OP0197 EVALUATION OF THE RELATIONSHIP OF LEPTIN WITH THE METABOLIC PHENOTYPE OF KNEE OSTEOARTHRITIS IN THE CONTEXT OF OBESITY THERAPY
Authors: E. Strebkova, L. Alekseeva
Journal: Annals of the Rheumatic Diseases (2021)

Background: Obesity and components of the metabolic syndrome (MS) play a key role in the pathogenesis of the metabolic phenotype of osteoarthritis (OA). Obesity is a process meta inflammation due to the synthesis of proinflammatory mediators (adipokines and adipocytokines). The severity of OA depends on the presence of obesity, adipokine activity, comorbidity, and the presence of MS. The problem of treatment of metabolic OA and obesity is very relevant, in connection with the obesity pandemic. Objectives: To evaluate the relationship of leptin with the clinical manifestations of OA and various components of MS in the context of obesity therapy. Methods: The study included 50 female patients aged 45-65 y.o. with Kellgren-Lawrence stage II-III knee OA and obesity (body mass index (BMI)&gt;30kg/m 2 ). The average age of the patients was 56.5 ± 5.86 years, the average duration of the disease was 7.43 ± 3.93 years. 62% of patients were diagnosed MS. Patients were randomly divided into 2 groups for the treatment of obesity. Patients from group 1 (n=25) took orlistat 120mg 3 times a day in combination with a hypocaloric diet and exercise for 6 months. Patients from group 2 (n=25) were on a hypocaloric diet in combination with exercise for 6 months. The groups were comparable in clinical parameters. The clinical course of OA was determined by the WOMAC and VAS. Anthropometric data (height, weight) were determined. All patients underwent a laboratory examination at 2 points (initially and after 6 months): a biochemical blood test, leptin was determined by PCR in peripheral blood. Results: 8% of patients had 1 MS component, 34% - 2 MS components, 34% - 3 MS components, 22% - 4 MS components, and 2% - 5 MS components at the beginning of the study. High leptin levels (p=0.001) were determined in patients with more than 3 MS components. The correlation analysis showed direct correlations of high leptin levels with the severity of knee WOMAC pain (r=0.36, p=0.02) and VAS pain (r=0.51, p=0.01). A positive correlation was determined between high leptin levels and body weight (r=0.56, p&lt;0.01) and waist circumference (r=0.38, p&lt;0.01). Patients from group 1 had a significant decrease of body weight by 10.07% (p&lt;0.05), the indicators of the WOMAC index improved: pain decreased by 52.5% (p&lt;0.05), stiffness by 47.98% (p&lt;0.05), joint functional failure by 51.55% (p&lt;0.05) after 6 months of drug therapy for obesity. Patients of group 2 had a not significant decrease of body weight by 0.84% (p&gt;0.05), and they were worse indicators of clinical manifestations of OA according to WOMAC compared to group 1 (p&lt;0.05). 24% of patients from group 1 showed a decrease in the number of MS components. 12% of patients from group 2 had a decrease in the number of MS components and 12% patients increase in MS components. Patients from 1 group with a significant decrease in body weight, there was a decrease in the level of leptin (p = 0.05) (graphic 1), in contrast to patients without weight loss on the background of non-drug therapy (p = 0.64). We found direct correlations between a decrease in leptin levels and a decrease in the WOMAC index (pain, stiffness, joint functional failure, total WOMAC) (r=0.5, p=0.01; r=0.4, p=0.04; r=0.4, p=0.03; r=0.5, p=0.01, respectively). Patients with a decrease in the number of MS components had a significantly lower leptin levels (p=0.01). Graphic 1. Dynamic of leptin. Conclusion: Leptin is a predictor of a worse course of the metabolic phenotype of OA associated with MS and obesity. High levels of leptin were observed with more MS components, and were associated with the severity of knee pain and body weight. We observed a decrease in the level of leptin, a decrease in the number of MS components, and an improvement in the clinical manifestations of OA against the background of a significant decrease in body weight. Thus, the treatment of obesity in patients with the metabolic phenotype of OA and other interventions aimed at reducing the level of leptin may contribute to reducing the progression of knee OA. Disclosure of Interests: None declared