Tirado-Sánchez A, Bonifaz A, Ponce-Olivera RM

Language: Spanish
References: 21
Page: 582-587
PDF size: 181.62 Kb.

ABSTRACT

Introduction: Dermatomyositis is an autoimmune disease and the most common idiopathic inflammatory myopathy. During patient follow-up, determining biochemical parameters is required in order to assess for disease activity and treatment efficacy. Objective: To determine the relationship between the degree of activation of the complement system through the soluble membrane attack complex (c5b-9), dermatomyositis clinical activity and its variations with conventional treatment. Method: Forty-five patients with active and inactive dermatomyositis were studied. Chemical parameters and clinical severity were established and correlated with ELISA-determined C5b-9 serum levels. Results: There was positive correlation between dermatomyositis cutaneous and muscular activity and C5b-9 serum levels, which was lower than with traditional biochemical markers. In the case of treatment response, C5b-9 showed significant reduction, similar to clinical severity; with biochemical parameters, the reduction was not significant at one month of treatment with systemic steroids. Conclusions: Serum levels of C5b-9 levels of C5b-9 are higher in patients with dermatomyositis than in healthy subjects; dermatomyositis active and inactive cases were determined by means of their measurement. They can be a reliable parameter of therapeutic response, more accurate than muscle enzymes measurement, particularly creatine phosphokinase.

REFERENCES

1. Findlay AR, Goyal NA, Mozaffar T. An overview of polymyositis and dermatomyositis. Muscle Nerve 2015;51:638-656.

2. Luo YB, Mastaglia FL. Dermatomyositis, polymyositis and immune-mediatednecrotising myopathies. Biochim Biophys Acta. 2015;1852 622-632.

3. Iaccarino L, Ghirardello A, Bettio S, Zen M, Gatto M, Punzi L, et al. The clinical features, diagnosis and classification of dermatomyositis. J Autoimmun. 2014;48-49:122-127.

4. Lahoria R, Selcen D, Engel AG. Microvascular alterations and the role of complement in dermatomyositis. Brain. 2016;139(Pt 7):1891-1903.

5. Kissel JT, Halterman RK, Rammohan KW, Mendell JR. The relationship of complement-mediated microvasculopathy to the histologic features and clinical duration of disease in dermatomyositis. Arch Neurol. 1991;48:26-30.

6. Serna M, Giles JL, Morgan BP, Bubeck D. Structural basis of complementmembrane attack complex formation. Nat Commun. 2016;7:10587.

7. Dudkina NV, Spicer BA, Reboul CF, Conroy PJ, Lukoyanova N, Elmlund H, et al. Structure of the poly-C9 component of the complement membrane attack complex. Nat Commun. 2016;7:10588.

8. Bayly-Jones C, Bubeck D, Dunstone MA. The mystery behind membrane insertion: a review of the complement membrane attack complex. Philos Trans R Soc Lond B Biol Sci. 2017;372:20160221.

9. Braczynski AK, Harter PN, Zeiner PS, Drott U, Tews DS, Preusse C, et al. C5b-9 deposits on endomysial capillaries in non-dermatomyositis cases. Neuromuscul Disord. 2016;26:283-291.

10. Sakuta R, Murakami N, Jin Y, Nagai T, Nonaka I, Nishino I. Diagnostic significance of membrane attack complex and vitronectin in childhood dermatomyositis. J Child Neurol. 2005;20:597-602.

11. Campo A, Hausmann G, Martí RM, Estrach T, Grau JM, Porcel JM, et al. Complement activation products (C3a and C5b-9) as markers of activity ofdermatomyositis. Comparison with usual biochemical parameters. Actas Dermosifiliogr. 2007;98:403-414.

12. Bohan A, Peter JB. Polymyositis and dermatomyositis (second of two parts). N Engl J Med. 1975;292:403-407.

13. Bohan A, Peter JB. Polymyositis and dermatomyositis (first of two parts). N Engl J Med 1975;292(7):344-7.

14. Isenberg DA, Allen E, Farewell V, Ehrenstein MR, Hanna MG, Lundberg IE, et al. International consensus outcome measures for patients with idiopathic inflammatory myopathies. Development and initial validation of myositis activity and damage indices in patients with adult onset disease. Rheumatology (Oxford). 2004;43:49-54.

15. Morgan BP. The membrane attack complex as an inflammatory trigger. Immunobiology. 2016;221:747-751.

16. Ballanti E, Perricone C, Greco E, Ballanti M, Di-Muzio G, Chimenti MS, et al. Complement and autoimmunity. Immunol Res. 2013;56:477-491.

17. Triantafilou K, Hughes TR, Triantafilou M, Morgan BP. The complement membrane attack complex triggers intracellular Ca2+ fluxes leading to NLRP3 inflammasome activation. J Cell Sci. 2013;126(Pt 13):2903-2913.

18. Zhao T, Gao J, Van J, To E, Wang A, Cao S, et al. Age-related increases in amyloid beta and membrane attack complex: evidence of inflammasome activation in the rodent eye. J Neuroinflammation. 2015;12:121.

19. Yin X, Han GC, Jiang XW, Shi Q, Pu CQ. Increased expression of the NOD-like receptor family, pyrin domain containing 3 inflammasome in dermatomyositis and polymyositis is a potential contributor to their pathogenesis. Chin Med J (Engl). 2016;129:1047-1052.

20. Kissel JT, Mendell JR, Rammohan KW. Microvascular deposition of complement membrane attack complex in dermatomyositis. N Engl J Med. 1986;314:329-334.

21. Máscaro JM, Hausmann G, Herrero C, Grau JM, Cid MC, Palou J, et al. Membrane attack complex deposits in cutaneous lesions of dermatomyositis. Arch Dermatol. 1995;131:1386-1392.