Background Adipokines are citkokines mainly secreted by adipose tissue and involved in a wide spectrum of processes including metabolism, insulin sensitivity, atherogenesis and immunity. Leptin is the first adipokine discovered and plays important immunological functions. Crescent scientific data confirm the leptin involvement in many human autoimmune diseases. We described leptin hyperexpression in sera of female SLE patients, especially in fertile age, in relation with metabolic parameters and disease activity

Objectives To evaluate the basal leptin levels in SLE patients who develop disease flares and damage accrual in 3 years follow-up.

Methods We performed a retrospective evaluation of basal serum leptin levels, metabolic parameters and SLE disease features in 20 female SLE patients. For all subjects, complete data concerning disease activity and damage were available over a period of almost 3 years after the baseline assessment. Metabolic parameters included basal insulin, glycaemia, HOMA-IR, plasma lipid profile, BMI, waist-hip ratio. SLE disease features were expressed as anti-dsDNA positivity, complement fraction C3 and/or C4 depletion, disease activity measured by SELENA SLEDAI and disease damage evaluated by SDI. SLE disease flares were assessed by revised SFI index. Number of disease flares was evaluated during the fist year of follow-up and at the end of a 3 years follow-up. SDI was measured at baseline and at the end of year 3.

Results We found hyperexpression of basal leptin levels in SLE patients who developed almost 1 flare at year 1 compared to patients without flares (p 0.002). Basal leptin in subject with almost 1 flare at the end of the 3 years of follow-up was higher in comparison with patients who didn't develop disease flares (p 0.0003). Basal leptin was increased in patients who presented almost 1 new point of SDI at the end of the 3 years follow-up versus patients without SDI increase (p 0.0003). The survival curve of the time without a lupus flare in subjects with leptin above 50 percentile significantly differed compared to subjects with leptin levels below 50 percentile (p 0.003). Patients with almost 1 flare at year 1 and year 3 and subject with almost 1 new SDI point at year 3 presented increased basal HOMA-IR, BMI and basal SELENA-SLEDAI. At baseline, leptin levels positively correlated with HOMA-IR (r 0.8, p<0.0001), BMI (r 0.8, p<0.0001) and SELENA SLEDAI (r 0.8, p<0.0001).

Conclusions We found basal leptin hyperexpression in SLE patients who developed disease flares and damage accrual in a 3 years follow-up period. These patients presented increased insulin-resistance and disease activity at baseline and leptin was tightly related to both these aspects. Further studies are required to evaluate the possible role of leptin as predictor of SLE prognosis

1. Margiotta DPE, Vadacca M, Navarini L, Basta F, Afeltra A. The complex role of leptin in SLE: is leptin a key link between metabolic syndrome, accelerated atherosclerosis and autoimmunity. Lupus: Open Access 2016; accepted.

2. Vadacca M, Margiotta DP, Navarini L, Afeltra A. Leptin in immuno-rheumatological diseases. Cell Mol Immunol 2011; 8:203–212.

3. Vadacca M, Margiotta D, Rigon A, Cacciapaglia F, Coppolino G, et al. Adipokines and systemic lupus erythematosus: relationship with metabolic syndrome and cardiovascular disease risk factors. J Rheumatol 2009; 36:295–297.

Disclosure of Interest None declared