A comparison of cardiovascular risk indices in patients with polycystic ovary syndrome with and without coexisting nonalcoholic fatty liver disease

Background Women with polycystic ovary syndrome (PCOS) have an adverse cardiovascular risk profile and an increased prevalence of nonalcoholic fatty liver disease (NAFLD), which is also associated with an adverse cardiovascular risk profile. Objective To compare the cardiovascular risk profile of women with PCOS alone and women with PCOS and NAFLD. Design, Setting and Participants Twenty-five oligoanovulatory women with PCOS were screened for NAFLD (including liver biopsy if appropriate) and had their cardiovascular risk factors measured which included the inflammatory marker C-reactive protein (CRP), endothelial function {measured using endoPAT 2000 and serum markers [intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin and P-selectin]}, clot structure and function [maximum absorbance (MA) and lysis potential (LT)]. Results Twelve patients had confirmed PCOS without evidence of NAFLD, and 13 patients had confirmed PCOS with evidence of NAFLD. The PCOS and NAFLD group were heavier (BMI 43 center dot 9 +/- 2 center dot 2kg/m(2)) compared with the PCOS alone group (BMI 37 center dot 6 +/- 1 center dot 4kg/m(2) P=0 center dot 03). There was no difference in CRP (7 center dot 57 +/- 0 center dot 95 vs 6 center dot 59 +/- 1 center dot 87mm P=0 center dot 62) or endothelial function (RH-PAT 1 center dot 96 +/- 0 center dot 1 vs 1 center dot 74 +/- 0 center dot 16 P=0 center dot 25), ICAM-1 (221 +/- 48 vs 250 +/- 60ng/ml P=0 center dot 19), VCAM-1 (2124 +/- 78 vs 2314 +/- 91ng/ml P=0 center dot 13), E-selectin (33 center dot 9 +/- 3 center dot 3 vs 39 center dot 5 +/- 15 center dot 5ng/ml P=0 center dot 31) and P-selectin (101 center dot 0 +/- 6 center dot 6 vs 95 center dot 9 +/- 10 center dot 2ng/ml P=0 center dot 69). There was no difference in clot formation or lysis. Conclusion The patients with PCOS and NAFLD were heavier compared with patients with PCOS alone. Despite this, we were unable to demonstrate differences in inflammatory markers, endothelial function or clot structure and function, suggesting that severity of steatosis is not the most important determinant of cardiovascular risk in PCOS.