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Related Concept Videos

Antihypertensive Drugs: Potassium-Sparing Diuretics01:28

Antihypertensive Drugs: Potassium-Sparing Diuretics

Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
Antihypertensive Drugs: Direct Renin Inhibitors01:25

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,...
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

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...
Drug Toxicity: Allergic Reactions01:30

Drug Toxicity: Allergic Reactions

Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial exposure to a...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

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...

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Related Experiment Video

Updated: May 25, 2026

Dioscin Mediated IgA Nephropathy Alleviation by Inhibiting B Cell Activation In Vivo and Decreasing Galactose-Deficient IgA1 Production In Vitro
14:18

Dioscin Mediated IgA Nephropathy Alleviation by Inhibiting B Cell Activation In Vivo and Decreasing Galactose-Deficient IgA1 Production In Vitro

Published on: October 13, 2023

Amlodipine-induced linear IgA disease.

L Low1, S Zaheri, S Wakelin

  • 1Department of Dermatology, Mint Wing A, St Mary's Hospital, London, UK. lynette_low@hotmail.com

Clinical and Experimental Dermatology
|February 4, 2012
PubMed
Summary
This summary is machine-generated.

This case report details a rare instance of drug-induced linear IgA dermatosis (LAD) linked to amlodipine. Prompt treatment with corticosteroids and dapsone led to the patient's recovery.

Related Experiment Videos

Last Updated: May 25, 2026

Dioscin Mediated IgA Nephropathy Alleviation by Inhibiting B Cell Activation In Vivo and Decreasing Galactose-Deficient IgA1 Production In Vitro
14:18

Dioscin Mediated IgA Nephropathy Alleviation by Inhibiting B Cell Activation In Vivo and Decreasing Galactose-Deficient IgA1 Production In Vitro

Published on: October 13, 2023

Area of Science:

  • Dermatology
  • Immunodermatology
  • Pharmacology

Background:

  • Linear IgA dermatosis (LAD) is a rare autoimmune blistering disease.
  • Drug-induced LAD is exceptionally uncommon, with vancomycin being the most frequently implicated agent.
  • Amlodipine, a calcium channel blocker, is not typically associated with LAD.

Observation:

  • A 58-year-old woman developed a pruritic rash with erythematous plaques and vesicles after starting amlodipine.
  • Skin biopsy revealed subepidermal blisters with eosinophils and neutrophils.
  • Direct immunofluorescence demonstrated IgA deposition along the basement membrane, confirming LAD.

Findings:

  • The patient's symptoms resolved following amlodipine discontinuation and treatment with prednisolone and dapsone.
  • This represents the first documented case of amlodipine-induced linear IgA dermatosis.
  • The findings highlight the potential for amlodipine to trigger rare dermatological reactions.

Implications:

  • Clinicians should consider amlodipine as a potential cause of LAD in susceptible individuals.
  • This case expands the spectrum of drugs known to induce LAD.
  • Further research is warranted to understand the mechanism of amlodipine-induced LAD.