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Prevalence of Anti-Cardiolipin and Anti-β2 Glycoprotein Antibodies in Indian Systemic Lupus Erythematosus Patients

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DOI: 10.4236/ijcm.2011.23059    3,756 Downloads   6,618 Views  

ABSTRACT

Anti-phospholipid antibodies (APA) like anti-cardiolipin antibodies (ACA) and anti-β2glycoprotien (anti-β2GP) are important cause of venous and arterial thrombosis and other occlusive vascular diseases. The prevalence of these antibodies in SLE patients at the time of diagnosis is not known in Indian SLE patients. This study was conducted to evaluate the prevalence of ACA and anti-β2GP autoantibodies in SLE patients and to correlate them with disease activity and immune parameters such as C3, C4 and CRP levels. where 85 SLE patients referred from Rheumatology Department, KEM hospital, Mumbai were studied. SLE disease activity was evaluated by SLE Disease Activity Index (SLEDAI) score at the time of evaluation. All patients studied were in an active stage of disease of which 37.6% patients had renal disorders, which were categorized as Lupus Nephritis (LN) and 62.3% patients did not show any renal manifestations (non-LN). ACA and anti-β2GP autoantibodies, to IgG and IgM subclasses were tested by ELISA. C3, C4 and CRP levels were detected by nephelometer. It was observed that 12.9% patients were IgG-ACA and IgM-ACA positive and ACA positivity was noted more among LN group Anti-β2GP autoantibody positivity was 27.1% for IgG and 31.8% for IgM., IgG-anti-β2GP antibodies were slightly higher in non-LN patients, whereas a higher incidence of IgM-anti-β2GP antibodies were detected in LN patients. Hence detection both ACA and anti-β2GP antibodies along with associated immune parameters were helpful to evaluate their possible association with disease severity in SLE patients. A long term follow up of patients having ACA and anti-β2GP antibodies without thrombotic event is also needed to detect their possible thrombotic event in future along with their clinical presentation.

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

V. Pradhan, A. Rajadhyaksha, P. Joshi, M. Patwardhan, S. Dighe and K. Ghosh, "Prevalence of Anti-Cardiolipin and Anti-β2 Glycoprotein Antibodies in Indian Systemic Lupus Erythematosus Patients," International Journal of Clinical Medicine, Vol. 2 No. 3, 2011, pp. 339-345. doi: 10.4236/ijcm.2011.23059.

