Understanding Drug-Induced Vasculitis: What Drugs Trigger Vasculitis?

October 6, 2025 •

4 min read

Drug-induced leukocytoclastic vasculitis (LCV), a common form of drug-related vasculitis, accounts for approximately 10% of all vasculitis cases [1.4.3]. Understanding what drugs trigger vasculitis is crucial for both patients and healthcare providers to recognize and manage this serious condition.

Quick Summary

A wide range of medications can cause drug-induced vasculitis (DIV), an inflammation of blood vessels. Key triggers include certain antibiotics, hydralazine, and propylthiouracil. Symptoms often start with a skin rash but can become systemic.

Key Points

Primary Cause: Drug-induced vasculitis (DIV) is an inflammation of blood vessels triggered by a reaction to medications or illicit drugs [1.4.4].
Common Triggers: Key drugs include hydralazine, propylthiouracil, minocycline, antibiotics, NSAIDs, and anti-TNF biologics [1.3.4, 1.6.1].
Illicit Drugs: Cocaine, especially when contaminated with levamisole, is a significant cause of severe ANCA-associated vasculitis [1.3.6].
Primary Symptom: The most common initial sign is a skin rash (cutaneous vasculitis), but it can become systemic and affect organs like the kidneys and lungs [1.3.4, 1.5.6].
Core Treatment: The most important step in management is stopping the suspected offending drug [1.5.1].
Severe Cases: Systemic or organ-threatening vasculitis often requires treatment with corticosteroids and other immunosuppressants [1.5.4].
Diagnosis: Diagnosis involves a detailed drug history, physical exam, lab tests for autoantibodies (like ANCA), and often a tissue biopsy for confirmation [1.3.2, 1.5.1].

What is Drug-Induced Vasculitis?

Drug-induced vasculitis (DIV) is the inflammation of blood vessel walls caused by a reaction to a pharmaceutical agent or illicit drug [1.4.4, 1.5.1]. This condition can affect blood vessels of any size—small, medium, or large—and can range from a mild, skin-limited issue to a life-threatening systemic disease involving multiple organs like the kidneys, lungs, and nervous system [1.3.4, 1.5.5].

The most common presentation of DIV is isolated cutaneous leukocytoclastic vasculitis (LCV), which primarily affects the skin [1.3.4]. Symptoms often appear with a temporal relationship to starting a new medication and can include fever, malaise, joint pain (arthralgia), muscle pain (myalgia), and a characteristic skin rash with red or purple spots (purpura) [1.5.1, 1.5.2, 1.5.7]. While many cases resolve after stopping the offending drug, a significant portion of patients may require further immunosuppressive therapy [1.3.4].

How Do Drugs Cause Vasculitis?

The exact mechanisms behind DIV are not fully understood but are believed to be immune-mediated [1.4.6]. Several theories exist:

Immune Complex Deposition: Some drugs may act as haptens, binding to proteins in the body and forming antigens. The immune system then creates antibodies to these complexes, which deposit in blood vessel walls, triggering a type III hypersensitivity reaction and inflammation [1.3.2].
ANCA-Associated Vasculitis (AAV): Certain drugs can lead to the production of antineutrophil cytoplasmic antibodies (ANCA). These antibodies mistakenly target and activate neutrophils (a type of white blood cell), causing them to release inflammatory substances that damage blood vessel walls [1.3.4, 1.6.5]. Propylthiouracil and hydralazine are classic examples of drugs that can induce AAV [1.6.1].
Abnormal NETosis: Studies suggest some drugs, like propylthiouracil, may cause neutrophils to form abnormal neutrophil extracellular traps (NETs). These NETs are resistant to normal degradation, leading to prolonged exposure of autoantigens to the immune system and triggering an autoimmune response [1.3.4].
Bypassing Immune Checkpoints: Newer cancer therapies, such as immune checkpoint inhibitors, can cause vasculitis by blocking the normal 'off' switches on T-lymphocytes. This leads to uncontrolled T-cell activation and subsequent inflammation of the vessel wall [1.3.4].

Common Medications That Trigger Vasculitis

Nearly every class of drug has been implicated in causing vasculitis [1.4.6]. The reaction can occur days to years after starting a medication [1.3.4]. The most frequently cited culprits vary depending on the type of vasculitis they induce.

Drugs Causing ANCA-Associated Vasculitis (AAV)

This is a serious form of vasculitis that often involves systemic symptoms. The classic drugs associated with AAV are:

Propylthiouracil (PTU): An antithyroid medication used to treat hyperthyroidism. It is one of the most reported causes of drug-induced vasculitis [1.2.9, 1.3.6].
Hydralazine: A vasodilator used to treat high blood pressure. The risk increases with higher doses and prolonged use [1.3.7].
Minocycline: A tetracycline antibiotic commonly used for acne. It can cause a medium-vessel vasculitis that mimics polyarteritis nodosa (PAN) and is often ANCA-positive [1.3.1, 1.3.4].
Cocaine: Often adulterated with levamisole, cocaine use is a major cause of ANCA-associated vasculitis. It can present with severe skin lesions, particularly on the ears, and systemic involvement [1.3.6, 1.6.8].
Allopurinol: Used to treat gout [1.3.3, 1.6.5].
Sulfasalazine: An anti-inflammatory drug used for rheumatoid arthritis and inflammatory bowel disease [1.6.5].

