Gastroesophageal reflux disease-related and functional heartburn: pathophysiology and treatment

被引:18
|
作者
Miwa, Hiroto [1 ]
Kondo, Takashi [1 ]
Oshima, Tadayuki [1 ]
机构
[1] Hyogo Coll Med, Dept Internal Med, Div Gastroenterol, Mukogawa Cho 1-1, Nishinomiya, Hyogo 6638501, Japan
关键词
acid pocket; ATP; esophageal epithelial cell; heartburn; prostaglandin E2; vonoprazan; RANDOMIZED CLINICAL-TRIAL; ESOPHAGEAL SPHINCTER RELAXATIONS; EPITHELIAL BARRIER FUNCTION; PLACEBO-CONTROLLED TRIAL; PROTON PUMP INHIBITORS; ACID-INDUCED HEARTBURN; EROSIVE ESOPHAGITIS; HEALTHY-VOLUNTEERS; VOLUNTARY MOVEMENT; BALLOON DISTENSION;
D O I
10.1097/MOG.0000000000000282
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Purpose of review Patients who continue to experience heartburn symptoms despite adequate-dose proton pump inhibitor therapy have unmet clinical needs. In this review, we focus on the most recent findings related to the mechanism of heartburn symptom generation, and on the treatment of gastroesophageal reflux disease related and functional heartburn. Recent findings The immunological mechanism in the esophageal mucosa has been addressed as a potential mechanism of the onset of esophageal mucosa damage and the generation of heartburn symptoms. Peripheral or central hypersensitivity in viscera is a potentially unifying pathophysiological concept in functional heartburn. Vonoprazan, a novel and potent first-in-class potassium-competitive acid blacker, is expected to prove useful in the treatment of reflux disease. Summary New findings in the mechanisms of heartburn symptom generation are emerging, including the immunological mediation of esophageal mucosal damage and the development of visceral hypersensitivity in functional heartburn. In the future, we anticipate the emergence of new and specific therapeutic options based on these mechanisms, with less dependence on acid-suppressing agents.
引用
收藏
页码:344 / 352
页数:9
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