Metabolic syndrome, plasma leptin and il - 1β concentrations in patients with primary knee osteoarthritis

IL-1β was a strong pro-inflammatory cytokine, important in the early stages of OA because it was not only increased cartilage catabolism (inhibiting type II collagen and aggrecan synthesis leads to substrate degeneration) but also inhibited cartilage anabolic. IL-1β stimulated IL-6 and IL-8 production; contributed to inflammation (localized in synovial or systemic inflammation). Chondrocytes were the main target cells of IL-1β, degenerative chondrocytes were higher sensitive to the effects of IL-1β 3 to 4-fold than normal chondrocytes. Only 1% of IL-1β receptors on active cartilage surface can convert

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fatty acids can cause insulin resistance. 1.3.4. Hypertension and osteoarthritis Hypertension caused endothelial dysfunction; reduction of neural dynamics, localized perfusion reduction in peripheral organizations including cartilage, reduction of oxygen and nutrient supply, reduction of metabolism in cartilage. In addition, local ischemia led to apoptosis of subcutaneous bone cells and subcortical bone abnormalities. 1.4. Recent researches 1.4.1. Metabolic syndrome and osteoarthritis researches According to the data of NHANES III, there were 7714 subjects, the prevalence of MS was 59% in OA group compared with 23% in the non-OA, one person with OA in middle age had a risk of MS increased 5.26-fold. 1.4.2. Leptin and osteoarthritis researches Leptin-deficient (ob/ob) and leptin receptor-deficient (db/db) female mice compared with wild-type mice were studied. Extreme obesity due to impaired leptin signaling induced alterations in subchondral bone morphology without increasing the incidence of knee OA. Systemic inflammatory cytokine levels remained largely unchanged in ob/ob and db/db mice. These findings suggest that body fat, in and of itself, may not be a risk factor for joint degeneration, because adiposity in the absence of leptin signaling is insufficient to induce systemic inflammation and knee OA in female mice (Griffin T.M.) 1.4.3. Leptin, metabolic syndrome and osteoarthritis researches Increased leptin levels in both women and men with MS. Leptin predicted that MS was independent of obesity. Leptin increased in MS, correlated with the number of components of MS and leptin was an important risk factor for KOA in women. Insulin resistance was associated with increased KOA in men, increased leptin levels was associated with increased KOA in women. 1.4.4. IL-1β and osteoarthritis researches Ning L. et al found IL-1β concentrations related to the severity of the disease so it was a marker for the severity of OA. Nguyen Ngoc Chau found that plasma IL-1β concentrations in OA patients was higher than the controls. CHAPTER 2: SUBJECTS AND METHODS 2.1. Subjects 582 primary KOA patients and 78 healthy control individuals were recruited during 2014 - 2019, at Bachmai hospital. 2.1.1. Study group Inclusion criteria: Diagnosed primary KOA based on the ACR 1991 and MS based on the IDF 2005 criteria. Exclusion criteria: secondary KOA, patients did not consent. 2.1.2. Controls 78 healthy individuals. 2.2. Research methods 2.2.1. Study design Prospective, descriptive cross-sectional study. 