Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019270 (hernia)
 15,856 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sliding hiatal hernia has long term been implicated as a cause of lower esophageal sphincter (LES) incompetence and gastroesophageal reflux. The physics of LES function in hiatal hernia were investigated in in vitro and in vivo experiments. In vitro models of sliding hernias were constructed from excised canine gastroesophageal specimens. A "sphincter" was simulated with a rubber band around the gastroesophageal junction. It was found that placement of a ligature "hernia ring" on the stomach increased the opening pressure of the model sphincter. Addition of a tissue "hernia sac" sutured to the esophagus above the sphincter further increased the opening pressure, the protective effect being related to the pressure transmitted from the stomach to the hernia sac. There was no fluid leakage from the hernia sac between the hernia ring and the stomach. In anesthetized dogs (in vivo model) gastric and esophageal pressures were measured during gastric infusion while the LES gas way to reflux. A ligature tied loosely around the stomach to simulate a "hernia ring" and a sliding hernia without a hernia sac increased both the opening and the closing pressures of the LES by 36 +/- 18% and 35 +/- 20% (mean +/- SD), respectively. The opening pressure was increased by a decrease in gastric wall tension at the gastroesophageal junction, which was caused by the decreased radius of the herniated portion of the stomach. Pressure transmitted from the stomach to the hernia sac added to the LES pressure, and thereby further increased the opening pressure of the sphincter. The results explain how gastroesophageal reflux may be prevented in patients with hiatal hernia. It was recognized that the hernia sac may protect the sphincter, provided that it inserts into the esophagus above the LES.
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PMID:Influence of hiatal hernia on lower esophageal sphincter function. 746 55

Sliding hiatal hernia is a common endoscopic finding with a prevalence that increases with the age of patients. Although nearly all patients with GERD have HH, only a minority of patients with hernia reports reflux symptoms. Our hypothesis is that H. pylori infection may be responsible for the high number of asymptomatic hernias. After exclusion of patients with peptic ulcer, 507 patients with an endoscopic diagnosis of hernia were considered. Patients were divided into three groups: A, < or = 45 years, 141 patients; B, 46-60 years, 144 patients; and C, > or = 61 years, 222 patients. Presence of reflux symptoms (questionnaire) and esophagitis, H. pylori status, and gastric histology were recorded. The prevalence of hernia in the total series was 11% in group A, 23% in B, and 38% in C. Aging was associated with a significant increase in H. pylori prevalence and corpus gastritis scores, and a parallel decrease of GERD symptom prevalence, which was 66.6% in group A, 52.1% in B, and 46.8% in C (P < 0.01). Taking the three groups together, prevalence of H. pylori infection was higher in patients without GERD than with GERD (66.4 vs 57.3%, P < 0.05), and higher in patients with nonerosive GERD than erosive GERD (62.8 vs 48.6%, P = 0.02); corpus gastritis scores were significantly higher in patients without GERD than those with GERD and in those with nonerosive than erosive GERD. In conclusion, H. pylori infection protects against development of GERD in subjects with hiatus hernia. This effect is significantly more evident in the elderly where, in spite of the high prevalence of hernia, only a small number of individuals develop GERD. The development of a corpus-predominant gastritis is probably responsible for this effect.
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PMID:Relationship of sliding hiatus hernia to gastroesophageal reflux disease: a possible role for Helicobacter pylori infection? 1274 48