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PubMed1987

Lamin B autoantibodies in sera of certain patients with systemic lupus erythematosus.

Sera from four patients with systemic lupus erythematosus containing antibodies that yield nuclear rim staining of HEp-2 cells by indirect immunofluorescence were identified and characterized. Each serum contained autoantibodies reacting strongly with lamin B on western blots. One of the four sera displayed weaker reactivity with lamins A and C, while the other three displayed only minimal reactivity with lamins A and C. Titers of antilamin antibodies ranged from 1:1,250 to 1:36,250. Two of the sera also reacted at a dilution of 1:20 with cytoplasmic filaments of PTK-2 cells, suggesting that a small fraction of the autoantibodies in these sera may bind to alpha-helical domains of the lamins that are homologous to those of intermediate filaments. The majority of the antilamin antibodies in these patients' sera are specific for portions of the lamin B molecule that are not homologous to lamins A and C, however. The findings suggest that autoantibodies to the nuclear lamina may, in some instances, be responsible for a rim pattern in the fluorescent antinuclear antibody assay. In addition, autoantibodies to the nuclear lamina in sera of certain patients with systemic lupus erythematosus may be useful for defining the molecular structure and biological functions of lamin B, as well as for studying mechanisms of autoimmunity.

Antibody Specificity↗
PubMed1997

Core decompression for osteonecrosis of the femoral head in systemic lupus erythematosus.

A cross sectional study was performed to try to identify various demographic and radiologic risk factors for disease progression in 50 patients (79 hips) with corticosteroid associated osteonecrosis of the femoral head who had a core decompression. Thirty-one of the hips were in 18 patients who had systemic lupus erythematosus and were compared with the remaining group of 48 hips in 32 patients who were taking corticosteroids for other reasons. All patients in the study had been taking greater than 30 mg of prednisone for at least 2 weeks at least 6 months before the onset of osteonecrosis. Patients underwent a core decompression and were then observed for an average of 12 years (range, 4-18 years). Overall, 42 of the 79 hips (53%) had satisfactory outcomes. Of the 31 hips in patients with systemic lupus erythematosus, 21 (68%) were converted to a total hip replacement. In the patients without systemic lupus erythematosus taking corticosteroids, 16 of 48 hips (33%) progressed to arthroplasty. A subset of 25 hips from each group (systemic lupus erythematosus and without systemic lupus erythematosus) were matched for age, gender, prednisone dose, Ficat and Arlet Stage, and length of followup. The matched group without systemic lupus erythematosus had 44% survival (11 of 25 hips), which was not statistically different when compared with the 36% survival (9 of 25 hips) found in the systemic lupus erythematosus group. The major risk factors for disease progression were late stage of disease (Stage III) at presentation and radiographic extent of the lesion (>200 degrees), regardless of diagnosis. None of the factors that have been found to be associated with osteonecrosis in patients with systemic lupus erythematosus could be associated with disease progression. Because cause seems to be less significant than the onset and extent of the disease, the clinician should make the diagnosis of osteonecrosis as promptly as possible so that treatment can be started at the earliest possible time, when it will be most efficacious.

Adolescent↗
PubMed1996

Similar Ro/SS-A autoantibody epitope and titer responses in annular erythema of Sjögren's syndrome and subacute cutaneous lupus erythematosus.

BACKGROUND AND DESIGN: Studies were conducted to determine whether certain types of Ro autoantibodies are unique to subacute cutaneous lupus erythematosus and annular erythema of Sjögren's syndrome. Ten American subacute cutaneous lupus erythematosus sera, 11 Japanese annular erythema of Sjögren's syndrome sera, and 39 control sera were tested by enzyme-linked immunosorbent assay with recombinant 52- and 60-kd Ro fusion proteins, native 60-kd Ro protein, and native La/SS-B protein. RESULTS: Japanese annular erythema of Sjögren's syndrome sera and American subacute cutaneous lupus erythematosus sera share several types of anti-52-kd and anti-60-kd Ro autoantibodies. However, these antibodies were found significantly more often and in significantly higher titers in sera from patients with Sjögren's syndrome who did not manifest these skin diseases. Patients with high Ro autoantibody titers were likely to have overt exocrine gland dysfunction. CONCLUSIONS: The failure to identify disease-specific Ro autoantibodies in subacute cutaneous lupus erythematosus and annular erythema of Sjögren's syndrome sera suggests that additional factors influence the development of these skin diseases. However, similarities in the Ro autoantibody responses and in the clinical features of subacute cutaneous lupus erythematosus and annular erythema of Sjögren's syndrome suggest that these two skin diseases might arise from a similar pathogenic process.

