Study the role of serum cartilage oligomericmatrix protein [comp] in the diagnosis of rheumatoid arthritis patients

Background: rheumatoid arthritis [RA] is a systemic autoimmune disease of unknown etiology. Cartilage oligomeric matrix protein [COMP] is one of markers used for early predicting joint destruction and disease activity in RA disease

Objective: in the present study we evaluated the role of COMP as diagnostic marker in RA patients in comparison with other traditional markers and its correlation with disease activity parameters

Patients and Methods: blood samples were collected from 50 patients newly diagnosed with rheumatoid arthritis [Group I] and also from 30 healthy subjectsas a control group [Group II].Serum level of COMP was measured by enzyme-linked immunosorbent assay [ELISA]

Results: there was a high significant difference between the RA patients group and the control group regardingserum COMP level.Also, there was a significant correlation between serum COMP level with clinical and laboratory data of active RA patients

Conclusions: serum COMP could be useful for early diagnosis of rheumatoid arthritis and also could be used as a marker of disease activity and joint destruction

Biochemical and genetic risk factors for atherosclerosis in systemic lupus erythematosus

Systemic lupus erythematosus [SLE] is associated with an increase in the risk of premature cardiovascular complications caused by accelerated atherosclerosis which significantly contributes to morbidity and mortality. Carotid ultrasonography is a very sensitive imaging tool to detect premature atherosclerosis and measurements of carotid intima-media thickness [IMT] assess the extent and the severity of systemic atherosclerosis. The pathogenesis of accelerated atherosclerosis in SLE is not clear; inflammation and endothelial dysfunction in addition to genetic risk factors represent important factors in the onset of atherosclerosis. To evaluate the relation between asymmetric dimethylarginine [ADMA], high sensitive C-reactive protein [hs-CRP], monocyte chemoattractant protein-1 [MCP-1] [both serum levels and the genotypes of the MCP-1 A-2518G polymorphism] with the development of carotid atherosclerosis in patients with SLE and their relation to disease activity. In the present study, 30 non-menopause SLE female patients and 20 healthy age-matched females were included. Both patients and controls were subjected to evaluation of body mass index [BMI], IMT, serum glucose, serum lipids, hs-CRP, ADMA, MCP-1 [both serum level and gene polymorphism]. Serum ADMA, hs-CRP, and MCP-1, levels were measured by enzyme-linked immunosorbent assay. MCP-1 genomic variants were detected by polymerase chain reaction followed by restriction enzyme-fragment analysis. Values for IMT, hs-CRP, ADMA and MCP-1 were significantly higher in patients with SLE than in healthy controls with more significant increase in SLE patients with IMT >/=1 mm than in those with IMT <1 mm. Carotid IMT was significantly positively correlated with all the studied variables except for age, BMI and FBS, but significantly negatively correlated with HDL-C in all SLE patients. G/G genotype of MCP-1 A-2518G gene was more frequent in SLE patients than controls. IMT, hs-CRP, ADMA and MCP-1 from patients with G/G phenotypes were markedly higher than those from patients with the A/A genotype. In multiple regression analysis, ADMA and MCP-1 were the strongest independent determinants of IMT in SLE patients. Assessment of high levels of ADMA, hs-CRP, MCP-1, in addition to the MCP-1 A-2518G polymorphism may play a role in the pathogenesis of accelerated atherosclerosis in SLE patients and would be useful in identifying the risk of developing cardiovascular disease. Development of a novel therapy targeting ADMA and MCP-1 may have a potential role in preventing the progression of increased IMT in SLE patients

Study of some biochemical and genetic risk factors for a therosclerosis in systemic lupus erythematososus patients

The aim of this study was to evaluate the relation between asymmetric dimethylarginine [ADMA], high sensitive C-reactive protein [hs-CRP], monocyte chemoattractant protein-1 [MCP-1] [both serum levels and the genotypes of the MCP-1 A-2518G polymorphism] with the development of carotid atherosclerosis in systemic lupus erythematosus patients [SLE]. Thirty non menopause SLE female patients and twenty healthy age-matched females were included. Both cases and controls were subjected to evaluation of body mass index [BMI], intimal-medial thickness [IMT], fasting blood sugar [FBS], serum lipids. Serum ADMA, hs-CRP, and MCP-1, levels were measured by ELISA. MCP-1 polymorphism was detected by PCR-RFLP. Our results showed that values foi IMT, hs-CRP, ADMA and MCP-1, were significantly higher in SLE patients than in healthy control with more significant increase in SLE patients with IMT >/= 1 mm than those with IMT <1 mm. Carotid IMT was significantly positively correlated with all the studied variables except for age, BMI and FBS, but significantly negatively correlated with HDL-C in all SLE patients. Genotype of MCP-1 [A-25 1 8G] showed that; GIG genotype was more frequent in SLE patients than controls. IMT, hs-CRP, ADMA and MCP-l from patients with G/G phenotypes were markedly higher than patients with the A/A or A/G genotype. In multiple regression analysis, ADMA and MCP-1 were the strongest independent determinants of IMT in SLE patients. In conclusion assessment of high levels of ADMA, hs-CRP, MPC-1, in addition to the MCP-l G allele may play a role in the pathogenesis of accelerated atherosclerosis in SLE patients and would be useful in identifying the risk of developing atherosclerosis

Mannose binding lectin: serum level, gene polymorphism in SLE patients and its relation to lupus nephritis

Systemic lupus erythematosus [SLE] is an autoimmune disease in which the complement system plays a crucial role in its pathogenesis. Mannan-binding lectin [MBL] is a recognition molecule of the lectin pathway of complement activation. The presence of several polymorphisms at the promoter and coding regions of the MBL-2 gene determines alterations at MBL serum concentration. MBL variant alleles that lead to low serum levels and/or functional deficits of MBL are postulated to contribute to the susceptibility of SLE. Moreover, the influence of MBL variation on antibodies production and renal involvement in SLE patients remains controversial. MBL serum level and genotypes were studied in SLE patients with evaluation of its role in auto antibodies production and lupus nephritis development. MBL genotypes and serum level were screened in a case control study included 30 SLE patients as well as 30 healthy controls. MBL polymorphism at exon 1 codons 54 and 57 was detected by PCR using sequence-specific priming [SSP] and serum MBL level was determined by ELISA technique. There was predominance of AA genotype [80%] in control group. Genotype frequencies of MBL variants in patients with SLE showed significant differences when compared with controls [AA 53.3% vs 80%, P=0.03, OR = 0.29 and A O+O O 46.6% vs 20%, P = 0.03, OR =3.5, respectively]. Serum MBL in SLE patients [900 ng/ml] was significantly lower than that of the control group [2750 ng/ml, P = 0.001] with positive correlation with low MBL genotypes. SLE patients with mutant alleles were more likely to produce anti dsDNA [92.8% vs 75%, OR = 4.3] and anti-Smith antibodies [35.7% vs 18.7%, OR = 2.3]. Patients carrying MBL-low genotypes have an increased risk of development of lupus nephritis than those carrying MBL-high genotypes [64.7% vs 35.2%, P - 0.02, OR= 2.4]. MBL gene polymorphism associated with low MBL serum levels that were found with significantly increased frequency in SLE patients may be one of the genetic factors that determine the susceptibility to develop lupus nephritis