Andrea E. Reid

Disparity in use of orthotopic liver transplantation among blacks and whites

Orthotopic liver transplantation (OLT) is the best treatment for end‐stage liver disease. Limited data exist on the access of minorities to OLT. The aim of this study was to determine whether disparities exist among black and white OLT patients. Data were collected from the United Network for Organ Sharing on black and white 18–70 year‐old OLT waiting list registrants (n = 29,013) and OLT recipients (n = 15,805) between 1994 and 1998. Standardized transplant ratios were generated by comparing the racial distribution of OLT patients with the US population. Demographic and clinical characteristics of OLT registrants were compared by race. Multivariate analyses were performed to identify predictors of time to OLT and the likelihood of dying or receiving OLT within 4 years, controlling for severity of illness and other factors. The standardized transplant ratio for black OLT recipients (0.65) was significantly lower than the standardized transplant ratio for white OLT recipients (1.05). Blacks were younger and sicker than whites. After adjustment for severity and other factors, time to OLT among recipients did not differ by race (P > .05). Blacks were more likely to die or become too ill for OLT while waiting (P < .001). Blacks were less likely to receive OLT within 4 years (P < .001). In conclusion, adult blacks were underrepresented among OLT patients. Although waiting times were similar once listed, black race affected outcomes while awaiting OLT. The process of referral and evaluation for OLT should be investigated further. (Liver Transpl 2004;10:834–841.)

Hepatitis c virus genotypes and viremia and hepatocellular carcinoma in the united states

ObjectiveHepatitis C virus (HCV) is a well recognized cause of hepatocellular carcinoma (HCC). The pathogenic significance of HCV genotypes in hepatocarcinogenesis is undefined. The aim of this study was to investigate the genotypic distribution and viremic level of HCV in patients with HCV-associated cirrhosis with or without HCC.MethodsA total of 28 HCV-infected patients with HCC (HCC+) and 38 patients with HCV-associated cirrhosis without HCC (HCC−) were studied. HCV genotype was assessed by the genotype-specific polymerase chain reaction (PCR) method of Okamoto and restriction fragment length polymorphism (RFLP) of the 5′ untranslated region (5′ UTR). Hepatitis C viremia was quantitated with the branched-chain DNA (bDNA) assay.ResultsUsing the Okamoto method, we found genotype 1b in 64% of the HCC+ group and 74% of the HCC− group, 36% of the HCC+ group and 16% of the HCC− group were coinfected with a combination of genotype 1b and another genotype. Using the RFLP method, we found genotype 1b in 41% of the HCC+ group and in 24% of the HCC− group. Other genotypes accounted for 18% of the HCC+ group and 55% of the HCC− group; no combination genotypes were identified. Poor concordance occurred between the two genotyping methods. Mean bDNA levels were not significantly different between the two groups.ConclusionsOur study demonstrates that no particular HCV genotypes were associated with HCC and genotype did not appear to influence the development of HCV-associated HCC.

Factors That Determine the Development and Progression of Gastroesophageal Varices in Patients With Chronic Hepatitis C

BACKGROUND & AIMS We aimed to identify the incidence and predictors of de novo gastroesophageal variceal formation and progression in a large cohort of patients with chronic hepatitis C and advanced fibrosis. METHODS All participants in the Hepatitis C Antiviral Long-Term Treatment against Cirrhosis Trial were offered an endoscopy before treatment and again after 4 years. Patients with varices at baseline also had an endoscopy at 2 years. Baseline laboratory and clinical parameters were analyzed as predictors of de novo variceal formation and variceal progression. RESULTS De novo varices developed in 157 of the 598 (26.2%) patients. Most of the new varices were small (76.4%) and only 1% of patients developed variceal hemorrhage. The likelihood of developing varices was associated with subject race (Hispanic > Caucasian > African American; P = .0005), lower baseline levels of albumin (P = .051), and higher levels of hyaluronic acid (P < .001) with an area under the receiver operating characteristic curve = .70. Among 210 patients with existing gastroesophageal varices, 74 (35.2%) had variceal progression or bleeding during follow-up. Patients with higher baseline ratios of serum aspartate/alanine aminotransferase (P = .028) and lower platelet counts (P = .0002) were at greatest risk of variceal progression (area under the receiver operating characteristic = .72). Prolonged, low-dose peginterferon-alpha2a therapy and beta-blockers did not influence the risk of developing new or enlarging varices. CONCLUSION Development of varices in patients with chronic hepatitis C is associated with patient race/ethnicity and laboratory markers of disease severity. Prolonged low-dose peginterferon-alpha2a therapy and beta-blockers do not reduce the risk of variceal development or progression.

Development and Progression of Portal Hypertensive Gastropathy in Patients With Chronic Hepatitis C

OBJECTIVES:The objective of this study was to determine the incidence and risk factors associated with new-onset and worsening portal hypertensive gastropathy (PHG) in patients with chronic hepatitis C (CHC).METHODS:A total of 831 CHC patients with bridging fibrosis or cirrhosis at the time of entry were prospectively monitored for clinical and histological liver disease progression while receiving either low-dose peginterferon α2a or no antiviral therapy in the HALT-C (Hepatitis C Antiviral Long-term Treatment against Cirrhosis) trial. Upper endoscopy with grading of PHG was performed at baseline and at year 4 of the study. The presence and severity of PHG were determined using the NIEC (New Italian Endoscopy Conference) criteria, and worsening PHG was defined as a score increase of ≥1 point.RESULTS:During a median follow-up of 3.85 years, 50% of 514 subjects without PHG developed new-onset PHG, whereas 26% of 317 patients with baseline PHG had worsening PHG. Independent predictors of new-onset PHG included higher alkaline phosphatase and being diabetic, whereas predictors of worsening PHG were Caucasian race, lower albumin, as well as higher serum aspartate transaminase/alanine transaminase ratio and homeostatic model assessment levels. New-onset and worsening PHG were significantly associated with clinical and histological progression. They were also associated with new-onset and worsening gastroesophageal varices.CONCLUSIONS:New-onset and worsening PHG develop at a rate of 12.9% per year and 6.7% per year, respectively, in non-responder CHC patients with advanced fibrosis. If confirmed in other studies, endoscopic surveillance for PHG may need to be tailored to individual patient risk factors.

The impact of race on liver transplant outcomes in the MELD era: still more questions than answers.

Liver transplantation is a life-saving therapy for patients with end-stage liver disease (ESLD); however, donor livers are scarce. Several studies have demonstrated racial disparities in access to liver transplant as well as patient and graft survival after liver transplantation. These studies used data gathered before the model for end-stage liver disease (MELD) was used to determine priority for liver transplant. In this issue of the journal, Drs. Ananthakrishnan and Saeian examine survival after transplant in the MELD era by race and ethnicity, and show that the racial disparities in posttransplant outcomes persist despite MELD. This study provides further evidence that race, which is likely a proxy for a variety of biological and sociological factors, must be considered in any prognostic model for liver transplantation. The impact of race on liver transplantation outcomes should be evaluated further in a well-designed, multicentered, prospective study.