Drugs Causing Cutaneous Vasculitis (LCV)

This form is often limited to the skin and is the most common type of DIV [1.3.4].

Antibiotics: Penicillins, cephalosporins, quinolones, and sulfonamides are frequent triggers [1.3.2].
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): This common class of pain relievers can be a cause [1.3.4, 1.3.8].
Anti-TNF-alpha agents: Biologics like infliximab, adalimumab, and etanercept, used for autoimmune conditions, can paradoxically induce vasculitis [1.2.7].

Comparison of Common Drug Triggers


Drug Class	Common Examples	Associated Vasculitis Type	Typical Onset
Antithyroid Drugs	Propylthiouracil, Methimazole	ANCA-Associated Vasculitis (AAV)	Can be soon after initiation or years later [1.3.4]
Antihypertensives	Hydralazine	ANCA-Associated Vasculitis (AAV)	Prolonged exposure (median 21 months) [1.3.4]
Antibiotics	Minocycline, Penicillins, Quinolones	Medium-Vessel (Minocycline), LCV	Variable, from days to years (Minocycline) [1.3.7]
Biologics	Infliximab, Etanercept (Anti-TNF)	LCV, IgA Vasculitis, AAV	Median 6 months after starting therapy [1.3.7]
Illicit Drugs	Cocaine (with Levamisole)	ANCA-Associated Vasculitis (AAV)	Can be at onset or years after abuse begins [1.3.4]
Gout Medication	Allopurinol	LCV, AAV	Variable

Diagnosis and Treatment

Diagnosing DIV is primarily one of exclusion [1.5.1]. A thorough medication history is paramount, focusing on any new drugs started in temporal proximity to the symptom onset. A physical exam, especially of the skin, and laboratory tests are performed. A skin or organ biopsy showing inflammation of blood vessels is the gold standard for confirmation [1.3.2, 1.5.2]. Blood tests may show elevated inflammation markers and the presence of ANCA, ANA, or other autoantibodies [1.3.4].

The cornerstone of management is to identify and withdraw the offending drug [1.5.4].

Mild Cases: For vasculitis limited to the skin, stopping the drug is often sufficient for resolution [1.4.2, 1.5.1].
Severe Cases: If there is systemic or organ-threatening involvement (e.g., kidney or lung), more aggressive treatment is needed. This typically involves corticosteroids and may include other immunosuppressive agents like cyclophosphamide or rituximab [1.5.4, 1.3.7].

Conclusion

Drug-induced vasculitis is a serious potential side effect of many common medications and illicit substances. Awareness of the drugs that can trigger vasculitis is the first step toward early diagnosis and intervention. While symptoms often begin with a skin rash, the condition can progress to affect vital organs. Prompt withdrawal of the causative agent is the most critical step in treatment and leads to a good prognosis in many cases, though severe instances require significant immunosuppressive therapy.

For more information from an authoritative source, you can visit the Vasculitis Clinical Research Consortium. [1.3.5]

Frequently Asked Questions

The most common symptom is a skin rash, often appearing as small red or purple spots (palpable purpura), particularly on the lower legs. Other general symptoms like fever, joint pain, and fatigue can also occur [1.5.1, 1.5.6].

Hydralazine (a blood pressure medication), propylthiouracil (an antithyroid drug), and minocycline (an antibiotic) are classically associated with drug-induced ANCA vasculitis. Cocaine laced with levamisole is also a major trigger [1.6.1, 1.3.4].

The onset of drug-induced vasculitis is highly variable. It can occur within days of starting a new medication or after months or even years of prolonged exposure [1.3.4].

In many cases, especially when the vasculitis is limited to the skin, the condition resolves after the offending drug is discontinued. However, severe cases with organ damage may have long-term consequences [1.5.1, 1.3.4].

Diagnosis relies on a combination of factors: a thorough medication history, physical examination, blood tests to check for inflammation and specific autoantibodies (like ANCA), and a biopsy of an affected tissue (usually skin) to confirm vessel inflammation [1.5.1, 1.3.2].

Yes, antibiotics are a common cause of drug-induced vasculitis, particularly cutaneous vasculitis. Penicillins, cephalosporins, quinolones, and sulfonamides are among the frequently implicated classes [1.3.2, 1.3.4].

The primary treatment is to stop taking the medication that caused the reaction. For mild skin-only symptoms, this may be enough. Severe cases with organ involvement often require treatment with corticosteroids or other immunosuppressive drugs [1.5.1, 1.5.4].