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[Studies on anti-DNA antibodies associated with renal involvement by enzyme-linked immunosorbent assay in patients with systemic lupus erythematosus].

It has been reported that a significantly higher incidence of lupus nephritis was found in patients with high avidity anti-DNA antibodies. Radioimmunoassay (Farr's assay) is a method which enables to detect high avidity anti-DNA antibodies, whereas enzyme-linked immunosorbent assay (ELISA) can detect anti-DNA antibodies from low to high avidity. There are, however some patients who had high levels of anti-DNA antibodies by Farr's assay without renal involvement. In this study, ELISA was developed to detect IgG anti-DNA antibodies highly associated with lupus nephritis by changing salt concentration of reaction buffer solution. Levels of a fraction, we call [0.1 M - 0.3 M] fraction, which was obtained from the antibody levels measured under 0.1 molar of sodium chloride (NaCl) subtracted by antibodies levels under 0.3 molar of NaCl solution were found to be significantly higher in patients with urinary protein (p = 0.0074) and low serum complement (C 3 less than 50 mg/dl; p = 0.0026, C 4 less than 10 mg/dl; p = 0.0280 and CH 50 less than 30 U/mL; p = 0.0662). Among the patients with hypocomplementemia, levels of [0.1 M - 0.3 M] fraction were significantly higher in patients with urinary protein than in patients without renal involvement. This fraction might be consistent with anti-DNA antibodies with intermediate avidity that are related to lupus nephritis. The ELISA procedure established in this study is showed to be a available method to detect anti-DNA antibodies associated with renal disease in patients with systemic lupus erythematosus.

Antibodies, Antinuclear↗

Selective decrease in antibody-dependent cell-mediated cytotoxicity in systemic lupus erythematosus and progressive systemic sclerosis.

With the use of two target cells (chicken erythrocytes and Chang cells), the antibody-dependent cell-mediated cytotoxicity (ADCMC) of peripheral blood mononuclear cells from patients with systemic lupus erythematosus (SLE) and progressive systemic sclerosis (PSS) was studied. Patients with active SLE had a significant reduction in ADCMC against Chang cells whereas cytotoxicity against chicken erythrocytes did not differ significantly from that of a control population. Similarly, a group of PSS patients with positive anti-DNP antibodies demonstrated a selective reduction in ADCMC against Chang cells. These findings support the concept that different effector cells mediate ADCMC against chicken erythrocytes and Chang cells, and indicate that in some patients with SLE and PSS there is a selective reduction or blockade of the ADCMC effector cell active against Chang cells.

Antibody-Dependent Cell Cytotoxicity↗

[Lupus erythematosus systemic and persistent pulmonary salmonellosis].

A 40-years-old woman with systemic lupus erythematosus and severe pulmonary nontyphoid salmonellosis (Salmonella Typhimurium), is reported. In addition the patient had incomplete septal cirrhosis. The authors pointed out a possible influence of Salmonella infection in the development of immune complex diseases.

Adult↗

Preliminary, dermatologic first step criteria for lupus erythematosus and second step criteria for systemic lupus erythematosus.

BACKGROUND: Comparisons of cases of systemic lupus erythematosus (SLE) with cases of rheumatoid arthritis and other rheumatologic disorders affords the basis of the 1982 revised criteria of the American Rheumatism Association (ARA) for classifying SLE cases. We address three questions: Do comparisons of LE cases with non-LE cases that have suggestive skin lesions yield criteria for use in dermatology clinics for primary classification of cases with photo distributions of skin lesions? Do comparisons of SLE with cutaneous LE cases yield the same or similar criteria to the revised ARA criteria for SLE? How should subacute cutaneous LE cases be evaluated for signs of significant systemic involvement? METHODS: Discriminant analyses on 168 cases with skin lesions suggestive of LE were performed using data based on the ARA criteria for SLE and study factors for cutaneous LE suggested by the European Academy of Dermatology and Venereology. RESULTS: These yielded two sets of criteria: (1) The 11 preliminary, dermatologic first step criteria (10 plus 1 for discoid lesions and histology) serve to classify cases as LE or non-LE. (2) The 11 preliminary, dermatologic second step criteria classify LE cases as cutaneous LE or systemic LE. Interestingly, 5 of 11 of these second step criteria differ from the 11 ARA criteria for systemic LE. These second step criteria afford a useful means of distinguishing between subacute cutaneous LE cases with or without significant systemic involvement. CONCLUSIONS: The study factors included in both the first and the second step criteria fall into three groups, notably clinical criteria, laboratory criteria, and "added study factors." The latter factors distinguish between the groups compared (LE vs. non-LE and cutaneous vs. systemic LE) but not as well as the study factors included as "criteria."

