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Clinical significance of immune deposits in the skin in SLE.

The lupus band test (LBT) was evaluated in 53 SLE patients. There was no significant correlation between the presence of a positive LBT and active clinical nephritis, renal histology, hypocomplementemia, or elevated anti-nDNA antibodies. In 14 patients the classes of immunoglobulins in the skin and the glomeruli were directly compared and differences were present in 11 patients. Repeat LBTs frequently became positive in patients after successful suppression of disease activity.

Adolescent↗
PubMed1986

Effect of plasmapheresis on E-rosette receptors in SLE patients.

The present study reports on the effects of plasmapheresis on both cellular (E-rosette receptor- and Fc receptor-bearing lymphocytes) and humoral (antilymphocyte antibodies) immunity in patients with active SLE. Ten untreated patients were studied before and after two plasma exchanges. The E-rosette receptor-positive cells were studied by OKT11 monoclonal antibody and Fc receptor-bearing cells by Leu15 monoclonal antibody. Antilymphocyte antibodies were studied before and after plasma exchange by an indirect immunofluorescence technique on autologous and normal lymphocytes. A reduction in OKT11+ and Leu15+ lymphocytes was observed in all patients before plasmapheresis. Antilymphocyte antibodies were detected in five patients. After plasma exchange, an increase in E-rosette receptor- and Fc receptor-bearing lymphocytes was observed along with a reduction in the amount of antilymphocyte antibodies.

Antibodies↗
PubMed1999

RNP positivity in Maltese SLE patients.

The SLE database at the Rheumatology Clinic, St. Luke's Hospital currently includes 62 patients. The presentation, clinical features, ACR criteria and laboratory findings in RNP positive lupus patients [14] were compared to RNP negative subgroup [33]. RNP positivity was significantly associated with Raynaud's phenomenon (p < 0.01), myalgia (p < 0.02), myositis (p < 0.05), neuropsychiatric features (p < 0.05) and Sm positivity (p < 0.01). RNP positive patients had a higher frequency of positive family history, mortality, malar and maculopapular rashes, nail-fold infarcts, telangiectasia, digital vasculitis, photo-sensitivity, arthritis, pleurisy, pericarditis, pericardial effusions, depression, headache, psychosis and TIA.

Autoantigens↗
PubMed1999

Male SLE patients in Malta.

The SLE patient database at the Rheumatology Clinic, St. Luke's Hospital includes 62 patients, 58 of which have complete data. The patients were grouped according to sex (7 males vs 51 females). The presentation, clinical manifestations, ACR criteria and laboratory findings of the 2 groups were analyzed and compared. Serositis as the initial manifestation at presentation was significantly commoner in males (29% vs 2%; p < 0.05). Cardiorespiratory problems such as pleurisy, pericarditis, pericardial effusions and myocarditis were more frequent in the male subgroup. Female patients had more arthritis, myositis, neuropsychiatric manifestations (depression, psychosis and headache) anemia, leucopenia and ENA positivity than their male counterparts. All 6 mortalities recorded were in the female subgroup.

Female↗
PubMed1982

Monocyte activation by immune complexes of patients with SLE.

1. IC precipitated by PEG from patients with SLE inhibit in vitro the FcR dependent reaction of normal monocytes with sSRBC, while the C3bR dependent reaction of the cells with sensitized yeast is reduced only by some of them. The monocytes were preincubated with the IC for 30 min at room temperature. 2. When the monocytes were incubated with the IC for 22 hours at 37 degrees C the reaction of FcR with sSRBC increased, while the C3bR dependent reaction did not altered. 3. Simultaneously with the increasing FcR dependent reaction, the secretion of lysosomal beta-glucuronidase of monocytes cultivated with IC is greater than those of the controls.

Antigen-Antibody Complex↗
PubMed1993

ANCA with specificity for lactoferrin in systemic lupus erythematosus (SLE).

Antibodies to lactoferrin were detected in about 20% of patients with SLE, irrespective of the presence of renal involvement and in 10% of patients with rheumatoid arthritis and in 19% of patients with scleroderma. We conclude that anti-lactoferrin antibodies may be found in different types of connective tissue disease. Their clinical significance in these diseases however remains to be elucidated.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1992

The genetic basis of Ro and La antibody formation in systemic lupus erythematosus. Results of a multicenter study. The SLE Study Group.

Antibodies against Ro and La, including recombinant La and recombinant 60 kD-Ro, were determined by counter immunoelectrophoresis and ELISA in over 300 central European systemic lupus erythematosus (SLE) patients. The presence of both Ro and La antibodies was strongly associated with the MHC haplotype B8-C4AQ0-DR3-DQ2, the association being strongest for DR3. After exclusion of all B8-DR3 positive patients only DR3 positive patients still showed an increased incidence of Ro and La antibodies, suggesting DR3 as the primary association factor. High titers of La antibody, but not of 60 kD-Ro antibody, were also significantly associated with the presence of DR3. Other DR and DQ antigens or heterozygous DQ combinations were not significantly associated with Ro and La antibodies.