References

[1] Y. Sherer, M. Blank and Y. Shoenfeld, “Anti-phospholipid syndrome (APS): where does it come from ?,” Best Pract Res Clin Rehumatol, Vol 21, No. 6, 2007, pp. 1071- 1078.
[2] E. M. Bevers, M. Galli, T. Barbui, et al., “Lupus anticoagulant IgG’s (LA) are not directed to phospholipids only, but to a complex of lipid-bound human prothrombin,” Thromb Haemost, Vol. 66, 1991, pp. 629-632.
[3] S. Miyakis, M.D. Lockshin, T. Atsumi, D.W. Branch, R.L. Brey and R. Cervera, “International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS),” J Thromb Haemost, Vol.4, 2006, pp. 295-306.
[4] H. P. McNeil, R. J. Simpson, C. N. Chesterman and S.A. Krilis, “Antiphospholipid antibodies are directed against a complex antigen that includes a lipid-binding inhibitor of coagulation: beta 2- glycoprotein 1 (apolipoprotein H),” Proc Natl Acad Sci USA, Vol. 87, 1990, pp. 4120-4125.
[5] P. L. Meroni, N. Del Papa, D. Gambini, A. Tincami and G. Balesterari, “Antiphospholipid antibodies and endothelial cells: an unending story,” Lupus, Vol. 4, 1995, pp.169-71.
[6] D. S. Pisetsky, G. Gilkeson and E. W. St. Clair, “Systemic Lupus Erythematosus. Diagnosis and Treatment,” Med Clin North Am, Vol.81, No. 1,1997, pp.113-128.
[7] G. S. Cooper, M.A. Dooley, E. L. Treadwell, E.W. St Clair, C. G. Parks and G.S. Gilkeson, “Hormonal, environmental, and infectious risk factors for developing Systemic Lupus Erythematosus,” Arthritis Rheum, Vol. 41, No. 10, 1998, pp.171417-24.
[8] V. D. D’Agati and G.B Appel, “Lupus Nephritis: Pathology and Pathogenesis,” D.J .Wallace, B.H. Hahn, eds. Dubois’ Lupus Erythematosus.7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007: 1094-111.
[9] H. Zheng, Y. Chen, W. Ao, Y. Shen, X. W. Chen, M. Dai, X. D. Wang, Y. C. Yan and C. D. Yang, “Antiphospholipid antibody profiles in lupus nephritis with glomerular microthrombosis: a prospective study of 124 cases,” Arthritis Res Ther, Vol.11, No. 3, 2009, R93. Epub 2009 Jun 22.
[10] J.P. Grande, “Mechanisms of progression of renal damage in lupus nephritis: pathogenesis of enal scarring,” Lupus, Vol. 7, No. 9, 1998, pp. 604-610.
[11] J. S. Levine, D. W. Branch and J. Rauch, “The antiphospholipid syndrome,” N Engl J Med Vol. 346, 2002, pp. 752-763.
[12] M.L. Davies, S.P. Young, K.Welsh, M.Bunce, B.P. Wordsworth, et al., “Immune responses to native β2-glycoprotein I in patients with Systemic Lupus Erythematosus and the anti-phospholipid syndrome,” Rheumatology, Vol 41, 2002, pp. 395-400.
[13] M. Jallouli, M. Frigui, M. B. Hmida, S. Marzouk, N. Kaddour and Z. Bahloul, “Clinical and immunological manifestations of Systemic Lupus Erythematosus: study on 146 south Tunisian patients,” Saudi J Kidney Dis Transpl, Vol. 19, No. 6, 2008, pp.1001-1008.
[14] E. Descloux, I. Durieu, P. Cochat, D. Vital Durand, J Ninet, N. Fabien and R. Cimaz, “Pediatric Systemic Lupus Erythematosus: prognostic impact of antiphospholipid antibodies,” Rheumatology (Oxford), Vol. 47, No. 2, 2008, pp.183-187.
[15] M. C. Hockberg, “Updating the American College of Rheumatology revised criteria for the classification of Systemic Lupus Erythematosus,” Arthritis Rheum, Vol. 40, 1997, pp. 1725.
[16] C. Bombardier, F. F. Gladmsn, M. B. Urowit, D. Caron and C. H. Chang, “Derivation of SLEDAI: a disease activity index for lupus patients. The committee on prognosis studies in SLE. Arch Rheum, Vol. 35, 1995, pp. 630-640.
[17] J. J. Weening, V. D. Agati, M. M. Schwartz, S. V. Seshan, C. E. Alpers and G. B. Appel, “The classification of glomerulonephritis in Systemic Lupus Erythematosus Re visited,” J Am Soc Nephrol, Vol.15, No. 2, 2004, pp. 241-250.
[18] J. R. Mueh, K. D. Herbst and S. I. Rapaport, “Thrombosis in patients with the lupus anticoagulant,” Ann Intern Med. Vol. 92, No. 2, 1980, pp. 156-159.
[19] L. O. Carreras, J. Vermylen, B. Spitz and A. Van Assche, “Lupus anticoagulant and inhibition of prostacyclin formation in patients with repeated abortion, intrauterine growth retardation and intrauterine death,” Br J Obstet Gynaecol, Vol. 88, No. 9, 1981, pp.890-894.
[20] M. L. Boey, C.B. Colaco, A. E. Gharavi, K. B. Elkon, S. Loizou and G. R. Hughes, “Thrombosis in Systemic Lupus Erythematosus: striking association with the presence of circulating lupus Anticoagulant,” Br Med J (Clin Res Ed, Vol. 8; No. 287(6398), 1983, pp. 1021-1023.
[21] E. N. Harris, A. E. Gharavi and M. L. Boey, “Anti cardiolipin antibody detection by radioimmunoassay and association with thrombosis in Systemic Lupus Erythematosus,” Lancet, Vol. 2, 1983, pp. 1211-1214.
[22] M. D. Lockshin and L. R. Sammaritano, “Lupus pregnancy,” Autoimmunity, Vol. 36, No. 1, 2011, pp.33-40.
[23] G. A. Mostafa, D.H. Ibrahim, A. A. Shehab and A.K. Mohammed, “The role of measurement of serum autoantibodies in prediction of pediatric neuropsychiatric Systemic Lupus Erythematosus,” J Neuroimmunol, Vol. 8, No. 227(1-2), 2010, pp.195-201.
[24] M. Petri, “Update on anti-phospholipid antibodies in SLE: the Hopkins’ Lupus Cohort,” Lupus, Vol. 19, No. 4, 2010, pp.419-423.
[25] M. Biggioggero and P.L. Meroni, “The geoepidemiology of the antiphospholipid antibody syndrome,” Autoimmun Rev, Vol. 9, No. 5, 2010, A299-304. Epub 2009 Nov 25.
[26] T. Gould, M. Tikly, R. Asherson, S. Loizou and S. Singh, “Prevalence and clinical correlates of anti-phospholipid antibodies in South Africans with Systemic Lupus Erythematosus,” Scand J Rheumatol, Vol. 35, No. 1, 2006, pp.29-34.
[27] A. S. Al Arfaj and N. Khalil, “Clinical and immunological manifestations in 624 SLE patients in Saudi Arabia,” Lupus, Vol.18, No.5, 2009, pp. 465-473.
[28] K. S. Woo, K.E. Kim, J.M. Kim, J. Y. Han, W. T. Chung and K. H. Kim, “Prevalence and clinical associations of lupus anticoagulant, anticardiolipin antibodies, and anti- beta2-glycoprotein I antibodies in patients with SLE,” Korean J Lab Med, Vol 30, No. 1, 2010, pp.38-44.
[29] A. Shrivastava, S. Dwivedi, A. Aggarwal and R. Misra, “Anti-cardiolipin and anti-beta2 glycoprotein I antibodies in Indian patients with Systemic Lupus Erythematosus: association with the presence of seizures,” Lupus, Vol. 10, No. 1, 2001, pp. 45-50.
[30] Z. S. Sarabi, E. Chang, R. Bobba, D. Ibanez, D. Gladman, M. Urowitz et al., “Incidence rates of arterial and venous thrombosis after diagnosis and Systemic Lupus Erythematosus,” Arthritis & Rheumatism, Vol. 53, No. 4, 2005, pp.609-612.
[31] D. Erkan,“ Lupus and thrombosis,” J Rheumatol, Vol 32, 2006, pp.1715-1717.
[32] M. Petri, M. Golbus, R. Anderson, Q. Whiting-O’Keefe, L. Corash and D. Hellmann, “Antinuclear antibody, lupus anticoagulant, and anticardiolipin antibody in women with idiopathic habitual abortion. A controlled prospective study of forty-four women,” Arthritis Rheum, Vol 30, 1987, pp.601-606.

  
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