Vergleichende Untersuchung angeborener und erworbener Risikofaktoren für Thrombosen in einer Patientenkohorte mit Thrombosen in atypischer Lokalisation
Dalia Khaddam (Bonn / DE), Hannah L. McRae (Bonn / DE), Nadine Schwarz (Bonn / DE), Johannes Oldenburg (Bonn / DE), Bernd Pötzsch (Bonn / DE), Sara Reda (Bonn / DE; Köln / DE), Heiko Rühl (Bonn / DE)
Thrombosis in atypical sites include splanchnic vein thrombosis (SVT), cerebral venous sinus thrombosis (CVST), and deep venous thrombosis (DVT) of the upper extremity. Their underlying mechanisms share similarities with typical venous thromboembolism (VTE), i.e. DVT of the lower extremity and/or pulmonary embolism, in addition to specific pathogenic factors. Compared with VTE in typical sites, their pathomechanisms are less understood.
Records of unselected patients with a history of VTE in typical sites (n=2,011), SVT (n=83), CVST (n=82), and DVT of the upper extremity (n=117), who were referred to the University Hospital Bonn for ambulatory thrombophilia testing, were retrospectively analyzed. In addition to demographic features, we comparatively assessed hereditary as well as site-specific and non-site-specific acquired thrombosis risk factors.
Compared with VTE in typical sites, SVT was more frequently associated with systemic inflammation, infection, or malignancy (2.2% vs. 12.2%; OR 6.2, 95% CI 3.0-12.6) and the JAK2 V617F mutation was present in 16.9%. In CVST compared with typical VTE, demographics and higher rates of oral contraception (43.2% vs. 57.6%; OR 1.9, 95% CI 1.1-3.2), and pregnancy (4.2% vs. 10.9%; OR 2.8, 95% CI 1.2-6.5) suggest a significant hormonal influence on its pathomechanism. DVT of the upper extremity was characterized by a particularly high rate (50.4%) of site-specific acquired risk factors. The prevalence of the F2 20210G>A mutation was higher in SVT and CVST (15.7% respectively 15.9%; OR 2.5, 95% CI 1.3-4.6 for both cohorts) than in VTE in typical sites (7.0%). The prevalence of the factor V Leiden mutation and of inhibitor deficiencies did not differ between cohorts.
The cohorts with thrombosis in atypical sites showed distinctive patterns of acquired risk factors. Further studies are warranted to provide additional mechanistic insight into the contribution of F2 20210G>A to the development of SVT and CVST, and the role of hormonal influence in CVST.
Nothing to disclose.