Related Experiment Video
Updated: May 5, 2026
04:48
Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment
Published on: January 7, 2015
6.9K
Cocaine- and Levamisole-Induced Vasculitis (CLIV)
1Internal Medicine, St. Luke's Hospital, Chesterfield, USA.
Cureus
|October 22, 2025
Summary
Cocaine- and levamisole-induced vasculitis (CLIV) is a severe condition affecting skin, kidneys, and lungs. Early recognition and stopping drug use are key to improving patient outcomes.
Area of Science:
- Rheumatology
- Toxicology
- Nephrology
Background:
- Cocaine- and levamisole-induced vasculitis (CLIV) is a specific drug-induced vasculitis.
- It is characterized by dual antineutrophil cytoplasmic antibody (ANCA) positivity, rapidly progressive glomerulonephritis (RPGN), and diffuse alveolar hemorrhage (DAH).
Purpose of the Study:
- To systematically review and synthesize current data on CLIV.
- To clarify clinical presentations, diagnostic methods, and management strategies for CLIV.
Main Methods:
- A systematic literature search was conducted on PubMed and Google Scholar (2015-2024).
- Keywords included "levamisole-induced vasculitis," "cocaine-associated vasculitis," "dual ANCA vasculitis," "RPGN," and "DAH."
- 18 relevant studies were included in the final analysis.
Main Results:
- The majority of patients exhibited cutaneous, renal, and pulmonary symptoms.
- Diagnosis involved ANCA serology (MPO, PR3), biopsy, and imaging.
- Corticosteroids were the primary treatment; severe cases needed rituximab, cyclophosphamide, or plasmapheresis.
Conclusions:
- Early diagnosis and cessation of cocaine and levamisole exposure significantly improve prognosis.
- Recognizing CLIV in cocaine users with ANCA-positive vasculitis is crucial for timely intervention.
Related Concept Videos
01:16Vascular Spasm
4.9K
The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last...
4.9K
01:24Drug Toxicity: Risk factors
229
Adverse Drug Reactions (ADRs) are potential complications that arise during pharmacotherapy, influenced by multiple risk factors. Age plays a significant role; both neonates and the elderly are at heightened risk due to their respective immature and diminished metabolic and elimination processes. Gender also impacts ADRs, with females experiencing a 1.5 to 1.7-fold greater risk than males, which may be linked to pharmacokinetic, pharmacodynamic, and hormonal differences. Notably, neonates, the...
229
01:30Drug Toxicity: Allergic Reactions
209
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...
209
01:16Drug toxicity: Idiosyncratic Reactions
220
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...
220
01:21Cytotoxic Edema: Pathophysiology
20
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...
20