2.2.2. Sampling method Sample size for aim 1: p = 0.59 d = 0.04 µ = 0.05 n = 580.8 We selected 582 patients in the KOA group n = Z2(1-µ/2) × p × (1-p) d2 Sample size for aim 2: σ = 0.3 d = 0.05 µ = 0.05 n = 138.3 n = Z2(1-µ/2) × σ2 d2 We selected 164 patients in the KOA* and 78 healthy individuals in the controls. The KOA* was similar to KOA about age, BMI, gender rate and the prevalence of MS. 2.2.3. Quantification of leptin and IL-1β plasma Plasma leptin test by the Human leptin ELISA kit of Sigma; plasma IL-1β test by Human IL-1β ELISA kit of Melsin, using human monoclonal antibodies. 2.3. Data processing Using medical statistics softwere: SPSS 20.0 2.4. Research diagram Diagnosis of KOA WC, blood pressure, HDL-C, triglyceride, glucose, HbA1c, insulin CONTROLS healthy people (n = 78) KOA* (n = 164) KOA (n = 582) Leptin, IL-1β 2. 2. To determine the relationship of plasma leptin and IL-1β concentrations with some clinical and subclinical features in patients with primary KOA. To determine the prevalence of MS, its components and the relationship with the stages of primary KOA. RECOMMENDATIONS CHAPTER 3: RESULTS 3.1. Demographic, anthropometric, biochemical and clinical characteristics in knee osteoarthritis group Table 3.1. In 582 KOA patients, women were 86.6%; mean ages were 56.7 ± 8.2 years; mean BMI was 24.0 ± 3.0 kg/m2. Table 3.6. No statistical differences between the mean ages, BMI, WC, WHR, hypertension, HbA1c, CRP between men and women groups. 3.2. The prevalence of metabolic syndrome and the relationship with the stages of primary knee osteoarthritis Table 3.8. The prevalence of MS and its components by sex Variables Total (n = 582) n (%) Women (n = 504) n (%) Men (n = 78) n (%) p women - men OR (95% CI) MS 301 (51.7) 279 (55.4) 22 (28.2) < 0.001 3.2 (1.9 - 5.3) High WC 415 (71.3) 392 (77.8) 23 (29.5) < 0.001 8.4 (4.9 - 4.2) Low HDL-C 314 (54.0) 283 (56.2) 31 (39.7) < 0.05 1.9 (1.2 - 3.2) Hypertension 374 (64.3) 321 (63.7) 53 (67.9) > 0.05 0.83 (0.5 - 1.4) High fasting glucose 254 (43.6) 220 (43.7) 34 (43.6) > 0.05 1.0 (0.6 - 1.6) High triglycerides 329 (56.5) 279 (55.4) 50 (64.1) > 0.05 0.7 (0.4 -1.1) Obese 201 (34.5) 175 (34.7) 26 (33.3) > 0.05 1.1 (0.6 -1.8) The prevalence of MS among KOA was 51.7%, it was statistically higher in women than men, with odds ratio was 3.2. The prevalence of high WC, low HDL-C in women with KOA was significantly higher than in men. No statistical differences of the prevalence of hypertension, high fasting glucose, high triglycerides, obese between men and women. Chart 3.1. The prevalence of MS and its components by obese The prevalence of MS, high WC, hypertension, high triglyceride, low HDL-C in the obese was higher than in the non-obese, but prevalence of hyperglycemia in two groups were the same. Chart 3.4. The prevalence of metabolic syndrome increased when the knee osteoarthritis stages increased. Table 3.13. The prevalence of MS, high WC, hypertension, high fasting glucose, high triglycerides in the late stage was statistically higher than in the early stage. Variables Late (n = 148) Early (n = 434) p OR (95% CI) n (%) n (%) MS 95 (64.2) 206 (47.5) < 0.001 2.0 (1.4 - 2.9) High WC 123 (83.1) 292 (67.3) < 0.001 2.4 (1.5 - 3.9) Hypertension 111 (75.0) 263 (60.6) < 0.05 2.0 (1.3 - 3.0) Hyperglycemia 76 (51.4) 178 (41.0) < 0.05 1.5 (1.04 - 2.2) High TG 96 (64.9) 233 (53.7) < 0.05 1.6 (1.1 - 2.3) Low HDL-C 83 (56.1) 231 (53.2) > 0.05 1.1 (0.8 - 1.6) 3.3. Plasma leptin and IL-1β concentrations 3.3.1. Characteristics of research groups Table 3.15. The KOA* was similar to the KOA in mean age, BMI, gender ratio and the prevalence of MS. The KOA* was similar to the controls in gender ratio, but the difference in mean age, BMI and the prevalence of MS. 