Allopurinol hypersensitivity syndrome
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| Allopurinol hypersensitivity syndrome | |
|---|---|
| Synonyms | N/A |
| Pronounce | N/A |
| Specialty | N/A |
| Symptoms | Rash, fever, eosinophilia, hepatitis, renal failure |
| Complications | Stevens-Johnson syndrome, toxic epidermal necrolysis, organ failure |
| Onset | Typically within weeks of starting allopurinol |
| Duration | Variable, depending on severity and treatment |
| Types | N/A |
| Causes | Hypersensitivity reaction to allopurinol |
| Risks | HLA-B*5801 allele, renal impairment, high starting dose of allopurinol |
| Diagnosis | Clinical evaluation, skin biopsy, blood tests |
| Differential diagnosis | Drug reaction with eosinophilia and systemic symptoms (DRESS), Stevens-Johnson syndrome, toxic epidermal necrolysis |
| Prevention | Genetic testing for HLA-B*5801 in high-risk populations, cautious dosing |
| Treatment | Discontinuation of allopurinol, supportive care, corticosteroids |
| Medication | N/A |
| Prognosis | Variable; can be life-threatening if not treated promptly |
| Frequency | Rare |
| Deaths | N/A |
Allopurinol Hypersensitivity Syndrome[edit]
Allopurinol hypersensitivity syndrome (AHS) is a rare but serious adverse reaction to the medication allopurinol, which is commonly used to treat gout and hyperuricemia. This syndrome is characterized by a combination of severe skin reactions, systemic symptoms, and internal organ involvement.
Clinical Features[edit]
AHS typically presents with a constellation of symptoms that may include:
- Severe skin reactions: These can range from maculopapular rash to more severe forms such as Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN).
- Fever: Patients often experience high fevers as part of the systemic response.
- Hepatitis: Liver involvement is common, with elevated liver enzymes indicating hepatic inflammation.
- Renal failure: Acute kidney injury can occur, often necessitating careful monitoring and management.
- Eosinophilia: An elevated eosinophil count is frequently observed in blood tests.
Pathophysiology[edit]
The exact mechanism of AHS is not fully understood, but it is believed to be an immune-mediated hypersensitivity reaction. Genetic factors, such as the presence of the HLA-B*5801 allele, have been associated with an increased risk of developing AHS, particularly in certain ethnic groups.
Diagnosis[edit]
Diagnosis of AHS is primarily clinical, based on the presentation of symptoms and a history of recent allopurinol use. Laboratory tests may show elevated liver enzymes, renal impairment, and eosinophilia. Skin biopsy can be performed to confirm severe cutaneous adverse reactions like SJS/TEN.
Management[edit]
The cornerstone of management is the immediate discontinuation of allopurinol. Supportive care is critical and may include:
- Hospitalization: Patients with severe reactions often require intensive care.
- Corticosteroids: These may be used to reduce inflammation and immune response.
- Hydration and renal support: Ensuring adequate hydration and monitoring renal function is essential.
- Treatment of skin lesions: In cases of SJS/TEN, specialized wound care is necessary.
Prevention[edit]
Screening for the HLA-B*5801 allele in high-risk populations before starting allopurinol can help prevent AHS. Alternative medications for managing hyperuricemia should be considered in patients with a positive genetic test.
