再発性アンジオテンシン変換酵素阻害剤 - 関連性血管内腫
N J Brown1, M Snowden, M R Griffin
1Department of Medicine, Vanderbilt University, Nashville, Tenn 37232-6602, USA. nancy.brown@mcmail.vanderbilt.edu
JAMA
|July 16, 1997
まとめ
血管新生腫後のACE阻害剤の継続的な使用は,再発のリスクを大幅に増加させます. 医師はしばしば,再発した血管腫を他の原因と誤って結びつけ,診断と適切な管理を遅らせます.
科学分野:
- 心血管薬理学について
- 薬物の副作用 薬物の副作用
- 臨床毒理学 臨床毒理学とは
背景:
- アンジオテンシン変換酵素 (ACE) 阻害剤は,血管腫と関連しています.
- ACE阻害剤の使用を継続した再発性血管内腫のリスクは十分に確立されていません.
研究 の 目的:
- ACE阻害剤-血管腫関連性の認識を調査する.
- ACE阻害剤治療を継続している患者における血管内腫の特徴を示すために.
主な方法:
- テネシー州メディケイド登録者 (15歳以上) の遡及コホート研究.
- ACE阻害剤 (1986-1992) を使用している間,最初の血管腫エピソードを持つ患者の分析.
- 1993年6月までの再発性血管腫エピソードのフォローアップ.
主要な成果:
- ACE阻害剤の使用中に最初の血管腫を発症した82人の患者を特定しました.
- 再発率は100患者年当たり8.5であった.
- 継続したACE阻害剤の使用は,治療中止 (1.8/100患者年;P=.001) と比較して,有意に高い再発率 (18.7/100患者年) を示した.
- 医師はしばしば,ACE阻害剤以外の原因による再発を原因とした.
結論:
- 血管腫にもかかわらずACE阻害剤の使用を継続すると,再発率が大幅に増加します.
- この再発は,著しい罹病率と関連しています.
- ACE阻害剤に誘発された血管腫の認識を改善することは,患者の安全性にとって極めて重要です.
関連する概念動画
Allergic Reactions
Overview
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
Antihypertensive Drugs: Angiotensin II Receptor Blockers
In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
Antihypertensive Drugs: Direct Renin Inhibitors
The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists
Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...


