MELD Score Is an Important Predictor of Pretransplantation Mortality in HIV-Infected Liver Transplant Candidates

Division of Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Gastroenterology (Impact Factor: 16.72). 09/2009; 138(1):159-64. DOI: 10.1053/j.gastro.2009.09.053
Source: PubMed


Human immunodeficiency virus (HIV) infection accelerates liver disease progression in patients with hepatitis C virus (HCV) and could shorten survival of those awaiting liver transplants. The Model for End-Stage Liver Disease (MELD) score predicts mortality in HIV-negative transplant candidates, but its reliability has not been established in HIV-positive candidates.
We evaluated predictors of pretransplantation mortality in HIV-positive liver transplant candidates enrolled in the Solid Organ Transplantation in HIV: Multi-Site Study (HIVTR) matched 1:5 by age, sex, race, and HCV infection with HIV-negative controls from the United Network for Organ Sharing.
Of 167 HIVTR candidates, 24 died (14.4%); this mortality rate was similar to that of controls (88/792, 11.1%, P = .30) with no significant difference in causes of mortality. A significantly lower proportion of HIVTR candidates (34.7%) underwent liver transplantation, compared with controls (47.6%, P = .003). In the combined cohort, baseline MELD score predicted pretransplantation mortality (hazard ratio [HR], 1.27; P < .0001), whereas HIV infection did not (HR, 1.69; P = .20). After controlling for pretransplantation CD4(+) cell count and HIV RNA levels, the only significant predictor of mortality in the HIV-infected subjects was pretransplantation MELD score (HR, 1.2; P < .0001).
Pretransplantation mortality characteristics are similar between HIV-positive and HIV-negative candidates. Although lower CD4(+) cell counts and detectable levels of HIV RNA might be associated with a higher rate of pretransplantation mortality, baseline MELD score was the only significant independent predictor of pretransplantation mortality in HIV-infected liver transplant candidates.

Download full-text


Available from: John Julian Fung, Oct 07, 2015
35 Reads
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: In the last two centuries, physical, chemical, and biological alterations of Lake Champlain have resulted in the loss of two species, addition of 15 fish species, and listing of 16 species as endangered, threatened or of special concern. The lake currently supports 72 native fish species; lake trout (Salvelinus namaycush) and Atlantic salmon (Salmo salar) were extirpated by 1900, American eel (Anguilla rostrata) and lake sturgeon (Acipenser fulvescens) populations are extremely low, and walleye (Sander vitreum) are declining. Dams on several rivers, and ten causeways constructed in the mid 1800s to early 1900s, cut off access to critical spawning areas and may have limited fish movements. Siltation and sediment loading from agricultural activity and urban growth have degraded substrates and led to noxious algal blooms in some bays. A commercial fishery targeting spawning grounds of lake whitefish (Coregonus clupeaformis), lake trout, and walleye probably reduced numbers of these species prior to its closure in 1912. Non-native species introductions have had ecosystem-wide impacts. Sea lamprey (Petromyzon marinus) populations were very high prior to successful control, possibly as a consequence of ecological imbalance and habitat changes. A paucity of historic survey data or accurate species accounts limits our understanding of the causes of current fish population trends and status; in particular, the effects of habitat fragmentation within the lake and between the lake and its watershed are poorly understood. Holistic, ecosystem management, including pollution reduction and examination of habitat impacts, is necessary to restore the general structure of native biological assemblages.
    Journal of Great Lakes Research 01/2012; 38. DOI:10.1016/j.jglr.2011.09.007 · 1.75 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: To review the recent literature on the prognostic value of biomarkers of liver fibrosis and impaired liver function in patients with chronic hepatitis C with or without HIV coinfection. A combination of standard blood tests seems to be useful in identifying patients at risk of liver-related complications. Findings from studies investigating the validity of the Model for End-Stage Liver Disease (MELD) score in HIV-infected liver transplant candidates are conflicting. Two large studies of HIV/hepatitis C virus (HCV) coinfected patients have shown that plasma levels of the fibrosis marker hyaluronic acid are a strong predictor of clinical complications. A smaller study found hyaluronic acid and two other fibrosis tests, aspartate aminotransferase-to-platelet ratio index (APRI) and Fib-4, to be independent predictors of mortality when included in models with the MELD or the Child-Pugh-Turcotte scores. Although the data are still limited, recent findings from large studies of the prognostic ability of fibrosis markers in hepatitis C patients provides hope that fibrosis markers, together with other noninvasive methods, one day, will replace liver biopsy as the gold standard for the prognostic evaluation of liver disease. The MELD score, and other prognostic factors, need further evaluation in HIV/HCV coinfected patients with end-stage liver disease.
    Current opinion in HIV and AIDS 11/2010; 5(6):517-23. DOI:10.1097/COH.0b013e32833e3ee6 · 4.68 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Hepatitis C virus (HCV) is the major cause of liver disease in haemophilia. Few data exist on the proportion with liver fibrosis in this group after long-term HCV and HIV co-infection. We conducted a cross-sectional multi-centre study to determine the impact of HIV on the prevalence and risk factors for fibrosis in haemophilic men with chronic hepatitis C. Biopsies were independently scored by Ishak, Metavir and Knodell systems. Variables were tested for associations with fibrosis using logistic regression and receiver operating curves (ROC). Of 220 biopsied HCV(+) men, 23.6% had Metavir ≥ F3 fibrosis, with higher mean Metavir fibrosis scores among HIV/HCV co-infected than HCV mono-infected, 1.6 vs. 1.3 (P = 0.044). Variables significantly associated with fibrosis included AST, ALT, APRI score (AST/ULN × 100/platelet × 10(9) /L), alpha-fetoprotein (all P < 0.0001), platelets (P = 0.0003) and ferritin (P = 0.0008). In multiple logistic regression of serum markers, alpha-fetoprotein, APRI and ALT were significantly associated with ≥ F3 fibrosis [AUROC = 0.77 (95% CI 0.69, 0.86)]. Alpha-fetoprotein, APRI and ferritin were significant in HIV(-) [AUROC = 0.82 (95% CI 0.72, 0.92)], and alpha-fetoprotein and platelets in HIV(+) [AUROC = 0.77 (95% CI 0.65, 0.88]. In a multivariable model of demographic and clinical variables, transformed (natural logarithm) of alpha-fetoprotein (P = 0.0003), age (P = 0.006) and HCV treatment (P = 0.027) were significantly associated with fibrosis. Nearly one-fourth of haemophilic men have Metavir ≥ 3 fibrosis. The odds for developing fibrosis are increased in those with elevated alpha-fetoprotein, increasing age and past HCV treatment.
    Haemophilia 01/2011; 17(1):103-11. DOI:10.1111/j.1365-2516.2010.02366.x · 2.60 Impact Factor
Show more