Serum sodium predicts mortality in patients listed for liver transplantation.

With the implementation of the model for end-stage liver disease (MELD), refractory ascites, a known predictor of mortality in cirrhosis, was removed as a criterion for liver allocation. Because ascites is associated with low serum sodium, we evaluated serum sodium as an independent predictor of mortality in patients with cirrhosis who were listed for liver transplantation and whether the addition of serum sodium to MELD was superior to MELD alone. This is a single-center retrospective cohort of all adult patients with cirrhosis listed for transplantation from February 27, 2002, to December 26, 2003. Listing laboratories were those nearest the listing date +/-2 months. Of the 513 patients meeting inclusion criteria, 341 were still listed, while 172 were removed from the list (105 for transplantation, 56 for death, 11 for other reasons). The median serum sodium and MELD scores were 137 mEq/L (range, 110-155) and 15 (range, 6-51), respectively, at listing. Median follow-up was 201 (range, 1-662) days. The risk of death with serum sodium <126 mEq/L at listing or while listed was increased, with hazard ratios of 7.8 (P < .001) and 6.3 (P < .001), respectively, and the association was independent of MELD. The c-statistics of receiver operating characteristic curves for predicting mortality at 3 months based upon listing MELD with and without listing serum sodium were 0.883 and 0.897, respectively, and at 6 months were 0.871 and 0.905, respectively. In conclusion, serum sodium <126 mEq/L at listing or while listed for transplantation is a strong independent predictor of mortality. Addition of serum sodium to MELD increases the ability to predict 3- and 6-month mortality in patients with cirrhosis.

Primary sclerosing cholangitis.

Primary sclerosing cholangitis (PSC) is an idiopathic, chronic cholestatic liver disease of uncertain etiopathogenesis commonly associated with inflammatory bowel disease (IBD) and is characterized by patchy inflammation of the biliary tree progressing to fibrosis and strictures. The natural history of PSC is highly variable but characteristically follows a progressive clinical course leading to biliary tree strictures, cholestasis, and choledocholithiasis. The course of the disease may be complicated by cholangitis, secondary biliary cirrhosis, liver failure, and cholangiocarcinoma. The diagnosis of PSC is based on typical cholangiographic findings, supported by nonspecific clinical signs and symptoms, cholestatic liver biochemical tests, and liver biopsy. Uncommon and usually clinically obvious secondary causes of sclerosing cholangitis are excluded before establishing the diagnosis of PSC. Therapeutic approaches that show promise include endoscopic therapy and ursodeoxycholic acid. The only accepted therapy for end-stage PSC that can improve long-term outcome is liver transplantation. The diagnosis of cholangiocarcinoma--often difficult and elusive--usually precludes liver transplantation because its prognosis is very poor.