Gastric Tissue Oxidative Changes in Portal Hypertension and Cirrhosis

Abstract

Gastric mucosal lesions are very common in portal hypertension and cirrhosis. The aim of this study was to assess for oxidative gastric tissue damage in cirrhosis and evaluate relations with portal hypertension and cirrhosis parameters. The study included 30 patients with cirrhosis and 30 controls. Each patient's history, physical examination, and laboratory findings were recorded, and multiple biopsies of the gastric antrum were obtained at endoscopy. A set of antral biopsies was also collected from each control subject. Each tissue specimen was analyzed for levels of glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase (CAT) activity and level of malondialdehyde (MDA). Patients' gastric GPX, SOD, and CAT levels were significantly lower, and MDA levels were higher, than in the control group. The GPX activity level in the specimens was moderately negatively correlated with portal vein diameter (P<0.05, r=-0.45) and spleen length (P<0.05, r=-0.45). In this study gastric tissue oxidative markers showed that antral oxidative factors worsen in cirrhosis. Oxidative stress may not be a clinical condition but it obviously shows gastric tissue damage and may explain many patients' gastric lesions and hemorrhage.

Quercetin attenuates, indomethacin-induced acute gastric ulcer in rats

“…These results are in agreement with the findings of Seckin et al [57]. Moreover, we also observed the destruction of the mucosal epithelial cells as well as a highly eosinophilic cytoplasm and pyknotic nuclei along the length of fundic glands from the neck to the base.…”

Effect of H pylori infection and its eradication on hyperammo-nemia and hepatic encephalopathy in cirrhotic patients

“…H pylori is known to produce copious amounts of ammonia due to its strong urease activity. Ammonia produced by H pylori has a role in the pathogenesis of hyperammonemia when this organism is widely distributed and present in large numbers in the stomach, particularly in the presence of liver cirrhosis [16][17][18][19] . We did not find a significant difference in age, liver impairment and complication rate (upper gastrointestinal bleeding, hepatorenal syndrome and ascites) between H pylori-positive and -negative groups.…”

Loss of parietal cell superoxide dismutase leads to gastric oxidative stress and increased injury susceptibility in mice

“…Mitochondria, however, are the major intracellular source of ROS, and mitochondrial dysfunction is a contributing casual factor in increased oxidative stress and a severe consequence of increased oxidative stress (38). In addition to their roles in the gastric injury caused by the ingestion of noxious agents and by H. pylori infection, ROS also play a causal role in the gastropathy that results from portal hypertension as a result of impaired antioxidant function, including SOD (42). Studies including our own indicate that the increased oxidative state of the portal hypertensive gastric mucosa predisposes it to injury induced by noxious agents, including, notably, alcohol (25,26).…”

“…In fact, reduced SOD2 activity and the resultant mitochondrial dysfunction have been linked to numerous human degenerative diseases, including Friedreich's ataxia (33), Alzheimer's disease (8), Parkinson's disease (50), and diabetes (49). Increased oxidative stress and reduced antioxidant function have also been characterized in portal hypertensive gastropathy (42). Indeed, parietal cell loss and impaired acid secretion have been reported as consequences of portal hypertensive gastropathy (1,24).…”