The authors define height- and sex-corrected normal values for spleen length and volume for women with a body height of 155-179 cm and men with a body height of 165-199 cm and propose validated algorithms to gauge the percentile of an individual's spleen size.

Background: It is still not clear whether native or platelet count adjusted platelet rich plasma (PRP) should be used for platelet aggregation measurements. Aim: To evaluate the necessity of using adjusted PRP in platelet function testing. Methods: Platelet aggregation with native PRP and adjusted PRP (platelet count: 250/nl, obtained by diluting native PRP with platelet poor plasma) was performed on the Behring Coagulation Timer (BCTH) using ADP, collagen, and arachidonic acid as agonists. Healthy subjects, patients on antiplatelet treatment, and patients with thrombocytosis (platelet counts in PRP . 1250/nl) were investigated. Results: No significant differences in the maximum aggregation response were seen when using either native or adjusted PRP from healthy subjects and patients on antiplatelet treatment. Nevertheless, some patients taking aspirin or clopidogrel showed reduced inhibition of ADP and arachidonic acid induced aggregation in adjusted PRP but not in native PRP. The maximum velocity of healthy subjects and patients on antiplatelet treatment varied significantly as a result of the degree of dilution of the adjusted PRP. Surprisingly, the BCT provided good results when measuring platelet aggregation of native PRP from patients with thrombocytosis, whereas commonly used aggregometers could not analyse platelet aggregation of native PRP in these patients. Conclusion:The time consuming process of PRP adjustment may not be necessary for platelet aggregation measurements. Moreover, using adjusted PRP for monitoring aspirin or clopidogrel treatment may falsify results. Therefore, it may be better to use native PRP for platelet aggregation measurements, even in patients with thrombocytosis.

Thrombophilic defects have been shown to be associated with an increased risk of venous thrombosis, fetal loss, and gestational complications. The knowledge about the clinical relevance of thrombophilic defects is increasing, and evidence-based indications for thrombophilia screening are therefore discussed in this review. Selective thrombophilia screening based on previous personal and/or family history of venous thromboembolism is more cost-effective than universal screening in all patient groups evaluated. In the majority of patients with acute venous thrombosis, the results of thrombophilia screening do not influence the duration of oral anticoagulation. The only patient population who clearly profits from thrombophilia screening in this situation are patients with a newly diagnosed antiphospholipid syndrome, because prolonged anticoagulation can avoid the high incidence of recurrence in this patient population. Because of the increased risk of venous thrombosis during pregnancy and the puerperium, thrombophilia screening is indicated in selected patients with a previous history of venous thrombosis or a positive family history. Significant associations with early and late pregnancy loss are observed for carriers of the heterozygous factor V Leiden mutation, the heterozygous prothrombin-mutation G20210A and anticardiolipin antibodies, while protein S deficiency is significantly associated with late pregnancy loss. Antithrombotic drugs like UFH, LMWH or low-dose aspirin may have a potential therapeutic benefit in patients with recurrent pregnancy loss and thrombophilia, but placebo-controlled, multicenter trials are urgently needed to clarify this issue. Although a supra-additive effect for the risk of venous thrombosis is observed between oral contraceptives and some thrombophilias, the absolute incidence of venous thromboembolism is low in premenopausal women and mass screening strategies are therefore unlikely to be effective. While antiphospholipid antibodies are known to be associated with arterial thrombosis, screening for heritable thrombophilias is not useful in arterial thrombosis, although subgroup analysis indicates that they may play a role particularly in young patients and children.

Cytomegalovirus (CMV) seems to contribute to the development of venous thromboembolism (VTE) in immunocompromised patients whereas literature data on the role in immunocompetent individuals are mainly limited to case reports. This study aimed to investigate if cytomegalovirus infection contributes to the development of VTE in immunocompetent individuals. CMV-IgG and CMV-IgM antibody titres, CMV-IgG avidity and CMV-DNA were identified in samples from 166 VTE patients and from 166 healthy blood donors matched for gender and age. CMV-IgG antibodies were found more frequently in VTE patients compared to controls [57.8% vs. 44.0%; adjusted OR 1.75 (95% CI 1.13-2.70); p = 0.016]. Accordingly, median CMV-IgG titres were significantly higher in the case group (89.4 vs. 1.8 AU/ml; p = 0.002). Although the overall rate was low, CMV-IgM antibodies were detected more often among cases than controls. The difference was significant in patients with an unprovoked VTE event [7.4% vs. 0.6%; adjusted OR 5.26 (95% CI 1.35-20.8); p = 0.017]. CMV-IgG antibodies of almost all VTE patients (98.9%) and controls (98.6%) were found to be of high avidity. The rate of positive CMV-DNA samples was low and not different between cases and controls. With the exception of age, no association was found between CMV seropositivity and established VTE risk factors within the VTE group. CMV infection seems to play a role in the development of VTE in immunocompetent patients. Recurrent infection might be more important than acute CMV infection.