intrinsic-factor and HIV-Infections

The mechanisms underlying acid secretory failure in patients with HIV disease are unknown. We evaluated, in a series of preliminary studies, changes associated with parietal cell structure and function in early and late HIV disease, in an attempt to elucidate possible underlying mechanisms. Gastric acid and intrinsic factor secretion, vitamin B12 absorption, and light and electron microscopic evaluation of gastric mucosa were evaluated in patients with early and late HIV infection (AIDS) and compared to non-HIV-infected controls. Immunolocalization of HIV-related antigens in gastric mucosa was also examined. Fasting gastric juice pH and intrinsic factor (IF) concentration in AIDS and HIV infected subjects were significantly different from controls (P = 0.012 and P = 0.025, respectively for pH, and 0.029 and 0.035 for IF; ANOVA LSD test). By contrast, maximal acid output (MAO) was significantly lower in AIDS, but not HIV-infected subjects (P = 0.043 and P = 0.322, respectively). Similarly, Schilling test phases 1 and 2 results were significantly lower in AIDS, but not HIV-infected subjects. Varying degrees of vacuolar degeneration of parietal cells were seen on light microscopy. On electron microscopy (EM), tubulovesicles were reduced and intracellular canaliculi dilated with striking loss of microvilli. Immunofluorescent staining with antibodies to gp120, gp41, p24, and p17 demonstrated positive punctate signals in the cytoplasm of gastric glands, which includes parietal cells. Immunogold EM with anti-gp120, localized predominantly to the microvilli of intracellular canaliculi in parietal cells. Abnormal secretory function of parietal cells occurs early in HIV disease, affects acid as well as intrinsic factor secretion, and is associated with morphological changes in the acid secretory apparatus.

Topics: Acquired Immunodeficiency Syndrome; Adult; Fluorescent Antibody Technique; Gastric Juice; Gastric Mucosa; HIV Antigens; HIV Enteropathy; HIV Infections; Humans; Intestinal Absorption; Intrinsic Factor; Lymphocytes; Male; Middle Aged; Parietal Cells, Gastric; Vitamin B 12

A prospective study of 60 consecutively admitted patients with HIV infection was performed to document the prevalence, etiology and manifestations of low serum vitamin B-12 in such patients. Low serum B-12 levels were found in 10 patients (16.7%). In 6, vitamin B-12 absorption was impaired and hog intrinsic factor addition did not improve it. Patients with low vitamin B-12 levels showed lower hemoglobin, leukocytes, lymphocytes, CD4 lymphocytes and CD4/CD8 lymphocyte ratio than HIV patients with physiological serum vitamin B-12 levels. However, bone marrow megaloblastosis was found in only 3 low vitamin B-12 patients and the deoxyuridine suppression test was pathological in only 1 case. In 7 patients, parenteral treatment was begun with variable response despite serum vitamin B-12 correction. In conclusion, low serum vitamin B-12 is often found in HIV-infected patients and it could be related to malabsorption, but clear megaloblastic abnormalities and treatment response could not be demonstrated. A decreased concentration of the serum binders due to disturbances in the leukocytes and related immunocompetent cell may play an additional role.

Topics: Adult; Anemia; Female; Gastric Acid; HIV Infections; Humans; Hydroxocobalamin; Intrinsic Factor; Leukocyte Count; Male; Prospective Studies; Vitamin B 12