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Hypernephroma with nonmetastatic liver dysfunction (Stauffer's syndrome) and hypercalcemia. Case report and review of the literature.

A case of renal carcinoma with hepatic dysfunction and hypercalcemia is described. The literature on Stauffer's syndrome has been reviewed and the pathogenesis of this syndrome discussed. It is stressed that the presence of hepatic dysfunction should not be considered a contraindication to surgery since its manifestations have been observed to regress in many cases following removal of the tumor.

Hepatomegaly↗

[Surgical stress and organ dysfunction: liver].

Various kinds of neuroendocrine responses occur to an extensive surgical stress such as major operation and severe trauma. Studies of the details of this response have focused on many endocrine systems for decades. Hypersecretion of the hormones results in metabolic and cardiovascular changes, particularly in catabolic condition. As hepatic circulation is affected by catecholamines such as norepinephrine, hepatic mitochondrial redox status highly reduced due to tissue hypoxia and to shortage in the energy substrate, even in the cases without apparent blood loss. This results in hepatic energy crisis. Although most of the conventional hepatic biochemical parameters failed to reveal, the crisis is often unexpectedly severe if one estimate it by measuring arterial ketone body ratio (AKBR), which reflects hepatic mitochondrial redox status. The energy crisis results in the disturbance of excretion of conjugated bilirubin from hepatocyte to bile canaliculi that has to occur against bilirubin concentration gradient. This explains one of the mechanisms of posttraumatic as well as postoperative hyperbilirubinemia. Recently, numerous studies focused on various kinds of physiologically active substances, such as monokines, eicosanoids, and oxygen radicals. They are released from various kinds of cell strains as humoral mediators in response to many kinds of stimuli and affect hepatic function. Studies to modulate the activity of such mediators are going on.

Catecholamines↗

Liver granulomas: a possible paraneoplastic manifestation of hypernephroma.

A patient with hypernephroma presented with signs of liver dysfunction. Liver biopsy disclosed the presence of granulomas. Extensive search for a known cause of hepatic granulomas was negative. The presence of granulomas in lymph nodes draining the neoplasm, the improvement of liver dysfunction after nephrectomy, and its aggravation preceding overt metastatic manifestation support the existence of a cause and effect relationship between the renal cell carcinoma and the liver granulomatous disease.

Aged↗

The spectrum of chronic liver disease in renal transplant recipients.

Chronic liver disease has been reported to be an important cause of late morbidity and mortality in renal transplant recipients. We have examined the prevalence and nature of chronic liver disease among 538 patients with functioning renal allografts managed at the Western Infirmary, Glasgow, between 1980 and 1989. Thirty-seven patients (7 per cent) satisfied biochemical criteria for chronic liver dysfunction. Liver biopsies were obtained from 24 of these, and autopsy tissue was available from three other patients. Chronic hepatitis of variable severity was present in 15 patients, haemosiderosis in 12 patients and nodular regenerative hyperplasia in five patients. Nineteen patients (51 per cent) had serological evidence of infection with the hepatitis C virus, and one of these developed chronic hepatitis B and D infection as well. Although a variety of chronic liver diseases occurred in our transplant population, the frequency of serious sequelae from liver dysfunction was much lower than that reported from transplant centres in other countries.

Chronic Disease↗

Evolution of HBeAg/anti-HBe status and its relationship to clinical and histological outcome in chronic HBV carriers in childhood.

Fifty-five Japanese HBV carriers under 15 yr of age were followed for 12 months or longer, during which time we investigated the evolution of HBeAg/anti-HBe status and clinical and histological aspects of the liver disease. Of 45 cases positive for HBeAg at the initial examination, 34 remained positive for HBeAg during the follow-up periods, while the remaining 11 lost HBeAg and eight of these seroconverted to anti-HBe. At the final observation, HBeAg positivity in serum was found in as many as approximately 90% of the HBV carriers under 6 yr, but had fallen to 48% in carriers between 12 and 15 yr. The serum transaminase values in 11 cases who lost HBeAg were abnormally elevated for variable periods, but eventually returned to normal. In six of these 11 who had liver dysfunctions, liver biopsy was performed during the HBeAg positive phase or shortly after the disappearance of HBeAg. The histologies of liver were chronic persistent hepatitis in two cases and chronic active hepatitis in four. Repeat liver biopsies of two cases with chronic active hepatitis at the first examination showed nonspecific reactive hepatitis 2 and 4 yr after seroconversion or disappearance of HBeAg. These results indicate that HBeAg-positive HBV carriers with overt liver dysfunctions in childhood are prone to lose HBeAg or to seroconvert to anti-HBe, followed by a marked histological regression, and therefore that special antiviral therapy is probably unnecessary.

Adolescent↗

Diclofenac associated hepatitis.

Diclofenac is a widely used non-steroidal anti-inflammatory drug, being the most commonly prescribed of its kind in the world. This paper describes five cases of hepatitis with clinical features indicating a direct link with diclofenac. All the patients presented with an acute hepatitis, three being jaundiced. They gave a history of taking diclofenac up to the time of presentation, four of the five having started the drug within the previous 3 months. There were no other features in the histories to suggest alternative causes for the liver dysfunction. Liver function tests were grossly abnormal in all cases, showing a hepatitic picture. A liver biopsy was performed in 4 cases, and showed features of an acute hepatitis with inflammation and hepatocyte damage dominating. The liver dysfunction returned to normal on drug withdrawal in four of the five cases, with full recovery by 3 months. One patient developed steroid-responsive chronic active hepatitis. Hepatotoxicity associated with diclofenac is documented, but previously only a few isolated cases have been described. The occurrence of five cases in one gastroenterology unit over a 12-month period suggests that hepatitis associated with diclofenac may be commoner than previously supposed.

Aged↗