Small Intestinal Structure and Function in Patients Infected with Human Immunodeficiency Virus (HIV): Evidence for HIV-Induced Enteropathy
- Reiner Ullrich, MB;
- Martin Zeitz, MD;
- Walter Heise, MD;
- Manfred L'age, MD;
- Gert Höffken, MD; and
- Ernst O. Riecken, MD
Excerpt
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 (β-glucosidase) activity in the duodenal brush border; when measurable, lactase (β-glucosidase) activity was decreased (P < 0.02). Alkaline phosphatase activity was normal. Crypt depth was greater (P < 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 < 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.
This 100-word excerpt has been provided in the absence of an abstract.
Acknowledgments
Acknowledgments: The authors thank Mrs. Ch. Brunn for technical assistance in doing the enzyme histochemical and immunohistochemical studies, Mrs. U. Feldmann for helping with the microdissection studies, and Dr. Stephen P. James, Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, for review of the manuscript.
Article and Author Information
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From the Free University of Berlin and Auguste-Viktoria Hospital, Berlin, Federal Republic of Germany. For current author addresses, see end of text.
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Grant Support: Supported by grant FKS 11-048-88 from the Bundesminister für Forschung und Technologie.
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Requests for Reprints: Martin Zeitz, MD, Medical Clinic, Department of Gastroenterology, Klinikum Steglitz, Hindenburgdamm 30, D 1000 Berlin 45, Federal Republic of Germany.
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Current Author Addresses: Drs. Ullrich, Zeitz, and Riecken: Medical Clinic, Department of Gastroenterology, Klinikum Steglitz, Hindenburgdamm 30, 1000 Berlin 45, Federal Republic of Germany.
Drs. Heise and L'age: Medical Department, Auguste-Viktoria Hospital, Rubensstrasse 125, 1000 Berlin 41, Federal Republic of Germany.
Dr. Hoffken: Medical Clinic, Department of Cardio-Pulmonary Diseases, Klinikum Steglitz, Hindenburgdamm 30, 1000 Berlin 45, Federal Republic of Germany.
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