Detección de mucinas ácidas en metaplasia gástrica de la vesícula biliar / Detection of acid mucins in gastric metaplasia of the gallbladder

BACKGROUND/AIM: In this paper we present a histological and histochemical study about the metaplastic changes in the gallbladder, and discussed the participation of the antral metaplasia in the genesis of gallbladder cancer. METHODS: We collected 43 pieces of colecistectomy whit antral metaplasia, intestinal metaplasia and displasia. Presence of mucins were demonstrated by the alcian blue stain to ph 3 and ph 0.5 ph. RESULTS: We found sulphated and not sulphated acid mucins. In all of the forms of antral metaplasia. The not freguent finding coas an intense staining of intracitoplasmie mucins in metaplastic cells. We alsa detected small globular deposits in isolated cells of surface epithelium. CONCLUSIONS: This finding seems to associate antral metaplasia with intestinal metaplasia, at least in the mucins production. Antral metaplasia could be one of the first steps involved in the sequence displasia-cancer in the gallbladder.

Objetivos: En este trabajo realizamos un estudio histológico e histoquímico de los cambios metaplásicos en la vesícula biliar, y discutimos la participación de la metaplasia antral en la secuencia displasia-cáncer. Materiales y métodos: Estudiamos 43 piezas de colecistectomía que en el examen histológico mostraron metaplasia antral, metaplasia intestinal y displasia. La presencia de mucinas fue establecida por la técnica de Alcian Blue a pH 3 y a ph 0,5. Resultados: Encontramos mucinas ácidas sulfatadas y no sulfatadas en todas las formas de metaplasia de tipo antral. El hallazgo más frecuente fue la marcación intensa y difusa de las mucinas intracitoplasmáticas en las células metaplásicas. Se apreciaron además pequeños depósitos globulares de mucinas en células aisladas del epitelio de superficie. Conclusión: La presencia de mucinas ácidas permite asociar a la metaplasia antral con la metaplasia intestinal, en cuanto, al menos, a la producción de mucinas. Pensamos que la metaplasia antral podría ser uno de los primeros eslabones en la secuencia displasia- cáncer de la vesícula biliar.

Na+i, K+i and Cl-i regulation of exocytosis in guinea-pig antral mucous cells

Effects of intracellular Na+, K+ and Cl- on Ca(2+)-regulated exocytosis activated by 10 microM acetylcholine (ACh) were studied in guinea-pig antral mucous cells which are permeabilized by nystatin treatment. Ca(2+)-regulated exocytotic events were modulated by [Na+]i, [K+]i and [Cl-]i via mediation of PTX-sensitive G proteins. Increases in [Na+]i and PTX inhibit G protein (G(Na)), which suppressed the exocytosis. Increases in [K+]i caused the exchange of G proteins (from G(Na) to G(K)) to increase, and GK evoked activation of the exocytosis and was inhibited by PTX. Increases in [Cl-]i and PTX inhibit G protein (G(Cl)), which stimulates exocytotic events. Based on these observations, the exocytosis in antral mucous cells were modulated by intracellular ions, concentration of which were increased or decreased by cell volume changes caused by Ach.

Antral gastrin cell population in patients with chagasic megaesophagus and megacolon

1. Patients with chronic Chagas' disease have abnormally low gastric acid secretion and increased gastrin release both during fasting and after different stimuli. Regardless of the relationship between intragastric acidity and gastrin secretion, it is uncertain whether hypergastrinemia in Chagas' disease is caused by an increased population of antral gastrin (G) cells (hyperplasia) or by enhanced cell activity (hyperfunction). 2. We therefore estimated G cell number in antral biopsies from 16 chagasic patients and 13 control subjects using a peroxidase-anti-peroxidase immunohistochemical technique. All subjects underwent a gastric secretion test to determine peak acid output following intravenous pentagastrin instillation. 3. Antral G cell number in Chagas' disease patients was not significantly different from that observed in the control group (number of cells/mm2, median and (range): 128 (44-284) vs 138 (65-285)). 4. In chagasic patients, peak acid output was significantly lower than in controls (mmol/h, median and (range): 9.819 (3.024-21.564) vs 17.490 (9.423-25.848)). 5. These results suggest that the increase in gastrin release associated with reduced gastric acid secretion in Chagas' disease is mediated by antral G cell hyperfunction rather than by hyperplasia

Immunohistochemical localization of insulin-like materials in antral gastric mucosa and intestinal epithelial cells of the turtles Chrysemys dorbigni and Phrynopshilarii

Immunoreactive insulinwas demonstrated immunohistochemically with antibodies to human and porcine insulin by the avidin-biotin-peroxidase complex method in open-type gastrointestinal cells from sections of the antral stomach and of the upper, midle and lower intestine of the turtles Chrysemys dorbigni and Phrynops hilarii.In both species the concentration of cells positive for insulin-like material was higher in the gastric antrummthan in the gut.The localization of insulin-like material in gastrointestinal mucosal cells of turtles is an unusual finding among vertebrates, because the insulin-containing cells migrate from the mucosal epithelium of the intestine early in vertebrate evolution to the acinar pancreas.The chemical nature of the gastrointestinal insulin-like material and its physiological role remainm to be determined