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Abstract: Objective: Data on C-reactive protein (CRP) as a risk indicator of venous thromboembolism are conflicting. A recent study reported higher CRP levels in homozygous carriers of a novel CRP gene polymorphism at the 3′ UTR (CRP +1444C>T). We investigated, whether homozygosity for CRP +1444C>T is associated with an increased risk of spontaneous venous thromboembolism (VTE). Methods and results: CRP +1444C>T genotype and plasma levels were assessed in 128 patients with deep venous thrombosis (DVT, 70 females/58 males), 105 with pulmonary embolism (PE, 58 females/47 males) and 122 healthy individuals (60 females/62 males). CRP +1444TT was significantly associated with increased CRP plasma levels in healthy individuals. CRP +1444TT was more frequent (14%) among controls than DVT patients (9%, p =0.26) or PE patients (6%, p =0.05), respectively. No significant deviation from Hardy–Weinberg equilibrium was observed in patients (p =0.8) or controls (p =0.3), respectively. CRP +1444C>T was not significantly associated with CRP levels in patients with VTE. Conclusions: Homozygous carriers of the CRP 3′ UTR +1444C>T polymorphism do not have a significantly increased risk of VTE. Our data support the assumption that a clinically relevant association between CRP and VTE is missing. [Copyright &y& Elsevier]

Background Knowledge of platelet function may assist in patient care in chronic autoimmune thrombocytopenia (cAITP). Materials and methods We evaluated the association of platelet function with haemorrhage in 41 patients, median age 41 years (range 14–82 years, 24 females) with chronic autoimmune thrombocytopenia (cAITP). Samples were investigated for platelet P-selectin, and adhesion and aggregate formation under high shear conditions. Data were compared to those from 28 healthy controls (median age 39 years, range 23–70 years, 17 females) and correlated with a bleeding score of 0 (no bleeding) to 3 (overt mucosal bleedings). Results P-selectin levels were higher in patients than in controls ( P < 0·0004). Compared to controls, the patients’ samples responded to high shear with decreased adhesion to the polystyrene surface ( P < 0·0001), but formed aggregates of normal size. P-selectin expression was neither correlated with platelet counts, nor platelet adhesion, nor the bleeding score. Only the size of formed aggregates correlated with P-selectin ( P = 0·01). Platelet counts (odds ratio 0·5, 95% confidence interval 0·22–0·88; P = 0·04) and adhesion (odds ratio 0·45, 95% confidence interval 0·17–0·87; P = 0·04) were independently inversely correlated with bleeding symptoms. Conclusion Platelet adhesion correlates with bleeding symptoms, while the size of aggregates that are formed under high shear correlates with in vivo platelet activation. The determination of these parameters may assist in estimating an individual bleeding risk and thus a decision for treatment. [ABSTRACT FROM AUTHOR]

Lupus anticoagulants (LA) prolong in vitro phospholipid-dependent coagulation tests, but are associated with thromboembolic disease (TE). However, a subgroup of individuals with LA has no TE, and it is therefore desirable to distinguish those at risk for TE from those without. Whether platelets have a primary role in the development of TE is not clear yet. We determined platelet autoantibodies to identify a specific platelet target which is associated with platelet activation in 97 patients with a long history of detectable LA, 65 patients with TE (LA/TE+), and 32 individuals without TE (LA/TE-). Thrombocytopenia was more common in the LA/TE- than in the LA/TE+ group (P < 0.05). Both groups had platelet antibodies, but the frequency of antibodies was lower in LA/TE+ than LA/TE- patients (P < 0.01), who had higher antibody titres against glycoprotein IIb/IIIa and glycoprotein Ib/IX (P < 0.05). Also, their platelets were more activated, as determined by PAC-1 binding (P < 0.01). These differences were also noted if patients with arterial thrombosis were evaluated separately. These findings in LA/TE- individuals were similar to those in patients with chronic autoimmune thrombocytopenia. However, there was no autoantibody target identifiable to distinguish between LA/TE- from LA-TE+ individuals. We therefore conclude that the presence of platelet antibodies, even if associated with platelet activation, is not sufficient to dispose LA patients to thromboembolic disease. [ABSTRACT FROM AUTHOR]