Влияние мелатонина на фактор дислипидемии при метаболическом фенотипе остеоартроза

Abstract

Introduction Osteoarthritis (OA) has long been considered from the mechanical point of view of etiology and pathogenesis, as a "wear and tear" disease. However, advances in fundamental medicine have changed the way we look at this disease. The role of systemic inflammation was determined in OA progression and risk factor related clinical phenotypes were differentiated as post-traumatic OA, age associated OA, genetic OA and metabolic syndrome associated OA. The development and progression of OA in metabolic disorders envision a concept of systemic regulation of osteocartilaginous and synovial tissues, and several studies showed that dysregulation of circadian rhythms may be involved in the development of dyslipidemia and systemic inflammation associated with obesity. The objective was to explore the effect of melatonin on the dynamics of lipid metabolism and the severity of clinical symptoms in patients with OA and insomnia based on the role of dyslipidemia in the pathogenesis of degenerative diseases. Materials and Methods The study included 36 individuals including 12 healthy volunteers and 24 inpatients of experimental groups with insomnia and Kellgren-Lawrence grades 2 and 3 gonarthrosis. Standard conservative treatment consisted of drug and physical therapy. Medical history, complaints were collected from the patients and physical examination performed to evaluate edema of the joint, alignment of the lower limb, range of motion in the joints and measure waist circumference, body height, body weight; body mass index. The biochemistry blood parameters measured included total cholesterol concentration (TCC), high-density lipoprotein cholesterol, low density lipoprotein cholesterol (LDL) and triglycerides (TG). VAS and Lequesne scale were used to assess pain and function of the joints. Results Patients with the metabolic OA showed statistically significant (p < 0.05) increase in TCC (6.23 (4.28 to 6.44) mmol/L, p < 0.0002), LDL fractions (4.52 (3.08 to 4.92) mmol/L, p < 0.00004), atherogenic coefficient (CA) (4.33 (3.15–4.8) mmol/L, p < 0.00003) and a decrease in the HDL fraction (1.08 (0.93 to 1.4) mmol/L, p < 0.01) before treatment in comparison with healthy individuals. The TG level remained within the normal range (0.73 [0.62 to 0.78] mmol/L). At a month, a statistically significant (p < 0.006) decrease in TC (4.62 [3.71 to 5.29] mmol/L), a decrease in atherogenic fractions of LP (LDL) (2.65 [1.90 to 3.05] mmol / L) (p < 0.002), an increase in the HDL fraction (1.49 [1.17 to 1.72] mmol/L) (p < 0.004) and a decrease in CA (2.07 [1.81 to 2.34] mmol/L) (p < 0.002) were observed in the experimental group of patients who received melatonin at the dose of 3 mg per day as an adjunctive therapy to the basic treatment. There was no significant dynamics of lipid metabolism in patients receiving standard treatment. The Lequesne's functional index significantly (p < 0.03) decreased in melatonin patients after treatment from 12 [12 to 13] to 10 (8.75 to 10.25) points and showed no significant dynamics measuring 10.5 [10 to 11.75] and 10 [10 to 19.25] points in patients receiving standard treatment. Although positive dynamics in VAS scores was observed in both experimental groups a greater improvement (p < 0.005) was seen in the drug group with VAS score improved from 4.5 [3.75 to 5] to 2.5 [2 to 3.25] mm versus 4.5 [4 to 5] and 3.5 [3 to 4] mm in the no-drug group (p < 0.01). Conclusion Melatonin incorporated into the basic therapy was shown to exert a positive effect on pain assessment, condition of the knee joint evaluated with knee rating scales and subjective instruments, objective examination. The moderate antiatherogenic effect facilitates the therapeutic regimen to be considered in management of metabolic osteoarthritis.