Which drugs cause vasculitis?

October 6, 2025 •

4 min read

Drug-induced vasculitis accounts for approximately 3% of all vasculitis cases [1.2.1]. This condition involves inflammation of blood vessels triggered by certain medications. Understanding which drugs cause vasculitis is the first step toward diagnosis and management.

Quick Summary

An overview of medications known to trigger vasculitis, an inflammatory condition of the blood vessels. This summary covers the primary drug classes, associated symptoms, and the importance of early diagnosis and drug cessation.

Key Points

Primary Cause: Drug-induced vasculitis is an inflammatory reaction in blood vessels triggered by medications, with antibiotics and NSAIDs being common culprits for skin-limited forms [1.4.4].
ANCA-Associated Vasculitis: Hydralazine, propylthiouracil, and cocaine (especially with levamisole) are classic drugs known to cause the more systemic ANCA-associated vasculitis (AAV) [1.7.1].
Key Symptoms: The most common symptom is a palpable purpuric rash on the skin, often accompanied by systemic signs like fever, joint pain, and muscle aches [1.5.1].
Diagnosis: Diagnosis relies on a careful medication history, physical examination, and often a skin biopsy. Stopping the suspected drug is a key diagnostic and therapeutic step [1.5.1, 1.5.2].
Treatment Cornerstone: The most critical step in management is discontinuing the offending drug, which often leads to resolution in mild cases [1.6.1].
Prognosis: The prognosis is generally excellent if the drug is stopped promptly. Severe cases with organ involvement may require corticosteroids or other immunosuppressants [1.6.5, 1.6.2].
Biologics and Vasculitis: TNF-alpha inhibitors, used to treat autoimmune diseases, can paradoxically induce vasculitis [1.3.4].

Understanding Drug-Induced Vasculitis

Drug-induced vasculitis (DIV) is an inflammatory condition affecting blood vessels that is directly triggered by a reaction to a medication [1.5.4]. It is considered a form of secondary vasculitis, meaning it has an identifiable cause, unlike primary vasculitis, which is often idiopathic [1.3.1]. While many cases are mild and resolve after stopping the offending drug, some can be severe, involving critical organs like the kidneys, lungs, and central nervous system [1.6.1, 1.5.1]. The most common presentation of DIV is cutaneous leukocytoclastic vasculitis (LCV), a small-vessel vasculitis that primarily affects the skin, causing palpable purpura (raised reddish-purple spots) [1.3.2, 1.4.4]. However, medications can induce vasculitis in small, medium, or large blood vessels [1.4.4].

Common Symptoms and Diagnosis

The clinical presentation of drug-induced vasculitis can vary widely. The most frequent signs are related to skin involvement, but systemic symptoms are also common.

Key Symptoms:

Skin Manifestations: Palpable purpura, petechial rash, skin necrosis (tissue death), and ulcers are common, especially on the lower extremities [1.5.1, 1.5.2].
Systemic Symptoms: Fever, malaise (general feeling of discomfort), arthralgia (joint pain), and myalgia (muscle pain) often accompany the skin rash [1.5.1].
Organ Involvement: In more severe cases, vasculitis can affect internal organs, leading to glomerulonephritis (kidney inflammation), interstitial lung disease, or neurological symptoms like headaches and seizures [1.3.6, 1.3.4].

Diagnosis is primarily one of exclusion [1.5.1]. A crucial first step is a thorough review of the patient's medication history to establish a temporal link between a drug's initiation and the onset of symptoms [1.5.1]. A skin biopsy is often performed to confirm the presence of vessel inflammation [1.5.2]. Blood tests may show elevated eosinophil counts or the presence of specific autoantibodies, such as antineutrophil cytoplasmic antibodies (ANCA), which are strongly associated with certain types of DIV [1.5.1, 1.3.5].

Major Drug Classes Implicated in Vasculitis

Almost any drug can potentially cause vasculitis, but some classes are more frequently implicated than others [1.3.7].

ANCA-Associated Vasculitis (AAV) Inducers

The drugs most classically associated with drug-induced AAV are:

Anti-thyroid Drugs: Propylthiouracil (PTU) is the most frequently reported drug in this class, followed by methimazole and carbimazole [1.7.4, 1.4.6]. PTU-induced AAV can occur years after starting the medication [1.3.6].
Hydralazine: An antihypertensive medication, hydralazine is a well-known cause of AAV, particularly with prolonged use and at higher doses [1.3.4, 1.7.1]. The risk is higher in females and those who are "slow acetylators" [1.3.4].
Minocycline: This tetracycline antibiotic, often used for acne, is frequently associated with a form of medium-vessel vasculitis that mimics polyarteritis nodosa (PAN) and is often ANCA-positive [1.4.1, 1.3.6].
Cocaine: Often contaminated with levamisole, cocaine use is a significant cause of AAV. Levamisole itself is a potent inducer of a severe vasculitis that can cause skin necrosis (particularly on the ears), arthralgia, and organ damage [1.3.8, 1.3.5].

