Gastric endocrine cells and gastritis in patients receiving long-term omeprazole treatment.

Gastric endocrine cells and gastritis in patients receiving long-term omeprazole treatment.
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接受长期奥美拉唑治疗患者的胃内分泌细胞与胃炎。

DOI:
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发表时间:
1992
期刊:
影响因子:
3.2
通讯作者:
R. Carlsson
R. Carlsson
中科院分区:
医学3区
文献类型:
--
作者:
E. Solcia;R. Fiocca;N. Havu;A. Dalväg;R. Carlsson

文献摘要

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对接受长期(几个月至4年)奥美拉唑治疗的448例患者中的443例胃黏膜活检标本中的嗜银内分泌细胞和胃炎进行了研究。所有患者均未出现内分泌或非内分泌肿瘤或异型增生。443例患者中123例(27.8%)在治疗前或治疗过程中有弥漫型(9.3%)、线型(4.1%)和微结节型(14.4%)内分泌增生。慢性萎缩性胃炎45例(10.2%),其中60%伴有小结节样增生。在慢性萎缩性胃炎患者中,96例活检组织中有49%出现小结节增生,相比之下,1083例非萎缩性慢性胃炎患者中有6%出现小结节增生,941例没有胃炎证据的患者中有2%出现小结节增生。在使用奥美拉唑至少330天的202例患者中,小结节增生的发生率从第一次活检的2.5%上升到最后一次活检的10.4%,慢性萎缩性胃炎的发生率从1.0%上升到13.0%。目前和平行的研究表明,胃炎的进展是酸相关疾病自然病程中固有的,而内分泌细胞的变化大多是胃炎相关腺体萎缩的继发性变化,没有致癌潜力。
Both argyrophil endocrine cells and gastritis were investigated in 2,120 biopsies of gastric corpus mucosa from 443 out of 448 patients receiving long-term (for periods ranging from several months to 4 years) omeprazole treatment. None of the patients showed neoplasia or dysplasia, either endocrine or non-endocrine. In 123 out of 443 patients (27.8%), endocrine hyperplasia of diffuse (9.3%), linear (4.1%) or micronodular (14.4%) type was detected either before or at some time during treatment. Chronic atrophic gastritis was found in 45 (10.2%) patients, 60% of whom also showed micronodular hyperplasia. In patients with chronic atrophic gastritis, micronodular hyperplasia occurred in 49% of 96 biopsies, compared with 6% of 1,083 biopsies from patients with non-atrophic chronic gastritis and 2% of 941 biopsies from patients with no evidence of gastritis. In 202 patients treated with omeprazole for at least 330 days, the incidence of micronodular hyperplasia increased from 2.5% at the first biopsy to 10.4% at the final biopsy, while the incidence of chronic atrophic gastritis increased from 1.0% to 13.0%. The present and parallel studies suggest that progression of gastritis is inherent in the natural history of acid-related diseases, while endocrine cell changes are mostly secondary to gastritis-related gland atrophy and have no tumorigenic potential.