Expression Of Macrophage Migration Inhibitory Factor And FKBP5in Patients With Immune Thrombocytopenia And Its Correlation With Glucocorticoid Resistance

Objective: To investigate the expression of macrophage migration inhibitoryfactor (MIF) in patients with primary immune thrombocytopenia(ITP) and itscorrelation with glucocorticoid resistance.Methods: The MIF mRNA expression was analyzed by semiquantitative real-timeRT-PCR in90newly diagnosed ITP patients. All the patients with ITP were dividedinto several subgroups according to glucocorticoid response, gengder, age, stages andseverity of desease, and difference between each pair of subgroups were analyzed. MIFprotein expression in serum was performed by ELISA.Results: We found no association of GC resistance and MIF mRNA and proteinexpression in ITP patients. According to the gengder, age, stages and severity ofdesease, the patients were further subdivided into8groups, no statistical difference wasfound.Conclusion: The present study suggested that the MIF expression does notcontribute to GC resistance in ITP. Objective: The FKBP5gene codes for the FK506-binding protein51(FKBP5), aco-chaperone of hsp90, which regulates glucocorticoid (GC) receptor sensitivity. TheFKBP5gene single nucleotide polymorphisms (SNP), rs1360780, has been found tomodulate GC sensitivity in stress-related psychiatric disorders. The aim of the presentstudy was to examine the effects of rs1360780on the treatment outcome of patientssuffering from idiopathic thrombocytopenic purpura (ITP) administered with GC.Methods: The polymorphism of FKBP5, rs1360780, was genotyped in55GC-resistant ITP patients,157GC-sensitive ITP patients and110unrelated healthyindividuals using real-time PCR and cycling probe technology with DNA extractedfrom peripheral blood.Results: No significant differences in FKBP5rs1360780genotypes (P=0.51) andalleles (P=0.89) were observed between the GC-resistant ITP patients and the healthycontrols. There were no significant differences observed between the GC-sensitive ITPpatients and the healthy controls (P=0.40for genotypes and P=0.62for T allele), as wellas between the GC-sensitive ITP patients and the GC-resistant patients (P=0.67forgenotypes and for T allele).Conclusion: The present study demonstrates that the FKBP5polymorphism maynot affect the response of ITP patients to GC treatment. Objective: Glucocorticoids (GCs) are considered the important drugs used intreatment of immune thrombocytopenia (ITP). However, about only10-30%patientswith ITP develop GC resistance after standard treatment with GC. Many studies hasbeen shown that the FKBP51overexpression and low expression of FKBP52affectedimmunosuppressive effects glucocorticoids. Here, we investigated the association of GCresistance with FKBP51and FKBP52mRNA expression in this case-control study.Methods:The FKBP51and FKBP52mRNA expression was analyzed bysemiquantitative real-time RT-PCR in90newly diagnosed ITP patients. All the patientswith ITP were divided into several subgroups according to glucocorticoid response,gengder, age, stages and severity of desease, and difference between each pair ofsubgroups were analyzed.Results: We found no association of GC resistance and FKBP51mRNAexpression in GC-resistant ITP patiences （26.20±5.18） compared with theGC-sensitive（27.80±5.99）. We found no association of GC resistance and FKBP52mRNA expression in GC-resistant ITP patiences （17.35±4.96）compared with theGC-sensitive（18.82±5.54）. According to gengder, age, stages and severity of desease,the patients were further subdivided into8groups, no statistical difference was found inGC-resistant ITP patiences compared with the GC-sensitive.Conclusion:The present study suggested that the FKBP51and FKBP52mRNAexpression does not contribute to GC resistance in ITP.