3.3.2. Plasma leptin and IL-1β concentrations in primary knee osteoarthritis compared with controls. Table 3.16.: Leptin, IL-1β, IL-1β/leptin in KOA* by sex Variables (n = 164) Total (n = 164) Men (n = 23) Women (n = 141) p Leptin (ng/mL) Median 9.5 4.0 10.6 < 0.001 Q1 - Q3 5.8 - 14.3 0.9 - 10.4 6.3 - 14.9 IL-1β (pg/mL) Median 10.0 9.7 10.0 > 0.05 Q1 - Q3 8.8 - 12.8 9.1 - 10.6 8.6 - 14.1 Tỉ số IL-1β/leptin Median 1.2 2.3 1.0 = 0.001 Q1 - Q3 0.7 - 2.2 1.1 - 9.9 0.6 - 2.0 KOA*: Leptin concentrations in women were higher than in men; IL-1β concentrations were not statistically different; IL-1β/leptin ratio in men was higher than in women. Table 3.17. Leptin, IL-1β, IL-1β/leptin in KOA* by obese Variables (n = 164) Obese (n = 59) Median (Q1 - Q3) Non obese (n = 105) Median (Q1 - Q3) p Leptin (ng/mL) 13.0 (10.4 - 15.8) 7.9 (4.5 - 11.5) < 0.001 IL-1β (pg/mL) 9.7 (8.8 - 12.1) 10.1 (8.6 - 13.4) > 0.05 IL-1β /leptin 0.8 (0.6 - 1.5) 1.4 (0.9 - 3.3) < 0.001 KOA*: Leptin concentrations in the obese were higher than in the non-obese; IL-1β were not statistically different. IL-1β/leptin ratio in the non-obese was higher than in the obese. Table 3.18. Leptin, IL-1β, IL-1β/leptin in KOA* by MS Variables (n = 164) OA with MS (n = 85) Median (Q1 - Q3) OA without MS (n = 79) Median (Q1 - Q3) p Leptin (ng/mL) 11.6 (8.7 - 15.7) 7.7 (3.9 - 11.4) < 0.001 IL-1β (pg/mL) 10.3 (8.9 - 13.5) 9.8 (8.6 - 12.0) > 0.05 IL-1β/leptin 1.0 (0.6 - 1.7) 1.4 (0.8 - 3.4) < 0.01 KOA*: Leptin concentrations in MS group were higher than the non-MS; IL-1β were not statistically different. IL-1β/leptin ratio in the KOA without MS was higher than the KOA with MS. Table 3.21. Leptin, IL-1β, IL-1β/leptin in controls Variables Tổng (n = 78) Men (n = 11) Women (n = 67) p Leptin (ng/mL) Median 0.5 0.1 0.5 < 0.001 Q1 - Q3 0.3 - 0.7 0.03 - 0.2 0.4 - 0.8 IL-1β (pg/mL) Median 6.9 6.6 6.9 > 0.05 Q1 - Q3 6.4 - 7.5 6.3 - 7.5 6.4 - 7.6 Tỉ số IL-1β /leptin Median 13.9 132.1 13.5 < 0.001 Q1 - Q3 9.6 - 24.9 27.2 - 227.5 9.4 - 19.2 Controls: Leptin concentrations in women was significantly higher than in men; IL-1β were not significantly different; IL-1β/leptin ratio in the men was higher than in the women. Table 3.22. Leptin, IL-1β, IL-1β/leptin in KOA* and controls Variables KOA* (n = 164) Median (Q1 - Q3) Controls (n = 78) Median (Q1 - Q3) p Leptin (ng/mL) 9.5 (5.8 - 14.3) 0.5 (0.3 - 0.7) < 0.001 IL-1β (pg/mL) 10.0 (8.8 - 12.8) 6.9 (6.4 - 7.5) < 0.001 IL-1β/leptin 1.2 (0.7 - 2.2) 13.9 (9.6 - 24.9) < 0.001 KOA*: Plasma concentrations of leptin and IL-1β were higher, IL-1β/leptin ratio was lower than in the healthy controls Table 3.23. Leptin, IL-1β, IL-1β/leptin in three groups Variables OA with MS (n = 85) OA without MS (n = 79) Controls (n = 78) p Leptin (ng/mL) Median (Q1 - Q3) 11.6 (8.7 - 15.7) 7.7 (3.9 - 11.4) 0.5 (0.3 - 0.7) < 0.001 IL-1β (pg/mL) Median (Q1 - Q3) 10.3 (8.9 - 13.5) 9.8 (8.6 - 12.0) 6.9 (6.4 - 7.5) < 0.001 IL-1β /leptin Median (Q1 - Q3) 1.0 (0.6 – 1.7) 1.4 (0.8 – 3.4) 13.9 (9.6 - 24.9) < 0.001 The concentrations of leptin and IL-1β tended to decrease in three groups: KOA with MS, KOA without MS and controls group (p < 0.001). In contrast, IL-1β/leptin ratio tended to increase. 