Gastroparesis.

Gastroparesis.
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DOI:
10.1053/j.gastro.2021.10.028
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发表时间:
2022-01
期刊:
影响因子:
29.4
通讯作者:
Sanders KM
Sanders KM
中科院分区:
医学1区
文献类型:
--
作者:
Camilleri M;Sanders KM

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胃轻瘫的特征是在没有机械性梗阻的情况下提示胃排空延迟的症状和客观证据。这篇综述主要基于动物研究,讨论了胃中固体和液体的正常排空,并详细介绍了生肌和神经肌肉控制机制,包括导致正常排空的幽门括约肌的特殊功能。要理解导致胃轻瘫的紊乱,必须清楚地了解基本机制,并且需要对人类胃肌肉进行更多研究。胃轻瘫的病理生理学部分考虑了影响非括约肌胃肌的神经肌肉疾病、导致胃轻瘫的外在神经控制障碍和幽门功能障碍。胃轻瘫的潜在细胞基础归因于氧化应激和炎症的影响,如在胃轻瘫患者的全层活检中观察到的,促炎细胞增加和常驻巨噬细胞减少。讨论了主要的诊断测试,包括测量胃排空、使用功能性管腔成像探头和高分辨率十二指肠窦测压来表征胃十二指肠交界处的异常运动功能。管理基于支持营养、饮食干预(包括物理减小固体食物的粒径)、药物(包括促动力剂和止吐剂)以及胃电刺激和幽门肌切开术等干预措施。对这些内容进行了简要讨论,并根据最佳胃排空测量和引起胃轻瘫的潜在病理生理学的客观记录,对未来个体化治疗的潜力进行了评论。
Gastroparesis is characterized by symptoms suggestive of and objective evidence of delayed gastric emptying in the absence of mechanical obstruction. This review addresses the normal emptying of solids and liquids from the stomach and details the myogenic and neuromuscular control mechanisms including the specialized function of the pyloric sphincter that result in normal emptying, based predominantly on animal research. A clear understanding of fundamental mechanisms is necessary to comprehend derangements leading to gastroparesis, and additional research on human gastric muscles is needed. The section on pathophysiology of gastroparesis considers neuromuscular diseases that affect non-sphincteric gastric muscle, disorders of the extrinsic neural control and pyloric dysfunction that lead to gastroparesis. The potential cellular basis for gastroparesis is attributed to the effects of oxidative stress and inflammation, with increased pro-inflammatory and decreased resident macrophages, as observed in full-thickness biopsies from patients with gastroparesis. Predominant diagnostic tests involving measurements of gastric emptying, the use of a functional luminal imaging probe and high-resolution antral duodenal manometry in characterizing the abnormal motor functions at the gastroduodenal junction are discussed. Management is based on supporting nutrition, dietary interventions including the physical reduction in particle size of solid foods, pharmacological agents including prokinetics and anti-emetics, and interventions such as gastric electrical stimulation and pyloromyotomy. These are briefly discussed, and comment is added on the potential for individualized treatments in the future, based on optimal gastric emptying measurement and objective documentation of the underlying pathophysiology causing the gastroparesis.
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