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PubMed1998

Childhood systemic lupus erythematosus and neonatal lupus syndrome.

Systemic lupus erythematosus in children can present with a wide spectrum of disease manifestations. Significant organ system involvement appears to be more severe in children than in adults. Central nervous system disease continues to be difficult to diagnose because of the lack of sensitive and specific diagnostic tests. Renal function is the major determinant of long-term prognosis and management in children with lupus. Identification of patients who are most at risk for progression of renal disease and aggressive treatment, including corticosteroids and immunosuppressive agents, are indicated. Genetic susceptibility studies in lupus reveal multiple contributions from HLA and non-HLA genes. Current concepts regarding apoptosis and DNA-protein complexes and autoreactive T-cell help for anti-DNA antibody production suggest novel directions for therapies. New understandings of the pathogenesis of neonatal lupus syndrome and congenital heart block reveals important information about prospective monitoring and management of mothers and fetuses at risk.

Cardiovascular Diseases↗
PubMed2004

Amelioration of lupus manifestations by a peptide based on the complementarity determining region 1 of an autoantibody in severe combined immunodeficient (SCID) mice engrafted with peripheral blood lymphocytes of systemic lupus erythematosus (SLE) patients.

A peptide based on the complementarity determining region (CDR)1 of a human monoclonal anti-DNA autoantibody (hCDR1) was shown to either prevent or treat an already established murine lupus in systemic lupus erythematosus (SLE)-prone mice or in mice with induced experimental SLE. The present study was undertaken to determine the therapeutic potential of hCDR1 in a model of lupus in severe combined immunodeficient (SCID) mice engrafted with peripheral blood lymphocytes (PBL) of patients with SLE. To this end, PBL obtained from lupus patients were injected intraperitoneally into two equal groups of SCID mice that were treated either with the hCDR1 (50 micro g/mouse) once a week for 8 weeks, or with a control peptide. Mice were tested for human IgG levels, anti-dsDNA autoantibodies, anti-tetanus toxoid antibodies and proteinuria. At sacrifice, the kidneys of the successfully engrafted mice were assessed for human IgG and murine complement C3 deposits. Of the 58 mice transplanted with PBL of SLE patients, 38 (66%) were engrafted successfully. The mice that were treated with the control peptide developed human dsDNA-specific antibodies. Treatment with hCDR1 down-regulated the latter significantly. No significant effect of the treatment on the levels of anti-tetanus toxoid antibodies could be observed. Treatment with hCDR1 resulted in a significant amelioration of the clinical features manifested by proteinuria, human IgG complex deposits as well as deposits of murine complement C3. Thus, the hCDR1 peptide is a potential candidate for a novel specific treatment of SLE patients.

Adoptive Transfer↗
PubMed2004

The study of the participation of basement membrane zone antibodies in the formation of the lupus band in systemic lupus erythematosus.

BACKGROUND: The lupus band test (LBT) is an important auxiliary method in the diagnosis of systemic lupus erythematosus (SLE), but the mechanism of its formation is still unknown. There are many kinds of autoantibodies, such as basement membrane zone autoantibodies (BMZ-Abs), in patients with SLE. AIM: To detect whether skin BMZ-Abs participated in the formation of the lupus band in SLE. Methods Immunoglobulin G (IgG)-type BMZ-Abs in 15 SLE patients were detected by means of immunofluorescence (IF), immunoblotting (IB), and immunoelectron microscopy (IEM). RESULTS: Direct immunofluorescence (DIF) on salt-split skin showed epidermal fluorescence in 12 of the 15 SLE patients. Two of the 12 patients also showed dermal fluorescence. Indirect immunofluorescence (IIF) on salt-split skin revealed that, in 12 of the 15 (80%) sera, antibodies were bound to the epidermal roof of the salt-split skin. IB showed that, in 14 SLE sera, autoantibodies reacted to 230, 200, 180, 130, and 97 kDa epidermal extracts and 75 kDa dermal extracts. Direct (DIEM) and indirect (IIEM) immunoelectron microscopy showed that gold particles were directed to every region of the BMZ, including hemidesmosomes, lamina lucida, lamina densa, and sublamina densa. CONCLUSIONS: BMZ-Abs in SLE sera may participate in the formation of the lupus band.

