Anti carbamylaed protein antibody is the role of systemic lupus and rheumatoid arthritis in diagnosis and its relation with prognosis

Objective: Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease characterized by numerous organ involvement. The normally deviated response of the natural immune system response is an important contributor to SLE pathogenesis. Natural immunity participates in SLE pathogenesis by stimulating both inflammatory cytokines and affecting adaptive immunity. Inflammatory cytokines and adaptive immune system cause tissue damage with the help of natural immunity. The natural immunization system contributes to the activation of autoreactive T and B cells, thus allowing a normally deviating immunoreaction in the adaptive immune system. Otoreactive B cells play an important role in the production of pathogenic autoantibodies, and these autoantibodies cause inflammation and damage to tissues and organs. In SLE, autoantibody development against nucleic acids and their binding proteins plays an important role in disease pathogenesis. Some of these autoantibodies are direct pathogenic. Pathogenic autoantibodies are a finding that reflect systemic impairment of immunological tolerance. Rheumatoid arthritis (RA) is the most common inflammatory rheumatic disease. It keeps joints frequently and, unlike other diseases that keep joints, it causes permanent joint damage (deformity, disability) in later periods. The disease can affect joints as well as organs such as the heart, lungs, eyes and skin. Although joint complaints such as pain and swelling in patients can be seen in few joints in the early period, in general, a large number of joints are kept. In seropositive rheumatoid arthritis together with rheumatoid factor and anti-ccp positivity is clinically diagnostic. The relationship between prognosis and course of antibody titer disorder has been shown in many studies. Recently a new autoantibody group; anti-carbamyl protein antibody; The carbamylation; isocyanic acid and post-translational modification processes resulting in non-enzymatic reaction protein production between specific functional groups. This reaction changes the structural and functional properties of the protein. Therefore, it contributes to molecular aging. Many studies have shown that carbamide proteins are present, especially in chronic diseases and atherosclerotic diseases. In particular, the anti-carbamyl protein antibody is an antibody that is developed against homotoclinic post-translational modification of lysine amino acid in the presence of cyanate. In the studies conducted, this antibody was detected in the sera of RA patients. Following detection of these antibodies, several predata showed that these antibodies may appear before and after ACPA development following the onset of symptoms. It has also been shown to predict the development of arthritis in patients with arthralgia. However, there is no clear indication of prognosis in relation to disease activation. At this level, the formation of carbamylation and / or anti- carbamyl antibodies is not known at this time what contributes to the disease processes of chronic inflammatory diseases such as kidney diseases, cardiovascular diseases and RA. Our purpose of this study is; the determination of the diagnostic value of anti- carbamyl antibody in patients with lupus and rheumatoid arthritis and the relationship with disease prognosis. Materials and Methods: Fifty-seven SLE patients (F / M 50/7; median age 40.913.7; median disease duration 2 years) were included in the study according to the 2012 SLICC SLE diagnostic criteria. 46 RA patients (F / M 38/8, median age 54.212.4 years, median duration of disease 2 years) selected according to 2010 ACR / EULAR diagnostic criteria were included. 30 healthy control groups were selected. The demographic and clinical laboratory findings of the patients were analyzed for age, sex, smoking, diagnosis, duration of diagnosis, treatment and follow up, disease acute phase response, hematological findings, organ involvement findings, disease activation scorings, side-effect complication profile, antibody level and follow-up) were recorded and recorded. Anti carP antibody Anti-carbamylated Protein Human anti-carbamylated Protein Antibody (ACP-Ab) ELISA Kit (SunRedBio, China) was used. Findings: The study population consisted of 133 subjects, 30 controls, 57 SLEs and 46 RAs. The mean age of SLE patients was found to be low compared to RA patients (40,9 ± 13,7 versus 54,2 ± 12,4; p <0,001). Gender distribution was similar in the patient groups(p=0,773). The proportion of active smokers was found to be higher in RA patients compared to SLE patients (19.6% versus 5.3%, p = 0.005). Mean age of diagnosis was found to be higher in RA patients than in SLE patients (50.0 ± 12.6 vs 37.7 ± 13.3; p <0.001). Median disease duration did not differ between RA and SLE patients (p = 0.759). The median CRP level in RA patients was higher than in SLE patients (8.8 versus 3.4; p <0.001). In patients with SLE, the SLEDAI value ranged from 1-9 and the median was 3. In RA patients, the DAS28 value was 2.9-6.6 and the median was 5. In patients with RA, anti CCP positivity was found to be higher (89.1% versus 8.1%, p <0.001) and anti-RF positive rate was higher in RA patient group (80.4% versus 17.8%, p < 0.001) Anti carP antibody was found to be 3.3% positive in the healthy control group. In contrast, anti carP antibody positivity was found as high as 17.4% in patients with RA. (p = <0.001), 54.4% were positive in the SLE patient group. (p = <0.001) Anti carP antibody predicted SLE patients with 54.4% sensitivity and 96.7% specificity compared to the healthy control group. (AUC: 0.755, p <0.001) Anti carP antibody predicted RA patients with 17.4% sensitivity and 96.7% specificity compared to the healthy control group (AUC: 0.570, p = 0.032). Anti carP antibody predicted SLE patients with 54.5% sensitivity and 82.6% specificity compared to healthy RA group (AUC: 0.685, p <0.001). AnticarP antibodies were found to be positive in all of the SLE patient groups with anti-CCP positivity. In addition, anti ds DNA median was higher than negative ones in patients who were positive for anticarP antibody but not statistically significant. Although the DAS28 median was higher in patients with RA than in the group negative to anticarP antibody, no statistical correlation was found (p = 0.467). There was no significant difference in organ involvement rates compared to the negative group in the anti-carp antibody positive group in SLE patients. However, the rate of CNS involvement (p = 0,395), hemolytic anemia rate (p = 0,368), thrombocytopenia rate (p = 0,233), renal involvement rate (p = 0,211) and GIS involvement rate p = 0,191). Anti-carP antibody positivity was assessed by ROC Curve analysis for the prediction of diagnostic performance of SLE patients compared to RA patients. Accordingly, Anti carP antibody positivity, ANA positivity and autoantibody positivity were found to have similar diagnostic performance. (AUC: 0.639) Conclusion: Antibody positivity was found to be 54.4% in SLE patient group. It is significantly higher in SLE compared to healthy control and RA patient group. In the SLE group, it is still a more significant diagnostic prognostic than the healthy control and RA group. Both SLE and RA patients have significant sensivity and specificity compared to the healthy control group. Key words: systemic lupus erythematosus, rheumatoid arthritis, anticarP antibody