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العنوان
Anticarbamylated protein antibody (Anti-Carp) and its relation to disease activity and radiological progression in patients with rheumatoid arthritis /
المؤلف
Ali, Randa Mahmoud.
هيئة الاعداد
باحث / راندا محمود علي
مشرف / محمد علي اسماعيل
مشرف / سحر عبد الرحمن السيد
مناقش / محمد اسماعيل عبد الكريم
مناقش / عصام محمد ابوالفضل
الموضوع
Rheumatoid arthritis. Antibodies. Proteins.
تاريخ النشر
2019.
عدد الصفحات
105 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الروماتيزم
تاريخ الإجازة
10/7/2019
مكان الإجازة
جامعة سوهاج - كلية الطب - الطب الطبيعي والروماتيزم والتأهيل
الفهرس
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Abstract

Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease affecting synovial joints. RA can be classified using the 2010 American College of Rheumatology/European League Against Rheumatism classification criteria (2010 ACR/EULAR criteria) for RA. The sensitivity of ACPA (~67 %) for RA is comparable to immunoglobulin (Ig)M-RF (~69 %) while their specificity (~95 %) is higher than that of IgM-RF (~85 %). Recently anti-carbamylated protein (anti-CarP) antibodies has been identified in both anti-cyclic citrullinated peptide 2 (anti-CCP2) antibody-positive and -negative RA patients. Anti-CarP antibodies target proteins that are modified through a post-translational modification named carbamylation.
Carbamylation is a post-translational modification resulting from the conversion of lysines into homocitrullines that requires the presence of cyanate. Cyanate is present in the body in equilibrium with urea. There are several conditions in which the concentration of cyanate (and therefore carbamylation) is increased, such as renal failure, chronic inflammation and heavy smoking. Carbamylation of proteins can lead to the loss of tolerance with formation of antibodies directed against carbamylated proteins (anti-CarP antibodies) in susceptible individuals.
The aim of our study was to evaluate anti-Carp antibody in serum of rheumatoid arthritis patients and its relation to radiological progression and disease activity.
Seventy rheumatoid arthritis patients and thirty-four controls were included in this study. The calculated cut off value of anti-carp antibody was 1.78ng/ml. 35.7% of RA patients had high titer of anti-carP antibodies above the cut off value. On the other hand, only 5.88% of controls had high titer of anti-carP antibodies above the cut off value. There was a significant difference (p < 0.01) in the mean value of anti-carP antibodies between patients and controls.
The patients were divided into two groups according to reactivity to anti-carP antibodies; patients who have anti-carP titer above the cut off value have been considered as positive and those who have titer less than the cut off value have been considered as negative. We found that there was a high significant (p < 0.001), (p < 0.05), (p < 0.05) (p < 0.001) difference between the mean of anti-carP, DAS28, Larsen (0) and Larsen (1) between the positive and negative groups respectively. On the other hand, we found that there was no significant difference in both RF and ESR. We tested the correlation between the parameters in the positive and negative groups. In the positive group, we found a high significant (p < 0.01) correlation between anti-carP titer and DAS28 and a significant (p < 0.05) correlation between anti-carP and both of Larsen (0) and Larsen (1), in addition we found that there was a significant and high significant (p < 0.01), (p < 0.001) correlation between duration and both of Larsen (0) and Larsen (1) respectively but we not demonstrated that there was correlation between anti-carP and both of RF and ACPA. On the other hand, we could not find any correlation with the studied parameters in the negative group.
In our study, we found that in the positive group there was a strong significant association between anti-carP antibody titer and joint erosions at both baseline and after one year, (r=0.460, 95% CI, 0.07921 to 0.7237, P<0.05) and (r=0.408, 95% CI, 0.01543 to 0.6918, P<0.05) respectively. On the other hand, we found that there was no significant correlation between anti-carP antibody titer and joint erosions in the anti-carP negative patients.
Conclusion
Anti-CarP antibodies were found to be significantly elevated in RA patients and significantly associated with the DAS28 which provides further evidence that anti-CarP antibodies could be a potential biomarker for severity of RA in patients. However, additional studies are required using a larger, multi-institutional cohort or meta-analysis to definitively measure differences between anti-CarP levels in RA patients and those in the healthy controls.
Our data denoted that serum anti-CarP antibody correlated with radiological erosions and severity which suggests that it may play a role in the pathogenesis of RA making it a valuable marker for disease progression. Therefore, anti-CarP antibodies might represent a promising marker to predict joint damage and disease activity in RA patients.