Related Experiment Video
Updated: Jun 28, 2026
03:40
Acupoint Catgut Embedding Therapy in Traditional Chinese Medicine for Managing Allergic Rhinitis
Published on: December 20, 2024
Recurrent severe angioedema associated with imidapril and diclofenac
1Department of Internal Medicine, Chulalongkorn University Hospital, Bangkok, Thailand. thatchai_k@yahoo.com
Summary
Angiotensin-converting enzyme inhibitors (ACEIs) can cause angioedema. Concomitant use with NSAIDs may worsen attacks, necessitating avoidance in patients with a history of angioedema.
Area of Science:
- Pharmacology
- Immunology
- Emergency Medicine
Background:
- Angiotensin-converting enzyme inhibitors (ACEIs) are commonly prescribed for hypertension and heart failure.
- ACEI-induced angioedema is a known, albeit infrequent, adverse effect.
- Angioedema can present with severe complications, including airway obstruction.
Observation:
- A 59-year-old female experienced recurrent tongue angioedema.
- The angioedema led to upper airway obstruction requiring endotracheal intubation.
- Laboratory tests, including complement levels, were unremarkable.
Findings:
- The patient's condition was attributed to ACEI-associated angioedema, potentially precipitated by NSAIDs.
- Discontinuation of imidapril (an ACEI) and diclofenac (an NSAID) resulted in clinical improvement.
- No other specific treatments were required for symptom resolution.
Implications:
- Patients with a history of angioedema should avoid ACEI therapy.
- Concomitant use of ACEIs and NSAIDs may increase the risk of severe angioedema.
- Clinicians should maintain a high index of suspicion for ACEI-induced angioedema, especially with NSAID co-administration.
Related Concept Videos
01:30Allergic Reactions: Anaphylaxis
Anaphylaxis is a severe, life-threatening hypersensitivity reaction mediated by Immunoglobulin E (IgE) antibodies. When IgE binds to allergens, it triggers the release of mediators– histamine, leukotrienes, and prostaglandins from mast cells and basophils. These mediators cause vasodilation, edema, and inflammation, leading to various symptoms.The primary allergens causing anaphylaxis include food items (e.g., peanuts, shellfish), drugs (e.g., penicillin, asparaginase, corticotropin, heparin),...
02:06Allergic Reactions
Overview
01:26Heart 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...
01:30Antihypertensive 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...
01:25Antihypertensive 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,...
01:30Antihypertensive 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...