Gastric acid secretion in HIV-1 infection.

It has been suggested that AIDS patients may have reduced gastric acid output. This is of concern because gastric acid may be required for absorption of oral antifungal agents that are important in AIDS management. The cause as well as the progression of reduced gastric acid output in AIDS patients is unclear. This study investigated gastric acid output in relation to the stage of non-AIDS HIV-1-infected patients. No statistical difference was found between nine control and 26 male HIV-infected subjects in basal acid output, maximal acid output, peak acid output, or fasting serum gastrin, regardless of stage. Likewise, no relationship between stage of HIV infection and gastric acid output was determined. We conclude that there is no impairment in basal and maximally stimulated gastric acid secretion in non-AIDS HIV-1-infected males. In addition, the clinical stage of non-AIDS HIV-1 infection has no effect on gastric acid secretion.

Bronchoalveolar lavage findings in patients seropositive for the human immunodeficiency virus (HIV).

To evaluate bronchoalveolar lavage (BAL) findings in patients infected with human immunodeficiency virus (HIV), 39 patients seropositive for the virus but with no history of opportunistic infection were studied. Opportunistic organisms such as Pneumocystis carinii were not found in any of the 35 BAL fluids sent for special stains and cultures. Three of 16 (18 percent) BAL fluids sent for HIV culture were positive compared with a 60.9 percent blood HIV culture positivity in the same group. To evaluate cellular recovery, the patients were divided into Walter Reed (WR) groups 1 and 2 (blood CD4 greater than or equal to 400/cu mm) and WR3 to WR5 (blood CD4 less than 400/cu mm). Compared with ten nonsmoking healthy controls, the WR1 and WR2 group had a greater overall cellular recovery but this was not statistically significant when the smokers were excluded. There was no difference in macrophage or lymphocyte percentages in either patient group compared with controls. T-cell subset analysis of a small group of WR1 to WR5 patient BAL fluids revealed no difference in CD4 numbers or the CD4/CD8 rate between WR1 and WR2 and WR3 to WR5 patients. We conclude that opportunistic pulmonary infection is unlikely in HIV-seropositive patients with normal chest roentgenograms despite symptoms of dyspnea on exertion. Also, HIV can be isolated from BAL fluid from these patients although not as often as from blood. Finally, there appears to be no distinct progression in BAL cellular findings before the onset of acquired immunodeficiency syndrome.