Asian People↗
PubMed2006

[Subacute cutaneous lupus erythematosus induced by terbinafine].

BACKGROUND: The onset of subacute cutaneous lupus erythematosus (SCLE) may be associated with the administration of a variety of drugs. Terbinafine, an oral antifungal agent, which rarely causes cutaneous eruptions, has been implicated as the cause or exacerbation of cutaneous lupus erythematosus in several patients. CASE: A 59-year-old man had received oral terbinafine for onychomycosis. The patient had a history of SCLE, which was in complete remission during the last 5 years. A month after initiating treatment with terbinafine the patient developed SCLE, which was diagnosed clinically and by histology. He had typical papulosquamous lesions. Immunological studies showed elevated titers of anti-nuclear antibodies. Following discontinuation of terbinafine therapy and under the treatment of systemic and topical steroids, a slow resolution of the eruption was noted over several weeks. CONCLUSIONS: This report, along with previous cases described, suggests the association between terbinafine therapy and the onset or exacerbation of SCLE often occurring in a patient with history of systemic lupus erythematosus or SCLE.

Antibodies, Antinuclear↗
PubMed1991

Strategies for reducing excess morbidity and mortality in blacks with systemic lupus erythematosus.

The epidemiology of systemic lupus erythematosus suggests that the excess morbidity and mortality in blacks with the disease is related to lower socioeconomic status. Poverty and factors associated with poverty are powerful predictors of poor outcome in a variety of chronic diseases, and lupus appears to be no exception. A body of studies in other illnesses suggests ways to neutralize, at least partially, the disadvantages of lower socioeconomic status, even though the root causes of poverty may be insurmountable. These include improving access to quality health care; targeting educational programs to promote recognition and understanding of the disease and the comorbid conditions that affect outcome; implementing programs to improve self-monitoring and adherence to medical regimens; developing opportunities to facilitate homemaking, childrearing, and working outside the home; and applying psychosocial interventions to enhance self-confidence and social support. Improved access to quality health care may actually lead to a decrease in health care costs.

Black or African American↗
PubMedDate not supplied

Family studies of B lymphocyte alloantigens in systemic lupus erythematosus.

In Caucasians with systemic lupus erythematosus (SLE), we have identified 3 risk markers in the HLA-D region -- HLA-DR2, HLA-DR3, and la-715 -- and have used these markers to probe 7 families in which more than 1 case of lupus had occurred. In 6 of the 7 families studied, persons with SLE were either homozygous for HLA-DR2, had 2 haplotypes carrying reactivity with la-715, or had at least 2 of the 3 risk markers HLA-DR2, HLA-DR3, and la-715. Several normal individuals in these kindreds also had these multiple risk markers but had no signs or symptoms of lupus. This limited study of lupus families suggests a role for coinheritance of HLA-D region genes as a factor in the development of SLE.

Adolescent↗
PubMed2001

Persistence of macroprolactinemia due to antiprolactin autoantibody before, during, and after pregnancy in a woman with systemic lupus erythematosus.

A woman with systemic lupus erythematosus (SLE) with marked increases in circulating 150-kDa PRL was studied from before conception, throughout pregnancy, and after pregnancy. The clinical features of the patient included idiopathic hyperprolactinemia without clinical symptoms such as amenorrhea and galactorrhea before pregnancy. No clinical lupus activity was present during follow-up. Serum PRL increase during pregnancy in this patient was considerably higher at weeks 27 and 33 than in normal pregnant women. In contrast, serum-free PRL levels were considerably lower at weeks 20, 27, and 33 than in normal pregnant women. A 150-kDa PRL (big big PRL) species persisted as the predominant circulating form of PRL throughout each measurement in this woman with SLE. In contrast, the predominant form of PRL in serum from healthy pregnant women was little PRL (or monomeric PRL). The nature of big big PRL was due to the presence of anti-PRL autoantibodies forming an IgG-23 kDa PRL complex, in accordance with the studies by affinity chromatography for IgG and Western blot analysis. The IgG-PRL complex was fully bioactive in vitro (Nb2 rat lymphoma cell assay). Injection of the serum into the rats demonstrated that the IgG-PRL complex was cleared more slowly than serum containing predominantly monomeric PRL. The data suggest that the IgG-PRL complex has biological activity; the absence of symptoms in this woman may be attributed to the fact that due to its large molecular weight, big big PRL does not easily cross the capillary walls. Delayed clearance may account for increased serum PRL levels in this SLE patient with anti-PRL autoantibodies.

