During the last decade great advances have been made of water retention and dilutional hyponatremia in human cirrhosis. Finally, the field of spontaneous infection of concerning the pathogenesis and treatment of ascites. A new hypothesis on the mechanism of renal dysfunction ascitic fluid (spontaneous bacterial peritonitis) is also experiencing major changes. The demonstration of intestiand ascites formation in cirrhosis has been proposed 1 and this has greatly stimulated research in this area. The nal bacterial translocation in experimental models of cirrhosis, 12 the potential role of cytokines in some discovery of the important role played by the vascular endothelium in the homeostasis of systemic hemodynam-complications associated with this infection, 13 the identification of subgroups of cirrhotic patients predisposed to ics and renal function 2,3 has also opened an important field of research into pathophysiology, and evidence has develop spontaneous bacterial peritonitis, 14 and the effectiveness of selective intestinal decontamination in the been presented implicating endothelial factors in the pathogenesis of systemic circulatory dysfunction in cir-primary and secondary prophylaxis of spontaneous bacterial peritonitis 15,16 are the most relevant developments. rhosis 4,5 and hepatorenal syndrome (HRS). 6 The reintroduction of therapeutic paracentesis has greatly modifiedIn clear contrast to these advances, little attention has been paid to the standardization of the nomenclathe treatment of cirrhotic patients with tense or refractory ascites. 7 The transjugular intrahepatic portosys-ture and diagnostic criteria of different syndromes associated with ascites in cirrhosis. The existence of a temic shunt is another therapeutic tool of potential interest in the management of refractory ascites. 8 The uniform language, however, is essential in modern medicine. It facilitates communication among clinisynthesis of orally-active specific antagonists of the tubular effect of antidiuretic hormone and inhibitors of antidi-cians and researchers and ensures unambiguous diagnoses and more confident prognoses. Moreover, it uretic hormone release will probably add new drugs to the pharmacological armamentarium for patients with improves pathophysiological and therapeutic investigations, simplifies the analysis of therapeutic trials, cirrhosis and ascites. These ''aquaretic drugs,'' which normalize renal water metabolism in experimental cirrhosis and stimulates multicenter studies. and ascites, 9-11 are of potential interest for the treatment PREVIOUS CONSENSUS DEFINITIONS OF HEPATORENAL SYNDROME AND

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Selective intestinal decontamination with norfloxacin partially reverses the hyperdynamic circulatory state in cirrhotic patients without harming splanchnic or renal hemodynamics.

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Cirrhosis of the liver is frequently associated with carbohydrate intolerance but it is unknown whether this intolerance is due to increased hepatic glucose production (HGP), decreased glucose utilization, or both. HGP and the MCR of glucose [(MCR)G] were measured at steady state, basally and during an infusion of insulin (25 mU/kg x h) and glucose (11 mumol/kg x min), in 11 cirrhotics and 8 controls using the technique of a primed constant infusion of [3H]3-glucose. HGP was also estimated at nonsteady state during an infusion of glucagon (8 ng/kg x min). Basal HGP was significantly lower in cirrhotics compared to controls (10.2 +/- 0.6 vs. 13.2 +/- 0.6 mumol/kg x min; P < 0.0025). During the insulin/glucose infusion, HGP was suppressed to the same degree in both groups [in controls by 83% (13.2 +/- 0.6 to 2.2 +/- 0.8 mumol/kg x min) and in cirrhotics by 87% (10.2 +/- 0.6 to 1.3 +/- 0.4 mumol/kg x min)]. After the glucagon infusion, HGP rose by a similar degree in cirrhotics and controls. In contrast, basal (MCR)G was significantly lower in the nondiabetic cirrhotics (2.1 +/- .02 ml/kg x min; P < 0.005) and diabetic cirrhotics (1.2 +/- 0.2 ml/kg x min; P < 0.0005) compared to that in the control subjects (2.8 +/- 0.2 ml/kg x min). Moreover, there was a highly significant (P < 0.001) negative correlation between basal (MCR)G and the fasting glucose level (r = 0.82), and the degree of glucose intolerance as expressed by the 2-h glucose level determined by the oral glucose tolerance test (r = 0.87). It is concluded that the glucose intolerance of cirrhosis is due to a defect in peripheral glucose utilization.

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Nineteen episodes of ischemic hepatitis were diagnosed by hepatitic liver function tests and characteristic liver pathology in 17 patients. All patients had an acute illness associated with a likely fall in cardiac output although only five episodes were associated with documented hypotension. Right ventricular failure was severe in only four, mild in six, and absent in nine whilst left ventricular failure was clinically apparent in 16. The hepatitic illness was usually mild. No patient died as a direct result of hepatic damage, prognosis depending on the underlying cardiac or systemic disease. Liver function tests were characterised by a marked rise in serum transaminase levels with a parallel increase in serum lactic dehydrogenase of hepatic origin and a short time course of the enzyme elevation lasting 3 to 11 days. It is concluded that ischemic hepatitis is caused by poor hepatic perfusion associated with an acute fall in cardiac output; is usually a subclinical illness with little influence on prognosis, and may be accurately differentiated from viral hepatitis on clinical and biochemical criteria alone.