Background Osteoarthritis (OA) is the most common joint disease. The most important factor not only in the development but also in the progression of OA is obesity. Higher incidence of OA in obese patients is associated with several factors. One of them is a large volume of fat mass, which increases the mechanical load on the joints. On the other hand, in obesity, hyperexpression of pro-inflammatory mediators (cytokines, adipokines) is observed, which negatively affect joint tissues, as well as provoke the development of low-level metabolic inflammation. Thus, the problem of OA and obesity is very relevant in modern rheumatology.

Objectives To determine features of clinical manifestations of OA in obesity and evaluate the effectiveness of obesity therapy in OA.

Methods The study included 73 patients (women) with knee OA (according to the ACR criteria) II-III X-ray stage by Kellgren-Lawrence: obese 50 (body mass index (BMI) > 30 kg/m2) and non-obese 23 (control group). Obese patients were divided into 2 groups: 1 group (n = 25) - received orlistat 120mg 3 times a day for 6 months in combination with non-medicamentous methods of controlling excess body weight and 2 group (n = 25), whose patients were recommended a diet and dosed exercise for 6 months. Monthly visits evaluated anthropometric measures, articular status, WOMAC. Initially and after 6 months, laboratory scores were evaluated in obese patients (determination of leptin, TNF-α, IL-6, CRP in peripheral blood).

Results In patients with OA and obesity, a more severe course of OA is determined compared to the control group (Table 1).

After 6 months of drug therapy of obesity in patients of group 1, a significant decrease in body weight by 10.07% (p < 0.05) was achieved. In patients of group 2, body weight decreased by 0.84% (p > 0.05). In patients of group 1, the indicators of the WOMAC index improved: pain decreased by 52.5% (p < 0.05), stiffness by 47.98% (p < 0.05), functional insufficiency by 51.55% (p < 0.05). In patients of group 2, there was also a decrease in the WOMAC index, however, these changes were worse than in patients with greater body weight loss. Analyzing laboratory data, in group 1 there was a significant decrease in the level of leptin (p = 0.05) and IL-6 (p < 0.05), in contrast to patients of group 2 (p = 0.64; p = 1.0, respectively). In the study of TNF-α, no significant changes in the two groups were determined. CRP level in 1 group of patients decreased by 23.74% (p > 0.05) compared to baseline data, in 2 group of CRP increased by 24.54% (p > 0.05). Correlation analysis revealed a direct relationship between a decrease in leptin level and a decrease in body weight (r = 0.5, p = 0.02) in patients with greater weight loss. Direct correlations of leptin reduction and WOMAC index decline (pain, stiffness, functional insufficiency, 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).

Conclusion The results of our study demonstrated a more severe clinical course of OA in obese patients. Drug therapy for obesity in patients with knee OA and obesity not only leads to a decrease in the presentation of clinical symptoms of OA, but also entails changes at the metabolic level: a decrease in leptin, IL-6 and CRP, which indicates a decrease in the intensity of metainflammation in obese patients. Thus, therapeutic interventions aimed at reducing body weight should be an integral part of knee OA therapy.

Disclosure of Interests None declared