Espessamento da camada média-íntima da carótida em pacientes com espondiloartrite

Autores

  • Thelma Larocca Skare Hospital Universitário Evangélico de Curitiba
  • Guilherme Cortez Verceze Hospital Universitário Evangélico de Curitiba
  • André Augusto de Oliveira Hospital Universitário Evangélico de Curitiba
  • Sonia Perreto Hospital Universitário Evangélico de Curitiba

Palavras-chave:

Espondiloartropatias, Doenças das artérias carótidas, Inflamação, Aterosclerose, Espondilite anquilosante

Resumo

CONTEXTO E OBJETIVO: A aterogênese acelerada tem se tornado um grande problema nas doenças reumáticas inflamatórias. O objetivo foi analisar a espessura da camada íntima-média (ECIM) da carótida em pacientes com espondiloartrite (ES) e relacioná-la com parâmetros clínicos e marcadores inflamatórios. TIPO DE ESTUDO E LOCAL: Estudo transversal analítico no Ambulatório de Reumatologia do Hospital Universitário Evangélico de Curitiba. MÉTODOS: A ECIM (medida por Doppler) de 36 pacientes com ES foi comparada com controles. A ECIM de pacientes com ES foi associada com marcadores inflamatórios, como velocidade de hemossedimentação (VHS), proteína C-reativa (PCR), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), e com parâmetros clínicos, como envolvimento axial e periférico, dactilite, HLA B27, ocorrência de uveíte, Bath Ankylosing Spondylitis Functional Index (BASFI) e perfil lipídico. RESULTADOS: A ECIM média em pacientes com ES foi de 0,72 ± 0,21 mm, enquanto nos controles foi de 0,57 ± 0,13 mm (P = 0,0007). Não se encontrou associação com VHS, PCR, BASDAI e dados clínicos. Em análise univariada, maior ECIM foi encontrado nos indivíduos com maior duração de doença (P = 0,014; R Pearson = 0,40; 95% intervalo de confiança, IC = 0,06 to 0,65), aumento nos triglicerídeos (P = 0,02; R Spearman = 0,37; 95% IC = 0,03 to 0,64) e maior idade (P = 0,0014; R Pearson 0,51; 95% IC = 0,21 to 0,72). CONCLUSÃO: Pacientes com ES têm maior grau de aterosclerose subclínica do que controles, dando suporte às evidências clínicas de aumento de risco cardiovascular em pacientes com doenças reumáticas.

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Biografia do Autor

Thelma Larocca Skare, Hospital Universitário Evangélico de Curitiba

MD, PhD. Head of Rheumatology Unit, Hospital Universitário Evangélico de Curitiba, Paraná, Brazil.

Guilherme Cortez Verceze, Hospital Universitário Evangélico de Curitiba

Student, School of Medicine, Faculdade Evangélica do Paraná (Fepar), Curitiba, Paraná, Brazil.

André Augusto de Oliveira, Hospital Universitário Evangélico de Curitiba

Student, School of Medicine, Faculdade Evangélica do Paraná (Fepar), Curitiba, Paraná, Brazil.

Sonia Perreto, Hospital Universitário Evangélico de Curitiba

MD. Cardiologist, Echocardiography Service, Hospital Universitário Evangélico de Curitiba, Curitiba, Paraná, Brazil.

Referências

Goodson NJ, Symmons DP, Scott DG, et al. Baseline levels of C-reactive protein and prediction of death from cardiovascular disease in patients with inflammatory polyarthritis: a ten-year followup study of primary care-based inception cohort. Arthritis Rheum. 2005;52(8):2293-9.

Huang AL, Vita JA. Effects of systemic inflammation on endothelium- dependent vasodilation. Trends Cardiovasc Med. 2006;16(1):15-20.

Salmon JE, Roman MJ. Subclinical atherosclerosis in rheumatoid arthritis and systemic lupus erythematosus. Am J Med. 2008;121(10 Suppl 1):S3-8.

Gonzalez-Gay MA, Gonzalez-Juanatey C, Piñeiro A, et al. High- grade C-reactive protein elevation correlates with accelerated atherogenesis in patients with rheumatoid arthritis. J Rheumatol. 2005;32(7):1219-23.

Heeneman S, Daemen MJ. Cardiovascular risks in spondyloarthritides. Curr Opin Rheumatol. 2007;19(4):358-62.

Gonzalez-Juanatey C, Vasquez-Rodriguez TR, Miranda-Filloy JA, et al. The high prevalence of subclinical atherosclerosis in patients with ankylosing spondylitis without clinically evident cardiovascular disease. Medicine (Baltimore). 2009;88(6):358-65.

van der Horst-Bruinsma IE, Lems WF, Dijkmans BA. A systematic comparison of rheumatoid arthritis and ankylosing spondylitis. Clin Exp Rheumatol. 2009;27(4 Suppl 55):S43-9.

Toussirot E, Wendling D. Late-onset ankylosing spondylitis and related spondylarthropathies: clinical and radiological characteristics and pharmacological treatment options. Drugs Aging. 2005;22(6):451-69.

Toussirot E. Late-onset ankylosing spondylitis and spondylarthritis: an update on clinical manifestations, differential diagnosis and pharmacological therapies. Drugs Aging. 2010;27(7):523-31.

Lehtinen K. Mortality and causes of death in 398 patients admitted to hospital with ankylosing spondylitis. Ann Rheum Dis. 1993;52(3): 174-6.

Choe JY, Lee MY, Rheem I, et al. No differences of carotid intima-media thickness between young patients with ankylosing spondylitis and healthy controls. Joint Bone Spine. 2008;75(5):548-53.

