Statin-induced liver injury in an area endemic for hepatitis B virus infection: risk factors and outcome analysis.

AIMS: Statin-induced liver injury (SILI) is quite rare, but may be severe. Little is known about the impact of chronic hepatitis B infection (CHBI) on SILI. We aimed to investigate the risk factors and outcome of SILI, with special reference to its interaction with CHBI. METHODS: Patients with SILI were recruited from our hospital, and three-to-one drug-matched controls were randomly selected. The clinical data of the patients were then compared. RESULTS: A total of 108 patients with SILI and 324 controls were enrolled. The patients with SILI were both older and had a higher statin dose than the controls. There was no predilection of liver injury associated with the seven available statins. Among the SILI patients, there was no statistical difference between the baseline and peak liver enzyme tests, and latency and severity between hepatitis B carriers (n = 16) and non-carriers (n = 92). High dose of statin and age were the two independent risk factors of SILI (OR and 95% CI: 1.93, 1.08-3.35, P = 0.025, and 1.73, 1.07-2.80, P = 0.027, respectively). Permanent discontinuation of statin was noted in 50 (46.3%) patients with SILI due to severe SILI or recurrent hepatotoxicity after rechallenge of other statins. CONCLUSION: High dose of statin and old age may increase patient susceptibility to SILI; however, CHBI and abnormal baseline liver tests are not risk factors of SILI. Nonetheless, SILI is still worthy of notice, because nearly half of the overt cases discontinued statin treatment due to severe hepatotoxicity in this study.

Superoxide Dismutase 2 Genetic Variation as a Susceptibility Risk Factor for Alcoholic Cirrhosis.

AIMS: Superoxide dismutase 2 (SOD2) is an important antioxidant phase 2 enzyme. The associations of SOD2 genetic variation and the risk of advanced alcoholic liver diseases are still debatable. We aimed to investigate the association of the main SOD2 genetic variant (47T>C) and the susceptibility to alcoholic cirrhosis. METHODS: A total of 80 patients with alcoholic cirrhosis (AC), 80 patients with alcoholic non-cirrhosis (ANC), 80 with viral hepatitis B-related cirrhosis (VC), and 165 healthy controls (HC) were enrolled into this study. A polymerase chain reaction was used to genotype their SOD2 47T>C (rs4880). RESULTS: There was no statistical difference in the frequency distribution of the three SOD2 47T>C genotypes among groups. However, if individuals with C variant were grouped together, the AC group had higher frequency of SOD2 C/C or C/T genotype than ANC, VC and HC groups had (38.7% vs. 21.3%, 26.3% and 21.8%, respectively, P = 0.010). After adjustment for confounders, the SOD2 C/C and C/T genotypes remained associated with the risk of AC (adjusted OR: 2.79 and 3.50, respectively, P < 0.03, compared with ANC and HC groups). In contrast, there was no significant difference of SOD2 genetic variation between VC and HC groups. CONCLUSIONS: Anti-oxidative enzyme SOD2 47T>C genetic variant may increase the susceptibility to AC. This suggests that oxidative stress plays a role in the development of AC.

Hepatitis, gallbladder hydrops, splenomegaly, and ascites in a child with scarlet fever.

We report a case of scarlet fever associated with hepatitis, gallbladder hydrops, splenomegaly, and ascites in a 15-year-old girl. The girl presented with fever and skin rash. Leukocyte, liver enzyme, and serum C-reactive protein concentrations were elevated. Ultrasonography revealed marked gallbladder wall thickening, diffuse liver parenchymal disease with moderate splenomegaly, and moderate ascites throughout the abdominal and pelvic cavities. Blood cultures for group A ß-hemolytic streptococci were negative. Complete recovery was facilitated with antibiotic treatment.