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[消化性溃疡、慢性十二指肠溃疡患者及其亲属中糖胺聚糖尿排泄的各种特征]

[Various characteristics of the urinary excretion of glycosaminoglycans in patients with peptic ulcer, chronic duodenal ulcer and in their relatives].

作者信息

Rabinovich P D, Gerasimovich A I

出版信息

Ter Arkh. 1985;57(2):28-30.

PMID:4002131
Abstract

The authors describe the results of studying secretion of glycosaminoglycans (GAG) with urine in 82 patients with peptic ulcer, 30 relatives and in 30 normal subjects with nonaggravated heredity. Patients with chronic duodenal ulcer during exacerbation and their normal relatives showed an essential reduction in the magnitude of the above indicator (1.6- and 1.8-fold, respectively, P less than 0.001) at the expense of a decrease in secretion of chondroitinsulfates (CDS) (2.4- and 2.1-fold, respectively, P less than 0.001). In peptic ulcer of the stomach, such a phenomenon was not recorded. During a disease remission there was an increase in GAG secretion with urine, linked with hyperheparinuria (13.1-fold, P less than 0.001). The data obtained indicate that the genetically determined impairment of CDS synthesis may be among one of the mechanisms by which hereditary aggravation in peptic ulcer of the duodenum is mediated. Hyperproduction of heparin during a disease remission is likely to play the role of one of the components of the defense-adaptation reaction responsible for ulcer healing.

摘要

作者描述了对82例消化性溃疡患者、30名亲属以及30名无遗传加重因素的正常受试者尿液中糖胺聚糖(GAG)分泌情况的研究结果。处于病情加重期的慢性十二指肠溃疡患者及其正常亲属,上述指标的数值显著降低(分别降低至1.6倍和1.8倍,P<0.001),这是由于硫酸软骨素(CDS)分泌减少所致(分别减少至2.4倍和2.1倍,P<0.001)。在胃溃疡患者中未观察到这种现象。在疾病缓解期,尿液中GAG分泌增加,这与高肝素尿有关(增加至13.1倍,P<0.001)。所获得的数据表明,遗传决定的CDS合成受损可能是十二指肠消化性溃疡遗传加重的介导机制之一。疾病缓解期肝素的过度产生可能是负责溃疡愈合的防御适应反应的组成部分之一。

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