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AAS and Your Liver

DrJMW

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An article from MEDLINE:




Androgenic/Anabolic steroid-induced toxic hepatitis.
J Clin Gastroenterol 2002 Oct;35(4):350-2 (ISSN: 0192-0790)
Stimac D; Milic S; Dintinjana RD; Kovac D; Ristic S
Division of Gastroenterology, Department of Internal Medicine, Clinical Hospital Center Rijeka, Rijeka, Croatia. [email protected].
Athletes and bodybuilders often misuse androgenic/anabolic steroids. When used in therapeutic doses, these drugs produce clinical jaundice in just a small number of recipients. We present a 26-year-old male bodybuilder who self-administered high doses of androgenic/anabolic steroids that induced liver damage. One month before admission to the hospital, he used testosterone enanthate (500 mg intramuscularly, twice weekly), stanozolol (40 mg/d), and methylandrostenediol (30 mg/d by mouth, for 5 weeks). On admission, his bilirubin level was 470 micromol/L (direct, 360 micromol/L), his aspartate aminotransferase (AST) level was 5,870 IU/L, his alanine aminotransferase (ALT) level was 10,580 IU/L, his alkaline phosphatase (ALP) level was 152 IU/L, his gamma-glutamyl-transpeptidase level was 140 IU/L, his albumin level was 27.6 g/L, and his prothrombin time was 29%. During the patient's prolonged hospitalization, multiple tests and liver biopsy were performed, showing only toxic hepatic lesions. The patient was provided with supportive medical treatment. Clinical signs and laboratory findings improved substantially 12 weeks after the patient discontinued androgenic/anabolic steroids. The reasons for presenting this case were the much higher values of AST and ALT levels than reported in other studies, although the values of bilirubin and ALP were similar to those found in the literature. To our knowledge, it is the first case of toxic hepatitis induced by androgenic/anabolic steroids with predominantly hepatocellular necrosis instead of intrahepatic cholestasis.
 
Wasn't methandriol known to be very hard on the liver? Then he added winny on top of that.

I'm curious, what exactly is "supportive medical treatment" in this situation. What can really be done? IV gluthion (sp)?
 
DrJMW said:
An article from MEDLINE:




Androgenic/Anabolic steroid-induced toxic hepatitis.
J Clin Gastroenterol 2002 Oct;35(4):350-2 (ISSN: 0192-0790)
Stimac D; Milic S; Dintinjana RD; Kovac D; Ristic S
Division of Gastroenterology, Department of Internal Medicine, Clinical Hospital Center Rijeka, Rijeka, Croatia. [email protected].
Athletes and bodybuilders often misuse androgenic/anabolic steroids. When used in therapeutic doses, these drugs produce clinical jaundice in just a small number of recipients. We present a 26-year-old male bodybuilder who self-administered high doses of androgenic/anabolic steroids that induced liver damage. One month before admission to the hospital, he used testosterone enanthate (500 mg intramuscularly, twice weekly), stanozolol (40 mg/d), and methylandrostenediol (30 mg/d by mouth, for 5 weeks). On admission, his bilirubin level was 470 micromol/L (direct, 360 micromol/L), his aspartate aminotransferase (AST) level was 5,870 IU/L, his alanine aminotransferase (ALT) level was 10,580 IU/L, his alkaline phosphatase (ALP) level was 152 IU/L, his gamma-glutamyl-transpeptidase level was 140 IU/L, his albumin level was 27.6 g/L, and his prothrombin time was 29%. During the patient's prolonged hospitalization, multiple tests and liver biopsy were performed, showing only toxic hepatic lesions. The patient was provided with supportive medical treatment. Clinical signs and laboratory findings improved substantially 12 weeks after the patient discontinued androgenic/anabolic steroids. The reasons for presenting this case were the much higher values of AST and ALT levels than reported in other studies, although the values of bilirubin and ALP were similar to those found in the literature. To our knowledge, it is the first case of toxic hepatitis induced by androgenic/anabolic steroids with predominantly hepatocellular necrosis instead of intrahepatic cholestasis.

