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In this study, we investigated the prognostic value of serum sodium and hyponatremia (<130 mEq/L) in 262 cirrhotic patients consecutively listed, 19 of which died (7%), 175 survived (67%), and 68 underwent liver transplantation (26%) during 3 months of follow-up. Hyponatremia was present in 63% of patients who died, compared to 13% of those who survived (P < .001), whereas the proportion with elevated creatinine (>1.4 mg/dL) was low and similar in both groups (10.5 vs. 3%). Prevalence of hyponatremia was higher than that of elevated serum creatinine across all model for end-stage liver disease (MELD) categories. Using logistic regression, hyponatremia and serum sodium were significant predictors of mortality with concordance statistics (c-statistics) .753 for hyponatremia, .784 for sodium, .894 for MELD, .905 for MELD plus hyponatremia (P ‫؍‬ .006 vs. MELD alone), and .908 for MELD plus serum sodium (P ‫؍‬ .026 vs. MELD alone). Risk of death across all MELD scores was higher for patients with hyponatremia than without hyponatremia. Cox regression considering data within 6 months of follow-up yielded qualitatively similar results, with hyponatremia being a significant predictor of greater mortality risk with an odds ratio of 2.65 (P ‫؍‬ .015). Each increase of 1 mEq/L of serum sodium level was associated with a decreased odds ratio of .95 (P ‫؍‬ .048). Our results indicate that hyponatremia appears to be an earlier and more sensitive marker than serum creatinine to detect renal impairment and / or circulatory dysfunction in patients with advanced cirrhosis. In conclusion, addition of serum sodium to MELD identified a subgroup of patients with poor outcome in a more efficient way than MELD alone and significantly increased the efficacy of the score to predict waitlist mortality. (Liver Transpl 2005; 11:336-343.)

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Early studies found that orthotopic liver transplantation (OLT) for hepatitis B virus (HBV)-related liver failure was associated with a very high rate of reinfection and severe and rapidly progressive liver disease, resulting in a significant decrease in graft and patient survival compared with patients transplanted for other causes of liver disease. 1,2 Various measures have been tried in an attempt to reduce the rate of reinfection. The most promising results have come from the use of long-term (Ն 6 months) high-dose hepatitis B immune globulin (HBIG). 3,4 However, this regimen is expensive, and a significant reduction in the rate of reinfection is mainly seen in patients who have nonreplicative infection pre-OLT. Reinfection despite HBIG immunoprophylaxis may be caused by inadequate neutralization of overwhelming amounts of wildtype HBV, or to breakthrough infection by immune escape mutants.The major B-cell epitopes of hepatitis B surface antigen (HBsAg) have been shown to reside in the 'a' determinant region located at amino acid positions 124-149. 5,6 This region is conformational and is thought to consist of two loops held by disulfide bridges between cysteines 124 and 137, and cysteines 138 and 147. 7 The second loop is more conserved and confers most of the antigenicity of the 'a' determinant; this loop is sometimes referred to as the major hydrophilic region (MHR). HBV can be classified into four major subtypes: adr, adw, ayr, and ayw. Antibodies to the 'a' determinant confer protection against all subtypes of HBV. 8 Mutations in the HBV S gene have been reported in OLT recipients who developed HBV reinfection despite prophylaxis with monoclonal or polyclonal hepatitis B surface antibody (anti-HBs). McMahon et al. found amino acid substitutions in the 'a' determinant in all three patients who were reinfected despite monoclonal anti-HBs prophylaxis, 9 while the incidence of mutations in the 'a' determinant in OLT recipients who were reinfected despite HBIG prophylaxis varied from 0% to 33%. 10-12 Some of these mutations, including the glycine-to-arginine substitution at codon 145, have been shown to decrease binding to monoclonal antiHBs, suggesting that the breakthrough infections were caused by immune escape mutants. 9,11,13 The number of patients cited in the above studies ranged from three to seven patients; therefore, the significance of S escape mutants in HBV reinfection post-OLT remains unclear. It is also possible that additional mutations may be present in the HBV S gene outside the 'a' determinant in patients who received polyclonal anti-HBs (HBIG). Unfortunately, there are very few data on the sequence in the rest of the S gene. In addition, to date, there are no data on the reversibility of these mutations after withdrawal of HBIG therapy.