Thrombopoietin: a potential diagnostic indicator of immune thrombocytopenia in pregnancy.

Xu Zhang,Ming Hou,Jihua Qiu,Fangmiao Jing,Xiaoqing Li,Lizhen Li,Jun Peng,Yajing Zhao,Panpan Han,Hai Zhou,Zhangyuan Kong

doi:10.18632/oncotarget.7106

Abstract

To evaluate whether the serum thrombopoietin levels in pregnancy-associated immune thrombocytopenia (ITP) differ from those in gestational thrombocytopenia, and reveal the possibility of thrombopoietin serving as a marker for differential diagnosis. Serum thrombopoietin concentration was determined in ITP in pregnancy (n = 35), gestational thrombocytopenia (n = 31), healthy pregnancy (n = 32), age-matched nonpregnant ITP (n = 32) and nonpregnant healthy controls (n = 35) by ELISA. The serum thrombopoietin level of ITP in pregnancy (1283 ± 646 pg/mL) was significantly higher than gestational thrombocytopenia (187 ± 64 pg/mL) (P < 0.01), although the platelet counts of these two disorders may overlap. Twenty-nine of 35 patients with ITP in pregnancy had thrombopoietin values >500 pg/mL, whereas none of the gestational thrombocytopenia patients' thrombopoietin levels exceeded 500 pg/mL. In addition, ITP in pregnancy presented a markedly higher thrombopoietin level than nonpregnant ITP (88 ± 41 pg/mL) (P < 0.01), indicating that the pathogenesis of pregnant and nonpregnant ITP was different. Our findings suggest that measurement of serum thrombopoietin concentration provides valuable diagnostic information for differentiating ITP in pregnancy from gestational thrombocytopenia. Thrombopoietin represents a reliable marker for ITP in pregnancy.

Highlights

Thrombopoietin (TPO), the ligand of c-Mpl protein, is the major physiological regulator of megakaryocyte maturation and platelet production.[1, 2] TPO enhances megakaryocyte colony formation; increases the size, number and ploidy of developing megakaryocytes; and results in increased platelet production.[3, 4] In turn, platelets become desialylated as they circulate and age in blood, the desialylated platelets bind to the hepatic Ashwell-Morell receptor (AMR) and induce hepatic TPO gene transcription and translation.[5]
Immune thrombocytopenia (ITP) is an autoimmune hematological disease characterized by thrombocytopenia caused by accelerated platelet destruction and suppression of platelet production,[10, 11] which is common in young women.[12]
Our study demonstrated that TPO levels of ITP in pregnancy patients are extremely elevated and significantly higher than those of gestational thrombocytopenia (GT) patients

Summary

Introduction

Thrombopoietin (TPO), the ligand of c-Mpl protein, is the major physiological regulator of megakaryocyte maturation and platelet production.[1, 2] TPO enhances megakaryocyte colony formation; increases the size, number and ploidy of developing megakaryocytes; and results in increased platelet production.[3, 4] In turn, platelets become desialylated as they circulate and age in blood, the desialylated platelets bind to the hepatic Ashwell-Morell receptor (AMR) and induce hepatic TPO gene transcription and translation.[5] TPO is expressed mainly in liver, and cleared from the circulation blood by binding to the c-Mpl ligands on platelets, megakaryocytes and their progenitors.[6] With a largely constitutive hepatic TPO production, the circulating TPO level is controlled by the total cell mass of the megakaryocyte lineage that expresses c-Mpl receptor.[7]. ITP appears in 1 to 2 pregnancies per thousand, and it may lead to www.impactjournals.com/oncotarget bleeding complications in both the mother and her infant. [13] the diagnosis of ITP in pregnancy is still indefinite so far, no laboratory test has been established to distinguish it from GT

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