Adult↗
PubMed2005

Effects of systemic lupus erythematosus on spatial cognition and cerebral regional metabolic reactivity in BxSB lupus-prone mice.

Brain-reactive auto-antibodies appear as key elements in the progressive CNS disturbances associated with systemic lupus erythematosus. The BxSB lupus prone mice are a model of this pathology, in which a gene located on the Y chromosome provokes a sex specific morbidity in males. This study was aimed to establish and characterize the relationships between behavioral disorders, neurological deficiencies and the aged-related immunological perturbations in this murine model. For this purpose, spatial and motor abilities were evaluated in male and female mice at six and 26 weeks of age. The results showed that the older males were greatly altered in their spatial abilities while the young ones and the females, whatever their age, were not. None of the animals had motor skill and motor learning disabilities. These spatial alterations were associated with modifications of basal neuronal activity measured by the cytochrome oxidase histochemical method in several areas directly or indirectly involved in spatial behavior, such as the hippocampus, the amygdala, the parietal and perirhinal cortex. Immunological study allowed us to correlate the behavioral abnormalities to the appearance of antibodies reactivities against cellular and nuclear components.

Animals↗
PubMed2001

Subacute cutaneous lupus erythematosus induced or exacerbated by terbinafine: a report of 5 cases.

BACKGROUND: Subacute cutaneous lupus erythematosus is a nonscarring, non-atrophy-producing photosensitive cutaneous disorder. Half of the patients have 4 or more of the criteria for classification as systemic lupus erythematosus. In some patients, drugs induce or exacerbate the cutaneous disease. OBSERVATION: We describe 5 patients who had either an exacerbation or a new onset of subacute cutaneous lupus erythematosus while taking terbinafine for presumed onychomycosis. CONCLUSION: In general, terbinafine is a safe drug, but perhaps patients with known lupus erythematosus or photosensitivity are predisposed to drug-induced or drug-exacerbated disease.

Adult↗
PubMed1996

Myocardial infarction as the presenting manifestation of systemic lupus erythematosus with antiphosphatidylserine antibodies.

BACKGROUND: The presence of antiphospholipid antibodies has been associated with thrombotic events in systemic lupus erythematosus and other diseases. Antiphosphatidylserine antibodies have been shown more recently to have clinical implications being noted in thrombocytopenia, positive VDRL test, prolonged partial thromboplastin time, and recurrent fetal loss. OBJECTIVE: To report a patient with systemic lupus erythematosus who presented with a myocardial infarction resulting from a single clot in the distal left anterior descending coronary artery and to discuss the merits of evaluating such patients for the presence of antiphospholipid antibodies. METHODS: Case report and review of the literature. RESULTS: A 55-year-old woman with no risk factors for coronary artery disease presented with a myocardial infarction. A distal left anterior descending coronary artery clot was seen on angiography. Evaluation for the presence of a hypercoagulable state revealed evidence for systemic lupus erythematosus. Although lupus anti-coagulant and anticardiolipin antibody titers were negative, antiphosphatidylserine IgA antibodies were detected. CONCLUSION: Because antiphosphatidylserine antibodies of the IgA isotype have been shown to be associated with thrombosis and other manifestations of systemic lupus erythematosus, a complete evaluation for antiphospholipid antibodies should include testing for all three isotypes.

Antibodies, Antiphospholipid↗
PubMed1996

Defective antigen-presenting cell function in patients with systemic lupus erythematosus.

