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M Elsakr

Publications and source records attributed to M Elsakr.

5 recordsLinked to original sources

Changes in parietal cell structure and function in HIV disease.

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.

Acquired Immunodeficiency Syndrome↗

Intercellular adhesion molecule-1 (ICAM-1) staining of reactive and neoplastic follicles. ICAM-1 expression of neoplastic follicle differs from that of reactive germinal center and is independent of follicular dendritic cells.

BACKGROUND: Intercellular adhesion molecule-1 (ICAM-1) is expressed on follicular dendritic cells (FDC), and the ICAM-1/LFA-1 pathway is essential for affinity selection of activated B-cells in germinal centers (GC). The expression of ICAM-1 has been studied by immunostaining methods in GC, but not in neoplastic follicles (NF). METHODS: The authors studied the expression of ICAM-1 by the avidin-biotin-peroxidase complex (ABC) method with frozen sections in GC of reactive nodes (n = 22) and NF of follicular lymphomas (n = 19), in comparison with FDC staining. RESULTS: GC stained uniformly for ICAM-1, with staining intensity varying little from node to node, and follicular borders were well demarcated from the surroundings. Endothelial cells within GC did not stain whereas those outside stained strongly. In contrast, NF stained variably from tumor to tumor, and in any given tumor. Characteristically, follicular borders were not demarcated, and stained areas were difficult to define due to the lack of demarcation, with the exception of large cell type with diffuse areas (n = 2). Endothelium of intrafollicular vessels stained prominently (12 of 19), and appeared to contribute to the staining intensity of the follicles. FDC staining revealed a meshwork pattern in GC which was similar to that of ICAM-1. The FDC mesh-work pattern was present in 15 tumors. The pattern was remarkably uniform with sharply defined borders, which contrasted starkly to the variable staining and lack of follicular borders in the ICAM-1 stain of the same tumors. CONCLUSIONS: The staining pattern of follicles for ICAM-1 was similar to that for FDC in reactive nodes, but distinct from the latter in follicular lymphomas. An appropriate expression of ICAM-1 appears to be essential for normal GC, as the alteration of the expression coincides with the malignant transformation of GC. The altered expression of ICAM-1 may be useful in distinguishing NF from reactive GC.

Adolescent↗

Gastropathy and ketoconazole malabsorption in the acquired immunodeficiency syndrome (AIDS).

STUDY OBJECTIVE: To correlate oral ketoconazole absorption with gastric acid secretion in patients with the acquired immunodeficiency syndrome (AIDS). DESIGN: Prospective measurement of maximal acid output and oral ketoconazole absorption with and without 0.1-N hydrochloric acid. SETTING: Hospital in-patients in university medical center. PATIENTS: Ten consecutive male patients with AIDS. INTERVENTION: Maximal acid output was determined after pentagastrin stimulation in all patients. Serum ketoconazole levels were measured the day after ingestion of a 200-mg ketoconazole tablet in the fasted state. On the final day, ketoconazole was ingested with 200 mL of 0.1-N hydrochloric acid. MEASUREMENTS AND MAIN RESULTS: Maximal acid output was below 15 mEq/h in 7 of 10 patients. In all 7, the area under the serum ketoconazole concentration-time curve was below normal (1.4 +/- 0.9 mg/h.L; mean +/- SE), and absorption was normalized by hydrochloric acid (9.9 +/- mg/h.L). Two of three patients with maximal acid outputs above 15 mEq/h had normal ketoconazole absorption (15.1 +/- 6.7 mg/h.L). CONCLUSIONS: The bioavailability of oral ketoconazole is reduced in patients with AIDS, largely as a result of gastric hypochlorhydria. Ketoconazole tablets should therefore be given with acid in these patients.

Acquired Immunodeficiency Syndrome↗

Seasonal variation of acute appendicitis: a 56-year study.

Over a period of 56 years, 12,686 appendectomies were done for acute appendicitis at the Jersey City Medical Center in Jersey City, New Jersey. We tabulated each appendectomy by the month and season of its occurrence. The spring and summer months had the highest incidence and the fall and winter the lowest. Using analysis of variance, however, we found no statistically significant variation in incidence.

Acute Disease↗