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Background and Aim: Hypoadiponectinemia and high tumor necrosis factor-alpha (TNF-α) levels are associated with the development of nonalcoholic fatty liver disease (NAFLD). This study aimed to investigate the genetic polymorphisms of adiponectin and TNF-α in Chinese NAFLD patients and their association with disease severity. Methods: Seventy-nine patients with histology-proven NAFLD (61 with simple steatosis and 18 with stage 2–4 fibrosis) and 40 controls were tested for the nucleotide polymorphisms at adiponectin −11 391, −11 377, +45, and +276 and TNF-α promoters −863, −308, and −238. Results: There was no significant deviation in the adiponectin and TNF-α gene polymorphisms between NAFLD patients and controls, or between patients with simple steatosis and those with stage 2–4 fibrosis. NAFLD patients with −11377G and +45G at the adiponectin gene were more likely to have hypertriglyceridemia. On multivariate analysis, older age, higher body mass index, and higher fasting glucose were independent factors associated with stage 2–4 fibrosis in NAFLD patients. Conclusions: Adiponectin and TNF-α gene polymorphisms were not shown to be associated with NAFLD or significant fibrosis in Chinese people. The adiponectin −11377G and +45G alleles were associated with hypertriglyceridemia in NAFLD patients. Since the current study is not adequately powered to detect smaller differences in allele frequencies, larger-sized studies in different ethnic groups are required. [ABSTRACT FROM AUTHOR]

Chan HL-Y, Chui AK-K, Lau W-Y, Chan FK-L, Yui AY, Rao ARN, Wong J, Lai EC-H, Sung JJ-Y. Outcome of lamivudine resistant hepatitis B virus mutant post-liver transplantation on lamivudine monoprophylaxis. Clin Transplant 2004: 18: 295–300. © Blackwell Munksgaard, 2004 We aimed to investigate the clinical outcome of patients who develop lamivudine resistant hepatitis B virus mutants (YMDD mutants) after liver transplantation. Patients who received liver transplantation for hepatitis B-related liver diseases from 1999 to 2002 were studied. All patients received lamivudine monotherapy before and after liver transplantation. HBsAg and HBV DNA were regularly monitored, and YMDD mutation was detected by direct sequencing. Twenty patients were followed up for median 94 wk (range: 15–177 wk) post-liver transplantation. Six patients developed YMDD mutants, and the cumulative probability of developing YMDD mutations post-liver transplantation was 21% in 1 yr and 34% in 2 yr. One patient developed YMDD mutants before liver transplantation and died of hepatitis reactivation and liver failure 15 wk post-transplantation. The other five patients developed YMDD mutants 32–72 wk after liver transplantation. Two of them developed severe hepatitis which responded promptly to adefovir dipivoxil. The remaining three patients with YMDD mutants had minimal to mild hepatitis. The cumulative survival for patients with YMDD mutants was 83% and 28% at 1 and 2 yr, respectively. Only one patient who did not develop YMDD mutants died at week 119 due to chronic rejection. The post-transplant survival for patients with YMDD mutants was significantly poorer than those without YMDD mutants (log rank test p = 0.083). The emergence of YMDD mutants after liver transplantation on lamivudine monoprophylaxis had wide range of clinical presentations and was associated with increased mortality. [ABSTRACT FROM AUTHOR]