Dougados M, van der Linden S, Juhlin R, et al. The European

Spondylarthropathy Study Group preliminary criteria for the classification of spondylarthropathy. Arthritis Rheum. 1991;34(10):1218-27.

Gonzalez-Gay MA, Gonzalez-Juanatey C, Lopez-Diaz MJ, et al. HLA-DRB1 and persistent chronic inflammation contribute to cardiovascular events and cardiovascular mortality in patients with rheumatoid arthritis. Arthritis Rheum. 2007;57(1):125-32.

Garrett S, Jenkinson T, Kennedy LG, et al. A new approach to defining disease status in ankylosing spondylitis: the Bath Ankylosing Spondylitis Disease Activity Index. J Rheumatol. 1994;21(12):2286-91.

Calin A, Garrett S, Whitelock H, et al. A new approach to defining functional ability in ankylosing spondylitis: the development of the Bath Ankylosing Spondylitis Functional Index. J Rheumatol. 1994;21(12):2281-5.

Torres TM, Ciconelli RM. Instrumentos de avaliação em espondilite anquilosante [Outcome measures in ankylosing spondylitis]. Rev Bras Rheumatol. 2006;46(Suppl 1):52-9.

van der Linden S, Valkenburg HA, Cats A. Evaluation of diagnostic criteria for ankylosing spondylitis. A proposal for modification of the New York criteria. Arthritis Rheum. 1984;27(4):361-8.

Moll JM, Wright V. Psoriatic arthritis. Semin Arthritis Rheum. 1973;3(1):55-78.

Kingsley G, Sieper J. Third International Workshop on Reactive Arthritis. 23-26 September 1995, Berlin, Germany. Report and abstracts. Ann Rheum Dis. 1996;55(8):564-84.

Cruzat V, Cuchacovich R, Espinoza LR. Undifferentiated spondyloarthritis: recent clinical and therapeutic advances. Curr Rheumatol Rep. 2010;12(5):311-7.

De La Mata J, Maese J, Martinez JA, Rosario P, Loza E. Current evidence of the management of undifferentiated spondyloarthritis: a systematic literature review. Semin Arthritis Rheum. 2011;40(5):421-9, 429.e1-3.

Sieper J, Rudwaleit M, Baraliakos X, et al. The Assessment of SpondyloArthritis international Society (ASAS) handbook: a guide to assess spondyloarthritis. Ann Rheum Dis. 2009;68 Suppl 2:ii1-44.

Bots ML, Grobbee DE, Hofman A, Witteman JC. Common carotid intima-media thickness and risk of acute myocardial infarction: the role of lumen diameter. Stroke. 2005;36(4):762-7.

O’Leary DH, Polak JF, Kronmal RA, et al. Carotid-artery intima and media thickness as a risk factor for myocardial infarction and stroke in older adults. Cardiovascular Health Study Collaborative Research Group. N Engl J Med. 1999;340(1):14-22.

Simon A, Gariepy J, Chironi G, Megnien JL, Levenson J. Intima-media thickness: a new tool for diagnosis and treatment of cardiovascular risk. J Hypertens. 2002;20(2):159-69.

Lorenz MW, Markus HS, Bots ML, Rosvall M, Sitzer M. Prediction of clinical cardiovascular events with carotid intima-media thickness: a systematic review and meta-analysis. Circulation. 2007;115(4): 459-67.

Tyrrell PN, Beyene J, Feldman BM, et al. Rheumatic disease and carotid intima-media thickness: a systematic review and meta-analysis. Arterioscler Thromb Vasc Biol. 2010;30(5):1014-26.

Mathieu S, Joly H, Baron G, et al. Trend towards increased arterial stiffness or intima-media thickness in ankylosing spondylitis patients without clinically evident cardiovascular disease. Rheumatology (Oxford). 2008;47(8):1203-7.

Gonzalez-Juanatey C, Llorca J, Amigo-Diaz E, et al. High prevalence of subclinical atherosclerosis in psoriatic arthritis patients without clinically evident cardiovascular disease or classic atherosclerosis risk factors. Arthritis Rheum. 2007;57(6):1074-80.

Peters MJ, van Eijk IC, Smulders YM, et al. Signs of accelerated preclinical atherosclerosis in patients with ankylosing spondylitis. J Rheumatol. 2010;37(1):161-6.

Silva LC, Ortigosa LC, Benard G. Anti-TNF- agents in the treatment of immune-mediated inflammatory diseases: mechanisms of action and pitfalls. Immunotherapy. 2010;2(6):817-33.

Castro KR, Aikawa NE, Saad CG, et al. Infliximab induces increase in triglyceride levels in psoriatic arthritis patients. Clin Dev Immunol. 2011;2011:352686.

Spanakis E, Sidiropoulos P. Papadakis J, et al. Modest but sustained increase of serum high density lipoprotein cholesterol levels in patients with inflammatory arthritides treated with infliximab. J Rheumatol. 2006;33(12):2440-6.

Vis M, Nurmorhamed MT, Wolbink G, et al. Short term effects of infliximab on the lipid profile in patients with rheumatoid arthritis. J Rheumatol. 2005;32(2):252-5.

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Publicado

2013-03-03

Como Citar

1.
Skare TL, Verceze GC, Oliveira AA de, Perreto S. Espessamento da camada média-íntima da carótida em pacientes com espondiloartrite. Sao Paulo Med J [Internet]. 3º de março de 2013 [citado 15º de outubro de 2025];131(2):100-5. Disponível em: https://periodicosapm.emnuvens.com.br/spmj/article/view/1284

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