Dynamic functional and ultrastructural changes of gastric parietal cells induced by water immersion-restraint stress in rats

AIM： To investigate the dynamic functional and ultrastructural changes of gastric parietal cells induced by water immersion-restraint stress （WRS） in rats.METHODS： WRS model of Sprague-Dawley （SD） rats was established. Fifty-six male SD rats were randomly divided into control group, stress group and post-stress group. The stress group was divided into 1, 2 and 4 h stress subgroups. The post-stress group was divided into 24, 48 and 72 h subgroups. The pH value of gastric juice, ulcer index （UI） of gastric mucosa and H^＋, K^＋- ATPase activity of gastric parietal cells were measured. Ultrastructural change of parietal cells was observed under transmission electron microscope （TEM）.RESULTS： The pH value of gastric juice decreased time-dependently in stress group and increased in post-stress group. The H^＋, K^＋-ATPase activity of gastric parietal cells and the UI of gastric mucosa increased time-dependently in stress group and decreased in poststress group. Compared to control group, the pH value decreased remarkably （P = 0.0001）, the UI and H^＋, K^＋- ATPase activity increased significantly （P = 0.0001, P = 0.0174） in 4 h stress subgroup. UI was positively related with stress time （r = 0.9876, P 〈 0.01） but negatively with pH value （r = -0.8724, P 〈 0.05）. The parietal cells became active in stress group, especially in 4 h stress subgroup, in which plenty of intracellular canalicular and mitochondria were observed under TEM. In post-stress group, the parietal cells recovered to resting state.CONCOUSION： The acid secretion of parietal cells is consistent with their ultrastructural changes during the development and healing of stress ulcer induced by WRS and the degree of gastric mucosal lesions, suggesting gastric acid play an important role in the development of stress ulcer and is closely related with the recovery of gastric mucosal lesions induced by WRS.

Gastric autoimmune disorders in patients with chronic hepatitis C before,during and after interferon-alpha therapy

AIM:To explore the prevalence of autoimmune gastritis in chronic hepatitis C virus (HCV) patients and the influence of α-interferon (IFN) treatment on autoimmune gastritis. METHODS:We performed a prospective study on 189 patients with positive anti-HCV and viral RNA enrolled in a 12-month IFN protocol.We evaluated:a) the baseline prevalence of autoimmune gastritis,b) the impact of IFN treatment on development of biochemical signs of autoimmune gastritis (at 3,6 and 12 months),c) the evolution after IFN withdrawal (12 months) in terms of anti-gastric-parietal-cell antibodies (APCA),gastrin,anti-thyroid,and anti-non-organ- specific antibodies. RESULTS:APCA positivity and 3-fold gastrin levels were detected in 3 (1.6%) and 9 (5%) patients,respectively,at baseline,in 25 (13%) and 31 (16%) patients at the end of treatment (both P<0.001,vs baseline),and in 7 (4%) and 14 (7%) patients 12 months after withdrawal (P=0.002 and P=0.01 respectively,vs baseline;P=not significant vs end of treatment).The development of autoimmune gastritis was strictly associated with the presence of autoimmune thyroiditis (P=0.0001),no relationship was found with other markers of autoimmunity. CONCLUSION:In HCV patients,IFN frequently precipitates latent autoimmune gastritis,particularly in females.Following our 12-month protocol,the phenomenon generally regressed.Since APCA positivity and high gastrin levels are associated with the presence of antithyroid antibodies, development of autoimmune thyroiditis during IFN treatment may provide a surrogate preliminary indicator of possible autoimmune gastritis to limit the need for invasive examinations.