在使用vonoprazan后,胃中出现网状粘液的患病率和相关因素
Satoshi Shinozaki1,2, Hirotsugu Sakamoto2, Hiroyuki Osawa2
1Shinozaki Medical Clinic, Utsunomiya, Tochigi 321-3223, Japan.
Biomedical reports
|December 25, 2024
概括
胃中的网状粘液是一种与诺普拉桑 (VPZ) 使用密切相关的新发现. 这种模式出现在VPZ开始后,与患者服用药物的时间无关.
科学领域:
- 胃肠病学 胃肠病学
- 内镜检查是指内镜检查.
- 药理学 药理学是指药理学的学科.
背景情况:
- 在上部内镜检查中观察到一种新的"网状粘液"模式.
- 这个图案在描述上类似于蜘蛛网或网.
- 它与药物和患者因素的关联需要调查.
研究的目的:
- 为了确定胃网状粘液的患病率.
- 确定与这种内镜发现相关的因素,特别是诺普拉桑 (VPZ) 的使用.
- 评估VPZ治疗的持续时间是否会影响粘液模式.
主要方法:
- 在547名接受食道胃二透镜检查的患者中进行了回顾性观察性研究.
- 审查医疗记录和内镜报告.
- 在VPZ用户和其他群体 (对照组,PPI,H2RA) 之间比较网状粘液的流行率.
主要成果:
- 网状粘液的总流行率为6% (33/547),其中诺普拉赞 (VPZ) 用户的发病率为97%.
- 与对照组和其他酸阻塞剂相比,使用VPZ (19%的患病率) 与网状粘液有显著的关联.
- VPZ使用是积极的预测因素,而胃缩和特定的损伤类型是负面的预测因素;VPZ治疗的持续时间没有显示任何关联.
结论:
- 胃网状粘液是一种与诺普拉桑 (VPZ) 使用密切相关的新发现.
- 这种粘液模式的存在并不取决于VPZ治疗的持续时间.
- 进一步的研究可能会阐明这种与VPZ相关的内镜发现背后的机制.
更多相关视频
05:23Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
Published on: March 7, 2025
225
05:50Author Spotlight: Point-of-Care Ultrasound for Gastric Content Assessment and Risk Stratification in Perioperative Care
Published on: September 22, 2023
2.5K
相关概念视频
01:30Peptic Ulcer Disease I: Introduction
81
Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
81
01:24Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
305
Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI) tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
305
01:26Peptic Ulcer Disease IV: Management
45
Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
45
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
476
Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
476
01:17Gastritis-II: Pathophysiology
160
Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
160
01:25Mucosal Barrier of the Stomach
411
The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
411