What drugs cause vasculitis? A look at drug-induced inflammation

October 6, 2025 •

6 min read

Drug-induced vasculitis accounts for up to 30% of cutaneous vasculitis cases, highlighting the need for vigilance when assessing a patient's medication history. Identifying what drugs cause vasculitis is critical, as this inflammatory condition of the blood vessels can range from mild skin rashes to life-threatening multiorgan damage.

Quick Summary

A diverse range of medications can trigger vasculitis, an inflammatory blood vessel disorder. Culprits include specific antibiotics, antihypertensives like hydralazine, and antithyroid medications. Symptoms vary but often include rashes and joint pain, with some cases involving major organs. Treatment centers on stopping the causative agent.

Key Points

Hydralazine is a well-known culprit: The antihypertensive drug hydralazine has a strong association with a lupus-like, ANCA-associated vasculitis, especially with long-term use at higher doses.
Antibiotics are a common trigger: Certain antibiotics, including penicillins, sulfonamides, and minocycline, are frequent causes of drug-induced leukocytoclastic vasculitis, primarily affecting the skin.
Antithyroid drugs pose a risk: Propylthiouracil (PTU) is a common cause of ANCA-associated vasculitis, and patients taking this medication require close monitoring for symptoms.
Anti-TNF agents can cause paradoxical vasculitis: Medications used to treat inflammation, such as adalimumab and etanercept, can paradoxically trigger vasculitis in a small number of patients.
Illicit drugs can cause severe reactions: Cocaine, especially when adulterated with levamisole, can cause a potent, ANCA-associated vasculitis with severe cutaneous and systemic manifestations.
Drug cessation is the primary treatment: The most important step in managing drug-induced vasculitis is identifying and stopping the causative medication, which often leads to remission, especially in mild cases.
Prognosis is generally favorable: While severe cases can occur, most instances of drug-induced vasculitis have a good prognosis, particularly when limited to the skin and addressed promptly.

Understanding Drug-Induced Vasculitis

Vasculitis is an inflammatory disorder that affects the blood vessels, causing changes such as thickening, weakening, or scarring of the vessel walls. This can restrict blood flow, leading to tissue and organ damage. While many cases of vasculitis are considered primary (idiopathic), a significant portion are secondary, meaning they are triggered by another condition or exposure, including certain medications. Drug-induced vasculitis (DIV) can affect vessels of any size, though it most commonly presents as small-vessel vasculitis, known as leukocytoclastic vasculitis (LCV). The clinical picture is often identical to that of primary vasculitis, making a thorough drug history essential for diagnosis.

Specific Drug Classes Linked to Vasculitis

Almost every class of medication has been anecdotally implicated in causing vasculitis, but certain drug classes have a more well-established association based on clinical evidence and case reports.

Antibiotics and Antimicrobials

Antibiotics are among the most frequent triggers of drug-induced vasculitis, primarily causing cutaneous LCV. The mechanism often involves the formation of immune complexes that deposit in small vessel walls, leading to inflammation.

Penicillins and Cephalosporins: These β-lactam antibiotics are well-known culprits for causing hypersensitivity reactions, including cutaneous LCV.
Sulfonamides (e.g., trimethoprim-sulfamethoxazole): These agents have a recognized association with DIV, sometimes progressing to more severe renal involvement.
Quinolones (e.g., ciprofloxacin): This class of antibiotics has also been reported to induce vasculitis, with some cases involving the kidneys.
Tetracyclines (e.g., minocycline): Commonly used for acne, long-term minocycline use is strongly linked to ANCA-associated vasculitis (AAV), sometimes mimicking a more systemic disorder like polyarteritis nodosa (PAN).
Other examples: Less common associations have been documented for antibiotics like vancomycin and tigecycline, highlighting that many different antimicrobial agents can pose a risk.

Anti-Hypertensive Drugs

Hydralazine: This vasodilator, used to treat high blood pressure, has a significant and well-documented link to AAV. The risk appears to be dose-dependent, with higher doses and prolonged use increasing the likelihood. Affected individuals often present with a lupus-like syndrome and test positive for antinuclear antibodies (ANA) and myeloperoxidase (MPO)-ANCA.

