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Related Concept Videos

Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
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Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Burn Injuries01:22

Burn Injuries

Burn injuries occur when the skin and underlying tissues are damaged due to exposure to heat, electricity, chemicals, radiation, or friction. They can vary in severity, from minor superficial burns to severe deep burns that can be life-threatening.
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Drug toxicity: Idiosyncratic Reactions01:16

Drug toxicity: Idiosyncratic Reactions

Idiosyncratic drug reactions represent abnormal chemical responses that vary significantly among individuals, ranging from extreme sensitivity to low doses to insensitivity to high doses. These reactions often occur due to the drug's covalent binding with serum proteins, forming a foreign hapten that triggers an immunotoxicological response. The variability in drug reactions has a strong pharmacogenetic foundation, with genetic differences crucial in how individuals metabolize drugs. For...
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Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...

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Updated: Jul 6, 2026

A Standardized Procedure of Dressing Management for Toxic Epidermal Necrolysis
07:22

A Standardized Procedure of Dressing Management for Toxic Epidermal Necrolysis

Published on: March 14, 2025

[Leflunomide-induced skin necrosis].

C Gros1, F Delesalle, S Gautier

  • 1Université de Lille-II et clinique de dermatologie, hôpital Claude-Huriez, CHRU de Lille, rue Michel-Polonovski, 59037 Lille cedex, France.

Annales De Dermatologie Et De Venereologie
|April 1, 2008
PubMed
Summary
This summary is machine-generated.

Leflunomide can cause rare but severe skin necrosis and ulcerations. Discontinuation of the drug and cholestyramine wash-out are crucial for healing, even with prolonged use.

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A Standardized Procedure of Dressing Management for Toxic Epidermal Necrolysis
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Granulocyte-dependent Autoantibody-induced Skin Blistering
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Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

Area of Science:

  • Rheumatology
  • Dermatology
  • Immunology

Background:

  • Leflunomide is an immunosuppressive drug commonly used for inflammatory rheumatic diseases.
  • Cutaneous adverse events associated with leflunomide are infrequently reported.
  • This case highlights a rare but severe dermatological complication attributed to leflunomide therapy.

Observation:

  • A 73-year-old woman developed abdominal ulcerations and hallux necrosis after one year of leflunomide treatment for psoriatic arthritis.
  • Initial treatment with corticosteroids for suspected vasculitis was ineffective, and the hallux necrosis necessitated amputation.
  • No other underlying causes such as immunological, vascular, or neoplastic conditions were identified.

Findings:

  • Discontinuation of leflunomide led to complete healing of the ulcerations within 12 weeks.
  • Seven similar cases of leflunomide-induced skin necrosis were identified in the literature.
  • Potential mechanisms include excessive immunomodulation or inhibition of epidermal growth factor receptor by leflunomide.

Implications:

  • Leflunomide should be considered as a potential cause of skin necrosis and ulcerations, even after extended treatment periods.
  • Prompt cessation of leflunomide and cholestyramine wash-out are recommended for managing these adverse effects.
  • Associated glomerulonephritis is a serious potential complication requiring careful monitoring.