3.3.3. Relationships between plasma leptin and IL-1β concentrations with some clinical and subclinical features in patients with primary knee osteoarthritis. Table 3.24. Correlation between leptin with metabolic syndrome components, obesity and some variables. Leptin and variables Women (n = 141) Men (n = 23) KOA* (n = 164) r p r p r p Components of metabolic syndrome SBP (mmHg) 0.134 > 0.05 0.030 > 0.05 0.036 > 0.05 DBP (mmHg) 0.091 > 0.05 0.004 > 0.05 -0.019 > 0.05 Glucose (mmol/L) 0.056 > 0.05 0.163 > 0.05 -0.013 > 0.05 Triglyceride (mmol/L) 0.080 > 0.05 0.047 > 0.05 0.014 > 0.05 HDL-C (mmol/L) 0.054 > 0.05 -0.217 > 0.05 0.087 > 0.05 WC (cm) 0.430 < 0.001 0.723 < 0.001 0.417 < 0.001 Weight (kg) 0.459 < 0.001 0.657 = 0.001 0.381 < 0.001 BMI (kg/m2) 0.514 < 0.001 0.548 < 0.01 0.489 < 0.001 Insulin (µU/mL) 0.420 < 0.001 0.668 < 0.001 0.403 < 0.001 HbA1c (%) 0.303 < 0.001 0.114 > 0.05 0.185 < 0.05 HOMA-IR 0.383 < 0.001 0.626 = 0.001 0.346 < 0.001 IL-1β (pg/mL) -0.046 > 0.05 -0.204 > 0.05 -0.046 > 0.05 CRP (mg/L) 0.113 > 0.05 -0.051 > 0.05 0.037 > 0.05 Age (năm) 0.113 > 0.05 -0.337 > 0.05 0.028 > 0.05 Leptin concentrations were positively correlated with markers of obesity and insulin resistance (WC, weight, BMI, insulin, HOMA-IR); were not correlated with MS components (except WC), IL-1β, CRP, age. Table 3.25. Multivariate regression equation between leptin with independent variables in women group Variables Beta coefficient standardized p Insulin (µU/mL) 0.760 < 0.001 BMI (kg/m2) 0.216 < 0.01 HOMA-IR -0.397 < 0.05 R2 = 0.298 và p ANOVA < 0.001 Leptin = 1.462*insulin + 0.638*BMI – 2.402*HOMA-IR -11.209 Women: insulin, BMI, HOMA-IR affected about 29.8% of the plasma leptin concentrations, in which insulin had the strongest effect. Table 3.26. Correlation between IL-1β, IL-1β/leptin with CRP and some other variables. Variables (n = 164) IL-1β Tỉ số IL-1β/leptin r p r p CRP (mg/L) -0.100 > 0.05 -0.009 > 0.05 VAS 0.086 > 0.05 0.204 < 0.01 Age (năm) 0.101 > 0.05 -0.012 > 0.05 Components of metabolic syndrome WC (cm) -0.086 > 0.05 -0.365 < 0.001 SBP (mmHg) -0.002 > 0.05 -0.057 > 0.05 DBP (mmHg) -0.064 > 0.05 -0.028 > 0.05 Glucose (mmol/L) -0.070 > 0.05 -0.047 > 0.05 Triglyceride (mmol/L) 0.153 = 0.05 0.066 > 0.05 HDL-C (mmol/L) -0.042 > 0.05 -0.118 > 0.05 BMI (kg/m2) -0.029 > 0.05 -0.390 < 0.001 HbA1c (%) -0.110 > 0.05 -0.218 < 0.01 Insulin (µU/mL) -0.180 < 0.05 -0.432 < 0.001 HOMA-IR -0.189 < 0.05 -0.388 < 0.001 IL-1β concentrations were not correlated with inflamatory marker (CRP), VAS, all components of MS, all markers of obesity and age; Weak negatively correlation with insulin, HOMA-IR. IL-1β/leptin ratio inversely correlatedwith WC, BMI, Insulin, HbA1c, HOMA-IR (r from -0,432 to -0,365; p < 0.01). Table 3.27. Variables (n = 164) Leptin (ng/mL) Median (Q1 - Q3) IL-1β (pg/mL) Median (Q1 - Q3) 4 stages of Xray 1 9 (4.2 - 13.1) 9.6 (8.6 - 14) 2 9.6 (5.8 - 14.8) 10.1 (8.7 - 13.6) 3 9.9 (5.7 - 14.3) 10.4 (9.1 - 12.5) 4 20.8 (9.4 - 40.5) 9.6 (9 - 11.4) p > 0.05 p > 0.05 Early and late Early 9.4 (5.7 - 14.0) 9.9 (8.7 – 13.8) Late 10.4 (6.0 - 14.6) 10.1 (9.1 - 12.2) p > 0.05 p > 0.05 Number of MS components 0 7.6 (1.2 - 11.1) 9.8 (8.3 - 10.4) 1 7.7 (1.7 - 12.4) 10 (8.5 - 17.9) 2 8.3 (4.2 - 11.4) 9.7 (8.4 - 11.8) 3 11.1 (6.0 - 15.0) 10.3 (8.4 - 14.3) 4 9.5 (6.1 - 15.7) 10.0 (9.1 - 12.4) 5 11.5 (7.5 - 16.2) 10.0 (9.0 - 15.3) p > 0.05 p > 0.05 Median of leptin or IL-1β concentrations were not statistically different in the groups of Xray, early and late, number of MS components. Table 3.28. Variables (n = 164) Leptin (ng/mL) Median (Q1 - Q3) IL-1β (pg/mL) Median (Q1 - Q3) BMI (kg/m2) < 23 6.2 (3.4 - 10.3) 10.2 (8.5 - 13.8) 23 - 24.9 9.4 (6.9 - 12.9) 10.1 (8.7 - 13) ≥ 25 13 (10.4 - 15.8) 9.7 (8.8 - 12.1) p < 0.001 p > 0.05 Number of KOA 1 knee 8.5 (4.0 - 11.9) 9.6 (8.2 - 12.2) 2 knees 10.5 (6.3 - 15.7) 10.3 (9 - 