Infection with human immunodeficiency virus (HIV) may lead to hemostatic imbalances. Forty-nine consecutive patients with acute opportunistic infections were screened for thrombophilic parameters. A follow-up investigation was performed after 10 +/- 8 weeks in 26 patients. In acutely ill patients, the incidence of protein S deficiency was 67% (33/49) and of protein C deficiency 25% (12/49), while at the follow-up visit the incidences were 54% (14/26) and 8% (2/26), respectively. Protein S and protein C levels increased significantly from initial to follow-up visit (p < 0.05). Lupus anticoagulants were not detected and anticardiolipin IgG antibodies were present in 11.4% (5/44). Three patients presented with deep venous thrombosis on admission; in two, protein S or protein C deficiency was observed. In conclusion, an acquired protein S and protein C deficiency often develop in patients with HIV and acute illness; this may be reversible after treatment for opportunistic infections.

SummaryThrombophilia is a well-established risk factor for a venous thromboembolic event (VTE), and it has been proposed that hereditary thrombophilia may substantially contribute to the development of VTE in young patients. We aimed to analyse the prevalence of thrombophilia with special regard to the age of VTE manifestation. The study cohort consisted of 1490 patients (58% females) with a median age 43 years at the time of their first VTE. At least one thrombophilic disorder was identified in 50Á1% of patients. The probability of detecting a hereditary thrombophilia declined significantly with advancing age (from 49Á3% in patients aged 20 years and younger to 21Á9% in patients over the age of 70 years; P < 0Á001). This may be primarily attributed to the decreasing frequencies of the F5 R506Q (factor V Leiden) mutation and deficiencies of protein C or protein S with older age at the time of the initial VTE event. Moreover, thrombophilia was more prevalent in unprovoked compared with risk-associated VTE (57Á7% vs. 47Á7%; P = 0Á001). The decline in the prevalence of hereditary thrombophilia with older ages supports the use of a selected thrombophilia screening strategy dependent on age and the presence or absence of additional VTE risk factors.

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.

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