Subtypes of Antiphospholipid Antibodies in Neurologic Disorders: An Observational Study

Author(s): Maryam Sahebari*, Maryam Rastin, Reza Boostani, Mohsen Forughipour, Kamila Hashemzadeh, Samira H. Sadeghi.

Journal Name: Current Rheumatology Reviews

Volume 15 , Issue 1 , 2019

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Abstract:

Background and Objectives: Concomitant neurologic manifestations and positive antiphospholipid antibodies (APAs) have been investigated in different manners. The present study aimed to investigate the association between neurologic manifestations and APAs.

Materials and Methods: This cross-sectional descriptive study was conducted on 100 consecutive patients with selected neurological manifestations and at least one positive APAs within the age range of 20-50 years, referred to the Rheumatic Diseases Research Center from the Northeast Central Neurology Department of Iran during August 2012 to March 2014.

Results: According to the results, 89% of the participants were persistently positive for APAs, including lupus anticoagulant, IgG anticardiolipin (aCL), IgM aCL, IgG β-2 glycoprotein 1 (β2- GP1), and IgM β2-GP1, observed in 16%, 41%, 42%, 17%, and 15% of the patients, respectively. Furthermore, 10% of the patients had concomitant lupus manifestations, and 37% of them showed anti-DNA. The IgG and IgM aCL were the most prevalent antibodies. Cerebral vascular accident (33%), retinal artery/vein occlusion (21%), and seizure (20%) were the most frequent presentations among the patients. In addition, the patients with multiple sclerosis (composing 3% of the subjects) were 100% positive for IgG and IgM aCL, as well as lupus anticoagulant. In addition, IgM anti-β2- GP1 was 100% positive in optic neuritis patients (composing 5% of the subjects) and was significantly associated with this neurologic disorder. IgM anti-β2-GP1 was also prevalent in the cases with Guillain-Barré syndrome. The most prevalent persistently positive antibody in the patients with cerebrovascular accident was IgM aCL.

Conclusion: The findings of this study revealed some associations between the subtypes of APAs and incidence of neurologic disorders. However, the exact correlation between those symptoms and APAs needs further investigations.

Keywords: Antiphospholipid antibody, antiphospholipid syndrome, anti-β2Glycoprotein1, lupus, central nervous system, neurological accident.

