In 1961, Stauffer described for the first time a syndrome associating abnormal liver function with RCC in the absence of metastatic disease (Stauffer 1961). The abnormalities returned to normal following nephrec-tomy. The incidence of Stauffer's syndrome ranged from 9 % to 33 %. Liver dysfunction is accompanied by hepatosplenomegaly in 50% of patients, including fever, fatigue, and weight loss. The biochemical abnormalities included elevated transaminases, elevated alkaline phosphatase, hypothrombinemia, prolonged partial thromboplastin time, elevated alpha 2 globulin levels, and hypoalbuminemia. The etiology of Stauffer's syndrome remains undefined. Some etiologic theories have been reported, including secretion of hepatoto-xins or lysosomal enzymes, which might also stimulate hepatic cathepsins, phosphatase, or beta glucuroni-dase. Attempts to reproduce this syndrome in animals by utilizing injections of tumor extracts have been unsuccessful (Hanash et al. 1971). Liver biopsies show a nonspecific reactive hepatitis with Kupffer cell proliferation, variable hepatocellular degeneration, and portal triaditis. There is no evidence of biliary obstruction to explain the elevated alkaline phosphatase (Hannash 1982). Following nephrectomy, reversal of liver function tests to normal is usually associated with favorable prognosis; their failure to normalize implies incomplete resection or unrecognized metastasis. Furthermore, patients whose liver function became normal following radical nephrectomy and subsequently revert to abnormal have tumor recurrence locally or distant metastasis (Warren et al. 1970).
Was this article helpful?