Autoantibodies↗
PubMed1981

Lupus nephritis and lupus band test.

Twenty-seven patients with histologically confirmed lupus nephritis were studied to identify the incidence of lupus band and its significance to histological patterns of nephritis and complement levels. It was found that the kidney involvement is 2.5 times more frequent in lupus band positive patients. The association of a positive lupus and low C3 level signifies the presence of diffuse proliferative glomerulonephritis rather than membranous glomerulonephritis. The results, together with earlier reports, are discussed.

Adolescent↗
PubMed1967

Immunopathologic studies of systemic lupus erythematosus. II. Antinuclear reaction of gamma-globulin eluted from homogenates and isolated glomeruli of kidneys from patients with lupus nephritis.

The gammaG-globulin eluted at acid pH from kidney cortex homogenates and isolated glomeruli of five of six patients with lupus nephritis was found to exhibit antinuclear activity, which was not dependent on presence of fresh human serum. Specificity, as demonstrated by absorption of antinuclear activity, was related to nucleoprotein in three glomerular acid eluates and to DNA in two acid eluates as well as in a deoxyribonuclease digest of disrupted glomeruli in one patient. Antinuclear activity was not found in acid eluates of kidneys from two patients with chronic liver disease and chronic discoid lupus, respectively, and one with lupus nephritis. These patients had a low titer of serum antinuclear factor and lesser amounts of kidney bound immunoglobulins. The presence of antinuclear activity in eluates of kidneys appeared to correlate with the amount of glomerular bound immunoglobulin and the level of antinuclear antibodies in serum. These findings suggest that in lupus nephritis, part of the glomerular bound immunoglobulin is derived from serum antinuclear factors possibly deposited as immune complexes.

Aged↗
PubMed2002

Prediction of lupus nephritis in patients with systemic lupus erythematosus using artificial neural networks.

Artificial neural networks are intelligent systems that have been successfully used for prediction in different medical fields. In this study, efficiency of neural networks for prediction of lupus nephritis in patients with systemic lupus erythematosus (SLE) was compared with a logistic regression model and clinicians' diagnosis. Overall accuracy, sensitivity and specificity of the optimal neural network were 68.69, 73.77 and 62.96%, respectively. Overall accuracy of neural network was greater than the other two methods (P-value < 0.05). The neural network was more specific in predicting lupus nephritis (P-value < 0.01), but there was no significant difference between sensitivities of the three methods. Sensitivities of all three methods were greater than their specificities. We concluded that neural networks are efficient in predicting lupus nephritis in SLE patients.

Algorithms↗
PubMed1978

Drug-induced lupus erythematosus with in vivo lupus erythematosus cells in pleural fluid.

Pleural involvement in drug-induced lupus erythematosus is not uncommon. Lupus erythematosus cells were found in vivo in the pleural of an elderly patient who had received procainamide (Pronestyl) hydrochloride (2 gm daily) for nine months. Patients who initially have pleural effusions while receiving drugs capable of inducing lupus erythematosus should have the fluid analyzed for lupus erythematosus cells to help clarify the cause of the effusion.

Aged↗
PubMed2005

Genetic dissection of systemic lupus erythematosus pathogenesis: partial functional complementation between Sle1 and Sle3/5 demonstrates requirement for intracellular coexpression for full phenotypic expression of lupus.

Sle1 on chromosome 1 and Sle3/5 on chromosome 7 are two of the most critical lupus susceptibility loci of the New Zealand Black/White-derived NZM2410 mouse strain. In contrast to C57BL/6 mice congenic for either Sle1 (B6.Sle1) or Sle3/5 (B6.Sle3/5), strains that express only a modest lupus-related phenotype, the bicongenic B6.Sle1.Sle3/5 strain has a robust phenotype, suggesting a critical role for epistatic interactions in lupus pathogenesis. Mixed chimera experiments indicated that the two loci are functionally expressed by different cell populations and predicted that phenotypic expression of the phenotypic features of the B6.Sle1.Sle3/5 strain could be fully reproduced with a combination of B6.Sle1 and B6.Sle3/5 bone marrow. Contrary to our expectations, there was only a partial functional complementation in these mixed chimeras. Spleen enlargement, CD4:CD8 ratio elevation, and epitope spreading of autoantibodies were fully developed in B6+B6.Sle1.Sle3/5 but not in B6.Sle1+B6.Sle3/5 mixed chimeras. This study is the first to present evidence that the pathways mediated by two critical lupus susceptibility loci derived from the New Zealand White strain must be integrated intracellularly for epistatic interactions to occur. Our mixed chimera approach continues to provide novel insights into the functional genetic pathways underlying this important murine model of systemic autoimmunity.