OBJECTIVE: Patients with systemic lupus erythematosus (SLE) who exhibit defective in vitro responses to recall antigens and normal responses to alloantigens have been shown to have an abnormality in antigen-presenting cell (APC) function. This study was undertaken to further characterize this defect in APC function in lupus patients. METHODS: Mononuclear cells (MNC) from the peripheral blood of patients with SLE and from normal individuals were cultured in the presence of either recall antigen tetanus toxoid (TT), anti-CD3 (OKT3) monoclonal antibody, or alloantigens, and proliferative or interleukin-2 responses were assessed. Cell surface expression of B7-1 was assessed by flow cytometry. RESULTS: MNC from all normal individuals and from 7 patients with SLE responded to both TT and alloantigen and were designated +/+. Twelve SLE patients did not respond to TT but did respond to alloantigen stimulation and were designated -/+. In both normal subjects and SLE patients, the ability to respond to OKT3 correlated strongly with the ability to respond to recall antigen. A defect in APC costimulatory function was suggested by data demonstrating that interferon-gamma-induced expression of B7-1 was significantly reduced in SLE patients compared with controls. Neither controls nor SLE patients expressed detectable amounts of surface B7-1 molecule on resting APC. Defective recall and anti-CD3-stimulated responses could be enhanced in SLE patients in the presence of B7/BBl-transfected P815 murine mastocytoma cells underscoring an SLE-associated defect in costimulatory activity. However, nontransfected P815 cells were also able to enhance responses to OKT3 in -/+ patients; blocking experiments showed that this was mediated through an IgG Fc receptor-dependent mechanism. CONCLUSION: These data indicate that SLE-associated defects in APC function in vitro can be accounted for by abnormalities in APC surface membrane molecules such as B7, IgG Fc receptors, and possibly others.

Adolescent↗
PubMedDate not supplied

[Hemorrhagic pericarditis and cardiac tamponade in systemic lupus erythematosus. A case report].

Systemic lupus erythematosus is a chronic inflammatory autoimmune disorder that can affect any organ or system. Although pericarditis is the most frequent cardiac manifestation of this entity, usually is not a life threatening situation. Pericardial effusion causing cardiac tamponade is a very rare complication in lupus, with an incidence less than 2%. We report a case of pericardial tamponade due to SLE with severe hemodynamic involvement in a 21-year-old woman associated to rapidly progressive glomerulonephritis, acute pancreatitis, acute acalculous cholecystitis, pleural effusion, hematologic, cutaneous and neurologic lupus activity. Recognition of this rare manifestation of SLE may be life saving.

Adult↗
PubMed1985

Cerebrospinal fluid immunoglobulin abnormalities in systemic lupus erythematosus.

Central nervous system (CNS) involvement is a common and important complication in systemic lupus erythematosus. The mechanisms for CNS involvement are poorly understood and reliable diagnostic procedures are lacking. Pairs of serum and cerebrospinal fluid (CSF) specimens from 17 patients with clinical and serological manifestations of systemic lupus erythematosus were analysed. All 11 patients with definite or suspect clinical CNS disorder revealed some kind of abnormality in the CSF, in contrast to three of seven systemic lupus erythematosus patients without CNS disorder. The most prominent findings in systemic lupus erythematosus patients with CNS disorder were immune aberrations with oligoclonal bands on agarose isoelectric focusing (AIF) and elevation of IgG and IgM index, probably reflecting intrathecal production of IgG and IgM respectively. Intrathecal production of antiviral antibodies was found in four of 12 patients by AIF followed by immunofixation and subsequent autoradiography. An enzyme-linked immunoabsorbent assay (ELISA) could not detect autoantibodies against structural brain antigens.

Adolescent↗
PubMed1983

Chronic infection with cutaneous herpes simplex in a patient with systemic lupus erythematosus.

A 68-year-old black woman with systemic lupus erythematosus being managed by systemic corticosteroids developed large ulcerated lesions in a dermatomal distribution on the flank and abdomen. Subsequently, large ulcers developed progressively in the perianal region, the buttocks, the perivaginal region, and the thighs. The clinical diagnosis was vasculitis of systemic lupus erythematosus. Biopsy from the margin of an ulcer showed changes in the epidermis that are specific for infections by herpesvirus. Electron microscopy revealed viral particles of herpesvirus. Cultures from the perianal lesions grew Herpesvirus hominis. This is the first report to our knowledge of "chronic cutaneous herpes infection" in a patient with systemic lupus erythematosus.

Aged↗