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PubMed2003

[Neuropsychiatric involvement in systemic lupus erythematosus. Part 2: diagnostic and therapy].

BACKGROUND: The diagnosis of neuropsychiatric lupus erythematosus (NPSLE) can be difficult and has to be differentiated from neurologic complications that result from hypertension, drugs, infection, uremia, and metabolic changes. DIAGNOSTICS: There is no single test which is diagnostic. Therefore, the clinical presentation, serologic tests and neuroimaging techniques have to be combined to support the diagnosis of cerebral lupus. Magnetic resonance imaging (MRI) is routinely used with a sensitivity of 50-87%. However, the abnormalities such as white matter lesions or brain atrophy are nonspecific and were also found in asymptomatic patients (16-52%). A negative MRI result does not exclude a diagnosis of cerebral lupus. Antibodies against phospholipids are an important immunoserologic marker due to the close association with thromboembolic events. Echocardiography and cerebrospinal fluid examination should be added to rule out cardiac embolic disease and CNS infection. Functional brain imaging techniques such as single-photon emission computed tomography, positron emission tomography, magnetization transfer imaging or magnetic resonance spectroscopy may be helpful especially in patients with unconspicuous MRI, but the findings are not SLE-specific. THERAPY: The treatment of cerebral lupus is empiric, due to a lack of randomized studies. Inflammatory brain lesions are treated with corticosteroids and immunosuppressive drugs (e. g., cyclophosphamide). Anticoagulant therapy with coumarins (at a target INR of 3.0-3.5) is recommended in cases of thrombotic events associated with antiphospholipid antibodies. However, no studies exist on patients with arterial thrombosis, including strokes, supporting this target INR.

Adrenal Cortex Hormones↗
PubMed2002

Objective evidence of abnormal regional cerebral blood flow in patients with systemic lupus erythematosus on Tc-99m ECD brain SPECT.

Technetium-99m ethyl cysteinate dimer (Tc-99m ECD) brain single photon emission computed tomography (SPECT) was used to detect abnormal regional cerebral blood flow (rCBF) in 78 SLE patients with neuropsychiatric manifestations. These patients were separated into two subgroups: group 1 including 48 cases with definite neuropsychiatric symptoms/signs and group 2 with 30 cases having no neuropsychiatric symptoms/signs. Tc-99m ECD brain SPECT demonstrated hypoperfusion brain lesions in 90% and 20% of patients in groups 1 and 2, respectively. In both groups, parietal lobe and cerebellum are the most and least common areas with hypoperfusion lesions, respectively. This study suggests that Tc-99m ECD brain SPECT may provide objective information for detection of hypoperfusion brain lesions in SLE patients.

Adult↗
PubMed2005

Damage did not independently influence mortality in childhood systemic lupus erythematosus.

OBJECTIVE: To analyze clinical, laboratory and treatment features associated with death in a childhood-onset SLE population. PATIENTS AND METHODS: Patients with childhood-onset SLE followed at the State University of Campinas, Brazil, between 1980 and 2002 were included. Data on clinical and laboratory features of the disease were collected regularly. Logistic regression was used for analyzing association between clinical and laboratory features and death. Kaplan-Meyer tests were used to estimate the survival curves. RESULTS: Of 61 patients identified, six were lost to follow-up during the first year of disease. The mean follow-up period of the remaining 55 patients was 3.25 years (SD=1.2). Mean SLICC/ACR-DI score was 4.9 (SD=3.4). Death occurred in 12 (21.8%) of 55 patients. Direct causes of death were: infection in six (50%), stroke in four (33.3%), and renal insufficiency in two (16.7%). Five patients (41.7%) died during the first 5 years of disease due to infection. Male gender (p=0.004; OR=9.1; 95% CI=7.6-21.0), infection (p=0.001; OR=4.2; 95% CI=1.6-15.2) and nephritis (p=0.02; OR=2.3; 95% CI=1.3-5.2) were independent factors associated with death in the multivariate analysis. The global survival rate adjusted for duration of disease was 93.9% in the first year of disease, 88.9% in the second year, 80.8% in the fifth year and 48.1% in 20 years of follow-up. When comparing survival curves, male gender, the presence of infection during the course of the disease and the presence of nephritis during follow-up had a worse survival. CONCLUSION: Male gender, the presence of infection and nephritis were independent risk factors for death in our Brazilian cohort. Damage did not independently influence survival in this study.

Adolescent↗
PubMed1996

Systemic lupus erythematosus with nephritis is strongly associated with the TNFB*2 homozygote in the Korean population.

To evaluate the association of TNFB NcoI polymorphism with SLE in the Korean population, we investigated the frequencies of the TNFB and HLADRB1 alleles in 281 controls and 97 SLE patients, including 56 patients with nephritis and 41 patients without nephritis. The frequency of the TNFB*2 homozygote in SLE was significantly increased over controls (43.3% vs 28.5%, RR = 1.9,p < 0.01). In SLE with nephritis, the TNFB*2 homozygote was more significantly increased (57.1% vs 28.5%, RR = 3.4,p < 0.0001), whereas there was no significant difference between SLE without nephritis and controls. The study of HLA-DRB 1 alleles revealed the increased frequencies of DRB1*02 and *03 (30.9% vs 18.2%, RR = 2.0,p < 0.01; 8.2% vs 2.1%, RR = 4.1,p < 0.05). There was no significantly different distribution of HLA-DRB1 alleles between SLE patients with nephritis and without nephritis. We found positive LD between TNFB*1 and HLA-DR1B1*13, and between TNFB*2 and the particular DRB1 allele: *15, *04, and *07 in controls and/or in SLE patients. After stratification for each HLADRB1 allele, SLE with nephritis showed a higher frequency of TNFB*2 homozygote compared with the corresponding controls in DRB1*15, *08, and *09 positives. Our results suggest that the TNFB*2 homozygote may be a strong susceptibility gene of SLE with nephritis in the Korean population.

Alleles↗
PubMed2000

Intermittent intravenous cyclophosphamide arrests progression of the renal chronicity index in childhood systemic lupus erythematosus.

OBJECTIVE: To assess prospectively the safety and efficacy of a 36-month course of systematic bolus intravenous cyclophosphamide therapy (IVCY) for children with lupus nephritis. STUDY DESIGN: Sixteen children with lupus nephritis were treated with IVCY for 36 months. Renal biopsies performed before and after treatment were scored for activity and chronicity. SLEDAI scores, laboratory measures, and prednisone dosage were recorded at the time of each treatment. RESULTS: After 36 months of IVCY therapy, the renal biopsy activity index decreased from 9 +/- 4 to 1 +/- 1 (P <.001) without a change in chronicity. The mean creatinine clearance increased from 90 +/- 23 to 107 +/- 23 mL/min/1.73 mol/L(2) (P <.01), and the mean 24-hour urine protein excretion decreased from 2.0 +/- 2.4 g/24 h to 0.5 +/- 0.7 g/24 h (P <.05). The mean SLEDAI score decreased from 19 +/- 5.2 to 2.9 +/- 3.1 (P <.001). The mean prednisone dosage decreased from 35.5 +/- 20 mg/d to 14.0 +/- 3 mg/d (P <.001). No significant complications occurred. CONCLUSIONS: Thirty-six months of systematic IVCY therapy led to decreased renal biopsy activity without progression of chronicity, with excellent disease control and a greater than 50% reduction in mean corticosteroid dose.

Adolescent↗