Splenectomy for HIV-related Immune Thrombocytopenia: Comparison with Results of Splenectomy for Non-HIV Immune Thrombocytopenic Purpura

Objective: To determine the effectiveness and safety of splenectomy for patients with human immunodeficiency virus (HIV)-related immune thrombocytopenia, using the results of splenectomy for patients with non-HIV immune thrombocytopenic purpura as a control group for comparison.

Design: Retrospective study.

Setting: Tertiary care university hospital.

Patients: Fourteen patients who underwent splenectomy for symptomatic, medically refractory HIV-related immune thrombocytopenia at this hospital from 1988 to 1997. During the same period, 20 patients had splenectomy for treatment of non-HIV immune thrombocytopenic purpura.

Intervention: Splenectomy.

Main Outcome Measures: Platelet response, need for postsplenectomy medical therapy, progression of HIV disease, and complications.

Results: All patients with HIV-related thrombocytopenia had a complete early platelet response to splenectomy, with an elevation of the platelet count to greater than 100X10(9)/L. After a median follow-up of 26.5 months, all but 1 patient had a sustained complete remission with no need for medical therapy for thrombocytopenia. Splenectomy was more effective in the HIV-related thrombocytopenia group than in the non-HIV immune thrombocytopenic purpura group, with significantly higher platelet counts at 1 week and 1 month after splenectomy in the HIV group (t test, P=.02 and P=.009, respectively). There were significantly fewer patients needing medical therapy for thrombocytopenia after splenectomy in the HIV group (chi2 test, P=.02). There were no remarkable short- or long-term complications in the patients with HIV infection, including no overwhelming postsplenectomy infections. Three patients have died, and 2 patients have developed AIDS since operation.

Conclusions: Splenectomy is effective treatment for patients with symptomatic HIV-related thrombocytopenia that is resistant to medical therapy. The effectiveness of this treatment suggests that the predominant mechanism of thrombocytopenia in HIV-infected patients is increased destruction of platelets because of platelet-associated immunoproteins.