All Title Author
Keywords Abstract


Atherosclerosis in Juvenile Idiopathic Arthritis

DOI: 10.1155/2012/714732

Full-Text   Cite this paper   Add to My Lib

Abstract:

Atherosclerosis is a chronic inflammatory disease of the arteries. Clinical consequences of the atherosclerotic process occur in the adult population, however atherosclerotic process begins in childhood. The classic risk factors for atherosclerosis include obesity, dyslipidaemia, age, gender or family history. In recent years, attention has been drawn to the similarity between atherosclerotic inflammatory processes and inflammatory changes in the course of systemic connective tissue disease, in particular systemic lupus etythematosus (SLE) or rheumatoid arthritis (RA). There is also observed the similarity of the pathogenetic background of development of atherosclerosis and juvenile idiopathic arthritis (JIA). Elevated levels of pro-inflammatory cytokines are observed in the course of juvenile idiopathic arthritis. Also homocysteine concentrations, which may play a significant role in the development of atherosclerotic lesions, are observed higher in patients with JIA. Some studies revealed higher carotid intima-media thickness (IMT) index values in children with JIA. In view of the fact that atherosclerotic process begins as early as in childhood, the introduction of appropriate preventive measures in children is a matter of utmost importance. 1. Introduction Atherosclerosis is a chronic inflammatory disease of the arteries. Clinical consequences of the atherosclerotic process, in the form of ischaemic heart disease, disorders of cerebral circulation, or circulatory disorders of peripheral arteries occur in the adult population; however atherosclerotic changes have their beginning in childhood. The severity of atherosclerosis correlates with the number and intensity of risk factors such as body mass index (BMI), systolic and diastolic arterial blood pressure, total cholesterol, LDL, HDL, triglyceride concentrations, and passive and active cigarette smoking. At present, much significance is attached to the inflammatory aetiology of atherosclerosis, which makes it an inflammatory disease, a vascular wall response to injury. Proinflammatory cytokines, such as IL-1b, IL-6, IL-8, or TNF-α, play a significant role in the development and progression of atherosclerotic lesions. Elevation of the concentrations of acute phase proteins, such as CRP, is also a reflection of the inflammatory process. An elevated homocysteine concentration also increases the risk of developing cardiovascular diseases. Awareness of the fact that initiation of the atherosclerotic process takes place very early in life underscores the need for identifying these changes as early as

