Neurological disease associated with antiphospholipid antibodies

Briley, Dennis; Coull, Bruce M.; Goodnight, Scott H.

doi:10.1002/ana.410250303

Cited by 227 publications

(105 citation statements)

References 44 publications

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“…18 These antibodies have been associated with systemic thrombotic problems including major arterial occlusions, deep-vein thrombosis, and pulmonary hypertension, as well as with thrombocytopenia and recurrent fetal abortion. 21 " 23 Asherson et al 24 reported a relation between CVD and antiphospholipid antibodies in patients with SLE and related disorders. Multiple episodes of cerebral infarction are common in patients with antiphospholipid antibodies, and some patients develop multi-infarct dementia during the course of their illness.…”

Section: Discussionmentioning

confidence: 99%

Stroke in systemic lupus erythematosus.

Kitagawa

Gotoh

Koto

et al. 1990

Stroke

135

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We investigated the clinical and pathologic characteristics of stroke in 234 patients with systemic lupus erythematosus. Thirteen patients (5.6%) developed cerebrovascular disease. Cerebral infarction was noted in eight, cerebral hemorrhage in two, and subarachnoid hemorrhage in three. In seven (54%) of these 13 patients, stroke occurred <5 years after systemic lupus erythematosus was diagnosed. Among the predisposing risk factors for stroke, hypertension was the most important. Lupus anticoagulant was detected in three (38%) and anticardiolipin antibody in three (43% of seven investigated) of the patients with infarction. Evaluation of the clinical manifestations and autoantibodies indicated that renal involvement and high titers of anti-deoxyribonucleic acid antibody were more frequent in the stroke group than in the non-stroke group. Autopsy studies on six of the patients with stroke revealed small infarcts and hemorrhages in all, but in no case was true angiitis observed. Libman-Sacks endocarditis was found in two of the three patients with infarction. In conclusion, the important contributory factor to the development of stroke in patients with systemic lupus erythematosus is considered to be hypertension mediated by immunologic abnormalities. 4 Although considerable knowledge has been accumulated concerning the clinical and serologic abnormalities associated with SLE, the pathogenesis of the cerebrovascular disease (CVD) that is occasionally associated with SLE remains uncertain. Several etiologic factors for CVD such as angiitis, antineuronal antibodies, cardiac diseases, and coagulopathies have been suggested. We analyzed the clinical and pathologic characteristics of the CVD occurring in SLE patients in an attempt to clarify its pathogenesis. Subjects and MethodsAll inpatient and outpatient medical records of 234 consecutive persons with SLE seen from 1972 to 1989 were retrospectively reviewed in detail for evidence of stroke. The diagnosis of SLE was made on the basis of the 1982 revised criteria for the classification of SLE.5 Stroke was diagnosed in SLE patients who had neurologic deficits with a corresponding lesion on a brain computed tomogram (CT scan). Cases in Received February 23, 1990; accepted July 16, 1990. which autopsy revealed a focus of cerebral infarction, cerebral hemorrhage, and/or subarachnoid hemorrhage were also included. Patients with transient ischemic attacks or neurologic signs and symptoms lasting for >24 hours, suggesting clinical stroke, but without corresponding CT lesions were excluded. Patients with asymptomatic infarcts encountered on brain CT scans or at autopsy were also excluded. The follow-up period ranged from 6 months to 15 years, with a mean of 6.7 years. Particular attention was paid to the presence of risk factors for CVD such as hypertension, diabetes mellitus, hypercholesterolemia, heart disease, antiphospholipid antibodies, and large doses of corticosteroid. The following definitions were formulated for the study: hypertension, blood pressure of > 160/95 m...

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Section: Discussionmentioning

confidence: 99%

Stroke in systemic lupus erythematosus.

