Lower Helicobacter pylori infection and peptic ulcer disease prevalence in patients with AIDS and suppressed CD4 counts.

OBJECTIVE: The prevalence of Helicobacter pylori (HP) has previously been reported to be lower in AIDS patients. This study evaluated the prevalence of HP and peptic ulcer disease in relation to absolute CD4 counts in HIV-seropositive patients with GI symptoms. DESIGN: Seventy-two patients (48 HIV-positive and 24 HIV-negative) with GI symptoms were evaluated with upper endoscopy and antral gastric biopsy. Samples were prepared with Giemsa stain and reviewed by a single pathologist to determine status of HP infection. The patients were stratified on the basis of HIV status and CD4 count: group A, HIV-positive patients with a CD4 count greater than 200, group B, HIV-positive patients with CD4 counts less than 200, and group C, an HIV-negative control group. RESULTS: The prevalence of HP infection in the three groups was as follows: group A 69% (11/16), group B 13% (4/32), and group C 63% (15/24). Peptic ulcer prevalence in group A was 19% (3/16), group B 3% (1/32), and group C 25% (6/24). CONCLUSIONS: The prevalence of HP in HIV-positive patients with a CD4 count less than 200 is significantly lower (p < 0.001) than that found in HIV-negative patients. The number of peptic ulcers in the HIV-positive group with CD4 < 200 was significantly less (p = 0.035) than that of the HIV-negative patients. These results suggest a role of CD4 cell and immune function in sustaining HP infection and HP-related peptic ulcer disease.

Helicobacter pylori prevalence in acquired immunodeficiency syndrome.

Helicobacter pylori is consistently reported with high prevalence in HIV-negative patients with chronic gastritis and active ulcer disease. This study is an evaluation of the prevalence of H. pylori in AIDS patients, and the association with chronic gastritis, erosions, and ulcer disease. Seventy-three AIDS patients referred for the evaluation of gastrointestinal symptoms underwent upper endoscopy and antral gastric biopsy. Histologic gastritis was diagnosed and degree of activity graded on hematoxylin-eosin stain. H. pylori organisms were identified by acridine orange stain. A single pathologist evaluated the biopsy specimens. H. pylori was found in 15% (11 of 73) of AIDS patients. Histologic chronic active gastritis was evident in 94.5% (69 of 73) of the study group. H. pylori was identified in 15.9% (11 of 69) of biopsy specimens with histologic chronic active gastritis. The organism was more common in biopsy specimens with a higher grade of activity in the chronic gastritis. Endoscopic erosions or ulcers were noted in 11 patients (seven gastric, four duodenal). H. pylori was present in 18% (2 of 11) of AIDS patients with erosions or ulcers. The prevalence of H. pylori in AIDS patients with histologic chronic active gastritis is much lower than the prevalence previously reported for HIV-negative patients with similar pathology. The low prevalence observed does not implicate H. pylori as the causal agent in most chronic active gastritis in the AIDS population. Impaired acid secretion may reduce colonization of gastric mucosa and explain the low rate of H. pylori observed.