患有川崎病的婴儿由于多次胃而出现胃肠出血
Takeru Kanazawa1, Tomokazu Nakagami1, Jyoji Yoshizawa1
1Children's Medical Center, Showa Medical University Koto Toyosu Hospital Tokyo Japan.
Journal of general and family medicine
|September 4, 2025
概括
尽管进行了预防性治疗,但婴儿患有严重的胃肠道出血,这是川崎病 (KD) 的罕见并发症. 这一案例凸显了对KD患者,特别是服用类固醇和NSAIDs患者进行仔细监测的必要性, 以防止出血.
科学领域:
- 儿童风湿病学
- 胃肠病学
- 系统性血管炎
背景情况:
- 川崎病 (KD) 是儿童获得心脏病的主要原因.
- 胃肠道症状在KD中很常见,但严重的胃肠道出血是罕见的并发症.
- 标准治疗包括静脉注射免疫球蛋白 (IVIG),阿司匹林和皮质类固醇.
研究的目的:
- 报告一个罕见的严重胃肠道出血病例,患者患有不完全的川崎病.
- 研究KD患者胃肠道出血的潜在原因,包括药物的副作用.
- 强调GI监测在KD管理中的重要性.
主要方法:
- 一个11个月大的女性被诊断出患有不完全的川崎病.
- 对临床表现,诊断和治疗过程的审查.
- 分析导致严重胃肠道出血的因素,包括药物.
主要成果:
- 患者出现多种胃和严重的肠道出血,需要输血.
- 尽管使用H2受体抗剂进行预防治疗,但仍发生出血.
- 发现的潜在因素包括KD本身以及皮质类固醇和NSAID的联合作用.
结论:
- 胃肠道出血可能是川崎病的直接和严重并发症.
- 皮质类固醇和NSAID可能会增加KD患者胃肠道出血的风险.
- 对胃肠道并发症的警监测以及对预防策略的进一步研究对于管理KD至关重要.
相关概念视频
Inflammatory Bowel Disease I: Ulcerative Colitis
308
Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
308
Esophageal Varices-II: Clinical Features and Management
133
Esophageal varices often manifest as gastrointestinal bleeding episodes, presenting symptoms like hematemesis (vomiting of blood), hematochezia (passing fresh blood via the rectum), and melena (black, tarry stools). Other signs can include weight loss, anorexia, abdominal discomfort, jaundice, pruritus, altered mental status, and muscle cramps.
In the initial assessment, a thorough review of the patient's medical history is vital to identify risk factors such as liver disease, alcohol...
In the initial assessment, a thorough review of the patient's medical history is vital to identify risk factors such as liver disease, alcohol...
133
Gastritis-II: Pathophysiology
537
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...
537
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
595
The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
595
Esophageal Varices-I: Introduction
324
Esophageal varices are dilated, tortuous veins which are found mainly in the submucosa of the lower esophagus but which may also appear higher up or extend into the stomach. They develop due to increased pressure in the portal venous system, often as a result of liver cirrhosis. This condition scars and damages the liver, impeding normal blood flow through the portal vein. To compensate, blood seeks alternative pathways, forming fragile new vessels (varices) in the esophagus and stomach. These...
324
Peptic Ulcer Disease I: Introduction
282
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...
282