Kitagawa

Gotoh

Koto

et al. 1990

Stroke

135

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“…Antiphospholipid antibodies of the immunotested negatively for anticardiolipin antibodies (n Å 37), globulin (Ig) G isotype show the strongest association but were present in 16.7% of those positive for anticard-with symptomatic disease. [1][2][3][4][5][6][7][8][9][10] iolipin (n Å 36) (P Å .01). In conclusion, anticardiolipin Anticardiolipin antibodies have been detected in a antibodies are frequently found in patients with chronic variety of infectious diseases, particularly of viral orihepatitis C and in these patients they may be implicated gin, such as human immunodeficiency virus infection, in the occurrence of thrombosis and in the development of thrombocytopenia.…”

Section: Titis C Patients the Presence Of Thrombocytopenia Portalmentioning

confidence: 99%

“…[3][4][5][6][7][8][9][10][11] The idea of a possible six patients, and the second determination was positive implication of antiphospholipid antibodies in thromboin three of them.…”

Section: Titis C Patients the Presence Of Thrombocytopenia Portalmentioning

confidence: 99%

Anticardiolipin antibodies in chronic hepatitis C: Implication of hepatitis C virus as the cause of the antiphospholipid syndrom

Prieto

1996

Hepatology

106

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Antiphospholipid antibodies are a type of autoanti-thematosus and other autoimmune disorders but are bodies that have been implicated in the occurrence of being increasingly detected in patients without apparthrombocytopenia and thrombotic events and have been ent underlying autoimmune disease.3,4 These autoantidescribed in autoimmune disorders and diverse viral bodies are strongly associated with recurrent spontanediseases. In this study anticardiolipin antibodies (immu-ous abortions, thrombocytopenia, and thrombotic noglobulin G [IgG] isotype) were determined in serum events including deep venous thrombosis with or withfrom 100 patients with chronic hepatitis C and 52 out pulmonary embolism, portal or hepatic vein thromhealthy controls. In addition, hepatitis C virus (HCV) bosis, large vessel arterial occlusions, myocardial inmarkers (anti-HCV and HCV RNA) were investigated in 73 patients with thrombotic disorders and no clinical farction, fixed or transient cerebral ischemic events, evidence of liver disease; of these patients 37 cases tested retinal arterial and venous occlusions, ischemic optic negatively for anticardiolipin antibodies and 36 posi-neuropathy, Degos disease, and nonbacterial thromtively. Anticardiolipin test was positive more frequently botic verrucous endocarditis.3-8 The combination of per-(22%) in the group of patients with chronic hepatitis C sistently positive antiphospholipid test results with than in healthy controls (1.9%; P õ .001). Using condi-any of these clinical manifestations is known as the tional logistic-regression analysis we found that in hepa-antiphospholipid antibody syndrome.9 This syndrome,

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“…The pathophysiology of spinal cord damage in these patients is unknown, but ischemia or direct interaction of aPL with CNS phospholipids has been suggested (43). Several studies suggest an association between aPL and Guillain-Barré syndrome, seizures, chorea (44) and migraine headaches (45).…”

Section: Neurological Complicationsmentioning

confidence: 99%

Origin and pathogenesis of antiphospholipid antibodies

Celli

Gharavi

1998

Braz J Med Biol Res

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Antiphospholipid antibodies (aPL) are a heterogeneous group of antibodies that are detected in the serum of patients with a variety of conditions, including autoimmune (systemic lupus erythematosus), infectious (syphilis, AIDS) and lymphoproliferative disorders (paraproteinemia, myeloma, lymphocytic leukemias). Thrombosis, thrombocytopenia, recurrent fetal loss and other clinical complications are currently associated with a subgroup of aPL designating the antiphospholipid syndrome. In contrast, aPL from patients with infectious disorders are not associated with any clinical manifestation. These findings led to increased interest in the origin and pathogenesis of aPL. Here we present the clinical features of the antiphospholipid syndrome and review the origin of aPL, the characteristics of experimentally induced aPL and their historical background. Within this context, we discuss the most probable pathogenic mechanisms induced by these antibodies.

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Neurological disease associated with antiphospholipid antibodies

Cited by 227 publications

References 44 publications

Stroke in systemic lupus erythematosus.

Stroke in systemic lupus erythematosus.

Anticardiolipin antibodies in chronic hepatitis C: Implication of hepatitis C virus as the cause of the antiphospholipid syndrom

Origin and pathogenesis of antiphospholipid antibodies

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