特发性胃轻瘫的病理生理学及其治疗意义。
Pathophysiology of idiopathic gastroparesis and implications for therapy.
作者信息
Bekkelund Mattis, Sangnes Dag A, Gunnar Hatlebakk Jan, Aabakken Lars
机构信息
a Faculty of Medicine, Department of Clinical Medicine , University of Oslo , Oslo , Norway.
b Department of Medicine , National Centre for Functional Gastrointestinal Disorders, Haukeland University Hospital , Bergen , Norway.
出版信息
Scand J Gastroenterol. 2019 Jan;54(1):8-17. doi: 10.1080/00365521.2018.1558280. Epub 2019 Jan 13.
OBJECTIVES
Idiopathic gastroparesis is a gastric motility disorder characterized by chronic upper gastrointestinal symptoms and delayed gastric emptying without an identifiable underlying condition. This review summarizes recent understanding of the pathophysiology and treatment of idiopathic gastroparesis.
MATERIALS AND METHODS
Structured literature search in the PubMed, Embase and ClinicalTrials.gov databases.
RESULTS
Idiopathic gastroparesis involves several alterations in gastric motility and sensation, including delayed gastric emptying, altered myoelectrical activity, impaired fundic accommodation, visceral hypersensitivity and disturbances in antropyloroduodenal motility and coordination. Multiple cellular changes have been identified, including depletion of interstitial cells of Cajal (ICC) and enteric nerves, as well as stromal fibrosis. The underlying cause of these changes is not fully understood but may be an immune imbalance, including loss of anti-inflammatory heme-oxygenase-1 positive (HO-1) macrophages. There is currently no causal therapy for idiopathic gastroparesis. The treatment ladder consists of dietary measures, prokinetic and antiemetic medications, and varying surgical or endoscopic interventions, including promising pyloric therapies. There are ongoing trials with several novel medications, raising hopes for future treatment.
CONCLUSIONS
Patients with idiopathic gastroparesis present several pathophysiological alterations in the stomach, where depletion of ICC is of special importance. Treatment is currently focused on alleviating symptoms through dietary adjustments, medication or surgical or endoscopic interventions.
目的
特发性胃轻瘫是一种胃动力障碍性疾病,其特征为慢性上消化道症状和胃排空延迟,且无明确的潜在病因。本综述总结了目前对特发性胃轻瘫病理生理学和治疗的认识。
材料与方法
在PubMed、Embase和ClinicalTrials.gov数据库中进行结构化文献检索。
结果
特发性胃轻瘫涉及胃动力和感觉的多种改变,包括胃排空延迟、肌电活动改变、胃底容受性受损、内脏高敏感性以及胃幽门十二指肠动力和协调性紊乱。已确定多种细胞变化,包括 Cajal 间质细胞(ICC)和肠神经的减少,以及基质纤维化。这些变化的根本原因尚未完全明确,但可能是一种免疫失衡,包括抗炎性血红素加氧酶-1 阳性(HO-1)巨噬细胞的缺失。目前尚无针对特发性胃轻瘫的病因治疗方法。治疗阶梯包括饮食措施、促动力和止吐药物,以及不同的手术或内镜干预,包括有前景的幽门治疗。目前有几种新型药物正在进行试验,为未来治疗带来了希望。
结论
特发性胃轻瘫患者的胃部存在多种病理生理改变,其中 ICC 的减少尤为重要。目前的治疗重点是通过饮食调整、药物治疗或手术或内镜干预来缓解症状。