Anti-Thyroid Medications

Propylthiouracil (PTU): This medication for hyperthyroidism is one of the most common causes of drug-induced AAV. Patients, often young females, may develop a vasculitis that mimics idiopathic AAV, though it is often less severe.
Methimazole and Carbimazole: These related antithyroid drugs have also been implicated in ANCA-associated vasculitis, though less frequently than PTU.

Anti-TNF-alpha Agents

Paradoxically, drugs designed to treat inflammatory conditions can sometimes trigger vasculitis. These agents, such as infliximab, adalimumab, and etanercept, can lead to the development of autoantibodies and various types of vasculitis, including AAV and IgA vasculitis.

Other Notable Drug Associations

Allopurinol: Used for uric acid metabolism disorders, allopurinol is linked to hypersensitivity vasculitis and Allopurinol Hypersensitivity Syndrome (AHS), which can involve multiple organs.
D-Penicillamine: This chelation and anti-inflammatory agent is known to cause AAV, sometimes leading to severe renal or pulmonary complications.
Illicit Drugs (Cocaine and Levamisole): The combination of cocaine and its common adulterant, levamisole, is a potent trigger for a severe form of ANCA-associated vasculitis. This is associated with characteristic purpuric rashes, sometimes on the ears, and can cause leukopenia and thrombosis.
Phenytoin: An anti-epileptic drug that has been occasionally reported to cause AAV.

Pathophysiology and Mechanisms

The exact mechanisms behind drug-induced vasculitis are complex and not fully understood, but several immune-mediated pathways have been identified.

Immune Complex Deposition: Many drugs can act as haptens, binding to proteins in the body to form neoantigens. The body's immune system then creates antibodies against these complexes, which can deposit in vessel walls. This triggers the complement system and inflammatory cascade, leading to leukocytoclastic vasculitis (LCV).
ANCA Production: Certain drugs, like hydralazine and propylthiouracil, are strongly linked to the production of antineutrophil cytoplasmic antibodies (ANCAs). These antibodies activate neutrophils, causing them to release inflammatory and cytotoxic substances that damage vessel walls.
Neutrophil Extracellular Trap (NET) Formation: Some medications, like PTU, may cause the formation of abnormal NETs, which expose neutrophil autoantigens to the immune system and can drive ANCA production.

Diagnosis and Clinical Presentation

The diagnosis of drug-induced vasculitis is primarily a diagnosis of exclusion and relies heavily on a detailed patient history, including a comprehensive review of all medications. Key indicators include a temporal relationship between starting a new drug and symptom onset, and resolution of symptoms upon drug discontinuation.

Common clinical features include:

Cutaneous Manifestations: Most commonly, a petechial or palpable purpuric rash, particularly on the lower extremities. This can also include urticarial lesions or skin ulcers.
Systemic Symptoms: Non-specific symptoms like fever, fatigue (malaise), and weight loss are often present.
Musculoskeletal Pain: Joint and muscle aches (arthralgia and myalgia) are common in DIV.
Internal Organ Involvement: In more severe cases, vasculitis can affect the kidneys (glomerulonephritis), lungs (pulmonary hemorrhage), or nervous system, leading to organ damage.

Diagnostic tools may include blood tests to assess inflammation (ESR, CRP), kidney function, and autoantibodies (ANCA, ANA). A skin or organ biopsy showing characteristic vascular inflammation is often the gold standard for confirmation.

Management and Prognosis

Management Steps

The cornerstone of treating DIV is the immediate withdrawal of the offending medication. For mild, skin-limited cases, this may be the only treatment required. However, in more severe presentations involving internal organs, immunosuppressive therapy is necessary.

Corticosteroids: Short-term, low-dose corticosteroids may be used for mild cases, while severe, organ-threatening vasculitis requires high-dose corticosteroids, often initiated with intravenous methylprednisolone.
Immunosuppressive Agents: For significant organ involvement, additional agents like cyclophosphamide or rituximab may be required.
Plasma Exchange: For life-threatening cases, such as massive pulmonary hemorrhage, plasma exchange may be used.