13.2) p < 0.05 p > 0.05 Duration Short 9.2 (5.4 - 13.3) 9.2 (8.7 - 14.0) Long 11.9 (8.7 - 15.6) 10 (8.9 - 11.0) p < 0.05 p > 0.05 Median of leptin concentrations increased gradually when BMI increased, number of KOA, the duration of KOA was long; median of IL-1β concentrations were not statistically different in these groups. Table 3.31. The cut-off point of plasma leptin to predict MS. Leptin (ng/mL) Cut-off point AUC 95% CI p Sensitivity Specificity Men n = 23 5.5 0.892 0.744 - 1.0 < 0.01 1.0 0.867 women n =141 8.7 0.643 0.55 - 0.736 < 0.01 0.779 0.516 The cut-off point of plasma leptin concentrations in men KOA was 5,5 ng/mL, in women KOA was 8.7 ng/mL to predict MS. CHAPTER 4: DISCUSSION 4.1. General characteristics of patients with knee osteoarthritis Anthropometric characteristics The mean age was 56.7 ± 8.2, from 37 to 81 years old. 86.6% were women. Many researchs found that OA was more common in women than men, especially after menopause, which may be related to estrogen deficiency or due to imbalance between bone formation and bone destruction related to leptin. Mean BMI was 24.0 ± 3.0 kg/m2, from 16.3 to 35.7 kg/m2; The proportion of overweight and obese accounted for 61.5%, similar to Bui Hai Binh's 60.7%. Mean BMI of men was similar to women group. Many researchs find the role of weight or BMI affecting the formation and development of OA, especially in the knee joint. Clinical and subclinical symptoms 582 KOA patients with 905 ostoarthritis of the knee joints, the right knee was 446 (49.3%), equivalent to the number of the left knee was 459 (50.7%). All patients had joint pain and short morning stiffness for less than 30 minutes or no stiffness. Symptoms of red, hot, swelling, muscular atrophy had below 20%. In addition, valgus was more common than varus deformity, the mean VAS and WOMAC scores were lower than the intervention studies. The mean plasma CRP concentrations was 2.9 ± 5.3 mg/L, similar to Sanchez-Ramirez D.C. was 2.9 ± 3.1 mg/L. The mean CRP in the MS group was higher than the non-MS. The rate of OA in the early stage (1 and 2) was 75.5%. 4.2. The prevalence of metabolic syndrome and the relationship with the stages of primary knee osteoarthritis Prevalence of metabolic syndrome in knee osteoarthritis MS was present in 51.7% KOA patients using the IDF criteria. This prevalence was similar to study of Shin D. in Korea (52.4%), ElSaid T.O. et al in Egypt (53.7%), Abourazzak F. et al in Morocco (48.5%); was higher than study of Xie D.X. et al in China (20.3%); was lower than study of Yerima A. et al in Nigeria (59.8%) and Puenpatom R.A. et al in the US (59%). In many researchs, the ratio of MS in OA was change from 20% to 60%, because the researches used different MS criteria, different OA criteria such as based on clinical and Xray or only based on Xray, different OA stages ... In women, the incidence of MS in KOA was 55.4%, it was higher than men (28.2%), an odds ratio of 3.2 and 95% CI of 1.9 - 5.3 (p < 0.001), similar to ElSaid T.O et al study (62.4% in women, higher than mens), differ from Niu J., et al the prevalence of MS in men OA was 26.7% higher than in women (22.9%) and Maddah S. et al, the prevalence of MS in mens (24.0%) was higher than women (18.3%). Firstly, due to the application of different criteria of MS, we used IDF to take WC as a compulsory standard, while other studies used NCEP to assess equally 5 criteria without mandatory criteria. Secondly, our women patients had a mean WC higher than the 80 cm, while the mean WC in the