Humans↗

Treatment of pulmonary hemorrhage in childhood systemic lupus erythematosus with mycophenolate mofetil.

Systemic lupus erythematosus is a chronic autoimmune disease of unknown etiology with multisystem involvement. Pulmonary hemorrhage is a major life-threatening manifestation in children and adolescents with systemic lupus erythematosus, as well as in adults. Treatment has traditionally been with high-dose corticosteroids, with or without the addition of cytotoxic agents. We report the response of a patient with childhood systemic lupus erythematosus with recurrent pulmonary hemorrhage to treatment with mycophenolate mofetil.

Adolescent↗

Diagnosis and management of patients with neuropsychiatric systemic lupus erythematosus (NPSLE).

Neuropsychiatric systemic lupus erythematosus (NPSLE) involves a wide range of focal and diffuse central and peripheral nervous system disorders and affects up to 75% of SLE patients. NPSLE can occur any time in the course of SLE, even during periods in which no SLE disease activity is detected, and is likely to be caused by multiple factors, including autoantibody production, microvasculopathy and pro-inflammatory cytokines. Central to the diagnosis of NPSLE is the question of whether the presenting neuropsychiatric symptoms are due to SLE-mediated organ dysfunction, infection, medication side-effects or metabolic abnormalities (e.g. uraemia), or are due to an unrelated condition. The diagnostic inference of NPSLE can be made only after these secondary causes have been excluded. There is no one single diagnostic tool specific to NPSLE, and clinical diagnostic impressions must be based on the combined use of immunoserological testing, functional and/or structural neuroimaging and standardized neurological, rheumatological, psychiatric and neuropsychological assessments. The management of NPSLE includes symptomatic and/or immunosuppressive treatment strategies depending on the specific presenting neuropsychiatric symptoms and whether these occur in the setting of an SLE disease activity flare.

Humans↗

[Drug-induced lupus erythematosus syndrome. Pathogenesis and relation to systemic lupus erythematosus].

The drug-induced lupus erythematodes syndrome is a heterogeneous group of exogenically caused transitory autoimmunopathies . Essential knowledge has been got concerning the pathomechanism of the syndromes evoked by hydralazine, procainamide, diphenylhydantoin and Venopyronum . Though there are analogies to the systemic lupus erythematosus, we must take into consideration a diversity of diseases. Antibodies against histone have a certain diagnostic as well as pathogenetic relevance.

Diagnosis, Differential↗

Impaired T-cell-independent B-cell maturation in systemic lupus erythematosus: coculture experiments in monozygotic twins concordant for Klinefelter's syndrome but discordant for systemic lupus erythematosus.

In a case of monozygotic twins discordant for systemic lupus erythematosus (SLE), coculture experiments with isologous (i.e., genetically identical) lymphocytes were performed. Adequate T-helper-cell function in the SLE twin was demonstrated. Lack of B-cell responsiveness to T-cell-dependent and T-cell-independent polyclonal activators points to a T-cell-independent B-cell maturation defect in the SLE twin.

Adolescent↗

Systemic lupus erythematosus. Diagnosis and treatment.