Other Significant Drug Classes

Antibiotics: Besides minocycline, other antibiotics like penicillins, cephalosporins, sulfonamides, and quinolones are among the most common triggers for cutaneous leukocytoclastic vasculitis [1.3.2, 1.3.7].
Tumor Necrosis Factor (TNF)-alpha Inhibitors: Biologics like infliximab, adalimumab, and etanercept, used for autoimmune conditions, can paradoxically induce vasculitis, including both cutaneous forms and IgA vasculitis [1.3.6, 1.3.4].
Nonsteroidal Anti-inflammatory Drugs (NSAIDs): These common pain relievers are a frequent cause of cutaneous vasculitis [1.4.4].
Immune Checkpoint Inhibitors: Newer cancer therapies like pembrolizumab and ipilimumab have been reported to cause various forms of vasculitis, including large-vessel vasculitis [1.3.6].


Drug Class	Common Examples	Associated Vasculitis Type
Anti-thyroid Drugs	Propylthiouracil, Methimazole	ANCA-Associated Vasculitis (AAV) [1.7.4]
Antihypertensives	Hydralazine	ANCA-Associated Vasculitis (AAV) [1.7.1]
Antibiotics	Minocycline, Penicillins, Sulfonamides	Cutaneous Vasculitis, AAV, PAN-like [1.3.2, 1.4.1]
TNF-alpha Inhibitors	Infliximab, Etanercept, Adalimumab	Cutaneous Vasculitis, IgA Vasculitis, AAV [1.3.6, 1.3.4]
Illicit Drugs	Cocaine (especially with Levamisole)	ANCA-Associated Vasculitis (AAV) [1.3.5]
NSAIDs	Ibuprofen, Naproxen	Cutaneous Leukocytoclastic Vasculitis [1.4.4]
Gout Medication	Allopurinol	AAV, Hypersensitivity Vasculitis [1.7.3, 1.3.4]

Treatment and Conclusion

The cornerstone of treatment for drug-induced vasculitis is the immediate withdrawal of the offending medication [1.6.1]. For many patients with mild, skin-only involvement, this may be sufficient to resolve the symptoms [1.5.2, 1.6.1].

In cases with more severe symptoms or systemic organ involvement, additional treatment is necessary. This often includes a course of corticosteroids like prednisone to control inflammation [1.6.7]. For life-threatening presentations, such as severe kidney or lung damage, stronger immunosuppressive agents like cyclophosphamide or rituximab may be required, sometimes in combination with plasmapheresis [1.6.2, 1.6.3]. The prognosis for DIV is generally good, especially when the causative drug is identified and stopped promptly [1.6.5]. Unlike primary vasculitis, long-term immunosuppressive therapy is usually not necessary [1.6.2].

In conclusion, a wide array of medications can trigger vasculitis. Heightened awareness among clinicians and patients is essential for prompt diagnosis. Recognizing the temporal association between a new medication and the onset of symptoms like a rash, fever, and joint pain is critical for initiating the most important step in management: stopping the drug.

For more information from an authoritative source, you may visit the Vasculitis Foundation.

Frequently Asked Questions

The most common sign is a skin rash, typically appearing as palpable purpura (raised, non-blanching red or purple spots), most often on the legs [1.5.1, 1.3.2].

The drugs most classically associated with causing ANCA-associated vasculitis (AAV) are the anti-thyroid drug propylthiouracil, the blood pressure medication hydralazine, and the illicit drug cocaine, especially when it is contaminated with levamisole [1.7.1, 1.7.4].

Diagnosis is a process of exclusion that involves taking a detailed medication history, performing a physical exam, and often a tissue biopsy of the affected area (usually the skin). A strong temporal relationship between starting a new drug and symptom onset is a key indicator [1.5.1, 1.5.2].

In most cases, drug-induced vasculitis resolves after the offending medication is discontinued. The prognosis is generally excellent, although severe cases might require additional treatment with corticosteroids [1.6.1, 1.6.5].

The primary and most crucial treatment is to stop taking the medication that is causing the reaction. For more severe cases with organ involvement, corticosteroids and other immunosuppressive drugs may be prescribed [1.6.1, 1.6.2].

Yes, antibiotics are one of the most common classes of drugs to cause cutaneous leukocytoclastic vasculitis. Penicillins, cephalosporins, and sulfonamides are frequently implicated [1.3.2, 1.3.7].

No, drug-induced vasculitis is typically not a lifelong condition. Once the triggering drug is removed, the condition usually resolves and does not require the long-term maintenance therapy often needed for primary vasculitis [1.6.2, 1.6.1].