men group was lower than the 90 cm, threshold, the prevalence of MS in the women OA was much higher than men. The incidence of MS in KOA with obesity was 72.6%, higher than non-obesity KOA (40.7%) with an odds ratio of 3.9. IDF considers obesity to be the main cause of MS. Obesity contributes to hyperglycemia, hypertriglyceridemia, insulin resistance, low HDL-C, hypertension. The incidence of MS increases when the OA stage was getting worse (Chart 3.4), which means that when OA was getting worse, the patient had more comorbid conditions such as hypertension, impaired fasting glucose, dyslipidemia. The incidence of MS in severe KOA was significantly higher than mild with OR by 2.0 and 95% CI from 1.4 to 2.9 (p < 0.001) (Table 3.13), similaly to Vasilic-Brasnjevic S. et al. 4.2.2. Relationship between obesity and knee osteoarthritis Obesity was the biggest risk factor for KOA and was an important component of MS. The incidence of MS in obesity was higher than the non-obesity group (72.6% vs 40.7%). In this study, the obesity rate was 34.5%; BMI was 24.0 ± 3.0 kg/m2; increased WC rate was 71.3%; the prevalence of MS in women group was higher than men because of the rate of increased WC in the women was higher than the men group. The incidence of both sides KOA in the obese was significantly higher than the one side group with odds ratio of 1.5; Similar conclusions of Sellam J. obesity increased the risk of KOA, especially OA knees on both sides. We also found abdominal obesity associated with OA but not BMI; Suitable for Vasilic-Brasnjevic et al, abdominal obesity or BMI ≥ 30 kg/m2 strongly correlated with the Xray stage. Obesity increased the chronic mechanical pressure at load bearing joints. Adipocytokine production, adipocytokines such as leptin, adiponectin ... they combined with pro-inflammatory cytokines such as IL-1β, TNF-α ... derived from adipose tissue, causing inflammation of synovial membranes, cartilage degradation; leptin acted directly on connective tissue to promote formation and progression of OA. 4.2.3. Relationship between hypertension and knee osteoarthritis The concept of "hypertension" according to the IDF criteria for MS, very differed from the JNC 8. According to IDF, the hypertension rate of KOA was lower than Puenpatom R.A. et al (64.3% vs 77.7%). There were very few studies that explain the relationship between hypertension and OA. A hypothesis hypertension caused endothelial dysfunction; reduction of neural dynamics, localized perfusion reduction in peripheral organizations including cartilage, reduction of oxygen and nutrient supply, reduction of metabolism between cartilage and covered cartilage. In addition, ischemia leaded to apoptosis of subchondral cells and turnover abnormalities. 4.2.4. Relationship between plasma sugar and knee osteoarthritis Glucose: The concept of "hyperglycemia" according to the IDF criteria for MS was different from IDF criteria for diabetes. The rate of hyperglycemia of patients with KOA was higher than Puenpatom R.A. study (43.6% vs 30.7%). It may be due to differences in size and age, glycemia concentrations increased with age. • Insulin concentrations: The insulin concentrations of the MS group were higher than the non-MS. • HOMA-IR: mean HOMA-IR in the MS group was higher than the non-MS, the men was lower than the women group. According to the two meta-analyzes of Louati and Williams, type 2 diabetes was a risk factor for OA. Of all components of MS, diabetes alone was considered an independent risk factor for progression of KOA. There were two types of type 2 diabetes mechanism acting on joint tissue. Firstly, chronic hyperglycemia causes oxidative stress, increased pro-inflammatory cytokine production, accumulation of AGEs in joint tissue, and differentiation of potential stem cells. Secondly, insulin resistance in local synovial membrane of diabetic patients and low-stage systemic inflammation associated with insulin resistance. 