Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.3.4.6 (urease)
 7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We aimed to determine the frequency of portal hypertensive gastropathy (PHG) in children with extrahepatic portal venous obstruction (EHPVO) and to find out the role of esophageal variceal obliteration by endoscopic injection sclerotherapy (EIS) and Helicobacter pylori (H. pylori) infection in the pathogenesis of PHG. Twenty consecutive children were studied before EIS and 20 after esophageal varices obliteration. Diagnosis of PHG was established by endoscopic assessment. Helicobacter pylori infection was diagnosed by rapid urease test, H. pylori culture, smear, and histopathologic examination of antral biopsy specimens. Portal hypertensive gastropathy was characterized and graded by endoscopy according to previously established criteria. In the pre-EIS group, eight (40%) had PHG (mild in all) compared with 16 (80%; mild in eight, severe in eight) in the post-EIS group (p < 0.05). Portal hypertensive gastropathy was more extensive in the post-EIS group. There was no significant difference between frequency of gastric varices and H. pylori infection in the pre-EIS and post-EIS groups. We conclude that PHG is common in children with EHPVO; its frequency, extent, and severity increase after esophageal variceal obliteration by EIS, and H. pylori infection does not play any role in its development.
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PMID:Portal hypertensive gastropathy in children with extrahepatic portal venous obstruction: role of variceal obliteration by endoscopic sclerotherapy and Helicobacter pylori infection. 881 18

An increased frequency of peptic ulcer disease is noted in patients with cirrhosis, but the role of H. pylori in this disorder remains to be determined. The diagnosis of cirrhosis was confirmed by a combination of clinical, biochemical, radiological, and histological methods. The severity of cirrhosis was assessed by Pugh's modification of Child's criteria. Upper gastrointestinal endoscopy was performed consecutively to evaluate the presence of varices and gastroduodenal mucosa. H. pylori status was assessed by histology, urease test, and serology. In all, 130 patients with cirrhosis were recruited into the study; there were 86 males and 44 females with a mean (SD) age of 54.4 (12.7) years. The H. pylori prevalence was 76.2%. There was no difference in age between the H. pylori-positive and -negative cirrhotics (P = 0.29). The H. pylori prevalence revealed no difference among cirrhotics with Child A (77.8%), Child B (72.9%), and Child C (78.6%) (P = 0.8), and neither was there a difference in H. pylori prevalence in cirrhotics with and without congestive gastropathy (77% vs 73.7%, P = 0.84). The prevalence of H. pylori in cirrhotics with and without varices did not show a statistical difference (75% vs 81.8%, P = 0.68). There also was no difference in the H. pylori prevalence between cirrhotic patients with and without peptic ulcers (84.4% vs 69.7%, P = 0.09). In conclusion, the prevalence of H. pylori or peptic ulcer is independent of the severity of cirrhotic liver disease. The association between H. pylori infection and peptic ulcer disease is weak in cirrhosis.
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PMID:Helicobacter pylori infection and peptic ulcer disease in cirrhosis. 963 11