+33%) and platelets (+38%) were significantly higher in A. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were higher, cholinesterase activity (CHE) lower in A (65+/-55, 38+/-27 and 3719+/-1528U/l) compared to ExA (24+/-10, 18+/-11 and 6345+/-975U/l; each P<0.001) with normal values for gamma-glutamyl transpeptidase (gamma-GT) and bilirubin. ALT, AST and CHE correlated significantly with the extent (duration and weekly dosage, expressed as a point score) of AAS abuse in A (r=0.68, 0.57 and -0.62; each P<0.01). Total and LDL-cholesterol were similar, HDL-cholesterol was distinctly lower in A than in ExA (17+/-11 and 43+/-11 mg/dl; P<0.001) and correlated negatively with the extent of AAS abuse (r=-0.50; P<0.05). Testosterone and estradiol were significantly higher, while LH, FSH and the sexual-hormone-binding (SHB) protein were lower in A than in ExA (each P<0.001). Two ExA had testosterone levels below the normal range.

INTERPRETATION:

The alterations in cell counts, HDL-cholesterol, liver function and most hormones of the pituitary-testicular axis induced by a long-term abuse of AAS were reversible after stopping the medication for over 1 year. In some ExA, an increased ALT activity and a depressed testosterone synthesis were found.

Editado Outubro 27, 2011 às 10:18 por quenca333

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