المستويات والانماط الجينية المتعددة لعامل نخر الورم ا الفا في مرضى التهاب المفاصل الرثوي في محافظة بابل == Tumor Necrosis Factor - Alpha ( - 308 G/A) Gene Polymorphisms and Levels in Rheumatoid Arthritis Patients in Babylon Province
Author name:
احمد خفيف خشان فرج
Supervisor name:
عبد السميع حسن الطائي | صباح جاسم الربيعي
General topic:
Medicine
Specific topic:
Clinical Biochemistry
Degree:
Master
University:
University of Babylon - Faculty Of Medicine
Language:
English
University location:
Babylon
First pages:
19T1713 - p.pdf
Abstract:
Rheumatoid arthritis is a systemic autoimmune disease affects 0.5 - 1% of the worldwide population, characterized by chronic inflammation of the synovial joints, hyperplasia and overgrowth of synoviocytes, with destruction of articular cartilage of unknown etiology that can cause serious weakness and inability to work. Tumor necrosis factor - α (TNF - α) proinflammatory cytokines, that plays an important role in the inflammatory and immune responses in several diseases, including RA are responsible for progress of RA.The present study aims to estimated the levels of TNF - α and anti - cyclic citrullinated peptide (ACCPA) in patients with RA and healthy controls in the case - control study.The present study also aims to investigate the possible association between TNF - α levels and ( - 308 G/A) TNF - α promoter polymorphism in patients with RA in Babylon Province.This study was designed as a case control. Forty - five (10 males and 35 females) patients with RA and forty - five ( 9 males and 36 females) apparently healthy persons as control with the compatible age and sex were enrolled in this study. Measurement the levels of TNF - α and (ACCP) antibodies were estimated by enzyme - linked immunoassay ELISA technique. Measurement of rheumatoid factor (RF) was assayed by use slide agglutination test for the qualitative and semi quantitative. Whereas, C - reactive protein (CRP) was determined using latex - enhanced nephelometry. Disease severity score of RA patients was determined by use DAS - 28. DNA was isolated from white blood cells (WBCs) and TNF - α ( - 308 G/A) gene promoter polymorphism was determined by polymerasechain reaction - restriction fragment length polymorphism (PCR - RFLP) technique.The present study was found a significantly high levels of serum TNF - α and ACCPA in patients with RA when compared to healthy controls. The RF of patients with RA in the present study was found to be positive in 69.3% and negative in 30.7 % in overall RA patients, whereas was negative in 97.2% and positive in 2.8% of healthy control. The CRP of patients with RA in the present study was found to be positive in 75% and negative in 25 % of overall patients with RA and was positive in 11% and negative in 89% of healthy control. Correlation between TNF - α levels with both of DAS - 28 and ACCPA in RA patients found to be a significant positive correlation. Correlation between DAS - 28 and ACCPA in RA patients was a significant positive correlation. The genotype of ( - 308 G/A) TNF - α gene promoter polymorphisms the GG genotype was 60% in RA patients and 42.2% in control group, while the GA genotype was 40% in RA patients and 53.3% in control group. The AA genotype was 0% in RA patients and 4.4% in control group. The relation between both of TNF - α levels and DAS - 28 with genotyping of ( - 308 G/A) TNF - α gene promoter polymorphism in RA patients were found to be a non - significant correlation.Based on the results of the present study, it can be concluded that Babylon RA patients may have different genetic or environmental factors contributing to the pathogenesis of RA. Further studies are necessary to search for other genetic polymorphisms and/or genes that contribute to the increased expression of TNF - α and hence the pathogenesis of RA in Babylon patients. The TNF - α ( - 308 G/A) promoter polymorphism may not be associated with the presence of RA in Babylon patients. An increase in the circulating TNF - α concentration, the capacity to produce TNF - α in the WBC, or the cytotoxic activity of TNF - α were found. Thus, other factors may be important in determining the circulating levels of TNF - α in RA. And this SNP cannot affect the serum level of TNF - α in RA patients. In addition, the different genotypes of TNF - α ( - 308 G/A) have no influence on disease activity of the disease.
