الفهرس 
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Abstract
Aim of the work
The aim of this study was to investigate the role of leptin, leptin receptor gene polymorphism and some adipokines in Egyptian female patients with knee OA.
Subjects and methods
This study was carried out on 95 Egyptian females, which were divided into;
group I: including 32 healthy females (BMI = 18.5–25 kg/m2), representing control group. group II: included 30 non obese female patients (BMI = 18.5–25 kg/m2), with confirmed knee OA in at least one knee. group III: included 33 obese female patients (BMI ≥ 30) with confirmed knee OA.
The diagnosis of OA was based on the symptomatic criteria of the American College of Rheumatology and the presence of radiographic signs (Kellgren-Lawrence (K/L) grading ≥ 2) for OA in at least one knee
Inclusion criteria included; obese osteoarthritis patients, osteoarthritis patients with normal BMI and healthy subjects. While, the following subjects were excluded from this study are those with; arthropathy due to gout, pseudogout, rheumatoid arthritis, with histories of corticosteroid medication, other forms of arthritis, cancer, or other chronic inflammation diseases.
Methods:
All the studied groups were subjected to the following:
1) Through history taking including checklist
2) Routine laboratory investigations including:
Erythrocyte sedimentation rate (ESR), fasting and postprandial blood glucose levels. lipid profile including total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein-cholesterol (LDL-C) .
3) Specific laboratory investigations including:
Serum Insulin level , HOMA ir value, nitric oxide (NO) level, leptin level, resistin level, adiponectin level and detection of LEPR gene polymorphism by quantities real time polymer chain reaction(PCR).
Results:
Results of current study indicated that NO, leptin and resistin levels were significantly increased in both osteoarthritic patients groups as compared to control. in addition, there were significant increase in obese OA patients as compared to non obese OA patients, suggesting that OA and obesity are related to promote inflammatory cytokines. While, adiponectin was significantly decreased in osteoartheritc patients groups compared to control, suggesting its protective role.
HOMA IR levels were significantly increased in obese OA patients as compared to non-obese OA patients and controls, which indicate that insulin resistance is associated with obesity.
As regard LEPR genetic polymorphism, the frequency of GG genotype was found to be significantly higher in group III when compared to group II and controls (26% to 4%,1%) (P<0.001); while AA genotype was the most frequent in the control group (75%) (P<0.001). Rs1137101 was correlated with knee OA in the dominant genetic model (GG + GA versus AA) in group II(OR=8, CL (2.6-24.2), p<0.001).Indicating that LEPR genetic polymorphism Rs1137101 may be associated with KOA incidence in Egyptian female patients.
Conclusions:
Our findings suggested that thegenetic variation in Rs1137101 may be involved in the pathogenesis of both obesity and knee osteoarthritis in Egyptian female patients. In addition, it seems that adipokines and oxidative stress are important factors linking obesity, adiposity, and inflammation in osteoarthritis.