500mg Test/week + 30mg Dball/day + 40mg Winstrol/day

AST = 5,870
ALT = 10,580

MEAN values for ALT and AST are between 20-60 IU/L

His liver values are downright astronomical for someone only using 70mg of 17 aa's/day.

And a GGT of 140......lol Thats the highest I have ever seen.

Fonz
 
DrJMW said:
An article from MEDLINE:
.......Clinical Hospital Center Rijeka, Rijeka, Croatia............. On admission, his bilirubin level was 470 micromol/L (direct, 360 micromol/L), his aspartate aminotransferase (AST) level was 5,870 IU/L, his alanine aminotransferase (ALT) level was 10,580 IU/L, his alkaline phosphatase (ALP) level was 152 IU/L, his gamma-glutamyl-transpeptidase level was 140 IU/L, his albumin level was 27.6 g/L, and his prothrombin time was 29%. ..........although the values of bilirubin and ALP were similar to those found in the literature.

Anyone know what lab values they use in Croatia where the study was done. I have a feeling his blood levels were not that bad. For example it says his albumin was 27.6 grams per liter. But in the USA we report albumin in grams per decaliter - so we would have to change the albumin values to 2.76 - which is low and reduced values are due to liver disease - otherwise it looks like his albumin is high off the charts . Albumin is fractionated in the liver so it is a good liver indicator. Dr. JMW, could the AST and ALT also be off by a factor of 10 due to Croatian values? If so a AST of 587 is darn bad, but I have seen that before and the patient recovered okay.

" Normal values for ALT may vary with method " - page 381, A Manual of Laboratory & Diagnostic Tests, 5th edition, Francis Fishbach.

Also levels of ALT and AST do not raise proportionate to liver damage. In other words 800 IU/L of AST is not necessarily twice as bad as 400. So the fact that his is 10,580 high does not necessarily indicate that the liver damage is worse that someone who is only 600, from what I have been taught.

Of course the real proof of liver damage was his liver biopsy.

Dr. JMW, what do they mean by the PT (prothrombin time) being "29%". I have never seen that designation before, but my experience in evaluating PT is perhaps inadequate. PT is measured in seconds as it is the amount of time it takes for prothrombin (which is produced in the liver) to be involved in the clot process in a lab (11-13 seconds normally), which is then often adjusted to INR's (international normalized ratio's) which is ideally often 2 to 2.5 times normal for patients with cardiac problems who are on warfarin or other such anticlotting drugs. SO what do they mean "29%" for the prothrombin time - 29% of what?.

At the end it says "although the values of bilirubin and ALP were similar to those found in the literature" - but they use different units than in the USA. In the USA bilirubin is reported in mg/ml and the Croatian values are reported in micromol/Liter. The Croatians apparently use the same lab values for ALP, but his are close to normal.

So I am not sure how bad of a picture this really paints. I have seen guys with ALT of 200 something and AST of 600 something who upon further examination (ultrasound etc) nothing really bad could be found.

The liver biopsy does not lie, but other contributing factors are not mentioned. Croatia and Serbia are very war torn or at least were recently. I use to know the statistics but in Russia something like 1/2 of all the deaths of men under the age of 50 are directly linked to alcohol (not alcohol related factors like car wrecks but directly to alcohol). I do not know about Croatia and Serbia but difficult conditions can increase alcohol and other such activity - so maybe this guy was washing his orals down with vodka?

I certainly don't want to underestimate the potential negative effect AAS can have on health, and the orals - especially crap like winstrol) is better off buried in the dirt - (and this abstract should create some s-e-r-i-o-u-s food for thought for all the casual self directed AAS users who might in the future write a post like "It looks like I am pissing coca cola, could something be wrong?") - but I am not sure we can adequately determine how serious of an impact his AAS had on his health and liver from this abstract.

This is a weakness of abstracts - they summarize a 5 page research article into a paragraph - with no other information or background. I like abstracts because they are short, but their very brevity makes them incomplete.
 
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