Effect of the treatment with alpha-macroglobulin on the development of experimental pancreatitis.

UNLABELLED: Alpha-macroglobulins are proteinase inhibitors. Monofluorophosphate increases alpha-macroglobulin levels in plasma, inducing a higher survival rate and lower pancreatic damage in rats with pancreatitis. The aim of this study was to evaluate the effect of alpha-macroglobulin on the development of pancreatitis. Pancreatitis was surgically induced in Sprague-Dawley rats divided into groups of 16 rats each and -subjected to the following intravenous treatments for 3 days: CONTROLS: pancreatitis without treatment, Enriched plasma: pancreatitis+-alpha-macroglobulin-enriched plasma, Normal plasma: pancreatitis+plasma with normal levels of alpha-macroglobulin, Saline Solution: pancreatitis+saline solution, Purified alpha-macroglobulin: pancreatitis+purified alpha-macroglobulin. After 14 days pancreatic damage was assessed using a score that measures: edema, fibrin, neutrophils, mononuclear leukocytes, necrosis, vascular congestion, thrombosis, hemorrhage and fibrosis. Pancreatic damage decreased and the percentage of animals with pancreatitis was lower in enriched-plasma and purified alpha-macroglobulin groups. We conclude that the intravenous administration of alpha-macroglobulins causes a reduction in the histological damage produced by pancreatitis.

[Enteroendocrine cells modifications in Helicobacter pylori gastritis]. / Modificaciones de las células enteroendócrinas en gastritis por Helicobacter pylori.

OBJECTIVE: The aim of the present study was to analyze the modifications in the number and distribution of enteroendocrine cells (EEC) in antrum of patients with Helicobacter pylori (HE) gastritis. We also wanted to demonstrate their possible participation in the immune response. MATERIAL AND METHODS: Twenty-six (26) biopsies of gastric antrum from patients between the ages of 40 and 60 were used. Slides were stained with H&E, Giemsa for HP, and chromogranin A to visualize EEC. Five (5) patients were normal controls. Eleven (11) patients had antral chronic gastritis (ACG) with different grades of activity, and ten (10) patients had multifocal atrophic gastritis (MAG), both groups associated to HP. EEC were quantified in relation to 100 epithelial cells. Results were statistically compared. RESULTS: In the normal control group, EEC were sparsely distributed, deep in antral glands, with an average 19.51 EEC/100 epithelial cells. In ACG there were 12.01/100. Besides EEC were irregularly distributed, close to inflammatory areas, or near lymphoid follicles. CONCLUSION: The decrease in EEC is probably due to degranulation and later to a disappearance or inhibition of stem cells by inflammatory products in HP gastritis. The proximity of EEC to prominent inflammatory zones may indicate EEC modulate the immune response. They produce and excrete peptides that interact with membrane receptors found in T lymphocytes and macrophages.

Modificaciones de las células enteroendócrinas en gastritis por Helicobacter pylori. / [Enteroendocrine cells modifications in Helicobacter pylori gastritis]

OBJECTIVE: The aim of the present study was to analyze the modifications in the number and distribution of enteroendocrine cells (EEC) in antrum of patients with Helicobacter pylori (HE) gastritis. We also wanted to demonstrate their possible participation in the immune response. MATERIAL AND METHODS: Twenty-six (26) biopsies of gastric antrum from patients between the ages of 40 and 60 were used. Slides were stained with H&E, Giemsa for HP, and chromogranin A to visualize EEC. Five (5) patients were normal controls. Eleven (11) patients had antral chronic gastritis (ACG) with different grades of activity, and ten (10) patients had multifocal atrophic gastritis (MAG), both groups associated to HP. EEC were quantified in relation to 100 epithelial cells. Results were statistically compared. RESULTS: In the normal control group, EEC were sparsely distributed, deep in antral glands, with an average 19.51 EEC/100 epithelial cells. In ACG there were 12.01/100. Besides EEC were irregularly distributed, close to inflammatory areas, or near lymphoid follicles. CONCLUSION: The decrease in EEC is probably due to degranulation and later to a disappearance or inhibition of stem cells by inflammatory products in HP gastritis. The proximity of EEC to prominent inflammatory zones may indicate EEC modulate the immune response. They produce and excrete peptides that interact with membrane receptors found in T lymphocytes and macrophages.