Research Institute of Internal and Preventive Medicine, Branch of the Institute of Cytology and Genetics, Siberian Branch, Russian Academy of Sciences

Abstract

The purpose of the study was to evaluate the clinical manifestations of osteoarthritis (OA) in combination with MS (OAMS) and their relationship with concentration of several circulating proinflammatory cytokines, the level of lipids in peripheral blood serum. Forty women patients with knee OA were examined: 19 patients from the experimental group in whom OA was combined with metabolic syndrome (MS), 21 patients with OA without MetS. All patients were elderly and overweight. In the first subgroup of patients, the absolute majority of people were obese, while in the second subgroup, overweight patients predominated. Patients in the experimental subgroup showed a statistically significant increase in waist circumference compared to patients without MS. The duration of OA did not differ in both subgroups. It has been established that the metabolic phenotype of gonarthrosis – OA in combination with metabolic syndrome – differs from patients with OA without MS in greater severity of pain, a decrease in the level of daily activity, an increase in the burden of the disease and other symptoms of OA. These core characteristics are associated with poor quality of life and clinically significant symptoms of depression. The metabolic type of gonarthrosis is characterized by more pronounced laboratory signs of systemic low-grade inflammation in comparison with patients without MS, as evidenced by a threefold increase in CRP content and an increase in the level of IL-6, IL-18 in PC serum. In addition, in patients with the metabolic phenotype of OA, a fivefold increase in the level of a specific humoral immune response to type 2 collagen (Col2Ab) and dyslipidemia – an increase in the content of LDL cholesterol and triglycerides, with a comparable reduced level of HDL cholesterol – were revealed. It is concluded that the phenotype of OA in combination with MS is probably due to the pathogenetic similarity of OA and MS (syntropy), which is based on low-grade inflammation. Studying the pathogenesis of the OAMS phenotype and developing new principles for the treatment of multimorbidity should be based on patient-oriented approaches.