[Changes in PT and APTT When Administrating Rivaroxaban, a Direct Inhibitor of Activated Factor X].

The effects of oral rivaroxaban (RX), a direct inhibitor of activated factor X (Xa), on prothrombin time (PT) and activated partial thromboplastin time (APTT) were examined. PT and APTT before and after administration of 15 mg RX in 10 healthy subjects were measured by using various reagents. In addition, the blood Xa inhibitor concentration was measured and its correlation with PT and APTT, as measured by each reagent, was examined. Furthermore, the relationship (sensitivity) between the prolongation ratio and FX activity was evaluated. Prolongation of both PT and APTT was observed after RX administration, and maximal prolongation was observed four hours after administration for each reagent. The prolongation ratio was different among the reagents used for examination, and the reagent with the highest sensitivity to FX and factor VII showed the largest prolongation ratio. PT and APTT were positively correlated with RX concentration when measured by any reagent. In this study, neither PT, APTT, nor RX concentration returned to the values measured prior to dosing even at 24 hours after administration of RX. Our results suggest that approximate concentration of remaining RX may be estimated by PT (second) when using a reagent showing a larger prolongation ratio.

Association between Helicobacter pylori infection and platelet count in mice.

Strong evidence for an association between idiopathic thrombocytopenic purpura (ITP) and Helicobacter pylori (HP) infection has been reported in humans. Chronic ITP is known to be improved by the eradication of HP. The purpose of this study was to reproduce these events by the experimental infection of several strains of mice with HP. BALB/c, C57BL/6, and DBA/2 mice were untreated or orally inoculated with HP. Two months later, platelet counts were compared in samples from HP-infected and noninfected mice. Platelet counts (mean ± SD, × 104 cells/µl) in blood samples from HP-infected BALB/c, C57BL/6, and DBA/2 mice were 102.28 ± 14.71, 99.65 ± 17.00, and 111.57 ± 16.20, respectively; the respective counts from noninfected mice were 121.80 ± 13.30, 104.35 ± 18.20, and 107.84 ± 14.33. A significant difference in platelet counts between HP-infected and noninfected mice was observed in BALB/c mice (P≤0.01) but was not observed in DBA/2 mice, even though the histocompatibility (H)-2 type of the DBA/2 was the same as that of BALB/c mice. According to ELISA results, the optical density value for the anti-HP antibody in HP-infected BALB/c mice was not correlated with the number of platelets (P>0.50). These results suggest that the decrease in platelet count caused by HP infection is not related to antibody titer and histocompatibility-2 type. Experimental infection of BALB/c mice with HP can reproduce the relationship between HP and ITP and serves as a good model to investigate the mechanistic basis for the effectiveness of HP eradication therapy for ITP treatment.

Evaluation of mouse red blood cell and platelet counting with an automated hematology analyzer.

An evaluation of mouse red blood cell (RBC) and platelet (PLT) counting with an automated hematology analyzer was performed with three strains of mice, C57BL/6 (B6), BALB/c (BALB) and DBA/2 (D2). There were no significant differences in RBC and PLT counts between manual and automated optical methods in any of the samples, except for D2 mice. For D2, RBC counts obtained using the manual method were significantly lower than those obtained using the automated optical method (P<0.05), and PLT counts obtained using the manual method were higher than those obtained using the automated optical method (P<0.05). An automated hematology analyzer can be used for RBC and PLT counting; however, an appropriate method should be selected when D2 mice samples are used.