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恰加斯病性巨食管和巨结肠患者的胃窦胃泌素细胞群

Antral gastrin cell population in patients with chagasic megaesophagus and megacolon.

作者信息

Troncon L E, Barbosa A J, Romanello L M, Toppa N H

机构信息

Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Brasil.

出版信息

Braz J Med Biol Res. 1994 Mar;27(3):645-53.

PMID:8081289
Abstract
  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.
摘要
  1. 慢性恰加斯病患者胃酸分泌异常低下,在禁食期间以及受到不同刺激后胃泌素释放均增加。尽管胃内酸度与胃泌素分泌之间存在关联,但尚不确定恰加斯病中的高胃泌素血症是由胃窦胃泌素(G)细胞数量增加(增生)还是细胞活性增强(功能亢进)所致。2. 因此,我们使用过氧化物酶 - 抗过氧化物酶免疫组织化学技术,对16例恰加斯病患者和13例对照受试者的胃窦活检组织中的G细胞数量进行了评估。所有受试者均接受了胃分泌试验,以确定静脉注射五肽胃泌素后的最大酸排量。3. 恰加斯病患者的胃窦G细胞数量与对照组相比无显著差异(细胞数/mm²,中位数及(范围):128(44 - 284)对138(65 - 285))。4. 在恰加斯病患者中,最大酸排量显著低于对照组(mmol/h,中位数及(范围):9.819(3.024 - 21.564)对17.490(9.423 - 答案25.848))。5. 这些结果表明,恰加斯病中与胃酸分泌减少相关的胃泌素释放增加是由胃窦G细胞功能亢进介导的,而非增生所致。

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