Extrinsic Venous Compression May Not Be a Sufficient Explanation for Venous Thromboembolism Due to Massive Fibroids.

The relationship between uterine leiomyomata (fibroids) and venous thromboembolism (VTE) is poorly characterised. Fibroids are smooth muscle cell tumours of the uterus; occuring in approximately 40% of women of reproductive age, they are twice as prevalent in women from African compared to Caucasian origin. It is assumed that massive leiomyomata (palpable beyond the level of the umbilicus) cause deep vein thrombosis as a consequence of a direct compressive effect on pelvic veins but this explanation may be insufficient. Other hypotheses for the thrombogenic nature of leiomyomata include the abnormal expression of type 1 basic FGF receptor, increased expression of thrombospondin 1 and nitrogen oxide synthase, abnormal oestrogen regulation and fibroid-induced polycythaemia. We describe the cases of seven women (mean age 41 yrs, range 29–46yrs) with VTE presumed secondary to massive fibroids. The majority of women (86%) were of African or Carribbean origin. Massive uterine leiomyomata were demonstrated in each patient by transvaginal ultrasound scanning. All cases had objectively confirmed (duplex ultrasound) symptomatic DVT, and two had CT-confirmed symptomatic pulmonary embolism (PE) at presentation. Direct venous compression by massive fibroids was demonstrated in only one case using magnetic resonance imaging (MRI)(case 1).

Interestingly the two cases with left sided proximal DVT (cases 2 and 5) revealed right-sided lateral and posterior uterine wall fibroids. Data on known acquired risk factors for VTE was recorded for each patient. Thrombophilia screening was performed in all cases at least four weeks following cessation of anticoagulation. Venous compression alone failed to explain six of the cases, where fibroids were not positionally related to the site of DVT. Of these, only one had significant additional risk factors for VTE (case 3). Whereas extrinsic compression of the pelvic veins may contribute to venous stasis and DVT formation in some cases, our findings suggest that it is unlikely that this is the only pathogenic mechanism. In conclusion, we suggest that the occurrence of VTE in women with massive fibroids is unlikely to be due solely to mechanical compression of the pelvic veins. It is possible that biological growth factors produced by the leiomyomata may trigger VTE formation and that oestrogen may have an independent growth promoting effect on both VTE and leiomyomata. Further research is required to characterise the prothrombotic state in these women.