[1]
Lim W. Antiphospholipid antibody syndrome. Hematology Am Soc 2013; 1: 675-80.
[2]
Uziel YLR, Blaser S, Andrew M, Schneider R, Silverman ED. Cerebral vein thrombosis in childhood systemic lupus erythematosus. J Pediatr 1995; 126(5): 722-7.
[3]
Ravelli AMA. Antiphospholipid syndrome. Pediatr Clin North Am 2005; 52(2): 469-91.
[4]
Cervera RPJ-C, Font J, Khamashta MA, et al. Antiphospholipid syndrome: Clinical and immunologic manifestations and patterns of disease expression in a cohort of 1,000 patients. Arthritis Rheum 2002; 46(4): 1019-27.
[5]
Arnson Y, Shoenfeld Y, Alon E, Amital H. editors. The antiphospholipid syndrome as a neurological disease. Semin Arthritis Rheum 2010; 40(2): 97-108.
[6]
Erkan D, Yazici Y, Peterson M, Sammaritano L, Lockshin M. A cross sectional study of clinical thrombotic risk factors and preventive treatments in antiphospholipid syndrome. Rheumatology 2002; 41(8): 924-9.
[7]
Kent M1 AF. Vogt E, Fyffe R, Ng AK, Rote N. Monoclonal antiphosphatidylserine antibodies react directly with feline and murine central nervous system. J Rheumatol 1997; 24(9): 1725-33.
[8]
Chapman J1 C-AM. Shoenfeld Y, Korczyn AD. Antiphospholipid antibodies permeabilize and depolarize brain synaptoneurosomes. Lupus 1999; 8(2): 127-33.
[9]
Brey RLAR, Curb JD, Sharp DS, et al. β2-Glycoprotein 1-dependent anticardiolipin antibodies and risk of ischemic stroke and myocardial infarction the honolulu heart program. Stroke Am Heart Assoc 2001; 32(8): 1701-6.
[10]
Mackworth-young CG. Antiphospholipid syndrome: Multiple mechanisms. Clin Exp Immunol 2004; 136(3): 393-401.
[11]
Cervera R, Piette JC, Font J, et al. Antiphospholipid syndrome: Clinical and immunologic manifestations and patterns of disease expression in a cohort of 1,000 patients. Arthritis Rheum 2002; 46(4): 1019-27.
[12]
Eriksson K, Peltola J, Keränen T, Haapala A, Koivikko M. High prevalence of antiphospholipid antibodies in children with epilepsy: A controlled study of 50 cases. Epilepsy research 2001; 46(2): 129-37.
[13]
Agrawal BL, Foa RP. Collagen vascular disease appearing as chorea gravidarum. Arch Neurol 1982; 39(3): 192-3.
[14]
Kittner S, Joseph C, Havstad S, et al. Anticardiolipin antibodies are an independent risk factor for 1st ischemic stroke. Neurology 1993; 43(10): 2069-73.
[15]
Miesbach W, Gilzinger A, Gökpinar B, Claus D, Scharrer I. Prevalence of antiphospholipid antibodies in patients with neurological symptoms. Clin Neurol Neurosurg 2006; 108(2): 135-42.
[16]
Tanne D, Hassin-Baer S. Neurologic manifestations of the antiphospholipid syndrome. Curr Rheumatol Rep 2001; 3(4): 286-92.
[17]
Harris E, Gharavi A, Asherson R, Boey M, Hughes G. Cerebral infarction in systemic lupus: Association with anticardiolipin antibodies. Clin Exp Rheumatol 1983; 2(1): 47-51.
[18]
Krause I, Lev S, Fraser A, et al. Close association between valvar heart disease and central nervous system manifestations in the antiphospholipid syndrome. Ann Rheum Dis 2005; 64(10): 1490-3.
[19]
Verrot D, San-Marco M, Dravet C, et al. Prevalence and signification of antinuclear and anticardiolipin antibodies in patients with epilepsy. Am J Med 1997; 103(1): 33-7.
[20]
Herranz MT, Rivier G, Khamashta MA, Blaser KU, Hughes GR. Association between antiphospholipid antibodies and epilepsy in patients with systemic lupus erythematosus. Arthritis Rheum 1994; 37(4): 568-71.
[21]
Chapman J, Cohen-Armon M, Shoenfeld Y, Korczyn A. Antiphospholipid antibodies permeabilize and depolarize brain synaptoneurosomes. Lupus 1999; 8(2): 127-33.
[22]
Wiechens B, Schröder JO, Pötzsch B, Rochels R. Primary antiphospholipid antibody syndrome and retinal occlusive vasculopathy. Am J Ophthalmol 1997; 123(6): 848-50.
[23]
Deschiens M-A, Conard J, Horellou MH, et al. Coagulation studies, factor V Leiden, and anticardiolipin antibodies in 40 cases of cerebral venous thrombosis. Stroke 1996; 27(10): 1724-30.
[24]
Sanna G, Bertolaccini M, Cuadrado M, Khamashta M, Hughes G. Central nervous system involvement in the antiphospholipid (Hughes) syndrome. Rheumatology 2003; 42(2): 200-13.
[25]
Brey RL. Differential diagnosis of central nervous system manifestations of the antiphospholipid antibody syndrome. J Autoimmun 2000; 15(2): 133-8.


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Article Details

VOLUME: 15
ISSUE: 1
Year: 2019
Page: [59 - 66]
Pages: 8
DOI: 10.2174/1573397114666180514125412
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