References

[1]  J. Cassidy and R. Petty, “Chronic arthritis in childhood,” in The Textbook of Pediatric Rheumatology, J. Cassidy, R. Petty, R. Laxer, and C. Lindsley, Eds., pp. 206–208, Sauders Elsevier, Philadelphia, Pa, USA, 5th edition, 2011.
[2]  A. Bor?sewicz and A. Skierczyńska, “Atherosclerosis: Disease of whole life and whole population of Eastern civilization countries,” Choroby serca i naczyń, tom. 3, nr. 1, pp. 1-6, 2006.
[3]  C. Napoli, F. P. D'Armiento, F. P. Mancini et al., “Fatty streak formation occurs in human fetal aortas and is greatly enhanced maternal, hypercholesterolemia. Intimal accumulation of low density lipoprotein and its oxidation precede monocyte recruitment into early atheroeclerotic lesions,” The Journal of Clinical Investigation, vol. 100, no. 11, pp. 2680–2690, 1997.
[4]  W. Palinski and C. Napoli, “The fetal origins of atherosclerosis: maternal hypercholesterolemia, and cholesterol-lowering or antioxidant treatment during pregnancy influence in utero programming and postnatal susceptibility to atherogenesis,” The FASEB Journal, vol. 16, no. 11, pp. 1348–1360, 2002.
[5]  C. Napoli, C. K. Glass, J. L. Witztum, R. Deutsch, F. P. D'Armiento, and W. Palinski, “Influence of maternal hypercholesterolaemia during pregnancy on progression of early atherosclerotic lesions in childhood: Fate of Early Lesions in Children (FELIC) Study,” The Lancet, vol. 354, no. 9186, pp. 1234–1241, 1999.
[6]  G. S. Berenson, S. R. Srinivasan, W. Bao, W. P. Newman III, R. E. Tracy, and W. A. Wattigney, “Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults,” The New England Journal of Medicine, vol. 338, no. 23, pp. 1650–1656, 1998.
[7]  L. S. Webber, S. R. Srinivasan, W. A. Wattigney, and G. S. Berenson, “Tracking of serum lipids and lipoproteins from childhood to adulthood. The Bogalusa Heart Study,” American Journal of Epidemiology, vol. 133, no. 9, pp. 884–899, 1991.
[8]  “Natural history of aortic and coronary atherosclerotic lesions in youth. Findings from the PDAY Study. Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 13, no. 9, pp. 1291–1298, 1993.
[9]  R. E. Kavey, V. Allada, S. R. Daniels et al., “Cardiovascular risk reduction in high-risk pediatric patients: a scientific statement from the American Heart Association expert panel on population and prevention science; the councils on cardiovascular disease in the young, epidemiology and prevention, nutrition, physical activity and metabolism, high blood pressure research, cardiovascular nursing, and the kidney in heart disease,” Circulation, vol. 114, no. 24, pp. 2710–2738, 2006.
[10]  J. Stańczyk, B. Kierzkowska, P. Podolec et al., “Polish forum for prevention guidelines on cardiovascular diseases prevention in children and adolescents,” Kardiologia Polska, vol. 68, no. 5, pp. 605–608, 2010.
[11]  R. Ross, “Mechanisms of disease: atherosclerosis- an inflammatory disease,” The New England Journal of Medicine, vol. 340, pp. 115–126, 1999.
[12]  N. J. Goodson, D. P. Symmons, D. G. Scott, D. Bunn, M. Lunt, and A. J. Silman, “Baseline levels of C-reactive protein and prediction of death from cardiovascular disease in patients with inflammatory polyarthritis: a ten-year followup study of a primary care-based inception cohort,” Arthritis and Rheumatism, vol. 52, no. 8, pp. 2293–2299, 2005.
[13]  M. A. Gonzalez-Gay, C. Gonzalez-Juanatey, A. Pi?eiro, C. Garcia-Porrua, A. Testa, and J. Llorca, “High-grade C-reactive protein elevation correlates with accelerated atherogenesis in patients with rheumatoid arthritis,” Journal of Rheumatology, vol. 32, no. 7, pp. 1219–1223, 2005.
[14]  M. A. Gonzalez-Gay, C. Gonzalez-Juanatey, M. J. Lopez-Diaz et al., “HLA-DRB1 and persistent chronic inflammation contribute to cardiovascular events and cardiovascular mortality in patients with rheumatoid arthritis,” Arthritis Care and Research, vol. 57, no. 1, pp. 125–132, 2007.
[15]  H. Maradit-Kremers, P. J. Nicola, C. S. Crowson, K. V. Ballman, and S. E. Gabriel, “Cardiovascular death in rheumatoid arthritis: a population-based study,” Arthritis and Rheumatism, vol. 52, no. 3, pp. 722–732, 2005.
[16]  C. Turesson, A. Jarenros, and L. Jacobsson, “Increased incidence of cardiovascular disease in patients with rheumatoid arthritis: results from a community based study,” Annals of the Rheumatic Diseases, vol. 63, no. 8, pp. 952–955, 2004.
[17]  D. H. Solomon, E. W. Karlson, E. B. Rimm et al., “Cardiovascular morbidity and mortality in women diagnosed with rheumatoid arthritis,” Circulation, vol. 107, no. 9, pp. 1303–1307, 2003.
[18]  M. T. Nurmohamed and B. A. C. Dijkmans, “Dyslipidaemia, statins and rheumatoid arthritis,” Annals of the Rheumatic Diseases, vol. 68, no. 4, pp. 453–455, 2009.
[19]  J. Lakatos and A. Harsagyi, “Serum total, HDL, LDL cholesterol, and triglyceride levels in patients with rheumatoid arthritis,” Clinical Biochemistry, vol. 21, no. 2, pp. 93–96, 1988.
[20]  M. Urban, E. Pietrewicz, A. Górska, and B. G?owińska, “Lipids and homocysteine level in juvenile idiopathic arthritis,” Polski Merkuriusz Lekarski, vol. 17, no. 99, pp. 235–238, 2004.