Antibodies, Antinuclear↗
PubMed1987

Increased presence of common systemic lupus erythematosus (SLE) anti-DNA idiotypes (16/6 Id, 32/15 Id) is induced by procainamide.

Sixty-seven patients on treatment with procainamide were examined for the presence of two common idiotypes of anti-DNA antibodies (16/6 Id and 32/15 Id). These idiotypes have been shown previously to have clinical relevance in patients with systemic lupus erythematosus (SLE). An enzyme-linked immunosorbent assay (ELISA) with rabbit anti-Id antibodies revealed increased concentrations of the 16/6 Id and 32/15 Id in 25 (37%) and 16 (24%) patients, respectively. Five of eight patients with drug-induced lupus had elevated titers of both idiotypes. A high correlation (R = 0.56, P less than 0.001 for 16/6 Id) was found between Id levels and anti-single-stranded DNA (ssDNA) antibody titers and between 16/6 Id titers and antihistone antibodies (IgG, R = 0.43; IgM, R = 0.25). It seems that procainamide, a component known to be associated with drug-induced lupus, may induce an increased production of common anti-DNA idiotypes in apparently normal subjects.

Antibodies, Viral↗
PubMed1989

Effects of dazmegrel, piroxicam and cyclophosphamide on the NZB/W model of SLE.

To investigate the potential importance of prostaglandins and thromboxane in systemic lupus erythematosus (SLE), the effects of a nonsteroidal antiinflammatory drug (piroxicam) and a thromboxane synthetase inhibitor (dazmegrel) were examined on survival, proteinuria, food consumption, body weight, and peripheral lymphocyte subset distribution in the NZB/W model of autoimmune lupus disease. The effect of an immunosuppressant (cyclophosphamide) known to be effective in the treatment of murine lupus on these parameters was also examined. Cyclophosphamide at 25 mg/kg ip weekly prolonged survival, inhibited proteinuria and prevented the characteristic decline in peripheral T cells and the relative increase in B cells seen in NZB/W lupus disease while having no apparent effect on body weight or food consumption. Neither dazmegrel at 50 or 200 mg/kg/day in the diet nor piroxicam at 2 mg/kg/day in the diet had any significant effects on these parameters.

Animals↗
PubMed1986

Arterial occlusion causing large bowel infarction--a reflection of clotting diathesis in SLE.

The patient, a 44-year old woman with systemic lupus erythematosus, (SLE), developed infarction of the bowel and spleen after occlusion of the inferior mesenteric and splenic arteries, necessitating colectomy and splenectomy. She had had previous cerebral thromboses and a lower limb deep vein thrombosis. Histological examination of the involved vessels showed the presence of thrombus only with the total absence of any vasculitis. The patient demonstrated antibodies to phospholipid - the "lupus anticoagulant" (LA) and antibodies to cardiolipin in serum, both strongly associated with thromboses.

Adult↗
PubMed1987

Autoimmune hepatitis or hepatic involvement in SLE?--A case report.

We report a patient with autoimmune hepatitis, who simultaneously satisfied the 1982 revised ARA criteria for systemic lupus erythematous and emphasize the difficulty in differentiating these two diseases. In addition, current concepts of a possible immunological distinction between autoimmune hepatitis and hepatic involvement in SLE are reviewed.

Autoimmune Diseases↗
PubMed1996

Lack of platelet response to collagen associated with autoantibodies against glycoprotein (GP) Ia/IIa and Ib/IX leading to the discovery of SLE.

An increased bleeding time and a prolonged APTT (activated partial thromboplastin time) observed in a 48-year-old woman led to the discovery of SLE confirmed by immunological tests. Platelet function and analysis of membrane glycoproteins revealed an isolated impaired collagen induced platelet aggregation and allowed the detection of autoantibodies directed against GpIa/IIa and GpIb/IX.

Antigens, CD↗
PubMed2004

Intravenous cyclophosphamide therapy in a case with refractory thrombotic microangiopathic hemolytic anemia and SLE.

The case of a 27-year-old woman who simultaneously presented with SLE and severe refractory thrombotic microangiopathic hemolytic anemia (TMHA) is reported. She had extremely high levels of platelet-associated IgG (PAIgG), and her TMHA was refractory to plasma exchange and corticosteroid therapy. However, the TMHA was effectively controlled by i.v. cyclophosphamide therapy. ITP and TTP are generally considered distinct diseases; however, TMHA may occur secondary to platelet aggregation via autoimmune mechanisms in certain cases. Immunosuppressive therapy at an early stage of the disease may be beneficial in refractory cases of TMHA with autoimmune features.

Adult↗
PubMed2005

Intracerebral hemorrhage in a patient with SLE and catastrophic antiphospholipid syndrome (CAPS): report of a case.

