Nonalcoholic steatohepatitis (NASH) may account for many cases of cryptogenic cirrhosis. If so, then steatosis might recur after liver transplantation. Two thousand fifty-two patients underwent primary liver transplantation for chronic liver disease between 1986 and 2004. Serial liver biopsy samples were assessed for steatosis and fibrosis. Two hundred fifty-seven patients (12%) had a pretransplant diagnosis of cryptogenic cirrhosis (239) or NASH (18). Fatty liver developed in 31% and was more common when the pretransplant diagnosis was NASH (45% at 5 years versus 23% for cryptogenic cirrhosis, P ¼ 0.007). NASH developed in only 4% and occurred exclusively when steatosis had already occurred. Steatosis after liver transplantation was associated with the baseline body weight and body mass index by univariate analyses, but no pretransplant or posttransplant characteristic independently predicted steatosis after liver transplantation because obesity was so common in all groups. Five percent and 10% developed bridging fibrosis or cirrhosis after 5 and 10 years, respectively, and this was more common after NASH (31%) than in those who developed steatosis alone (6%) or had no fat (3%, P ¼ 0.002). One-, 5-, and 10-year survival was the same in patients who underwent transplantation for cryptogenic cirrhosis or NASH (86%, 71%, and 56%) and in patients who underwent transplantation for other indications (86%, 71%, and 53%; not significant), but death was more often due to cardiovascular disease and less likely from recurrent liver disease. In conclusion, fatty liver is common after liver transplantation for cryptogenic cirrhosis or NASH but is twice as common in the latter group; this suggests that some cryptogenic cirrhosis, but perhaps not all, is caused by NASH. Posttransplant NASH is unusual, and steatosis appears to be a prerequisite. Advanced fibrosis is uncommon, and survival is the same as that of patients who undergo transplantation for other causes. Liver Transpl 16:431-439,

Chronic hepatitis C is often asymptomatic and undiagnosed yet can progress to liver failure or hepatocellular carcinoma. This study determined the prevalence of hepatitis C in Texas and estimated the progression of disease in this cohort. National Health and Nutrition Evaluation Survey III data on the national prevalence of an antibody to the hepatitis C virus were extrapolated to Texas using census data weighted for local characteristics. A Markov model estimated the progression of liver disease. Results showed that 387,395 Texans (1.79%) are infected with the hepatitis C virus. County prevalence varied from 1.25% to 2.63%, with higher rates concentrated along the US-Mexico border. However, most cases of infection were located near major Texas cities. The number of infected persons will decline in the future. However, the proportion of cases progressing to cirrhosis will increase, resulting in more complications such as liver failure and hepatocellular carcinoma. Thus, chronic hepatitis C is common in Texas and will result in an increase in complications of cirrhosis in coming years. The disease will tax health care facilities and transplant units in the state.

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