Performance of a point-of-care device in determining prothrombin time in supra-therapeutic INRs.

INTRODUCTION: Point-of-care (POC) devices have been widely adopted for monitoring prothrombin time (PT) (INR) following the demonstration of their accuracy compared to standard INR determination. However, guidelines suggest confirmation of POC results when INRs increase above therapeutic range, due to concerns regarding possible inferior performance of POC devices in high INR levels. Unfortunately, patients with supra-therapeutic INRs are underrepresented in studies that validated these devices. METHODS: We performed a prospective evaluation of the performance of a POC device in monitoring oral anticoagulation in patients with INR values above 3.5 in a University outpatient anticoagulation clinic. During a 6-month period, 2322 INR determinations were performed with a POC device, and results above 3.5 were immediately repeated on an automated coagulometer. RESULTS: Dual INR determinations by two methods were obtained in 160 visits, with a mean INR from the POC device of 4.52 ± 0.96. Both classical statistics and clinical concordance analysis yielded satisfactory results when the two methods were compared. CONCLUSION: Our results demonstrate that POC devices present good correlation with standard laboratory methods for PT determination in supra-therapeutic INRs and that differences in clinical management do not support the need for systematic confirmation of these results in nonbleeding patients.

The impact of the search for thrombophilia risk factors among antiphospholipid syndrome patients with thrombosis.

Thrombosis is a major clinical feature of the antiphospholipid syndrome. Interactions between genetic and acquired factors could contribute to thrombosis development. In this study, we evaluated 40 patients with antiphospholipid syndrome and thrombosis, 31 primary and nine secondary to systemic lupus erythemathosus, to estimate the carrier rates of factor V Leiden, 20210A --> G prothrombin variant and 677C --> T in the MTHFR gene. Protein C, protein S and antithrombin were measured in 30 patients, with a median of 100.66 +/- 23.86, 93.57 +/- 36.44 and 98.8 +/- 5.67%, respectively. None of the patients were deficient on these natural anticoagulants. No significant variation was found between the patient group and the controls, regarding the prevalence of homozygotes for the mutated 677T allele (2.5 versus 5.4%), or heterozygotes for factor V Leiden (0 versus 0.7%). Despite the fact that these mutations are relatively common in Brazilian thrombophilic patients, its low prevalence in this cohort of patients suggest that these genetic alterations are not risk factors for thrombosis in antiphospholipid syndrome. The prevalence of the mutated allele 20210A of the prothrombin gene was higher in patients when compared with controls (5 versus 0.7%; P = 0.01), suggesting that prothrombin variant could increase the risk of thrombosis in patients with antiphospholipid syndrome.

Study of hemostasis in pediatric patients with portal vein thrombosis.

We describe the behavior of hemostatic variables in children with portal vein thrombosis (PVT) and in a control pediatric population. Hereditary protein C (PC) or protein S (PS) deficiency was not a etiologic factor for PVT in children. Minor signs of consumption of coagulation factors II, V, fibrinogen and hyperfibrinolysis were detected. One child had lupus anticoagulant (LA).

Studies on the components of the contact phase system in patients with acute nonlymphoblastic leukemia.

The objective of the present study was to evaluate factors of the plasma kallikrein system in patients with acute nonlymphoblastic leukemia (ANLL), and compare the results to a normal control group. A prospective study was performed in the Tertiary Health Care Institution, Hemocentro, Campinas State University, Campinas, São Paulo, Brazil. Thirty-five patients, diagnosed as ANLL between 1988 and 1991, were considered for participation. Eleven patients were not eligible, according to the exclusion criteria: infection/septicemia, previous treatment or blood transfusion. The study was performed with 24 ANLL patients, average age 34 years (16-69 years), 14 men and 10 women. Nineteen healthy volunteers, workers from the Hematology Center, average age 32 years (21-59 years), 11 men and 8 women, were the control group. Plasmatic prekallikrein, C1-inhibitor, alpha 2-macroglobulin, activated partial thromboplastin time, prothrombin time, factor XII, factor XI, factor V and prealbumin were measured. Plasmatic prekallikrein (p = 0.02) and prealbumin (p = 0.03) were significantly decreased, and prothrombin time increased (p = 0.003) in the patient group when compared to the control. Significant correlation (r = 0.49, critical value = 0.43, p < 0.05) between prekallikrein and prealbumin, and between prothrombin time and factor V (r = 0.54, critical value = 0.44, p < 0.05) was demonstrated in the patient group. No correlation was found between parameters analysed and circulant blast count or leukemia subgroups. Statistical analysis was performed by the Wilcoxon test. Correlation between the parameters was also verified. These results suggest activation of the contact system or impaired liver synthesis in patients with ANLL, and could contribute to disease complications.