4.2.5. Relationship between dyslipidemia and knee osteoarthritis Degenerative cartilage reduced regulating gene expression, absorption of cholesterol into cells causes accumulation of cholesterol in chondrocytes (Tsezou A. et al). Increasing free fatty acids can cause insulin resistance. Treatment of dyslipidemia with statins in OA patients for 2 years that reduce in progress of OA (Wang Y). • Triglyceride: The prevalence of triglyceride in KOA patients was 56.5%, there were no difference between men and women. The rate of hypertriglyceride in the obese was statistically higher than the non-obese group; in the group with MS was statistically higher than the non-MS, in the late was statistically higher than early stage. • Low HDL-C: The rate of low HDL-C in the MS group was statistically higher than without MS group. There was no difference in rate of low HDL-C between late and early groups. The rate of increased triglyceride (56.5%) was equivalent to the low HDL-C (54%), similar to Bui Hai Binh study (52.4%). Compared to Gweressus E.D. et al, our mean triglyceride was higher, the mean HDL-C was lower. This difference may be due to race, Vietnamese people tend to eat more starch, so they tend to have a higher rate of increased triglycerides and lower HDL-C. Plasma leptin and IL-1β concentrations Characteristics of disease groups, disease groups*, controls KOA group and KOA* group were similar to gender, age, BMI and rate of MS indicate that the KOA* group was representing the KOA group. KOA* group and controls were similar to rate of sex but differences in BMI and rate of MS 4.3.2. Plasma leptin 4.3.2.1. Leptin concentrations in patients with primary knee osteoarthritis KOA* group: leptin concentrations was between 0.07 - 75.8 ng/mL, median 9.5 ng/mL; interval quartile 5.8 - 14.3 ng/mL; mean 11.5 ± 10.0 ng/mL; it was similar to result of Zheng S. (10.65 ± 13.10 ng/mL); lower than most published results, probably due to differences in obesity criteria, mean BMI in these studies were higher in our study, which leptin correlated with BMI. Leptin concentrations in KOA* group had median value and inter-quartile range of 9.5 (5.8 - 14.3) ng/mL, significantly higher than the controls of 0.5 (0.3 - 0.7) ng/mL. Leptin concentrations were highest in the KOA group with MS, higher than the KOA group without MS, the lowest in the healthy controls (p < 0.001). This suggests that leptin had an intermediate role in the relationship between leptin and MS and OA. However, this was a cross-sectional study, so it was not possible to determine the causal relationship of leptin-induced OA or OA causing increased leptin-associated MS. 4.3.2.2. Factors affecting leptin concentrations in KOA patients • Leptin and sex: In women, leptin concentrations were higher than men in both KOA* and controls groups. In women, leptin was always higher than men, regardless of OA status. Due to the effects of sex hormones, leptin was two to three-fold higher in women than men, who had the same amount of fat. • The correlation be

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