Henoch–Schönlein Purpura During Treatment with Fluoxetine

To the Editor:

Selective serotonin reuptake inhibitors (SSRI) have rarely been reported to be related to vasculitis in young or adult subjects (Margolese et al. 2001; Welsh et al. 2005). Herein we present an adolescent boy who developed Henoch–Schönlein purpura (HSP) during treatment with fluoxetine.

Case Presentation

A boy aged 15 years was referred to emergency clinic with widely spread skin rash on his lower legs and pain in his ankles and knees. The lesions were palpable and purpuric, which made the clinician consider the diagnosis of vasculitis. He was started on fluoxetine treatment by his family doctor 1 week ago. Blood tests for complete blood count, blood chemistry, liver function tests, total serum immunoglobulin E, immunoglobin M, immunoglobulin A, and coagulation tests (the activated partial thromboplastin time and prothrombin time) were within normal limits. His urine analysis revealed slight proteinuria. D-dimer level was 3468 μg/L (<550), fibrinogen level was 332.02, which were consistent with vasculitis. Due to these clinical findings, he was diagnosed as having HSP, and fluoxetine treatment was stopped. He was treated with methylprednisolone 40 mg qd and ranitidine 100 mg qd.

The patient reported bereavement symptoms for 2 months since the death of his father. He had irritability, sleep problems, and excessive crying episodes that made the doctor consider depression and start with fluoxetine treatment. He had no previous psychiatric or medical diagnoses. His developmental history and psychometric assessment were within normal limits. After the emergency visit fluoxetine was ceased. Weekly supportive visits were arranged and his vasculitic symptoms resolved in 2 months.

Discussion

There are some case reports describing adult patients with urticarial and leukocytoclastic vasculitis related to SSRI treatment (Margolese et al. 2001; Welsh et al. 2005). Paroxetine and fluoxetine have been reported to be related to leukocytoclastic vasculitis, which develops within a few weeks after the initiation of SSRI treatment (Margolese et al. 2001; Welsh et al. 2005). However, to our knowledge, there is no report of vasculitis related to SSRIs in children or adolescents.

In our case, vasculitis emerged after 1 week of fluoxetine treatment. HSP is also a type of leukocytoclastic vasculitis of childhood that results in a triad of symptoms, including a purpuric rash occurring on the lower extremities, abdominal pain, or renal involvement and arthritis. Although the etiology and pathophysiology of HSP remain unclear, infectious agents, drugs, and vaccinations have been implicated as possible triggers for HSP (Trapani et al. 2005). We could not find any abnormal standard laboratory results or medical problems in his history that could be related to any other possible cause of HSP. Therefore, fluoxetine was considered the only possible causative factor related to vasculitis in this adolescent boy. Naranjo causality scale score was 6 revealing probable causative association (Naranjo et al. 1981).

In conclusion, clinicians should be aware of HSP as an adverse effect of SSRI. More research is warranted regarding psychopharmacological mechanisms of SSRI-related vasculitis.