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Stevens-Johnson Syndrome Induced by Allopurinol

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Abstract Background and Objective: Adverse drug reaction leading to Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis(TEN) is a rare and potentially life-threatening adverse effect of allopurinol. Before allopurinol initiation, screening for patients with HLA-B*58:01 is recommended to avoid the risk of complications. Case description: An 85-year-old man was admitted to our hospital after initiating allopurinol for treating hyperuricemia, presenting with diffuse maculopapular rash on entire body. The level of inflammatory indicators such as C-reaction protein(CRP), erythrocyte sedimentation rate (ESR) and procalcitonin and the amount of eosinophilic granulocyte were decreased after discontinuation of allopurinol and corticosteroid administration, while deterioration of the situation occurred after quick glucocorticoid withdrawal. Reinstitution of the glucocoritcoids with immunoglobulin showed clinical improvement. Despite the amelioration of SJS, the patient died after 40 days of hospitalization with the acute coronary syndrome. Conclusion A case of allopurinol-induced SJS/TEN syndrome suggests that clinicians should prescribe allopurinol to hyperuricemia patients with caution. Detection of HLA-B*58:01 for allopurinol hypersensitivity among high-risk individuals is warranted. Timely treatment with glucocosteroid and immunoglobulin might be helpful in the management of this rare but serious adverse reaction.
Title: Stevens-Johnson Syndrome Induced by Allopurinol
Description:
Abstract Background and Objective: Adverse drug reaction leading to Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis(TEN) is a rare and potentially life-threatening adverse effect of allopurinol.
Before allopurinol initiation, screening for patients with HLA-B*58:01 is recommended to avoid the risk of complications.
Case description: An 85-year-old man was admitted to our hospital after initiating allopurinol for treating hyperuricemia, presenting with diffuse maculopapular rash on entire body.
The level of inflammatory indicators such as C-reaction protein(CRP), erythrocyte sedimentation rate (ESR) and procalcitonin and the amount of eosinophilic granulocyte were decreased after discontinuation of allopurinol and corticosteroid administration, while deterioration of the situation occurred after quick glucocorticoid withdrawal.
Reinstitution of the glucocoritcoids with immunoglobulin showed clinical improvement.
Despite the amelioration of SJS, the patient died after 40 days of hospitalization with the acute coronary syndrome.
Conclusion A case of allopurinol-induced SJS/TEN syndrome suggests that clinicians should prescribe allopurinol to hyperuricemia patients with caution.
Detection of HLA-B*58:01 for allopurinol hypersensitivity among high-risk individuals is warranted.
Timely treatment with glucocosteroid and immunoglobulin might be helpful in the management of this rare but serious adverse reaction.

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