This study aims to investigate the incidence of hepatitis B virus (HBV) reactivation in inflammatory arthritis (IA) patients with HBV infection using anti-tumor necrosis factor (TNF) agents and evaluate the efficacy of antiviral therapy in reducing the risk of viral reactivation in chronic HBV infection. IA patients using anti-TNF agents from six centers were enrolled. Their HBV infection conditions and ALT and HBV-DNA levels were monitored periodically. Among the six chronic hepatitis B patients, HBV reactivation was found in two patients without antivirus prophylaxis and no viral replication was detected in the other four patients with antivirus prophylaxis. In the 31 inactive carriers, the increase of viral load was detected in 6 of 22 (27.3 %) patients without antiviral prophylaxis, and there was no viral reactivation in the other 9 patients with antiviral prophylaxis. HBV reactivation was not found in the 50 patients with resolved HBV infection. It is suggested that anti-TNF therapy might increase the risk of HBV reactivation in patients with chronic HBV infection, and antiviral prophylaxis could effectively decrease the risk. Anti-TNF agents seem to be safe in patients with resolved HBV infection.

Alcoholic hepatitis is a severe liver disease with a high mortality rate, and hepatic failure, gastrointestinal bleeding and infection are the three main causes of death.

The results indicate that baicalin regulates immune balance and relieves the ulcerative colitis-induced inflammation reaction by promoting proliferation of CD4(+)CD29(+) cells and modulating immunosuppressive pathways.

Our study indicates that avidity of anti-MPO antibodies might be more closely associated with clinical vasculitis than titre.

Abstract.A number of studies have shown that cyclooxygenase-2 (COX-2) gene polymorphisms were associated with gastric cancer. However, the results from different research groups have not been consistent. The present study aimed to investigate the association between polymorphisms of the cyclooxygenase-2 promoter region (-1195G>A, -765G>C) and gastric cancer patients with various degrees of relationship in the Chinese Han population. COX-2-1195G>A and COX-2-765G>C polymorphisms in 296 gastric cancer patients and 319 control family members were genotyped using polymerase chain reaction-restriction fragment length polymorphism. An increased risk of gastric cancer was observed in subjects with the COX-2-1195AA genotype (OR=2.03; 95% CI, 1.27-3.22), and the association strength decreased as the degree of relationship decreased. Stratification analysis revealed that the OR value of COX-2-1195AA genotype and A carriers exhibited synergy with Helicobacter pylori (H. pylori) infection (AA genotype: OR=2.96; 95% CI, 1.57-5.58; A carriers: OR=2.04; 95% CI, 1.18-3.52). No significant difference was found in each genotype of COX-2-765G>C between gastric cancer patients and control family members, as well as gastric cancer patients with various degrees of relationship. Our study demonstrated that the polymorphism of COX-2-1195AA genotype may be a risk factor for gastric cancer patients with various degrees of relationship among the Chinese Han population. H. pylori infection therefore may enhance the risk of gastric cancer in individuals with the COX-2-1195 AA genotype. IntroductionGastric cancer occurs with a variable geographic distribution worldwide, and the incidence is high in China (1). Helicobacter pylori (H. pylori) infection is an established risk factor in gastric cancer, triggering chronic inflammation of the stomach and leading to stepwise development of the malignancy (2,3). However, a number of previous studies have demonstrated that H. pylori is involved in gastric cancer tumorigenesis in a small proportion of individuals infected with the organism, indicating that individual genetic susceptibility may also play a critical role in gastric cancer (4). Subsequent studies further indicated that single nucleotide polymorphism (SNP) may have an effect on gastric tumorigenesis (5). Determinants of the host response to H. pylori infection continue to focus on polymorphisms in genes related to innate and acquired immune responses, including TLR-4, NOD2 and COX-2 (5-7).Cyclooxygenase-2 (COX-2) is known as an inducible enzyme that catalyzes conversion of arachidonic acid to prostaglandins in response to various inflammatory stimuli (8). Progression from initial gastric lesions to gastric cancer has been correlated with COX-2 over-expression, providing evidence that its activity may be involved in the onset of gastric carcinogenesis (9). Previous studies demonstrated that COX-2 is also associated with proliferation and apoptosis markers and that it is an independent prognostic factor in gastric cancer (10). At present, 2 ...