Systemic lupus erythematosus is a multisystem inflammatory disease characterized by antinuclear antibody production. The diagnosis of this disease is established on the basis of a constellation of clinical and serologic features. Therapy is directed to specific disease manifestations and involves an array of anti-inflammatory and immunosuppressive agents that are administered judiciously to limit toxicity.

Anti-Inflammatory Agents↗

Crusted scabies in a child with systemic lupus erythematosus.

A child with systemic lupus erythematosus who has been treated with prednisone for three years, developed crusted scabies. Scrapings from lesions revealed Sarcoptes scabiei adult mites mad eggs. The patient died with septicemia and renal failure soon after starting topical 20% sulfur. A marked improvement was observed in the cutaneous lesions.

Biopsy↗

Profiles of antibodies to poly(ADP-ribose), left-handed Z-DNA, and other nuclear constituents in systemic lupus erythematosus and progressive systemic sclerosis.

A simple and sensitive method was developed for detection of antibodies to histones using a modification of the enzyme-linked immunosorbent assay (ELISA) for antibodies to nucleic acids. The antigens used for antibody assay were poly(ADP-ribose), left-handed Z-DNA, double-stranded DNA (dsDNA), single-stranded DNA (ssDNA), and calf thymus histones. These five antigen-antibody systems were used to examine the antibodies in patients with systemic lupus erythematosus (SLE) and progressive systemic sclerosis (PSS). A positive correlation was found between the antibody titers in patients with PSS. However, weak correlation was found between the titers of antibodies to these nuclear antigens in the SLE patients, except for correlations between the titers of antibodies to left-handed Z-DNA and histones, and those to ssDNA and dsDNA. From these data, it is suggested that presentation of modified chromatin to immune systems is involved in antinuclear antibody formation in PSS patients, whereas spontaneous expansion of clones for antinuclear antibodies may occur in SLE patients under certain conditions.

Adenosine Diphosphate Ribose↗

Complement system protein C4 and susceptibility to hydralazine-induced systemic lupus erythematosus.

21 patients with systemic lupus erythematosus induced by long-term treatment with hydralazine were investigated to see whether susceptibility to this syndrome was associated with deficiency of the classical pathway complement protein, C4. 16 of 21 (76%) patients had one or more C4 null (ie, non-productive) alleles compared with 35 of 82 normal subjects (43%). This difference was significant. The HLA-DR4 antigen, known to be in linkage disequilibrium with the C4B null allele, was also significantly more frequent in the patients (14 of 21 patients compared with 31 of 81 normal subjects). Susceptibility to hydralazine-induced lupus, as in idiopathic systemic lupus erythematosus, may depend partly upon genetically determined C4 levels.

Alleles↗

Placental pathology in systemic lupus erythematosus: a prospective study.

OBJECTIVES: Systemic lupus erythematosus and antiphospholipid antibody, often identified in patients with systemic lupus erythematosus, are associated with poor pregnancy outcome. This study distinguishes between the effect of each of these factors on gestational outcome and placental pathologic conditions in pregnant patients with systemic lupus erythematosus. STUDY DESIGN: Thirty-seven pregnancies and 40 placentas from 33 women with systemic lupus erythematosus were studied prospectively. RESULTS: Systemic lupus erythematosus alone, but not systemic lupus erythematosus activity, was associated with increased spontaneous abortions, preterm gestations, and fetal growth restriction. Placental correlates were ischemic-hypoxic change, decidual vasculopathy, decidual and fetal thrombi, chronic villitis, and decreased placental weight. Extensive infarction and fetal death were important antiphospholipid antibody-related findings. CONCLUSIONS: Decidual vasculopathy/coagulopathy appears to mediate the antiphospholipid antibody-related and much of the systemic lupus erythematosus-related deleterious effect on the placenta and gestational outcome. The presence of antiphospholipid antibody largely, but not invariably, predicts fetal death. Antiphospholipid antibody-independent chronic villitis may represent a second mechanism of systemic lupus erythematosus-related change.

Adult↗