Research Article: Clinical Features, Treatment, and Outcome of HIV-Associated Immune Thrombocytopenia in the HAART Era

Date Published: May 28, 2012

Publisher: Hindawi Publishing Corporation

Author(s): Kimberley L. S. Ambler, Linda M. Vickars, Chantal S. Leger, Lynda M. Foltz, Julio S. G. Montaner, Marianne Harris, Viviane Dias Lima, Heather A. Leitch.

http://doi.org/10.1155/2012/910954

Abstract

The characteristics of HIV-associated ITP were documented prior to the HAART era, and the optimal treatment beyond HAART is unknown. We performed a review of patients with HIV-associated ITP and at least one platelet count <20 × 109/L since January 1996. Of 5290 patients in the BC Centre for Excellence in HIV/AIDS database, 31 (0.6%) had an ITP diagnosis and platelet count <20 × 109/L. Initial ITP treatment included IVIG, n = 12; steroids, n = 10; anti-RhD, n = 8; HAART, n = 3. Sixteen patients achieved response and nine patients achieved complete response according to the International Working Group criteria. Median time to response was 14 days. Platelet response was not significantly associated with treatment received, but complete response was lower in patients with a history of injection drug use. Complications of ITP treatment occurred in two patients and there were four unrelated deaths. At a median followup of 48 months, 22 patients (71%) required secondary ITP treatment. This is to our knowledge the largest series of severe HIV-associated ITP reported in the HAART era. Although most patients achieved a safe platelet count with primary ITP treatment, nearly all required retreatment for ITP recurrence. New approaches to the treatment of severe ITP in this population are needed.

Partial Text

An association between immune thrombocytopenia (ITP) and the acquired immune deficiency syndrome (AIDS) was first recognized in 1982 [1]. Prior to the advent of highly active antiretroviral therapy (HAART), the incidence of HIV-associated thrombocytopenia was estimated at 10–30%, and thrombocytopenia was the initial manifestation of HIV in approximately 10% of cases [2, 3]. The incidence varied according to the definition of thrombocytopenia and the characteristics of the baseline population; for example, it was more common in HIV-infected intravenous drug users (IDUs) compared to HIV-infected men who have sex with men [2]. Although thrombocytopenia may occur at any time during the course of HIV infection, the incidence generally correlates with the degree of immunosuppression and is more prevalent in individuals with clinical AIDS [4–6].

We searched the BC Centre for Excellence in HIV/AIDS (CFE) database to identify patients with HIV who had at least one platelet count <100 × 109/L since January 1996; the year HAART use was widely adopted in British Columbia. For this paper, we chose to focus on patients with severe HIV-associated ITP. Although the International Working Group (IWG) definition of severe ITP includes only patients with clinically relevant bleeding [14], since it would be impossible to identify this group of patients retrospectively from our database, we defined severe thrombocytopenia as at least one platelet count <20 × 109/L. We chose this approach because, at our institution, these patients are routinely referred to hematology and generally require treatment, whereas patients with HIV-associated ITP and higher platelet counts are usually managed by their primary care physician or HIV specialist. We reviewed all charts from patients with a platelet count <20 × 109/L. For the analysis, we included only patients with a diagnosis of HIV-associated ITP made by a hematologist. Patients were excluded if they had pancytopenia, were taking medications that cause thrombocytopenia, had another documented cause of thrombocytopenia, or did not have documentation of assessment by a hematologist. Coinfection with hepatitis B or C was defined as serologic evidence of hepatitis B or C infection prior to or at the time of ITP diagnosis. Chronic liver disease was defined as radiologic or laboratory evidence of chronic liver dysfunction prior to the time of ITP diagnosis. Of 5290 patients in the CFE database since 1996, 1357 (26%) had at least one platelet count <100 × 109/L, 417 (8%) had at least one platelet count <50 × 109/L, 151 (3%) had at least one platelet count ≤20 × 109/L, and 31 patients (0.6%) were diagnosed with HIV-associated ITP and had a platelet count ≤20 × 109/L, see Figure 1. In this study, although the incidence of thrombocytopenia in HIV-infected individuals was high (26%), the incidence of severe HIV-associated thrombocytopenia was only 0.6%. These results are similar to those of studies performed in the era prior to the widespread use of HAART, in which the incidence of platelet count less than 150 × 109/L was 10–30% in HIV-infected individuals, and the incidence of a platelet count less than 50 × 109/L was 1.5–9% [2, 4, 15]. Approximately two-thirds of patients in our study had a CD4 count over 200 cells/μL. Although this seems contrary to previous studies that showed an increased incidence and severity of thrombocytopenia with lower CD4 counts [4–6], in our study, the higher number of patients with CD4 count greater than 200 cells/μL is most likely a reflection of the composition of the baseline population in the HAART era. Importantly, our study shows that control of HIV infection alone is not sufficient to prevent ITP in all patients. HIV-associated ITP remains an important clinical problem in the era of the widespread use of HAART. Although most patients respond to primary ITP treatment and there are few treatment-related complications, nearly all patients require retreatment for recurrent ITP. Inferior response to treatment was associated with a history of IDU. New approaches to the treatment of HIV-associated ITP in this patient population are needed. The authors have no relevant conflict of interests to disclose.   Source: http://doi.org/10.1155/2012/910954

 

Leave a Reply

Your email address will not be published.