Animals↗
PubMed1999

Toxoplasma infection in systemic lupus erythematosus mimicking lupus cerebritis.

An opportunistic infection is a known, although under-diagnosed, complication of systemic lupus erythematosus (SLE). A 48-year-old woman with a recent diagnosis of SLE was admitted to the hospital because of a fever, confused state, and convulsive episode. Her symptoms were interpreted as being compatible with lupus cerebritis. Treatment with methylprednisolone resulted in a temporary improvement in the patient's condition. Nevertheless, during the next few weeks, her physical and mental condition deteriorated, and she died of massive pulmonary emboli. An autopsy revealed no signs of lupus cerebritis; however, disseminated cerebral toxoplasmosis was found. Cerebral toxoplasmosis is a rare complication of SLE that may be misdiagnosed as lupus cerebritis.

Autopsy↗
PubMedDate not supplied

[Lupus band test: diagnostic value in disseminated lupus erythematosus].

By direct immunoflurescence, deposits of immunoglubins and complement were investigated at the dermal epidermal junction in skin specimens from 210 patients divided into three groups: A--134 patients without lupus; B--54 patients with Systemic Lupus Erythematosus (SLE); C--22 patients with Discoid Lupus Erythematosus. Twenty two patients from group B were submitted to renal biopsy: 20 of these demonstrated a positive lupus band test and data suggested a positive correlation between the intensity of immunoglobulin and complement deposition at the dermal epidermal junction with more severe renal involvement. The other 32 patients were not submitted to renal biopsy; in sediment and band test, may be of value in the prevision of patients with higher probability of developing more serious renal lesions. Our results revealed a high specificity (85.5%) and sensitivity (87%). Test positivity was uninfluenced by steroid and immunosuppressive therapy. The test appears to be of great interest for use on all patients who fail to meet the criteria for the diagnosis of SLE but whose condition suggest such a diagnosis.

Epidermis↗
PubMed1994

Depressive symptoms in patients with systemic lupus erythematosus: association with central nervous system lupus and Sjögren's syndrome.

OBJECTIVE: To determine if patients with systemic lupus erythematosus (SLE) with depressive symptoms differ in regard to organ involvement and serological activity from other patients with SLE. METHODS: Disease manifestations were compared between 71 patients with SLE with a history of depressive symptoms and 278 patients without a history of depressive symptoms by univariate analysis and multiple logistic regression. RESULTS: Both univariate and logistic regression analysis revealed an association of depressive symptoms with neuropsychiatric lupus and secondary Sjögren's syndrome (SS). Patients with neuropsychiatric lupus had an adjusted odds ratio of 3.43 (95% CI 2.55, 4.63; p = 0.00005), and patients with secondary SS had an adjusted odds ratio of 2.97 (95% CI 2.08, 4.25; p = 0.0006) for depressive symptoms. No other organ involvement or serological abnormality was associated with depressed mood. CONCLUSION: These discrete associations of depressive symptoms with neuropsychiatric lupus and secondary SS suggest that depression does not occur purely as a response to social stresses, and may be a manifestation of autoimmune disease in some patients.

Adult↗
PubMed1997

Association of the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index with measures of disease activity and health status in patients with systemic lupus erythematosus.

