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The risk of venous thromboembolism associated with long-haul flights is the subject of controversy. In a prospective, controlled study, we examined 160 passengers before and after return from a long-haul flight and 160 age-matched and sex-matched, non-travelling volunteers using venous compression ultrasound. Deep vein thrombosis was not observed in either group. Isolated calf muscle vein thrombosis (ICMVT) was present in 4/160 (2.5%) flight passengers and in 1/160 (0.6%) controls. All subjects with ICMVT were clinically asymptomatic, and ICMVT was located in the soleal muscle veins in all four subjects. Three of the four passengers with ICMVT had other risk factors for thrombosis.

Coagulation factor V has been at the centre of investigation for several years. In addition to factor V Leiden, various other polymorphisms are becoming the object of interest. Different results have been published about the association of the HR2 haplotype with decreased factor V levels and with reduced response to activated protein C (APC). Due to the central position of factor V in the clotting process, its activity can be determined in both thromboplastin-based and activated partial thromboplastin time (aPTT)-based assays. A multitude of assays are known for the determination of APC response. The aim of our study was to investigate whether different methods disclose genotype-dependent differences in factor V activity as well as APC response. Three wild-type carriers, three carriers homozygous for the R2 allele (4070G), and three carriers homozygous for the G allele (2391G, 2663G, 2684G, 2863G) were investigated. For each individual plasma sample, the factor V activity was determined using 12 different reagent combinations of three different thromboplastins, three different aPTT reagents, and two different factor V deficient plasma sources. The determination of factor V activity in the thromboplastin system revealed differences between the genotypes. These differences were independent of the thromboplastin reagent and the factor V-deficient plasma. The aPTT system exhibited a dependency on the aPTT reagent and the factor V-deficient plasma. Analysis of APC response disclosed genomic differences in specific test systems only. One type of assay could be more appropriate than other types in dependence of the position of genomic variations. Therefore, the applied assay is an important influential factor in investigations of functional consequences of genomic variations.

Different assays for the assessment of protein S (PS) functional activity are commercially available. We were able to show that, considering the influence of factors known in respect of PS, good agreement can be reached between the results of the determination of free PS as obtained using an immunoassay with monoclonal antibodies and the determination of PS activity as obtained using a test based on activated factor X (factor Xa). However, values of PS activity higher than free PS concentration were obtained in plasma samples taken from patients undergoing therapy with low molecular weight (LMW) heparin. An in vitro incubation of plasma samples with LMW heparin in varying concentrations led, in every case, to an increase of clotting times and thus to an increase of PS activity. In all investigations, the ratios of clotting time with heparin to that without heparin were higher in plasma samples containing PS than in PS-deficient plasma. This result was independent of the use of commercially deficient plasma or the blocking of PS in reference plasma by addition of polyclonal PS antibodies. Obviously, heparin blockers in commercially available assays only neutralize the effect of conventional heparin, and the prolongation of the clotting time is mainly caused by the inhibition of factor Xa by LMW heparin. The reason for the stronger effect in plasma containing PS than in the same plasma after the blocking of PS with polyclonal antibodies as well as in PS-deficient plasma is unclear. Due to the unrecognizable influence of LMW heparin on global clotting assays, the assessment of PS activity values without clear documentation of the application of LMW heparin can lead to improper diagnoses.