Steroid induced liver failure

Treatment: If a pancreatic or liver tumor is identified and able to be surgically excised, the skin lesions may normalize for an extended period of time, but because these tumors metastasize (spread to other areas of the body) quickly, surgery is not curative. In cases of end stage liver disease, surgery is not possible, and the goal of therapy is to increase quality of life and decrease uncomfortable skin lesions with supportive care and addressing the nutritional abnormalities. Supportive care includes supplementing protein and necessary minerals and enzymes through the diet and oral supplements or by weekly intravenous amino acid infusions that are performed in the hospital on an outpatient basis until improvement in the skin is noted. Unfortunately, despite the supportive care, the disease will progress.

A very typical case of severe cholestasis due to anabolic steroid use.  Because the steroids were being used without medical supervision, the dose and actual duration of use of each preparation was unclear, but cholestasis usually arises within 4 to 12 weeks of starting a C-17 alkylated androgenic steroid.  The jaundice can be severe and prolonged and accompanied by severe pruritus and marked weight loss.  The serum enzymes are typically minimally elevated except for a short period immediately after stopping therapy.  The pattern of enzyme elevations can be hepatocellular, cholestatic or mixed.  Liver biopsy shows a “bland” cholestasis with minimal inflammation and hepatocellular necrosis.  Ma Huang has also been implicated in cases of drug induced liver injury, but is associated with an acute hepatocellular pattern of injury.

This case demonstrates how significant hepatic fibrosis and portal hypertension can arise during methotrexate therapy without accompanying symptoms or significant elevations in serum aminotransferase levels.  Also characteristic was the mild and nonprogressive nature of the cirrhosis despite continuation of methotrexate.  A possible noninvasive marker for the development of significant fibrosis in this case was the decrease in platelet count, which fell from 181,000/μL at baseline to 105,000 μ/L one year later–a 47% decline and a “platelet slope” of -74,000/year.  In analyses of serial platelet count determinations in patients who developed portal hypertension, a platelet slope of -9,000/year was found to be indicative of the development of portal hypertension and hepatic dysfunction.  Whether leflunomide contributed to the toxicity of methotrexate is not clear, but the findings are compatible with the duration and total dose of methotrexate received.  The patient did not have typical risk factors for developing methotrexate related fibrosis such as excessive alcohol use, underlying viral hepatitis, renal insufficiency or diabetes (no mention is made of body weight or presence of obesity).  While this patient did not qualify for undergoing surveillance liver biopsies (according to the criteria of the American College of Rheumatology), noninvasive tests such as PIIIP, hepatic imaging or elastography would have been appropriate and would likely have suggested the presence of significant fibrosis much earlier.

The treatment of fatty liver depends on its cause, and, in general, treating the underlying cause will reverse the process of steatosis if implemented at an early stage. Two known causes of fatty liver disease are an excess consumption of alcohol and a prolonged diet containing foods with a high proportion of calories coming from lipids. [17] For the patients with non-alcoholic fatty liver disease with pure steatosis and no evidence of inflammation, a gradual weight loss is often the only recommendation. [3] In more serious cases, medications that decrease insulin resistance, hyperlipidemia , and those that induce weight loss have been shown to improve liver function. [4]

Steroid induced liver failure

steroid induced liver failure

The treatment of fatty liver depends on its cause, and, in general, treating the underlying cause will reverse the process of steatosis if implemented at an early stage. Two known causes of fatty liver disease are an excess consumption of alcohol and a prolonged diet containing foods with a high proportion of calories coming from lipids. [17] For the patients with non-alcoholic fatty liver disease with pure steatosis and no evidence of inflammation, a gradual weight loss is often the only recommendation. [3] In more serious cases, medications that decrease insulin resistance, hyperlipidemia , and those that induce weight loss have been shown to improve liver function. [4]

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