Patterns of Care and Association of Response with Rituximab among Patients of Immune Thrombocytopenia Purpura in a Rural Practice

Research Article

Ann Hematol Oncol. 2017; 4(11): 1182.

Patterns of Care and Association of Response with Rituximab among Patients of Immune Thrombocytopenia Purpura in a Rural Practice

Bulbul A1,2*, Rashad S1, Tsao-Wei D3, Huber M4 and Weitz IC3

1Department of Hematology & Oncology, Kymera Independent Physicians, USA

2Division of Internal Medicine, Department of Hematology/Oncology, Texas Tech University Health Sciences Center School of Medicine, USA

3Jane Anne Nohl Division of Hematology, University of Southern California, Keck School of Medicine, USA

4New Mexico State University, USA

*Corresponding author: Bulbul A, Department of Hematology/Oncology, Division of Internal Medicine, Kymera Independent Physicians, Texas Tech University Health Sciences Center School of Medicine, USA

Received: October 12, 2017; Accepted: November 16, 2017; Published: December 07, 2017


Immune thrombocytopenia (ITP) is a heterogeneous disorder of immune dysregulation of T and autoreactive B cells leading to the immune-mediated destruction of platelets due to the eventual loss of immune tolerance against platelet epitopes.

Keywords: Immune thrombocytopenia; Thrombocytopenia; Dexamethasone


ITP results from antiplatelet antibodies targeting primary platelet glycoproteins such as GP IIb/IIIa. Production of crossreactive antiplatelet antibodies by autoreactive B cells in response to infection and impaired expression of inhibitory Fc receptors have been implicated [1,2]. Beyond the effects on circulating platelets, these antibodies are also directed against platelet glycoproteins on the surface of megakaryocytes, inducing apoptosis-like programmed cell death and reducing platelet production [3-5]. In certain settings, such as inflammation, Antigen-presenting cells APCs create cryptic epitopes that can escape negative selection. Furthermore, the T cells observed are primarily against cryptic rather than native epitopes [6]. Supporting a role for APCs as critical cells in the development of ITP. In addition, patients with ITP demonstrate an increased Th1/Th2 ratio favoring autoreactive B-cell [7].

Treatment of ITP has evolved from blocking platelet clearance with corticosteroids, intravenous immunoglobulin (IVI g) or removing the site of clearance with splenectomy, to B and T cell modulation, as well as thrombopoietin agonists to boost platelet production. Several studies have examined whether more intensive dosing of steroids in newly-diagnosed ITP leads to more durable remissions. Although there has been some success with HD Dexamethasone [8,9] the role of B cell modulation with rituximab in improving sustained platelet response (SR) across different lines of treatment is unclear. Some studies demonstrate higher sustained response (SR) with the addition of rituximab to HD, 60%-76% compared to 30-36% with Dexamethasone alone [10-12] as well as improved responses. However, other studies fail to reproduce the composite end points of platelets >50x109/L, reduction of significant bleeding or rescue treatment once standard treatment of HD Dexamethasone was stopped [13]. In this study, we look at responses in ITP patients in rural community setting receiving rituximab vs alternative therapies.


A retrospective review of three hundred sixty-two patients with thrombocytopenia (ICD 9 287.5 and 287.31; ICD 10 D 69.6, D 69.3) seen between Jan 1990 to June 2016 across three rural community practices in southeastern NM was performed.

Patients with Secondary Non-immune thrombocytopenia due to chronic liver disease related to Alcohol, Hepatitis C, Cirrhosis, hypersplenism, leukemia, CLL, Lymphoma, and or drug-related thrombocytopenia were excluded from the statistical analysis N=88 (24%). Secondary Immune related thrombocytopenia that were included in secondary analysis were patients with ANA >1:640 and or clinical features of collagen vascular disorders N=41 (11%). Fisher exact test was used to determine the association of treatment and response in both primary and secondary ITP. The International Working Group (IWG-2011) classification and criteria were used to assess response [14]. Sustained Response (SR) was defined as a platelet count of >50,000 per cubic millimeter six months after treatment [8,14].

Complete response (CR)

Platelet count ≥100×109/L and absence of bleeding.

Partial response (PR)

Platelet count ≥30×109/L and at least 2-fold increase the baseline count and absence of bleeding.

No response (NR): Platelet count <30×109/L or less than 2-fold increase of baseline platelet count or bleeding. Relapse was any platelet below 50×109/L or bleeding.

Loss of CR

Platelet count below 100×109/L or bleeding (from CR).

Persistent ITPs

3-12-month duration. Different criteria are used to describe chronic ITP in different papers >6 months to >12 months. [14,15]. The protocol was approved and study in accordance with the IRB at Texas Tech University Health Sciences Center.


Two hundred thirty-three patients (64%) had primary ITP 41 (11%) had secondary immune related ITP as described. The demographic and clinical baseline characteristics are outlined in (Table 1). Median age of diagnosis was 61 and median platelet on diagnosis was 90 (0-148). The median platelet count in patients <50 was lower at 77. One hundred seventy (73%) patients with primary ITP did not have a bone marrow biopsy, 63 patients (27%) did have bone marrow biopsy to confirm the diagnosis. Megakaryocytic hyperplasia was the most common diagnostic finding in primary ITP (n=15).