STUDY OBJECTIVE: To determine small intestinal mucosal structure and function in patients with human immunodeficiency virus (HIV) infection. DESIGN: Prospective, consecutive sample study. SETTING: Referral-based medical clinics at a municipal and a university medical center. PATIENTS: Forty-five HIV-infected patients (44 men, 1 woman) with gastrointestinal complaints. INTERVENTIONS: All patients had esophagogastroduodenoscopy. Distal duodenal biopsy samples were examined morphometrically and by quantitative enzyme histochemical techniques. Immunohistologic studies were done to determine whether HIV antigen p24 was present. Biopsy and stool samples were examined for enteric pathogens and patients were evaluated for malabsorption. MEASUREMENTS AND MAIN RESULTS: Malabsorption was common in HIV-infected patients. In 15 of 38 patients mononuclear cells infected with HIV were found in the mucosa. In 15 of 25 patients there was no detectable lactase (beta-glucosidase) activity in the duodenal brush border; when measurable, lactase (beta-glucosidase) activity was decreased (P less than 0.02). Alkaline phosphatase activity was normal. Crypt depth was greater (P less than 0.05), villous surface area was slightly smaller, and mitotic figures per crypt were not different in HIV-infected patients compared with controls. Patients without additional intestinal infection had a reduced number of mitotic figures per crypt (P less than 0.05) and normal crypt depth. The reduction in mitotic figures was most pronounced in patients with mucosal HIV antigen p24. CONCLUSIONS: The HIV-infected patients with gastrointestinal symptoms show low-grade small bowel atrophy and a maturational defect in enterocytes, which may be caused exclusively by HIV. An additional intestinal infection can mask this mucosal atrophy.
STUDY OBJECTIVE: To determine small intestinal mucosal structure and function in patients with human immunodeficiency virus (HIV) infection. DESIGN: Prospective, consecutive sample study. SETTING: Referral-based medical clinics at a municipal and a university medical center. PATIENTS: Forty-five HIV-infectedpatients (44 men, 1 woman) with gastrointestinal complaints. INTERVENTIONS: All patients had esophagogastroduodenoscopy. Distal duodenal biopsy samples were examined morphometrically and by quantitative enzyme histochemical techniques. Immunohistologic studies were done to determine whether HIV antigen p24 was present. Biopsy and stool samples were examined for enteric pathogens and patients were evaluated for malabsorption. MEASUREMENTS AND MAIN RESULTS:Malabsorption was common in HIV-infectedpatients. In 15 of 38 patients mononuclear cells infected with HIV were found in the mucosa. In 15 of 25 patients there was no detectable lactase (beta-glucosidase) activity in the duodenal brush border; when measurable, lactase (beta-glucosidase) activity was decreased (P less than 0.02). Alkaline phosphatase activity was normal. Crypt depth was greater (P less than 0.05), villous surface area was slightly smaller, and mitotic figures per crypt were not different in HIV-infectedpatients compared with controls. Patients without additional intestinal infection had a reduced number of mitotic figures per crypt (P less than 0.05) and normal crypt depth. The reduction in mitotic figures was most pronounced in patients with mucosal HIV antigen p24. CONCLUSIONS: The HIV-infectedpatients with gastrointestinal symptoms show low-grade small bowel atrophy and a maturational defect in enterocytes, which may be caused exclusively by HIV. An additional intestinal infection can mask this mucosal atrophy.