Prognosis

The prognosis for most cases of DIV is good, with complete remission often occurring after discontinuing the culprit drug.
However, cases with severe systemic involvement can lead to critical illness and, rarely, death. End-organ damage, particularly to the kidneys, can sometimes be irreversible despite successful treatment.

Comparison of Drug-Induced Vasculitis Types


Feature	ANCA-Associated Vasculitis (e.g., Hydralazine, PTU)	Immune Complex-Mediated Vasculitis (e.g., many antibiotics, NSAIDs)
Primary Mechanism	Autoantibody (ANCA) production leading to neutrophil activation and vessel damage.	Formation and deposition of immune complexes in vessel walls.
Typical Vessels Affected	Small vessels, but can include medium-sized vessels in some cases.	Small vessels, commonly limited to the skin.
Autoantibodies	High likelihood of ANCA positivity (especially anti-MPO), often alongside other autoantibodies like ANA and anti-histone antibodies.	ANCA typically negative, though other antibodies may sometimes be present.
Common Presentation	Can involve skin, kidneys (glomerulonephritis), lungs (hemorrhage), and nervous system. Can mimic systemic lupus erythematosus (SLE).	Most often presents as cutaneous leukocytoclastic vasculitis (LCV), with palpable purpura and rash. Systemic involvement is less common but possible.
Treatment Focus	Drug discontinuation plus immunosuppressive therapy for moderate to severe cases.	Drug discontinuation often sufficient for skin-limited disease; corticosteroids for persistent or widespread cutaneous disease.
Prognosis	Generally favorable upon drug cessation, but may have a less predictable course and risk of organ damage in severe cases.	Often self-limited and resolves quickly with drug discontinuation. Recurrence is likely upon re-exposure.

Conclusion

Identifying what drugs cause vasculitis is a crucial diagnostic step in rheumatology and dermatology, and awareness of this adverse reaction is key for all clinicians. While a wide range of medications, from common antibiotics to specific antihypertensives and antithyroid agents, have been linked to vasculitis, prompt recognition and discontinuation of the offending agent are the most critical interventions. For many patients, particularly those with skin-limited disease, removing the drug is all that is needed for a full recovery. However, in more severe, systemic cases, immunosuppressive therapy may be required to prevent permanent organ damage. A thorough drug history, coupled with clinical assessment and targeted diagnostic testing, is essential for correctly identifying and managing this potentially serious condition.

Frequently Asked Questions

Drug-induced vasculitis is an inflammation of the blood vessels triggered by a reaction to a specific medication. It occurs when the immune system mistakenly attacks the vessel walls after exposure to a drug, leading to changes in the vessel structure and function.

Diagnosis of DIV requires a detailed review of the patient's medical history and current medications, a physical examination, and potentially a skin or organ biopsy to confirm vascular inflammation. Blood tests for inflammatory markers and specific autoantibodies like ANCA are also used.

Common symptoms include a skin rash, most often a petechial or palpable purpura (tiny red or purple spots), frequently on the lower legs. Other signs can include joint pain, fever, fatigue, and, in severe cases, damage to internal organs like the kidneys or lungs.

Yes, cocaine, particularly when it is mixed with the veterinary drug levamisole, is known to cause a severe form of ANCA-associated vasculitis. It can result in distinctive skin rashes and potentially life-threatening systemic involvement.

The most important treatment is discontinuing the medication suspected of causing the reaction. For mild cases, this may be enough. In more severe cases, corticosteroids and other immunosuppressive drugs may be needed to control the inflammation and prevent organ damage.

In many cases of drug-induced vasculitis, especially those limited to the skin, symptoms will resolve with the discontinuation of the offending drug. However, recovery can vary depending on the severity and extent of the reaction.

Risk factors can vary by drug. For example, higher doses and prolonged use of hydralazine, as well as a specific genetic metabolic profile (slow acetylator status), increase risk. Some cases are idiosyncratic and can affect anyone.