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Potent anabolic androgenic steroids (AAS) are often illegally present in commercially available body building supplements (BBS) and may cause drug induced liver injury (DILI) with different phenotypes. AAS induced DILI typically presents with a prolonged cholestatic liver injury with pruritus and a typical enzyme pattern of elevated transaminases that rapidly fall as alkaline phosphatase slowly increases. Liver biopsy reveals bland cholestasis that usually does not have chronic sequalae. Pathophysiology is unknown and genetic variants in genes associated with cholestatic syndromes were observed in a minority of patients. Chemical analysis of BBS have identified controlled AAS, which were not documented on the label. More frequent use of BBS in males to enhance physical performance is predicted to increase the incidence of cholestatic DILI. The typical presentation of AAS induced liver injury in an at risk populations should prompt careful assessment of BBS exposure.

Anabolic androgenic steroids (AAS) have several adverse effects on the cardiovascular system that may lead to a sudden cardiac death (SCD). We herein report a case involving a 24-year-old male, AAS abuser with intramuscular delivery in the 6 months before, who suffered a cardiorespiratory arrest at home’s bathtub when returning from New Year’s party. A forensic autopsy was performed according to the guidelines of the Association for European Cardiovascular Pathology (AECVP). The body showed hypertrophy of skeletal musculature, with low amount of subcutaneous fat and no signs of injury (body mass index, BMI: 26.8 kg/m2). On internal examination, there were multiorgan congestion, acute pulmonary edema, and cardiomegaly (420 g) with severe coronary atherosclerosis and superimposed acute occlusive thrombosis at the left main trunk and left anterior descendant. Areas of scarring were located at the intersection between the posterior wall and the posterior third of the septum (postero-septal). At histology, acute myocardial infarction at the anterior third of the septum and the anterior wall, and subacute myocardial infarction at apical septum and apical posterior wall were detected. Other findings were small intramyocardial vessel disease and myocytes hypertrophy. Chemicotoxicological analysis in blood showed ethanol ((0.90 ± 0.05) g/L), stanazolol (11.31 µg/L), nandrolone (2.05 µg/L) and testosterone (

Aims The real effects of the chronic consumption of anabolic-androgenic steroids (AASs) on cardiovascular structures are subjects of intense debate. The aim of the study was to detect by speckle tracking echocardiography (STE) right ventricular (RV) and left ventricular (LV) dysfunction at rest and during exercise stress echocardiography (ESE) in athletes abusing AAS. Methods and results One hundred and fifteen top-level competitive bodybuilders were selected (70 males), including 65 athletes misusing AAS for at least 5 years (users), 50 anabolic-free bodybuilders (non-users), compared to 50 age- and sex-matched healthy sedentary controls. Standard Doppler echocardiography, STE analysis, and lung ultrasound at rest and at peak supine-bicycle ESE were performed. Athletes showed increased LV mass index, wall thickness, and RV diameters compared with controls, whereas LV ejection fraction was comparable within the groups. left atrial volume index, LV and RV strain, and LV E/Em were significantly higher in AAS users. Users showed more B-lines during stress (median 4.4 vs. 1.25 in controls and 1.3 in non-users, P Conclusions In athletes abusing steroids, STE analysis showed an impaired RV systolic deformation, closely associated with reduced functional capacity during physical effort, and—during exercise—more pulmonary congestion.

Anabolic–androgenic steroids (AAS) are used by power athletes to improve performance. However, the real effects of the chronic consumption of AAS on cardiovascular structures are subjects of intense debate. To detect by speckle tracking echocardiography (STE) underlying left atrial (LA) dysfunction in athletes abusing AAS and assess possible correlation between LA myocardial function and exercise capacity during cardiopulmonary stress test. 65 top-level competitive bodybuilders were selected (45 males), including 35 athletes misusing AAS for at least 5 years (users), 30 anabolic-free bodybuilders (non-users), compared to 40 age- and sex-matched healthy sedentary controls. Standard Doppler echocardiography, STE analysis and bicycle ergometric test were performed to assess LA myocardial function and exercise capacity. Athletes showed increased left ventricular (LV) mass index, wall thickness and stroke volume compared with controls, whereas LV ejection fraction, LV end-diastolic diameter and transmitral Doppler indexes were comparable between the three groups. Conversely, LA volume index, LV and LA strain and LV E/Em were significantly increased in AAS users. By multivariate analyses, LV E/Em (beta = − 0.30, p < 0.01), LA volume index (− 0.42, p < 0.001) and number of weeks of AAS use per year (− 0.54, p < 0.001) emerged as the only independent determinants of LA lateral wall peak STE. In addition, a close association between LA myocardial function and VO2 peak during cardiopulmonary exercise testing was evidenced (p < 0.001), showing a powerful incremental value with respect to clinical and standard echocardiographic data. STE represents a promising technique to assess LA myocardial function in athletes abusing steroids. AAS users showed a more impaired LA deformation, associated with reduced functional capacity during physical effort.

