Joint Damage in ANCA-Associated Systemic Vasculitis Message I. Microscopic Polyangiitis
Articular syndrome is one of the main signs of the microscopic polyangiitis (MPA), which in some regions of the Earth accounts for over 90 % of all systemic vasculitis (SV), associated with antineutrophil cytoplasmic antibodies (ANCA). It was found that 5 years after the manifestation of MPA, a progressive reduction of the para-articular (epiphyseal) bone mineral density and destruction of the joints begin to form. Many questions related to the nature of the course of joint pathology in specific ANCA-SV require further study. Objective: to evaluate joint damage in patients with MPA and the relationship with extra-articular pathology. Material and methods. We study involved 89 patients with MPA aged 18–78 years old, among which there were 44 % men and 56 % women. The duration of the disease from the first signs of manifestation was 7 years. Acute or subacute course of MPA has been registered in 27 % of cases, and in the rest — chronic one; I degree of the activity of pathological process has been detected in 10 % of cases, II —in 32 %, III — is 58 %. Results. The joint involvement is observed in 60 % of patients with MPA, in 40 % of cases it occurs in the form of oligoarthritis, depends on the presence of pathology in skeletal muscles, pneumopathy or peripheral neuropathy. Clinical, radiological and sonographic signs of articular pathology in MPA are closely associated with patients’ age, disease duration, lesions of the heart, kidneys and skin. In the pathogenetic structures of arthropathy in patients with MPA, C-reactive protein (CRP) and circulating immune complexes (CIC) are involved, and the nature of ANCA (antibodies to myeloperoxidase and proteinase-3) is of small value, while the high blood levels of rheumatoid factor (RF) have certain prognosis-negative significance in terms of the severity of joint pathology. Conclusion. Unfavorable prognostic criteria for the development of joint pathology in patients with MPA are indicators in the blood: CRP > 20 mg/l and CIC > 130 с.u., and the RF values > 60 IU/ml are considered the risk factors for severe arthropathy.
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Eleftheriou D. Eosinophilic granulomatosis with polyangiitis in childhood: retrospective experience from a tertiary referral centre in the UK / D. Eleftheriou, H. Gale, C. Pilkington [et al.] // Rheumatology. — 2016. — Vol. 29, № 3. — E. 029.
Gibelin A. Epidemiology and etiology of Wegener granulomatosis, microscopic polyangiitis, Churg-Strauss syndrome and Goodpasture syndrome: vasculitides with frequent lung involvement / A. Gibelin, C. Maldini, A. Mahr // Semin. Respir. Crit. Care Med. — 2011. — Vol. 32, № 3. — P. 264-273.
Itabashi M. Long-term damage assessment in patients with microscopic polyangiitis and renal-limited vasculitis using the vasculitis damage index / M. Itabashi, T. Takei, T. Moriyama [et al.] // Mod. Rheumatol. — 2014. — Vol. 24, № 1. — P. 112-119.
Li J. Clinical analysis of 43 patients with eosinophilic granulomatosis with polyangiitis / J. Li, L. M. Zhang, W. Zhao [et al.] // Zhonghua Yi Xue Za Zhi. — 2016. — Vol. 96, № 10. — P. 787-791.
Mohammad A. J. Incidence and survival rates in Wegener’s granulomatosis, microscopic polyangiitis, Churg-Strauss syndrome and polyarteritis nodosa / A.J. Mohammad, L.T. Jacobsson, K.W. Westman, G. Sturfelt // Rheumatology. — 2012. — Vol. 48, № 12. — P. 1560-1565.
Oiwa H. Janeway lesions in eosinophilic granulomatosis with polyangiitis / H. Oiwa, K. Nishioka // Intern. Med. — 2016. — Vol. 55, № 5. — P. 549-550.
Pamuk Ö.N. The epidemiology of antineutrophil cytoplasmic antibody-associated vasculitis in northwestern Turkey / Ö.N. Pamuk, S. Dönmez, G.B. Calayir, G.E. Pamuk // Clin. Rheumatol. — 2016. — Vol. 18, № 3. — P. 143-149.
Puéchal X. Therapeutic immunomodulation in eosinophilic granulomatosis with polyangiitis (Churg-Strauss) / X. Puéchal // Joint Bone Spine. — 2016. — Vol. 83, № 1. — P. 7-10.
Shuai Z.W. Clinical analysis of patients with myeloperoxidase antineutrophil cytoplasmic antibody-associated vasculitis / Z.W. Shuai, Y.F. Li, M.M. Zhang, Z.Y. Hu // Genet. Mol. Res. — 2015. — Vol. 14, № 2. — P. 5296-5303.
Tsuchiya N. Genetics of ANCA-associated vasculitis in Japan: a role for HLA-DRB1*09:01 haplotype / N. Tsuchiya // Clin. Exp. Nephrol. — 2012. — Vol. 23, № 11. — P. 132-136.
Wada T. Pathophysiology and laboratory findings in patients with ANCA-associated vasculitis / T. Wada // Rinsho Byori. — 2015. — Vol. 63, № 10. — P. 1213-1219.
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