A 31-year-old woman was admitted to the hospital for investigation of left lower limb thrombophlebitis. History, physical examination, and laboratory investigations led to the diagnosis of systemic lupus erythematosus (SLE), complicated by secondary antiphospholipid syndrome (APS). Treatment included steroids, azathioprine, aspirin, and low molecular weight heparin. Sixty-three days later, she was admitted to the hospital again because of high fever, macroscopic hematuria, and dyspnea. Laboratory testing showed anemia and impaired renal function. High-resolution chest computed tomography (CT) revealed bilateral multiple peribronchial infiltrates with hemorrhage. Magnetic resonance imaging (MRI) angiography of the kidneys revealed left renal vein thrombosis combined with ischemia of the left kidney. Cyclophosphamide and methylprednisolone pulse treatment as well as intravenous immunoglobulins were started immediately. Despite intensive immunosuppressive and supportive treatment, she suffered three relapses of alveolar hemorrhage and died on day 40, due to severe intracerebral bleeding. The final diagnosis was catastrophic APS with diffuse alveolar hemorrhage and kidney involvement. The unusual combination of recurrent alveolar hemorrhage and death from intracerebral hemorrhage rather than thrombosis in a CAPS patient is discussed.

Adult↗
PubMed2006

Nocardia brain abscesses in a male patient with SLE: successful outcome despite delay in diagnosis.

We report a 37-year-old African-American man with systemic lupus erythematosus (SLE) diagnosed in May 2001 when he presented with biopsy-proven nephritis. He had been treated intermittently from May 2001 to November 2004 with intravenously (i.v.) administered cyclophosphamide and high doses of prednisone due to unrelenting proteinuria. In November 2004, he was admitted to the hospital because of deterioration of renal function and massive proteinuria (21 g dl(-1) 24 h(-1)) and treated with pulses of methylprednisolone and two courses of i.v. administered cyclophosphamide. His hospital course was complicated by cellulitis and bacteremia with Pseudomonas spp. and Streptococcus bovis. He was discharged on prednisone 60 mg daily, ciprofloxacin, augmentin, and hemodialysis. He was readmitted a week later with new onset of seizure activity, slurred speech, and left-sided hemiparesis. Magnetic resonance imaging of the brain revealed multiple ringlike enhancing foci in the frontal and occipital lobes. Brain biopsy was performed, and Gram stain and initial cultures were negative. Empiric tobramycin, cefepime, and metronidazole were administered. Diagnosis was delayed for several months, but culture eventually grew Nocardia asteroides. Trimethoprim-sulfomethoxazole and linezolid therapy was begun. This was followed by slow, but steady, clinical improvement. Risk factors, diagnostic clues, and treatment are reviewed.

Adult↗
PubMed1992

Production of antibodies specific for double stranded antigen DNA cloned from immune complexes in plasma of a SLE patient.

The antigenicity of antigen DNA isolated from immune complexes in plasma of a SLE patient was examined. DDY mice were immunized with the cloned antigen DNA carrying a sequence homologous with a part of bacteriophage f1 (KS8 DNA) by the coupling method, and the antibody response was estimated by radioimmunoassay. Antibodies specific to double stranded DNA were elicited. Moreover, the antibodies showed preferential binding to KS8 DNA than other DNA derived from Escherichia coli. These results suggest that KS8 DNA has a significant antigenicity in mice.

Antibodies, Heterophile↗
PubMed1991

Modulation of SLE induction in naive mice by specific T cells with suppressor activity to pathogenic anti-DNA idiotype.

T cells (CD8+) with specific suppressor activity against anti-dsDNA antibody (16/6 Id+) were generated in vitro. The cells were established from BALB/c-enriched T cells exposed in vitro to silica beads coated with the pathogenic anti-DNA idiotype, 16/6. The idiotype specificity of the suppressor cells was demonstrated by (a) specific induction of a decrease in proliferative response of T helper cell lines specific for the pathogenic idiotype (16/6 Id), when exposed to the idiotype, with no effect on T cell lines with other specificities, e.g., against human IgM or synthetic polypeptide. (b) Effectively suppressing in vitro antibody production of anti-16/6 antibody, employing 16/6-primed B cells and specific helper T cell line. The 16/6 Id-specific Ts cells were found to be MHC restricted. Weekly intravenous injections of 10(7) 16/6 Id-specific Ts cells given to BALB/c mice at different stages of experimental SLE disease prevented the clinical, serological, and pathological manifestations. This effect was characterized by decreased titers of autoantibodies (e.g., anti-DNA, anti-Sm antibodies) in the sera, by abolishment of the proteinuria, leukopenia, and the increased ESR, followed by decreased immunoglobulin deposition in the kidneys. Treating the mice with control IgM-specific T cells did not affect the above parameters. These studies demonstrate the ability to generate Ts cells specific for pathogenic idiotypes. The method might be employed therapeutically to modulate the course of autoimmune conditions.

Animals↗