相关实验视频

Updated: May 6, 2026

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache

Published on: June 2, 2014

质子抑制剂使用与偏头痛之间的关联:系统性审查和元分析

Prakasini Satapathy^1,2, Mahalaqua Nazli Khatib³, Nasir Vadia⁴

¹Center for Global Health Research, Saveetha Institute of Medical and Technical Sciences, Saveetha Medical College and Hospital, Saveetha University, Chennai, India. prakasini.satapathy@gmail.com.

The journal of headache and pain

|March 29, 2025

概括

质子抑制剂 (PPI) 的使用与整体偏头痛没有显著联系. 然而,在男性中发现了显著的关联,但在女性中没有,这需要进一步调查潜在的性别特异性影响.

科学领域:

神经学神经学
药理学药理学是指药理学的学科.

背景情况:

偏头痛是一种流行的神经系统疾病.
质子抑制剂 (PPI) 广泛用于与酸有关的胃肠道疾病.
防护剂使用与偏头痛发病率之间的联系尚未得到充分证实.

研究的目的:

系统地审查和元分析PPI使用与偏头痛发病率之间的关联.
根据性别和偏头痛亚型,调查这种关联中的潜在差异.

主要方法:

在PubMed,Embase和Web of Science的系统文献搜索到2024年1月.
五项研究的元分析,包括超过150万参与者.
随机效应模型用于计算聚合调整的赔率比率 (aORs) 和置信区间 (CI).
根据性别和偏头痛亚型进行子组分析;用于证据确定性的GRADE方法.

主要成果:

在PPI使用和偏头痛之间没有显著的总体关联 (aOR,2.508;95% CI,0.790-7.969).
在男性 (aOR,3.875;95% CI,2.413-6.222) 中观察到显著的关联,但在女性中没有 (aOR,2.475;95% CI,0.563-10.890).
在偏头痛有光环和没有光环的亚型之间没有发现显著差异.
级别评估表明证据的确定性非常低.

结论:

总的来说,PPI使用与偏头痛没有显著的关联.
特别是在男性中,发现PPI使用和偏头痛之间存在显著的关联.
需要进一步的研究来阐明偏头痛的因果关系和性别特异性机制.

关键词:

进行元分析分析.偏头痛是一种偏头痛.质子抑制剂的使用系统性审查系统性审查

更多相关视频

Investigating Migraine-Like Behavior Using Light Aversion in Mice

Investigating Migraine-Like Behavior Using Light Aversion in Mice

Published on: August 11, 2021

Dural Stimulation and Periorbital von Frey Testing in Mice As a Preclinical Model of Headache

Dural Stimulation and Periorbital von Frey Testing in Mice As a Preclinical Model of Headache

Published on: July 29, 2021

相关概念视频

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...

Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids

Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids

In the complex environment of the gastric lumen, excessive acid secretion can lead to the formation or worsening of ulcers within the delicate mucosal layer. Antacids, such as sodium bicarbonate and calcium carbonate, provide relief by neutralizing this acid, transforming it into harmless salt and water. This neutralization process raises the gastric pH from a highly acidic level of 1 to a more basic 3-4, reducing the acidity within the stomach.
However, this neutralization reaction between...

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

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...

Drugs Affecting GI Tract Motility: Dopamine Receptor Antagonists

Drugs Affecting GI Tract Motility: Dopamine Receptor Antagonists

Prokinetic agents are specialized medications that stimulate gastrointestinal (GI) motility, promoting food movement through the GI tract. Dopamine, an inhibitory neurotransmitter, plays a significant role in this process, reducing GI motility and indirectly controlling the speed of digestion. Dopamine receptor antagonists, such as metoclopramide and domperidone, offer a unique advantage as prokinetic agents. By blocking the dopamine receptors, these drugs increase GI motility, improving food...

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy. SP binds and activates...