[21]  R. Gon?alves Marangoni, A. L. Hayata, E. F. Borba, P. M. Azevedo, E. Bonfá, and C. Goldenstein- Schainberg, “Decreased high- density lipoprotein cholesterol levels in polyarticular juvenile idiopathic arthritis,” Clinics, vol. 66, no. 9, pp. 1549–1552, 2011.
[22]  A. D. Tselepis, M. Elisaf, S. Besis, S. A. Karabina, M. J. Chapman, and A. Siamopoulou, “Association of the inflammatory state in active juvenile rheumatoid arthritis with hypo-high-density lipoproteinemia and reduced lipoprotein- associated platelet-activating factor acetylhydrolase activity,” Arthritis and Rheumatism, vol. 42, no. 2, pp. 373–383, 1999.
[23]  A. Bakkaloglu, B. Kirel, S. Ozen, U. Saat?i, R. Topalo?lu, and N. Be?ba?, “Plasma lipids and lipoproteins in juvenile chronic arthritis,” Clinical Rheumatology, vol. 15, no. 4, pp. 341–345, 1996.
[24]  R. Palomino-Morales, C. Gonzalez-Juanatey, T. R. Vazquez-Rodriguez et al., “A1298C polymorphism in the MTHFR gene predisposes to cardiovascular risk in rheumatoid arthritis,” Arthritis Research and Therapy, vol. 12, no. 2, article R71, 2010.
[25]  K. S. McCully, “Vascular pathology of homocysteinemia: implications for the pathogenesis of arteriosclerosis,” American Journal of Pathology, vol. 56, no. 1, pp. 111–128, 1969.
[26]  M. Gon?alves, V. D'Almeida, E. M. Guerra-Shinohara, L. C. Galdieri, C. A. Len, and M. O. Hilário, “Homocysteine and lipid profile in children with Juvenile Idiopathic Arthritis,” Pediatric Rheumatology, vol. 5, article 12, 2007.
[27]  E. Pietrewicz and M. Urban, “Early atherosclerosis changes in children with juvenile idiopathic arthritis,” Polski Merkuriusz Lekarski, vol. 22, no. 129, pp. 211–214, 2007.
[28]  H. K. Choi, M. A. Hernán, J. D. Seeger, J. M. Robins, and F. Wolfe, “Methotrexate and mortality in patients with rheumatoid arthritis: a prospective study,” The Lancet, vol. 359, no. 9313, pp. 1173–1177, 2002.
[29]  R. Kleemann, S. Zadelaar, and T. Kooistra, “Cytokines and atherosclerosis: a comprehensive review of studies in mice,” Cardiovascular Research, vol. 79, no. 3, pp. 360–376, 2008.
[30]  M. Gattorno and A. Martini, “The immune system and inflammatory response,” in The Textbook of Pediatric Rheumatology, J. Cassidy, R. Petty, R. Laxer, and C. Lindsley, Eds., pp. 55–57, Sauders Elsevier, Philadelphia, Pa, USA, 5th edition, 2011.
[31]  S. Prahalad, T. B. Martins, A. E. Tebo et al., “Elevated serum levels of soluble CD154 in children with juvenile idiopathic arthritis,” Pediatric Rheumatology, vol. 6, article 8, 2008.
[32]  M. Yilmaz, S. G. Kendirli, D. Altintas, G. Bing?l, and B. Antmen, “Cytokine levels in serum of patients with juvenile rheumatoid arthritis,” Clinical Rheumatology, vol. 20, no. 1, pp. 30–35, 2001.
[33]  A. Burger-Kentischer, H. Goebel, R. Seiler et al., “Expression of macrophage migration inhibitory factor in different stages of human atherosclerosis,” Circulation, vol. 105, no. 13, pp. 1561–1566, 2002.
[34]  E. F. Morand and M. Leech, “Macrophage migration inhibitory factor in rheumatoid arthritis,” Frontiers in Bioscience, vol. 10, no. 1, pp. 12–22, 2005.
[35]  E. F. Morand, M. Leech, H. Weedon, C. Metz, R. Bucala, and M. D. Smith, “Macrophage migration inhibitory factor in rheumatoid arthritis: clinical correlations,” Rheumatology, vol. 41, no. 5, pp. 558–562, 2002.
[36]  R. López-Mejias, M. Garcia-Bermúdez, C. Gonzalez-Juanatey, et al., “Lack of association between IL6 single nucleotide polymorphisms and cardiovascular disease in Spanish patients with rheumatoid arthritis,” Atherosclerosis, vol. 219, no. 2, pp. 655–658, 2011.
[37]  R. Palomino-Morales, C. Gonzalez-Juanatey, T. R. Vazquez-Rodriguez et al., “Lack of association between macrophage migration inhibitory factor-173 gene polymorphism with disease susceptibility and cardiovascular risk in rheumatoid arthritis patients from northwestern Spain,” Clinical and Experimental Rheumatology, vol. 28, no. 1, pp. 68–72, 2010.
[38]  A. M. van Sijl, M. J. Peters, D. K. Knol et al., “Carotid intima-media thickness in rheumatoid arthritis as compared to control subjects: a meta-analysis,” Seminars in Arthritis and Rheumatism, vol. 40, no. 5, pp. 389–397, 2011.
[39]  C. Gonzalez-Juanatey, J. Llorca, J. Martin, and M. A. Gonzalez-Gay, “Carotid intima-media thickness predicts the development of cardiovascular events in patients with rheumatoid arthritis,” Seminars in Arthritis and Rheumatism, vol. 38, no. 5, pp. 366–371, 2009.
[40]  M. Urban, E. Pietrewicz, A. Górska, W. Szczepański, and M. Baran, “Correlation between intima-media thickness in carotid artery and markers of epithelial cell dysfunction in patients with juvenile idiopathic arthritis,” Medycyna Wieku Rozwojowego, vol. 13, no. 4, pp. 277–282, 2009.
[41]  A. Górska, L. Rutkowska-Sak, E. Musiej-Nowakowska, S. Chlabicz, and S. Górski, “Nailfold videocapillaroscopy—a useful tool for screening patients with juvenile idiopathic arthritis at the risk of development of premature atherosclerosis,” Postepy Higieny i Medycyny Doswiadczalnej, vol. 64, pp. 296–302, 2010.

Full-Text

comments powered by Disqus