Abstracts

Epileptic seizures have been observed in 10-15% of patients with systemic lupus erythematosus (SLE) and are associated with great morbidity and mortality.
To evaluate the frequency of epileptic seizures in a large cohort of patients with systemic SLE and to determine whether clinical and laboratory factors are associated with its occurrence.
The records of 519 patients with four or more criteria for SLE diagnosis according to the American Collage of Rheumatology (1982), followed at the Rheumatology and Neurology Unit of the State University of Campinas, had their medical histories, clinical and serological characteristics prospectively documented in computer database programs.
To determine the risk factors for occurrence of seizures the clinical manifestations, serologic features and treatment strategies were analyzed at disease onset and during follow-up. The following clinical manifestations were analyzed: malar rash, discoid lesions, subacute cutaneous lesions, photosensitivity, oral ulcers, arthritis, serositis, nephritis, stroke, thrombocytopenia, hemolytic anemia, fever, Raynaud's phenomenon, thrombosis, myositis, lung involvement and lymphadenopathy.
Sixty-five (12.5%) patients with seizures were identified (77 women), with ages ranging from 7 to 69 years (mean=32). Five patients had epilepsy before the diagnosis of SLE. In 19 (3.7%) seizures occurred at onset of SLE symptoms. Seizures occurred after the onset of SLE in 41 of 519 (7.9%) patients. Fifty-eight (11.2%) patients had acute symptomatic seizures and 7 (1.4%) had recurrent seizures. Variables associated with acute epileptic seizures at SLE onset were the occurrence of stroke (p=0.0004; OR=10.36; CI=95%), the presence of antiphospholipid antibodies (p=0.0013; OR=6.69; CI=95%) and the absence of malar rash (p=0.0272; OR=3.57; CI=95%). Seizures during follow-up period were related to nephritis (p=0.0021; OR=3.04; CI=95%) and seizures at disease onset (p=0.0003; OR=7.26; CI= 95%). Recurrence of seizures was observed in only 7 (36.84%) patients. All these patients presented clinically with antiphospholipid syndrome.
Stroke and antiphospholipid antibodies were the clinical and laboratory features strongly related to seizures at SLE disease onset. During the follow-up period, patients with renal flares were at greater risk for acute symptomatic seizures. SLE patients with seizures should be carefully evaluated for subclinical stroke and for the presence of antiphospholipid antibodies