Campylobacter pyloridis gastritis: the past, the present, and speculations about the future.
Campylobacter pyloridis infection of the stomach has been associated with gastric ulcer, duodenal ulcer, nonulcer dyspepsia, and gastritis. The etiological role of C. pyloridis in most of those conditions remains unclear. We reviewed what is known about C. pyloridis infections in man. Considerable clinical data on C. pyloridis infections was available in older literature concerning gastritis and gastric urease. C. pyloridis causes a form of type B gastritis. In some individuals the acute infection is associated with abdominal pain and transient hypochlorhydria. C. pyloridis infection is difficult to eradicate with current therapies. The mechanisms by which C. pyloridis infection may lead to development of peptic ulcers, nonulcer dyspepsia, or atrophic gastritis are discussed. Recent technological advances, such as the 13C-urea breath test, provide rapid noninvasive methods of identifying active C. pyloridis infection. These methods will permit the rapid execution of definitive investigations of the epidemiology, transmission patterns, and possible reservoirs of C. pyloridis infection and will delineate the spectrum of C. pyloridis-associated disorders.
D000126:Achlorhydria / Q000209:etiology; D001284:Atrophy / Q000473:pathology; D002167:Campylobacter / Q000201:enzymology; D002169:Campylobacter Infections / Q000150:complications*; D004415:Dyspepsia / Q000209:etiology; D005756:Gastritis / Q000209:etiology*; D006801:Humans; D010437:Peptic Ulcer / Q000209:etiology; D013270:Stomach / Q000382:microbiology / Q000473:pathology; D013272:Stomach Diseases / Q000150:complications*; D014510:Urease / Q000378:metabolism
D014510:Urease