Anti-CCP antibody levels are not associated with MS: results from a case-control study.

Mahmut Alpayci,Veysel Delen,Yasemin Bayram,Huseyin Guducuoglu,Aysel Milanlioglu,Mehmet Nuri Aydin

doi:10.1155/2015/817427

Mahmut Alpayci, Veysel Delen + Show 4 more

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https://doi.org/10.1155/2015/817427

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Abstract

Citrullinated proteins have been suggested to play a critical role in the pathogenesis of multiple sclerosis (MS). Anticyclic citrullinated peptide (anti-CCP) antibody is used in the early diagnosis of rheumatoid arthritis (RA). The objective of this study was to investigate the presence of anti-CCP antibody in patients with MS compared to RA patients and healthy controls. Fifty patients with MS (38 females, 12 males; mean age 36.72 ± 8.82 years), 52 patients with RA (40 females, 12 males; mean age 40.87 ± 10.17 years), and 50 healthy controls (32 females, 18 males; mean age 38.22 ± 11.59 years) were included in this study. The levels of serum anti-CCP antibody were measured using an enzyme-linked immunosorbent assay (ELISA). The results of the study showed that anti-CCP antibody levels were significantly higher in RA patients versus MS or healthy controls (P < 0.001). Moreover, anti-CCP antibody was positive in 43 (83%) patients with RA, while it was negative in all MS patients as well as in all healthy controls. Also, no significant correlation was found between the anti-CCP levels and EDSS scores (r = −0.250). In conclusion, the results of this study did not support a positive association between serum anti-CCP antibody and MS.

Highlights

Multiple sclerosis (MS) is a chronic inflammatory autoimmune demyelinating disorder of the central nervous system (CNS) [1]
Multiple sclerosis was diagnosed according to the McDonald 2005 revised criteria [10], and rheumatoid arthritis (RA) was diagnosed according to the American College of Rheumatology (ACR) 1987 revised criteria [11]
Anti-CCP antibody was positive in 43 (83%) patients with RA, while it was negative in all MS patients as well as in all healthy controls

Summary

Introduction

Multiple sclerosis (MS) is a chronic inflammatory autoimmune demyelinating disorder of the central nervous system (CNS) [1]. It is believed that these attacks result from acute focal inflammation of the CNS and cause disease progression, but specific factors initiating this inflammation are still unknown [1, 2]. Myelin basic protein (MBP) is the only essential structural protein for the formation of myelin and is considered as the crucial molecule for myelination [5]. Glial fibrillary acidic protein (GFAP) is another main protein molecule that plays a key role in astrocytic functional processes [6]. It has been suggested that citrullinated CNS proteins, including GFAP and MBP, may trigger autoimmune mechanisms, contributing to MS pathogenesis [5,6,7]. Citrullination is a posttranslational modification resulting in the conversion of arginine to citrulline and catalyzed by peptidyl arginine deiminase (PAD) enzyme [6, 7]

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