Sinnathamby Evan S, Urban Bretton T, Clark Robert A, Roberts Logan T, De Witt Audrey J, Wenger Danielle M, Mouhaffel Aya, Willett Olga, Ahmadzadeh Shahab, Shekoohi Sahar, Kaye Alan D, Varrassi Giustino
School of Medicine, Louisiana State University Health Sciences Center (LSUHSC) New Orleans, New Orleans, USA.
School of Medicine, Louisiana State University (LSU) Health, Shreveport, USA.
Cureus. 2024 Feb 1;16(2):e53400. doi: 10.7759/cureus.53400. eCollection 2024 Feb.
Edema is an accumulation of fluid in the body's tissues that affects millions of Americans yearly. It can affect multiple body parts, for example, the brain or eyes, but often occurs in the periphery, including the feet and legs. Medications, such as dihydropyridine and thiazolidinediones (TZDs), can be the etiology of edema. Edema can develop in association with problems in the vasculature or lymphatic flow. In recent years, a better understanding of these drug-induced mechanisms has been appreciated. Specifically, dihydropyridines can increase hydrostatic pressure and cause selective pre-capillary vessel vasodilation. TZDs can cause edema through increased vascular permeability and increased hydrostatic pressure. Specifically, peroxisome proliferator-activated receptor gamma (PPARγ) stimulation increases vascular endothelial permeability, vascular endothelial growth factor (VEGF) secretion, renal sodium, and fluid retention. Other drugs that can cause edema include neuropathic pain agents, dopamine agonists, antipsychotics, nitrates, nonsteroidal anti-inflammatory (NSAIDS), steroids, angiotensin-converting enzyme (ACE) inhibitors, and insulin. There are various clinical presentations of edema. Since multiple mechanisms can induce edema, it is important to understand the basic mechanisms and pathophysiology of drug-induced edema. Edema can even become fatal. For example, angioedema can occur from ACE inhibitor therapy. In this regard, it is considered a medical emergency when there is laryngeal involvement. This review aims to thoroughly appreciate the multiple causes of drug-induced edema and the ways it can be treated or prevented.
水肿是指体液在人体组织中的积聚，每年影响数百万美国人。它可累及身体多个部位，例如大脑或眼睛，但通常发生在身体外周，包括足部和腿部。药物，如二氢吡啶类和噻唑烷二酮类（TZDs），可能是水肿的病因。水肿可与血管系统或淋巴液流动问题相关联。近年来，人们对这些药物诱导机制有了更好的认识。具体而言，二氢吡啶类可增加流体静压并导致选择性毛细血管前血管舒张。噻唑烷二酮类可通过增加血管通透性和流体静压导致水肿。具体来说，过氧化物酶体增殖物激活受体γ（PPARγ）的刺激会增加血管内皮通透性、血管内皮生长因子（VEGF）分泌、肾脏钠潴留和液体潴留。其他可导致水肿的药物包括神经性疼痛药物、多巴胺激动剂、抗精神病药物、硝酸盐、非甾体抗炎药（NSAIDS）、类固醇、血管紧张素转换酶（ACE）抑制剂和胰岛素。水肿有多种临床表现。由于多种机制均可诱发水肿，因此了解药物性水肿的基本机制和病理生理学很重要。水肿甚至可能致命。例如，血管性水肿可由ACE抑制剂治疗引起。在这方面，当喉部受累时，它被视为医疗紧急情况。本综述旨在全面了解药物性水肿的多种病因以及治疗或预防方法。