Background/Aim. Long-term intensive training is associated with distinctive cardiac adaptations which are known as athlete?s heart. The aim of this study was to determine whether the use of anabolic androgenic steroids (AAS) could affect echocardiographic parameters of left ventricular (LV) morphology and function in elite strength and endurance athletes. Methods. A total of 20 elite strength athletes (10 AAS users and 10 non-users) were compared to 12 steroid-free endurance athletes. All the subjects underwent comprehensive standard echocardiography and tissue Doppler imaging. Results. After being indexed for body surface area, both left atrium (LA) and LV end-diastolic diameter (LVEDD) were significantly higher in the endurance than strength athletes, regardless of AAS use (p < 0.05, for both). A significant correlation was found between LA diameter and LVEDD in the steroid-free endurance athletes, showing that 75% of LA size variability depends on variability of LVEDD (p < 0.001). No significant differences in ejection fraction and cardiac output were observed among the groups, although mildly reduced LV ejection fraction was seen only in the AAS users. The AAS-using strength athletes had higher A-peak velocity when compared to steroidfree athletes, regardless of training type (p < 0.05 for both). Both AAS-using and AAS-free strength athletes had lower e? peak velocity and higher E/e? ratio than endurance athletes (p < 0.05, for all). Conclusions. There is no evidence that LV ejection fraction in elite athletes is altered by either type of training or AAS misuse. Long-term endurance training is associated with preferable effects on LV diastolic function compared to strength training, particularly when the latter is combined with AAS abuse.

Since the increased prevalence of anabolic androgenic steroids abuse in last few decades is usually accompanied by various exercise protocols, the scope of our study was to evaluate the effects of chronic nandrolone decanoate administration in supraphysiological dose and a prolonged swimming protocol (alone and simultaneously with nandrolone decanoate) on depressive state in male rats. Simultaneously, we investigated the possible alterations in neuropeptide Y (NPY) content in blood and the hippocampus, in order to determine the role of NPY in the modulation of depressive-like behavior.Exercise induced antidepressant effects in tail suspension test (decrease of the total duration of immobility), as well as significant increase in the number of hippocampal NPY-interneurons in CA1 region. Chronic nandrolone decanoate treatment attenuated the beneficial antidepressant effects of exercise as measured by the tail suspension test parameters. Simultaneously, nandrolone decanoate treatment resulted in diminution of NPY content both in blood (decreased serum levels) and in hippocampus (the significant decrease in NPY expression in all three investigated hippocampal regions-CA1, CA2/3 and DG). Our findings indicate that alterations in serum and hippocampal NPY contents may underlie the changes in depressive state in rats. The exercise was beneficial as it exerted antidepressant effect, while chronic nandrolone decanoate treatment resulted in depressive-like behavior. Furthermore, the behavioral indicators of depression showed strong correlations with the serum levels and the hippocampal content of NPY.

Abuse of anabolic-androgenic steroids (AAS) is a widespread problem throughout Western society. The secretive nature of AAS makes it difficult to study the potential consequences with recognised scien

Chronic use of anabolic adrogenic steroids (AAS) has been known to cause serious adverse effects. While the effects of AASs on cardiovascular system are well known, toxicity on other organs has received less attention. A doserelated nephrotoxic effect has been proposed and a wide variety of morpho-functional damages have been observed, but the exact pathophysiological mechanism of action is still not well known. In the present minireview, we highlight the remaining issues through an analysis of the pertinent literature. As with HSPs toxic agents their overexpression could be considered a protective reaction against AAS abuse however, comprehensive studies concerning the whole range of Hsps/chaperones expressions in all organs after long term use of AAS are needed.

In the athletes the wide use of Anabolic Androgenic Steroids (AAS) cause series damage in various organs, in particular, analyzing the liver, elevation on the levels of liver enzymes, cholestatic jaundice, liver tumors, both benign and malignant, and peliosis hepatis are described. A prolonged AAS administration provokes an increase in the activities of liver lysosomal hydrolases and a decrease in some components of the microsomal drug-metabolizing system and in the activity of the mitochondrial respiratory chain complexes without modifying classical serum indicators of hepatic function. Liver is a key organ actively involved in numerous metabolic and detoxifying functions. As a consequence, it is continuously exposed to high levels of endogenous and exogenous oxidants that are by-products of many biochemical pathways and, in fact, it has been demonstrated that intracellular oxidant production is more active in liver than in tissues, like the increase of inflammatory cytokines, apoptosis and the inhibitors of apoptosis NF- κB and Heat Shock Proteins.

Long-term side effects of high doses of anabolic androgenic steroids self-administration were evaluated in this study. Twenty male bodybuilders, voluntarily starting steroid self-administration, were followed every 6 months over 2 years. Physical examination, haematological, metabolic and endocrine variables, semen analysis, hepatic and prostate ultrasound and echocardiographic evaluations were performed. LH values (baseline 3.43 +/- 1.75) were suppressed at 18 (1.98 +/- 1.99) (p = 0.026) and 24 (2.43 +/- 2.17) (p = 0.026), and FSH (3.95 +/- 2.01) at 6 (3.01 +/- 2.16) (p = 0.031), 12 (2.45 +/- 2.54) (p = 0.029), 18 (2.02 +/- 2.29) (p = 0.032) and 24 (3.42 +/- 2.64) (p = 0.032) months and SHBG (34.11 +/- 10.88) values significantly lowered at 12 (24.81 +/- 12.49) (p < 0.05), 18 (21.28 +/- 11.15) (p < 0.01), 24 months (25.42 +/- 11.16) (p < 0.01). A significant decrease in spermatozoa count (p < 0.01), and fertility index (p = 0.01) occurred. HDL-cholesterol (baseline 56.94 +/- 13.54) was reduced at 18 (41.86 +/- 14.17) (p < 0.01) and 24 (43.82 +/- 18.67) (p < 0.05) months and Apo A-1 at 12 (p < 0.001), 18 (p = 0.05) and 24 (p = 0.05) months. The most important long-term adverse effects were lower fertility and the impairment of lipid profile associated with an increased cardiovascular risk.