Antiphospholipid antibodies in leprotic patients: a correlation with disease manifestations.

OBJECTIVES Previous studies showed that antiphospholipid antibodies (aPL) are frequent in the sera of leprosy patients and are most probably directed against body tissue cardiolipins. Some groups have demonstrated differences between the binding specificity of "autoimmune-aPL" and "non-autoimmune-aPL". It is widely accepted that a plasma protein, beta 2-Glycoprotein I (beta 2-GPI), is required for the binding of autoimmune anticardiolipin antibodies (aCL) to cardiolipin. However, some reports suggested heterogeneity of leprosy aCL with respect to their beta 2-Glycoprotein I (beta 2GPI) dependency, although no thromboembolic complications have been reported. This study was designed to assess the specificity of aPL by investigating the prevalence of aCL, anti-phosphatidylserine (aPS), anti-phosphatidylinositol (aPI), anti-beta 2GPI and antiprothrombin (aPT) antibodies, and evaluate their clinical significance in a group of patients with lepromatous leprosy. PATIENTS AND METHODS 35 lepromatous leprosy patients were selected randomly from an Egyptian leprosarium as a study group. 35 normal household contact controls were selected matching the study group for both sex and age. aCL, aPS, aPI, aPT, anti-beta 2GPI and beta 2-dependent aCL antibodies were investigated by ELISA in all patients and controls. RESULTS aCL antibodies were more frequent in leprosy patients than in controls [13/35 (37%) vs. 3/35 (9%), respectively, p = 0.02] and significantly correlated with Raynaud's phenomenon, skin nodules, chronic skin ulcers and urticarial skin rash. No association was found with hypopigmentation, hyperpigmentation and saddle nose. None of the patients presented aPS nor aPI. Only 1 subject from the control group presented aPI along with aCL. aPT were present in 2/35 (5.7%) and anti-beta 2GPI in 1/35 (2.9%) leprotic patients. None of the individuals from the control group presented aPT nor anti-beta 2GPI. CONCLUSIONS An association was found between the presence of aCL and certain dermatological manifestations of leprosy, such as Raynaud's phenomenon, skin nodules, chronic skin ulcers and urticarial skin rash. As in other infectious diseases, there was a lack of beta 2GPI-dependency and an absence of thrombotic complications.

[1]  E. Nunzi,et al.  beta 2-Glycoprotein I-dependence of anticardiolipin antibodies in multibacillary leprosy patients. , 1998, Leprosy review.

[2]  G. Hughes,et al.  Multiple antiphospholipid tests do not increase the diagnostic yield in antiphospholipid syndrome. , 1998, British journal of rheumatology.

[3]  G. Hughes,et al.  Autoantibodies to human prothrombin and clinical manifestations in 207 patients with systemic lupus erythematosus. , 1998, The Journal of rheumatology.

[4]  G. Hughes,et al.  Specificity of ELISA for antibody to beta 2-glycoprotein I in patients with antiphospholipid syndrome. , 1996, British journal of rheumatology.

[5]  G. Hughes,et al.  Antiphospholipid antibodies and antiphospholipid syndrome , 1995, Current opinion in rheumatology.

[6]  Y. Shoenfeld,et al.  Anticardiolipin Antibodies in Infections are Heterogenous in Their Dependency on β 2-Glycoprotein I: Analysis of Anticardiolipin Antibodies in Leprosy , 1994, Lupus.

[7]  R. Roubey.  Autoantibodies to phospholipid-binding plasma proteins: a new view of lupus anticoagulants and other "antiphospholipid" autoantibodies. , 1994, Blood.

[8]  A. Mukherjee,et al.  Anticardiolipin antibodies in leprosy. , 1994, Indian journal of leprosy.

[9]  T. Yasuda,et al.  Anticardiolipin antibodies recognize beta 2-glycoprotein I structure altered by interacting with an oxygen modified solid phase surface , 1994, The Journal of experimental medicine.

[10]  松浦 栄次.  Anticardiolipin antibodies recognize β[2]-glycoprotein I structure altered by interacting with an oxygen modified solid phase surface , 1994 .

[11]  G. Hughes.  The antiphospholipid syndrome: ten years on , 1993, The Lancet.

[12]  P. Sandra,et al.  Lipid composition of leprosy-derived corynebacteria, a distinct group of corynebacteria, and of a reference Corynebacterium. , 1993, Biotechnology therapeutics.

[13]  J. Buyon,et al.  Lupus anticoagulant activity of autoimmune antiphospholipid antibodies is dependent upon beta 2-glycoprotein I. , 1992, The Journal of clinical investigation.

[14]  C. R. Wang,et al.  Autoantibodies and related immunity of leprosy patients from leprosarium in Taiwan. , 1992, Zhonghua Minguo wei sheng wu ji mian yi xue za zhi = Chinese journal of microbiology and immunology.

[15]  Hunt,et al.  A Phospholipid-β2-Glycoprotein I Complex Is an Antigen for Anticardiolipin Antibodies Occurring in Autoimmune Disease But Not with Infection , 1992, Lupus.

[16]  S. Krilis,et al.  New aspects of anticardiolipin antibodies. , 1990, Clinical and experimental rheumatology.

[17]  M. Lockshin,et al.  Antiphospholipid antibody syndrome: immunologic and clinical aspects. , 1990, Seminars in arthritis and rheumatism.

[18]  J. Goudevenos,et al.  High prevalence of anti-cardiolipin and other autoantibodies in a healthy elderly population. , 1987, Clinical and experimental immunology.

[19]  G. Hughes,et al.  Evaluation of the anti-cardiolipin antibody test: report of an international workshop held 4 April 1986. , 1987, Clinical and experimental immunology.

[20]  W H Jopling,et al.  Clinical aspects of leprosy. , 1982, Tubercle.