Do not take alpha drol dangerous
[QUOTE=Owen70;82849083]just letting u know before hand you're gonna get your ass handed to you for cycling PH's under 21, but in all honesty everything looks good.
pick up some SAM-e in 400mg caplets, take those 4 hours away from when you take your caps of alpha drol. TAKE THE SAM-E on an [I]empty stomach[/I]
btw, 150mg of trenadrol is quite a bit man combined with 30mg phera, you may wanna stick to 100mg.[/QUOTE]
Over the counter (OTC) medicines are commonly used in the United States despite a lack of scientific evidence for clinical utility and toxicity associated with their use. A case of jaundice and IgA nephropathy as a consequence of use of a muscle enhancing OTC supplement that was advertised as innocuous with no hormonal activity is described. IgA nephropathy has not been described previously in association with the use of testosterone. The case highlights that, besides adulteration, the misrepresentation of chemicals present in OTC medications and supplements can create confusion and a false sense of security with their use.
(Am J Gastroenterol 2006;101:2659?2662)
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Various renal disorders including glomerulonephritis, cryoglobulinemia, polyarteritis nodosa, renal tubular acidosis, interstitial nephritis, renal papillary necrosis, nephrotic syndrome, acute tubular necrosis, and IgA nephropathy have been described in association with a variety of liver disorders (1). Specifically, IgA nephropathy has been reported in patients with alcoholic, viral, autoimmune, and α1-antitrypsin related liver diseases (2). The use of testosterone has been reported to produce cholestatic jaundice that spontaneously resolves within a few weeks of its onset (3). Herein is reported a case of jaundice and IgA nephropathy in an individual who was using a muscle enhancing OTC supplement that was advertised as having no hormonal ingredients.
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A 23-yr-old Hispanic male bodybuilder without any known past medical history presented at the Maricopa Medical Center (MMC) with a 2-wk complaint of nausea, vomiting, decreased appetite, jaundice, RUQ a**ominal pain, pale stools, dark urine, and itching. Two months before the onset of his clinical symptoms, he had started using an OTC nutritional supplement for bodybuilders named anabolic extreme (superdrol) having methasteron as its active ingredient. He consumed 72 10-mg pills of superdrol, starting at one tablet daily for 2 wk followed by two tablets daily. He did not exceed the maximal suggested dose of 126 pills (10 mg each) that was recommended over a 6-wk period. He stopped using superdrol with the onset of diffuse skin itching. He did not report any history of alcohol, recreational drugs, or tobacco use. There was no family history of liver disease. He did not have any drug allergies.
On physical examination, his vital signs were stable. He was deeply icteric with several scratch marks noted throughout the trunk and lower extremities. He was overweight with a BMI of 28. The a**omen was slightly tender in the right upper quadrant with no evidence of ascites, hepatosplen*****ly, or a Murphy's sign.
At presentation, labs revealed a total bilirubin of 36.2 g/dL, an AST of 57 U/L, ALT of 93 U/L, alkaline phosphatase of 224 U/L, total protein of 9.1 g/dL (6.3?8.2), and IgG of 669 mg/dL (751?1,560). The hepatitis viral antibodies including HAV-IgM, HB core-IgM, HBS-AG, HBV core-AB IgG, HIV-1 AB, HDV-AG as well as HCV-RNA, and HBV-DNA by polymerase chain reaction were negative. The ceruloplasmin was 76 mg/dL. Smooth muscle, antinuclear, myeloperoxidase, and LKM antibodies were negative. Alpha-fetoprotein was normal. A hepatitis A IgG-AB was positive. A 24-h urinary copper was 166 μg/dL. A urinalysis did not reveal proteinuria or hematuria. The rest of his lab reports are summarized in Table.
The patient was hospitalized for one day and discharged on oral ursodeoxycholic acid at 600 mg twice daily and hydroxyzine at 25 mg three times daily to be used as needed for pruritus. Two weeks later, he presented to the hospital because of vomiting and unrelenting skin itching. He was hypertensive with a blood pressure of 189/86 mmHg, and the use of metoprolol at a dose of 50 mg twice daily normalized his blood pressure.
A liver biopsy showed features of marked intrahepatic cholestasis, mild portal inflammation consisting predominantly of lymphocytes, foci of lobular inflammation with balloon degeneration, mild Kupffer cell iron deposition and pericellular fibrosis. There was no evidence of granulomas, peliosis, hepatic rosettes, portal fibrosis, or bile duct injury (Fig. 1). The hepatic iron index was 1.19. An a**ominal ultrasound showed mild liver enlargement at 18 cm. The gallbladder and bile duct were normal. The kidneys were slightly echogenic. The CT scan of the a**omen with IV and oral contrast did not show any liver lesion, ascites, or biliary obstruction. A kidney biopsy showed interstitial edema containing a mild lymphohistiocytic infiltrate with numerous esoinophils. An immunofluoresecence stain showed diffuse granular mesangial staining for IgA (2+) (Fig. 2). After 1 wk of hospitalization, the patient was discharged and readmitted 4 days later because of rectal bleeding and a hemoglobin level of 7.9 gm/dL with an MCV of 89 fL. The upper and lower gastrointestinal endoscopies did not reveal any varices. After receiving 2 units of packed red blood cells, his hemoglobin increased to 9.4 g/dL and he was discharged home. Two wk later, he followed up in the outpatient clinic, feeling better without any itching and near-normalization of his lab reports including both kidney and liver function.
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