OBJECTIVE: To examine the internal consistency and validity of the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI) with respect to disease activity, health status, and medication score. METHODS: A prospective cross sectional study of patients with systemic lupus erythematosus (SLE) attending a specialist lupus outpatient clinic between July 1994 and February 1995. The internal consistency of the SDI components was examined using Cronbach's coefficient alpha. The associations of the SDI components with disease activity measured by the British Isles Lupus Assessment Group (BILAG) index, health status measured by the Medical Outcomes Study (MOS) Short Form 20, and with a medication score were analyzed using Spearman's rank correlation coefficient (p). RESULTS: 133 women and 8 men ranging in age from 20.1 to 88.7 years (mean 41.1, SD 12.5) were studied. With few exceptions, the components of the SDI that reflect damage in different organ systems were not associated with each other. We found a significant although weak relationship between some related SDI and BILAG components (p 0.25 to 0.28; p < 0.01). While damage to the musculoskeletal system was associated with limitations in physical functioning measured with the MOS Short Form 20 (p-0.30; p < 0.01) and renal damage inversely with fatigue (p-0.23; p < 0.01) there was no significant relationship of other SDI components with the MOS Short Form 20. Renal and neuropsychiatric damage were associated significantly with the medication score (p 0.27 and 0.23; p < 0.01). CONCLUSION: The components of the SDI are valid in that they are associated with disease activity in the respective organ systems and some of them with a medication score. However, damage in different organ systems in SLE does not follow a common pattern. It is thus suggested that the SDI profile be used in addition to the SDI total score as an endpoint in clinical and epidemiological studies.

Adult↗
PubMed1989

[Antiphospholipid antibodies in systemic lupus erythematosus: incidence, significance and relation to lupus nephritis].

The prevalence of three different types of antiphospholipid antibody in 88 consecutive patients with systemic lupus were 27.2% for lupus anticoagulant (LAC), 31.8% for anticardiolipin antibody (aCL), and 13.6% for falsely positive serologic tests for syphilis (FPSTS). The three tests were correlated, thus confirming the overlapping specificities of this family of antibodies. Although FPSTS was not associated with any particular manifestation of systemic lupus, aCL correlated with thrombosis (p = 0.0001), thrombopenia (p = 0.009), neuropsychiatric features (p = 0.02) and membranous nephropathy (p = 0.001), while LAC correlated with thrombosis (p = 0.001) and hemolytic anemia (p = 0.04). The previously unreported association between membranous nephropathy and aCL might explain some features of the former, particularly the higher incidence of thromboembolic complications and the poorly known relation with renal vein thrombosis.

Adolescent↗
PubMed1985

The lupus anticoagulant. A disease marker in antinuclear antibody negative lupus that is cross-reactive with autoantibodies to double-stranded DNA.

The lupus anticoagulant (LA) was demonstrated in 37% of 52 consecutive systemic lupus erythematosus (SLE) patients and patients with lupus-like syndromes, who were referred to our unit. The LA was found to be associated with a biologic false-positive VDRL (P less than 0.005), and the apparently paradoxical association of LA with vascular thromboses was confirmed (P less than 0.05). The presence of LA and a biologic false-positive VDRL defined a group of 7 antinuclear antibody negative patients with characteristic features of recurrent thromboses, spontaneous abortions, neurologic involvement, and renal disease. Further studies on 6 selected sera demonstrated LA in all 6 IgM fractions and in 3 of 6 IgG fractions. Inhibition of LA was shown in 6 of 9 Ig fractions after absorption with double-stranded DNA (dsDNA). Anticardiolipin antibody was shown by immunodiffusion in 3 LA positive IgG fractions from VDRL negative sera. Cardiolipin micelles partially inhibited anti-dsDNA binding of 4 IgG fractions, 3 of which were LA negative. In this report we discuss the overlapping specificities due to cross-reactivity between LA, anticardiolipin, and anti-dsDNA antibodies in human SLE, and we suggest that LA be considered equivalent to the biologic false-positive VDRL as a criterion for the diagnosis of SLE.

Antibodies, Antinuclear↗
PubMed1998

Immunological and molecular analysis of three monoclonal lupus anticoagulant antibodies from a patient with systemic lupus erythematosus.

