first thing that pops out to me is that it refers directly to 17-alpha alkylated AAS, i know that isn't the case with 2BigFred, he has stated many times he used orals only twice, but it is something that everyone needs to realize. they are NOT SAFE. its the first thing mentioned in the article. it says "These hepatic alterations are caused almost exclusively by 17-alkylated AAS."
ok here's the first guy:
he's taken AAS for 15 years, primarily 8 week cycles with 2 week breaks. he's taken stanozolol, oxymetholone, nandrelone decanoate, testosterone enanthate, and methenolone enanthate. first thing there that pops out to me is that he
didn't use trenbolone. and this guy's oral dosaging was INSANE. i dont know the accuracy of this information, but it claims he took 400mg/day of orals and 600mg/2-3 times a week depending on the cycle. didnt smoke, didnt drink. liver values were a little off, but not bad. he had 2 large liver lesions.
The absence of any other risk factor and the previous history of AAS consumption at high doses allowed us to establish the aetiology of the liver tumours: hepatic adenomas secondary to AAS abuse.
i think this is really important:
At present, 4 years after the diagnosis and subsequent to further ecographic examinations, to our surprise, there has been a slight decrease in the size of the tumours (of about 1–2 cm in the tumour in the left lobe and 3–4 cm in the tumour in the right lobe) (not shown). Liver function has also clearly improved. Serum levels of transaminases have returned to normal, as have the other serum markers of liver function. As in previous examinations, coagulation tests and serum levels of AFP were absolutely normal. On the other hand, the serum levels of sex hypophyseal hormones (FSH and LH) were evaluated and found to be normal, thus suggesting that the withdrawal of AAS may have induced the total recovery of the hypothalamic-hypophyseal axis. However, the patient continues in the above mentioned liver transplantation program and undergoes periodic examination because of the enormous size and the potential malignant transformation of the liver lesions.
apparently his body recovered almost fully after he stopped his usage and is trying to fix itself...
second guy:
again 8 week cycles with 2 weeks in between. this guy is 23. he used stanozolol, oxymetholone, nandrolone decanoate, testosterone phenylpropionate, and boldenone. again, NO TREN. The patient began to show symptoms after 6 months of treatment with AAS and 1 month of treatment with diuretics and a restrictive diet. again, didnt smoke or drink. the guy was a mess when he came in, had acute renal failure, muscle damage, metabolic alkalosis, hypokaliaemia, and hypernatraemia.
The marked hypokaliaemia suffered by the patient could be explained by the fact that this bodybuilder did not maintain an adequate Na+, K+ and water intake over the training periods, and, furthermore, self administered a loop diuretic. This marked hypokaliaemia favoured muscle damage and rhabdomyolisis. Furthermore, the high doses of self administered AAS presumably promoted aggression and other changes in attitude that could explain the excess training despite muscle weakness due to hypokaliaemia. This situation resulted in multiple ruptures of muscle fibres (increasing serum values of CPK, AST, ALT, LDH, and elevation of blood levels of myoglobin and myoglobinuria). The increase in myoglobin renal excretion, with subsequent cylinder formation in the nephron or/and direct toxicity to tubular cells, led to acute renal failure.
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