Polycystic ovary syndrome: focus on platelets and prothrombotic risk.

OBJECTIVES

Subjects with polycystic ovary syndrome (PCOS) were shown to carry an increased long-term cardiovascular risk. Systemic inflammation and reactive leukocytosis have also been described in PCOS. Recent research suggests the presence of an increased thrombotic risk in these patients.

METHODS

We describe a cohort of PCOS patients presenting with persistent thrombocytosis. Our cohort included women aged 20-37 who also had moderate leukocytosis and neutrophilia. They showed normal mean platelet volume and platelet aggregation. We excluded any myeloproliferative conditions in all patients.

RESULTS

The mean platelet count and standard deviation (SD) at presentation were 587 ± 61 × 10/L (normal 140-440 × 10/L). Median C-reactive protein (CRP) was 1.66 (range 1.2-2.2, normal <1 mg/dL). The platelet counts did not correlate with the CRP levels in our patients (Pearson correlation coefficient 0.171 and 0.170, respectively, P = 0.08).

CONCLUSION

While the inflammatory state of PCOS could play a role in triggering an increased platelet count, the persistent thrombocytosis in our patients did not correlate with the CRP levels. Therefore, from an etiological perspective, thrombocytosis appears to be at least partially independent from the classical pathways of systemic inflammation. The preexisting procoagulant state in PCOS due to coagulation cascade stimulation, platelet activation, and endothelial dysfunction may be further fueled by the presence of persistent thrombocytosis. We propose a unique model for cardiovascular risk assessment in women with PCOS to include not only the classic cardiovascular risk factors, but also the parameters related to the proinflammatory and procoagulant tendencies manifested in PCOS.