goa1175
New member
So this dude has two types of hepatitis, and some other liver disease. He goes to the hospital for another liver ailment and BAM! it's the steroids that destroyed his liver! Certainly not the completely unrelated liver ailments. Suprised I haven't seen this story on the 6 o'clock news. :frustrate
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Clin Alert, Sept 15, 2005 v43 i17 p2(1)
Anabolic steroid abuse: vanishing bile duct syndrome and inflammatory pseudotumor.
Full Text: COPYRIGHT 2005 Sage Publications, Inc.
No. 239
A 32-year-old male patient was admitted to the hospital for jaundice (aminotransferase levels 3 to 4 times the upper normal limit) with asthenia and malaise 2 weeks following discontinuation of anabolic steroid abuse (3-month history). Medical history included acute hepatitis B, acute hepatitis of unknown origin, and a positive HAV-Ab IgG. The patient had been treated for primary hypogonadism with testosterone undecanoate (40 mg x 4 times per day for 3 years). Laboratory findings included a total bilirubin level of 639 mmol/L to 688 mmol/L with a direct bilirubin level of 530 mmol/L, aspartate aminotransferase of 81 U/L, alanine aminotransferase of 182 U/L, [gamma]-glutamyltransferase of 148 U/L, alkaline phosphatase of 212 U/L, international normalized ratio of 0.96, activated partial thromboplastin time of 0.87, blood urea nitrogen of 5.67 mmol/L, and creatinine level of 80 mmol/L. Abdominal ultrasound and magnetic resonance imaging revealed abnormal hepatic pattern and right lobal hypoechoic subcapsular lesion (5 x 5 cm) similar to a carcinoma with undilated bile ducts. Liver biopsy showed dilated portal tracts with edema and inflammation due to severe cholestasis and vanishing interlobular ducts in greater than 50% of portal tracts. The patient was treated with prednisone (1 mg/kg) and urso deoxy cholic acid (900 mg/d) leading to improvement of symptoms and laboratory test results. Clinical improvement resulted from surgical resection of the liver mass, which revealed inflammatory pseudotumor.
The authors concluded that this patient experienced anabolic steroid-induced vanishing bile duct syndrome. Severe destruction of at least half of interlobular ducts is a characteristic of vanishing bile duct syndrome. The pathogenesis of vanishing bile duct syndrome is unknown; however, the role of immune-mediated damage and generation of cytotoxic T cells and/or antibody-producing B cells and possible genetic component has been proposed.
Anabolic Steroids [Synthetic derivatives of testosterone]
Capra F et al (F Capra, Medicina Interna A Policlinico GB Rossi, Univ di Verona, Piazzale LA Scuro 10, 37134 Verona, Italy) Vanishing bile duct syndrome and inflammatory pseudotumor associated with a case of anabolic steroid abuse. Dig Dis Sci 50:1535-1537 (Aug) 2005
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Clin Alert, Sept 15, 2005 v43 i17 p2(1)
Anabolic steroid abuse: vanishing bile duct syndrome and inflammatory pseudotumor.
Full Text: COPYRIGHT 2005 Sage Publications, Inc.
No. 239
A 32-year-old male patient was admitted to the hospital for jaundice (aminotransferase levels 3 to 4 times the upper normal limit) with asthenia and malaise 2 weeks following discontinuation of anabolic steroid abuse (3-month history). Medical history included acute hepatitis B, acute hepatitis of unknown origin, and a positive HAV-Ab IgG. The patient had been treated for primary hypogonadism with testosterone undecanoate (40 mg x 4 times per day for 3 years). Laboratory findings included a total bilirubin level of 639 mmol/L to 688 mmol/L with a direct bilirubin level of 530 mmol/L, aspartate aminotransferase of 81 U/L, alanine aminotransferase of 182 U/L, [gamma]-glutamyltransferase of 148 U/L, alkaline phosphatase of 212 U/L, international normalized ratio of 0.96, activated partial thromboplastin time of 0.87, blood urea nitrogen of 5.67 mmol/L, and creatinine level of 80 mmol/L. Abdominal ultrasound and magnetic resonance imaging revealed abnormal hepatic pattern and right lobal hypoechoic subcapsular lesion (5 x 5 cm) similar to a carcinoma with undilated bile ducts. Liver biopsy showed dilated portal tracts with edema and inflammation due to severe cholestasis and vanishing interlobular ducts in greater than 50% of portal tracts. The patient was treated with prednisone (1 mg/kg) and urso deoxy cholic acid (900 mg/d) leading to improvement of symptoms and laboratory test results. Clinical improvement resulted from surgical resection of the liver mass, which revealed inflammatory pseudotumor.
The authors concluded that this patient experienced anabolic steroid-induced vanishing bile duct syndrome. Severe destruction of at least half of interlobular ducts is a characteristic of vanishing bile duct syndrome. The pathogenesis of vanishing bile duct syndrome is unknown; however, the role of immune-mediated damage and generation of cytotoxic T cells and/or antibody-producing B cells and possible genetic component has been proposed.
Anabolic Steroids [Synthetic derivatives of testosterone]
Capra F et al (F Capra, Medicina Interna A Policlinico GB Rossi, Univ di Verona, Piazzale LA Scuro 10, 37134 Verona, Italy) Vanishing bile duct syndrome and inflammatory pseudotumor associated with a case of anabolic steroid abuse. Dig Dis Sci 50:1535-1537 (Aug) 2005