Endocrine Abstracts

Introduction: Non-alcoholic fatty liver disease (NAFLD) has become the leading cause of chronic liver disorders in Western countries, encompassing a spectrum of diseases ranging from simple steatosis to liver fibrosis and cirrhosis. Polycystic Ovary Syndrome (PCOS), the most common endocrine disorder of women during the reproductive period, is often implicated with NAFLD.

Aim: To investigate the potential involvement of PCOS on the aggravation of NAFLD by investigating the associations among insulin resistance (IR) or hyperandrogenism with the degree of liver fibrosis as expressed by liver stiffness (LS) and specific markers (hepatokines).

Methods: Forty-nine women with PCOS (based on the National Institutes of Health criteria) and 32 age- and BMI- matched healthy controls were included. IR was defined by the AUC-GLU, AUC-INS, HOMA-IR, QUICKI and FIRST-SECOND PHIS calculated from oral glucose tolerance tests. Hepatokines (fetuin-A, adiponectin, FGF-21) were measured. LS was assessed by Transient Elastography.

Results: For all participants, median age was 27 (range: 20-35) years, median BMI was 25 (19-35.2) kg/m² and median waist circumference (WC) was 94 (60-125) cm. All patients with PCOS had statistically significant greater LS values compared to controls (6.1±0.9 vs 5.5±0.9 kPa; P=0.05). According to BMI, patients and controls were subdivided in normal-weight controls (n=14; 17.3%), overweight controls (n=18; 22.2%), normal-weight PCOS (n=26; 32.1%) and overweight PCOS (n=23; 28.4%). Regarding LS, normal-weight PCOS, overweight controls and overweight PCOS, all had statistically significant greater LS values compared to normal-weight controls (5.5±0.9, 6±0.5, 6.2±0.8 vs 4.7±0.7 kPa, respectively; P< 0.05 for each comparison), whereas LS values were significantly greater in overweight PCOS compared to normal-weight PCOS (6.2±0.8 vs 5.5±0.9 kPa; P< 0.05). Statistically significant correlation was found between LS values and Δ4α (r=0.242, P=0.03), but not with testosterone concentrations. Regarding LS and IR markers, statistically significant correlations were found in overweight PCOS between LS and AUC GLUC (r=0.517 P=0.07); in normal-weight controls between LS and adiponectin (r=-0.537, P=0.05), and in overweight controls between LS and HOMA IR, QUICKI, FIRST PHIS, SECOND PHIS, AUC INS, and adiponectin, respectively (r=0.743 P=0.001, r=0.727 P=0.001, r=0.504 P=0.03, r=0.510 P=0.03, r=0.475 P=0.05, r=-0.646 P=0.04, respectively).

Conclusions: PCOS and obesity are related to development of LS. The role of IR seems pivotal in the development of LS, whereas that of hyperandrogenism seems moderate. Interestingly, it appears that the co-existence of PCOS and obesity potentially promote more intensely the progression of LS.