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[Definitie:] "An ergogenic aid is any substance or phenomenon that enhances performance."
(Wilmore and Costill) 
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2 4 - 1 1 - 2 0 0 5 Vanishing bile duct syndrome and inflammatory pseudotumor associated with a case of anabolic steroid abuse
Capra F, Nicolini N, Morana G, Guglielmi A, Capelli P, Vantini I. We describe a case of vanishing bile duct syndrome (VBDS) associated with an inflammatory pseudotumor caused by a C-17 alkylated agent. A 32-year-old man was admitted to our department for jaundice, aminotransferase levels three to four times the upper limit of normal, asthenia, and malaise. The patient had previously been treated for 3 years with testosterone undecanoate (40 mg × 4/day) for primary hypogonadism. There was also a history of acute hepatitis B in 1997 and acute hepatitis of unknown origin in 1998. The patient was positive for HAV-Ab IgG. During the 3 months before hospitalization the patient had been taking several drugs in order to improve his bodybuilding. These drugs were stopped because of gynecomasty. Two weeks after stopping them the patient reported the appearance of worsening jaundice. At admission to hospital blood tests showed a total bilirubin level of 639µmol/L, increasing to 688µmol/L, with direct bilirubin of 530 µmol/L; aspartate aminotransferase, 81 U/L; alanine aminotransferase, 182 U/L; ? -glutamyltransferase, 148 U/L; alkaline phosphatase, 212 U/L; INR, 0.96; aPTT, 0.87; BUN, 5.67 mmol/L; and creatinine, 80µmol/L. Abdominal ultrasonography (US) revealed an abnormal hepatic pattern similar to acute hepatitis with starry sky image and a hypoechoic subcapsular lesion 5 × 5 cm in diameter in the right lobe. The focal lesion resembled a hepatocellular carcinoma (HCC). Bile ducts were not dilated. Magnetic resonance imaging confirmed the presence of a lesion with a central area of necrosis, suggestive of HCC
Moreover, we performed a liver biopsy far from the lesion to identify the parenchymal damage. The liver specimen, analyzed by an expert pathologist, showed severe cholestasis, particularly in the centrilobular area (acinar zones 2–3), characterized by bile pigment material in the canaliculi, and brown granules in the hepatocytes and in the Kupffer cell cytoplasm. The portal tracts were dilated with edema and mild inflammation. Moreover, the typical hallmark of VBDS was found: disappearance of interlobular ducts in more than 50% of the portal tracts. These findings were associated with a mild degree of necrosis of hepatocytes The patient was treated with corticosteroids (prednisone, 1 mg/kg) and UDCA (900 mg/day). The symptoms and the laboratory values began to improve 10 weeks after the appearance of the icterus. As soon as liver function tests returned to normal he underwent surgical resection of the liver mass.
During surgery a liver ultrasonographywas performed, without evidence of other lesions. The surgical specimen was mostly composed of an inflammatory infiltrate of plasma cells, foam cells, and giant cells and there was mild miofibroblastic proliferation. This histological image was representative of inflammatory pseudotumor. Clinical improvement was demonstrated by evaluation of the surrounding liver tissue, which showed an important reduc- tion of the inflammatory infiltrate and, in the portal tracts, focal biliary damage. Anabolic steroid abuse is the main cause of “pure” toxic cholestasis. The spectrum of drug-induced cholestasis ranges from mild, reversible, and acute forms to severe chronic cases. Bile duct damage may be present or absent. Approximately 1% of patients who develop drugassociated cholestatic hepatitis develop progressive destruction of cholangiocytes, with the result so-called VBDS. In this syndrome the lesion of the biliary epithelium involves the loss of interlobular ducts located between the cholangioles and second- or third-generation septal bile ducts, causing ductopenia; this is defined as severe destruction of at least half of the interlobular ducts. There are two main types of VBDS: a major and a minor form. The minor form is more frequent and its prognosis is good, since symptoms (jaundice and pruritus) and blood test abnormalities disappear rapidly. In the major form some cases are irreversible, with persistent jaundice and developement of biliary cirrhosis complicated by liver failure and/or portal hypertension leading to death or liver transplantation. In this form the biochemical abnormalities are very important, with high levels of ?GT, ALP, bilirubin, bile acids, and cholesterol. Hepatosplenomegaly, xanthelasmas, and xanthomas may be present. While in the minor and in the major form without biliary cirrhosis, the therapy is mainly limited to the treatment of symptoms and to the consequences of prolonged cholestasis, liver transplantation must be considered in patients who develop secondary biliary cirrhosis. The pathogenesis of VBDS is unknown as the mechanisms of biliary epithelial cell injury and interlobular duct loss have not been explained. Growing evidence in the literature supports the importance of immune-mediated damage once the involved part of the biliary tract is a preferential target of the immune system; class II HLA molecules might represent the first step in immune damage by the generation of cytotoxic T cells and/or antibody producing B cells. A genetic predisposition is probably involved, since only a minority of subjects exposed to possible causal agents develop immunization and hepatocholangitis. Other mechanisms that could be involved include inhibition of Na and K adenosine triphosphatase (ATPase), increased paracellular permeability and regurgitation of bile constituents into plasma, impaired function of the cytoskeleton, alteration of intracellular calcium homeostasis, and alteration of dislocation of canalicular carriers and/or ductular obstruction. |
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