Antiphospholipid antibodies (APA), including lupus anticoagulants (LAC; as detected by in vitro blood clotting tests) and anti-cardiolipin antibodies (ACA; as assayed by solid-phase immunoassay), are strongly associated with recurrent thrombosis, thrombocytopenia, and recurrent fetal loss in some patients with systemic lupus erythematosus (SLE). The combined presence of APA and these clinical manifestations is termed antiphospholipid syndrome (APS). LAC and ACA comprise heterogeneous and somewhat overlapping autoantibody subsets. To date, it is unclear what degree of heterogeneity is present in an individual patient and between patients. To begin to address these issues, we generated three monoclonal LAC antibodies from a patient with SLE and APS. These antibodies were studied for their binding specificities and variable (V) region nucleotide sequences. All three LAC were unreactive with DNA, cardiolipin or other phospholipids. Sequence analysis of these antibodies revealed extensive overlap in their Ig V genes with anti-DNA antibodies and other autoantibodies characteristic of lupus. These data provide the first V gene sequence information on a group of SLE-derived LAC without ACA activity, representative of a similar subset of LAC found in patients with APS.

Adult↗
PubMed1997

Lupus vulgaris in a patient with systemic lupus erythematosus and persistent IgG deficiency.

We present the case of a patient with juvenile onset systemic lupus erythematosus (SLE) who developed a persistent, acquired hypogammaglobulinaemia with IgG deficiency. The hypogammaglobulinaemia was probably a complication of high dose corticosteroid treatment. The serum IgG level remained subnormal despite intravenous immunoglobulin therapy. Lupus vulgaris, which developed on the nasal cartilage in this patient with SLE, is not an expected finding. This patient is probably the first reported case of SLE associated with lupus vulgaris.

Adult↗
PubMed2000

An unusual case of systemic lupus erythematosus, lupus nephritis, and transient monoclonal gammopathy.

A 23-year-old female patient suffering from active systemic lupus erythematosus (SLE) was treated with azathioprine (2 mg/kg per day) and prednisone. Lupus nephritis class III with increasing proteinuria developed 28 months after disease onset. Treatment was switched to monthly pulse cyclophosphamide administered intravenously for 6 months (total dose 6.3 g), followed by oral azathioprine and low-dose prednisone to maintain partial remission. Eight months later, the patient developed an acute exacerbation of SLE with fever, proteinuria of 9.1 g/day, pancytopenia, and cerebral involvement with cephalgias and a grand mal seizure. She responded well to high-dose corticosteroids (500 mg prednisolone pulses over 3 days, i.v.) and was azathioprine switched from to methotrexate (12.5-15 mg per week). Under this treatment, lupus activity gradually decreased and the patient felt well again. Five years after the initial diagnosis of SLE, a rapidly increasing immunoglobulin G-kappa type (IgG-kappa) monoclonal gammopathy developed, reaching a maximal serum paraprotein concentration of 73.5 g/l. Bone marrow biopsy revealed 15% of moderately abnormal, highly differentiated plasma cells arranged in small clusters and expressing IgG-kappa. No bony lesions were detectable on skeletal radiographs. Pulses of dexamethasone (40 mg) were administered and led to a transient decrease of paraproteinemia to a minimum of 31.9 g/l, followed by an increase to 62 g/l. At that point, high-dose chemotherapy supported by autologous stem cell transplantation was considered. Due to an intermittent pneumococcal septicemia, methotrexate was discontinued and dexamethasone was replaced by 5-10 mg cloprednol. At this point, totally unexpectedly, the paraprotein decreased spontaneously without any further cytostatic treatment and was no longer detectable 1 year later. Concomitantly, plasma cell counts in bone marrow biopsies fell to below 5%. As SLE remained inactive, the patient became pregnant and gave birth to a healthy child. During late pregnancy, SLE activity flared up with rising proteinuria and blood pressure. Therefore, after delivery, cyclophosphamide (100 mg/day, orally) was readministered for 4 months, resulting in an improvement of kidney function with stable proteinuria of 1-2 g/l to date. Paraproteins are no longer detectable. In conclusion, this case report documents the rare event of transient paraproteinemia in a patient with SLE. A self-limiting regulatory defect in the control of a terminally differentiated B-cell clone may be the origin of this phenomenon.

Adult↗