Short paper Relation between 3435C N T multidrug resistance 1 gene polymorphism with high dose methylprednisolone treatment of childhood acute idiopathic thrombocytopenic purpura Mehmet Akin a, ⁎, Sebahat Turgut b, 1 , Ceylan Ayada b, 1 , Yusuf Polat c, 2 , Yasemin Isik Balci d, 3 , Firat Erdoğan e, 4 a Denizli State Hospital, Department of Pediatric Hematology, Denizli, Turkey b Pamukkale University, Faculty of Medicine, Department of Physiology, Turkey c Denizli State Hospital, Department of Microbiology, Denizli, Turkey d Pamukkale University, Faculty of Medicine, Department of Pediatric Hematology, Turkey e Medipol University, Department of Pediatric, Istanbul, Turkey abstract article info Article history: Accepted 11 June 2011 Available online 21 June 2011 Received by A.J. van Wijnen Keywords: MDR1 Idiopathic thrombocytopenic purpura High dose methylprednisolone The current study was conducted to assess 3435CNT multidrug resistance 1 gene polymorphism and the efficacy of high dose methylprednisolone (HDMP) in childhood acute idiopathic thrombocytopenic purpura patients. Methods: A total of 31 childhood acute Idiopathic thrombocytopenic purpura patients (17 females, 14 males) between the ages of 2 and 16 years of age were included in the study. High-dose methylprednisolone was given at a dose of 30 mg/kg/day for 3 days and 20 mg/kg/day for 4 days, consecutively and intravenously. Polymerase chain reaction–restriction fragment length polymorphism was used for the detection of C3435T single nucleotide polymorphism. Fragments obtained were 238 bp to T/T genotype, 172 bp and 60 bp fragments to the C/C genotype, and 238 bp, 172 bp and 60 bp to the C/T genotype. Results: The distribution of CC, CT, and TT genotypes were 19.0%, 61.3%, and 19.4%, respectively. Both allele frequencies of C and T were the same — 50%. There was no significant difference in genotype and allele distribution between the patients with ITP and the control group (χ 2 = 0.84 p = 0.65, χ 2 = 0.2 p = 0.63, respectively). There were no significant differences in age, gender, and pre- and post-treatment platelet counts between CC, CT, and TT genotypes of the MDR gene. Response to treatment shows no significant difference between genotype and allele groups. Conclusion: In our study, there was no difference in the HDMP treatment response between MDR1 gene genotypes. However, it should be noted that this study includes a small group of patients. Our data should therefore be considered preliminary, awaiting further confirmatory studies on an expanded patient base. © 2011 Elsevier B.V. All rights reserved. 1. Introduction Childhood acute Idiopathic thrombocytopenic purpura (ITP) is a common pediatric hematologic disorder characterized by increased destruction of antibody-sensitized platelets with normal to increased megakaryocytes in the bone marrow, as well as the presence of thrombocytopenia with otherwise normal red cells and leukocytes, absence of splenomegaly and the absence of other causes of thrombocytopenia (Cines and Blanchette, 2002; Kühne et al., 2003). Multidrug resistance-1 (MDR-1) is characterized by the over- function of P-glycoprotein (P-gp), a pump molecule that decreases intracellular drug concentration by effluxing them from the intracel- lular space. P-gp is expressed in the apical membrane of cells with excretory functions, such as those in the liver, kidney, small intestine, stomach, and the blood–brain barrier (Lum and Gosland, 1995). Functional P-gp is found in several types of human leukocytes and stem cells. Among hematological cells, P-gp expression is highest in natural killer cells, CD4+ and CD8+ lymphocytes, and bone marrow progenitor cells (Klimecki et al., 1994). Single nucleotide polymorphisms (SNPs) of the MDR1 gene have been identified and correlate with P-gp expression (Hoffmeyer et al., Gene 487 (2011) 80–83 Abbreviations: HDMP, High dose methylprednisolone; ITP, Idiopathic thrombocy- topenic purpura; MDR-1, Multidrug resistance-1; P-gp, P-glycoprotein; SNPs, Single nucleotide polymorphisms; IVIG, Intravenous immune globulin; R, response; NR, No response. ⁎ Corresponding author. Tel.: + 90 505 3945276; fax: + 90 258 2619206. E-mail addresses: drmehmetakin@yahoo.com.tr (M. Akin), sturgut@pau.edu.tr (S. Turgut), drypolat@gmail.com (Y. Polat), firaterdogan@yahoo.com (F. Erdoğan). 1 Tel.: +90 258 2962492; fax: +90 258 2962433. 2 Tel.: +90 505 3937160; fax: +90 258 2619206. 3 Tel.: +90 505 3136592; fax: +90 258 2962433. 4 Tel.: +90 505 6763484. 0378-1119/$ – see front matter © 2011 Elsevier B.V. All rights reserved. doi:10.1016/j.gene.2011.06.019 Contents lists available at ScienceDirect Gene journal homepage: www.elsevier.com/locate/gene