Anabolic steroid-induced hepatotoxicity: is it overstated?

[heavyiron]

This abstract shows that measuring GGT and CK as well as ALT and AST determines liver stress or muscle stress. Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels may have been overstated



Clin J Sport Med. 1999 Jan;9(1):34-9.

Anabolic steroid-induced hepatotoxicity: is it overstated?

Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ.
The Department of Biomedical Science, University of North Texas Health Science Center, Fort Worth 76107-2699, USA.

Abstract

OBJECTIVE: There have been numerous reports of hepatic dysfunction secondary to anabolic steroid use based on elevated levels of serum aminotransferases. This study was conducted to distinguish between serum aminotransaminase elevations secondary to intense resistance training and anabolic steroid-induced hepatotoxicity in elite bodybuilders.

DESIGN: This was a case-control study of serum chemistry profiles from bodybuilders using and not using anabolic steroids with comparisons to a cohort of medical students and patients with hepatitis.

PARTICIPANTS: The participants were bodybuilders taking self-directed regimens of anabolic steroids (n = 15) and bodybuilders not taking steroids (n = 10). Blood chemistry profiles from patients with viral hepatitis (n = 49) and exercising and nonexercising medical students (592) were used as controls.

MAIN OUTCOME MEASURES: The focus in blood chemistry profiles was aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (GGT), and creatine kinase (CK) levels.

RESULTS: In both groups of bodybuilders, CK, AST, and ALT were elevated, whereas GGT remained in the normal range. In contrast, patients with hepatitis had elevations of all three enzymes: ALT, AST, and GGT. Creatine kinase (CK) was elevated in all exercising groups. Patients with hepatitis were the only group in which a correlation was found between aminotransferases and GGT.

CONCLUSION: Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels may have been overstated, because no exercising subjects, including steroid users, demonstrated hepatic dysfunction based on GGT levels. Such reports may have misled the medical community to emphasize steroid-induced hepatotoxicity when interpreting elevated aminotransferase levels and disregard muscle damage. For these reasons, when evaluating hepatic function in cases of anabolic steroid therapy or abuse, CK and GGT levels should be considered in addition to ALT and AST levels as essential elements of the assessment.


PMID: 10336050 [PubMed - indexed for MEDLINE]

 

[heavyiron]

Excercise significantly increases liver enzymes for 1 week.


Br J Clin Pharmacol. 2008 Feb;65(2):253-9. Epub 2007 Aug 31.

Muscular exercise can cause highly pathological liver function tests in healthy men.

Pettersson J, Hindorf U, Persson P, Bengtsson T, Malmqvist U, Werkström V, Ekelund M.
AstraZeneca R&D Lund, Lund, Sweden.


Comment in:

• Br J Clin Pharmacol. 2008 Nov;66(5):725.

Abstract

What is already known about this subject: The occurrence of idiosyncratic drug hepatotoxicity is a major problem in all phases of clinical drug development and the leading cause of postmarketing warnings and withdrawals. Physical exercise can result in transient elevations of liver function tests. There is no consensus in the literature on which forms of exercise may cause changes in liver function tests and to what extent. What this study adds: Weightlifting results in profound increases in liver function tests in healthy men used to moderate physical activity, not including weightlifting. Liver function tests are significantly increased for at least 7 days after weightlifting. It is important to impose relevant restrictions on heavy muscular exercise prior to and during clinical studies.

AIM: To investigate the effect of intensive muscular exercise (weightlifting) on clinical chemistry parameters reflecting liver function in healthy men.

METHODS: Fifteen healthy men, used to moderate physical activity not including weightlifting, performed an 1 h long weightlifting programme. Blood was sampled for clinical chemistry parameters [aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LD), gamma-glutamyl transferase (gamma GT), alkaline phosphatase (ALP), bilirubin, creatine kinase (CK) and myoglobin] at repeated intervals during 7 days postexercise and at a follow-up examination 10-12 days postexercise.

RESULTS: Five out of eight studied clinical chemistry parameters (AST, ALT, LD, CK and myoglobin) increased significantly after exercise (P < 0.01) and remained increased for at least 7 days postexercise. Bilirubin, gamma GT and ALP remained within the normal range.

CONCLUSION: The liver function parameters, AST and ALT, were significantly increased for at least 7 days after the exercise. In addition, LD and, in particular, CK and myoglobin showed highly elevated levels. These findings highlight the importance of imposing restrictions on weightlifting prior to and during clinical studies. Intensive muscular exercise, e.g. weightlifting, should also be considered as a cause of asymptomatic elevations of liver function tests in daily clinical practice.

Figure 1
Individual changes over time for aspartate aminotransferase (µkat l−1). 1, (○); 2, (□); 3, (

); 4, (+); 5, (◊); 6, (

); 7, (??); 8, (•); 9, (

); 10, (

); 11, (+); 12, (♦); 13, (

); 15 (??)

Figure 2
Individual changes over time for alanine aminotransferase (µkat l−1). 1, (○); 2, (□); 3, (

); 4, (+); 5, (◊); 6, (

); 7, (??); 8, (•); 9, (

); 10, (

); 11, (+); 12, (♦); 13, (

); 15 (??)

Figure 3
The aspartate aminotransferase/alanine aminotransferase ratio during the study period. Each box shows the median and the interquartile range values; lines show the total range​

​

PMID: 17764474 [PubMed - indexed for MEDLINE]PMCID: PMC2291230

 

[heavyiron]

J Am Osteopath Assoc. 2001 Jul;101(7):391-4.

Evaluation of aminotransferase elevations in a bodybuilder using anabolic steroids: hepatitis or rhabdomyolysis?

Pertusi R, Dickerman RD, McConathy WJ.
Department of Medicine, University of North Texas Health Science Center, 3500 Camp Bowie Blvd, Fort Worth, TX 76107-2699, USA.

Abstract

The use of anabolic steroids among competitive athletes, particularly bodybuilders, is widespread. Numerous reports have noted "hepatic" dysfunction secondary to anabolic steroid use based on elevated serum aminotransferase levels. The authors' objective was to assess whether primary care physicians accurately distinguish between anabolic steroid-induced hepatotoxicity and serum aminotransferase elevations that are secondary to acute rhabdomyolysis resulting from intense resistance training. Surveys were sent to physicians listed as practicing family medicine or sports medicine in the yellow pages of seven metropolitan areas. Physicians were asked to provide a differential diagnosis for a 28-year-old, anabolic steroid-using male bodybuilder with an abnormal serum chemistry profile. The blood chemistries showed elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatine kinase (CK) levels, and normal gamma-glutamyltransferase (GGT) levels. In the physician survey (n = 84 responses), 56% failed to mention muscle damage or muscle disease as a potential diagnosis, despite the markedly elevated CK level of the patient. Sixty-three percent indicated liver disease as their primary diagnosis despite normal GGT levels. Prior reports of anabolic steroid-induced hepatotoxicity that were based on aminotransferase elevations may have overstated the role of anabolic steroids. Correspondingly, the medical community may have been led to emphasize anabolic steroid-induced hepatotoxicity and disregard muscle damage when interpreting elevated aminotransferase levels. Therefore, when evaluating enzyme elevations in patients who use anabolic steroids, physicians should consider the CK and GGT levels as essential elements in distinguishing muscle damage from liver damage.


PMID: 11476029 [PubMed - indexed for MEDLINE]