Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2004) 8 P32

1Department of Endocrinology, Sandwell and West Birmingham Hospitals NHS Trust, West Midlands, U.K.; 2Department of Endocrinology, Princess Royal Hospital, Telford, Shropshire, U.K.


Anabolic steroids enhance performance in atheletes, but can lead to life threatening consequences. We report a 33-year-old male amateur body-builder using anabolic steroids, presenting with acute inferolateral myocardial infraction and marked hyperlipidaemia. He had no known cardiovascular risk factors. Despite rapid thrombolysis, peak creatinine kinase was 3,348 iu/l, signifying significant myocardial damage and a markedly raised total cholesterol of 10.6 mmol/l, with a low HDL of 0.9 mmol/l. As he had on going chest pain, a coronary angiogram was performed, which revealed stenoses and ectasia in the left circumflex, which were successfully stented. Our patient has remained off steroids since his first presentation and is symptom free and well, with a marked reduction of his total cholesterol to 4.6mmol/l (HDL 1.0 mmol/l) within 6 weeks (on simvastatin 40 mg). Screening of family members has negated the possibility of an underlying familial hyperlipidaemia. With no other cardiovascular risk factors and the remarkable reduction of total cholesterol within 6 weeks of stopping the anabolic steroids, it seems highly likely that both the ectaticcoronary artery changes and the hyperlipidaemia seen in our patient were secondary to his steroid abuse. In weight training athletes, anabolic steroid abuse is associated with an average reduction of 55% in HDL along with an average increase of 66% in LDL. In addition to atherogenesis, hypercholesterolemia can mediate arterial occlusion by enhancing coronary artery responsiveness to norepinephrine and enhancing platelet aggregation, potentially setting the stage for in situ thrombosis, coronary spasm, or both. The structural effect of anabolic steroids in the form of hypertrophy of heart muscles is well known, although structural alterations like ectasia secondary to decrease in elastin and increase in fibrous tissue are also being increasingly recognized. The wide spread usage of these drugs suggests a new risk factor for coronary heart disease may be emerging.

Volume 8

195th Meeting of the Society for Endocrinology joint with Diabetes UK and the Growth Factor Group

Society for Endocrinology 

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