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At least 955 records · Page 53Linked to original sources
PubMed1982

Bullous systemic lupus erythematosus.

Two patients with established systemic lupus erythematosus developed bullous dermatoses clinically suggestive of bullous pemphigoid (BP). Direct immunofluorescence demonstrated linear staining at the dermoepidermal junction for IgG and C3 in a pattern typical for BP. However, immunoelectron microscopy demonstrated deposits of IgG largely below the basal lamina, with little if any deposit present within the lamina lucida. These findings are consistent with systemic lupus erythematosus (SLE) and effectively rule out BP. In addition, the leukocyte attachment assay, an in vitro assay of the functional activity of tissue-deposited immune complexes, demonstrated strong attachment of leukocytes to the dermoepidermal junction of patients' skin, suggesting that the immune reactants were functional immune complexes of possible importance to the pathogenesis of the bullous lesions. To our knowledge, this is the first time that immunoelectron microscopy has been performed on skin from patients suspected of manifesting concurrent SLE and BP. Our findings cast doubt on previous such reports by demonstrating the existence of a bullous form of SLE resembling BP both clinically and by direct immunofluorescence.

Adolescent↗
PubMed1994

Rapid appearance of severe mitral regurgitation under high-dosage corticosteroid therapy in a patient with systemic lupus erythematosus.

Survival of patients with systemic lupus erythematosus has increased with corticosteroid therapy. However, adverse effects of corticosteroid therapy on cardiovascular structures, such as scarring and shrinking of affected valves, are not well known. We report the case of a 19-year-old patient who developed severe mitral insufficiency within a few weeks after high-dosage corticosteroid therapy had been instituted for an acute relapse of systemic lupus erythematosus. The rapid development of severe mitral regurgitation was documented by sequential colour Doppler echocardiography.

Adult↗
PubMed2003

[Primary central nervous system lymphoma in a patient with systemic lupus erythematosus].

A 36 year-old woman with systemic lupus erythematosus was admitted to our hospital with headache, brachiocrural hemiparesis and hemianesthesia. She had been treated with prednisone and cyclophosphamide. CT scan and MRI revealed a 15 mm nodular mass enhanced with gadolinium in left frontal convexity. CNS biopsy was performed and a diffuse large B-cell lymphoma was diagnosed. She was treated with radiation therapy without response and died. There are few reports of erythematosus systemic lupus associated with primary central nervous system lymphoma.

Adult↗
PubMed1977

Serum factors releasing serotonin from normal platelets: relation to the manifestations of systemic lupus erythematosus.

In 13 patients with systemic lupus erythematosus, globulin fractions of sera from serial bleedings were assayed for the induction of serotonin release from normal platelets. Releasing activity appeared at some time in the sera of seven patients, five of whom had episodes of thrombocytopenia. Conversely, only one patient manifested thrombocytopenia without the occurrence of serotonin releasing activity at any time. In three patients with episodes of thrombocytopenia, increases in serotonin releasing activity temporally coincided with drops in platelet count. These data show that levels of circulating platelet serotonin releasing factor(s) vary in the course of systemic lupus erythematosus and these variations may be inversely related to the platelet count in particular patients.

Adult↗
PubMed1990

Glycoprotein specificity of cold-reactive IgM antilymphocyte autoantibodies in systemic lupus erythematosus.

Sera from patients with systemic lupus erythematosus frequently contain IgM antibodies to glycoproteins of Mr 46,000 and approximately 200,000 isolated from nonionic detergent lysates of mature T cells by affinity chromatography with solid-phase wheat germ agglutinin. Autoantibodies of this specificity correlate strongly with the presence of IgM anti-T cell autoantibodies, as determined by independent indirect immunofluorescence and complement-dependent microcytotoxicity assays, and are specifically absorbed by incubation of patient serum with viable T cells. Collectively, the data suggest that gp46 and, to a lesser extent, gp approximately 200 represent major targets of IgM antilymphocyte autoantibodies in systemic lupus erythematosus.

Antibody Specificity↗
PubMed1991

Haemostatic factors associated with vascular thrombosis in patients with systemic lupus erythematosus and the lupus anticoagulant.

To elucidate the mechanism of vascular thrombosis in patients with systemic lupus erythematosus and the lupus anticoagulant changes in factors associated with haemostasis were investigated. The lupus anticoagulant was associated with an increased incidence of thrombosis, particularly cerebral thrombosis. Concentrations of fibrinopeptide A and fibrinopeptide B beta 15-42 were significantly raised in the plasma of patients with systemic lupus erythematosus and the anticoagulant compared with concentrations in patients without the lupus anticoagulant. The tendency towards formation of thrombosis was not found in all lupus patients with the anticoagulant, however. Concentrations of thromboxane B2 were remarkably raised in the plasma of the two patients with the lupus anticoagulant who had recently had thrombosis. Concentrations of 6-keto-prostaglandin F1 alpha, protein C, antithrombin III, and plasminogen were similar in both groups. No significant decrease in serum stimulatory activity on prostacyclin production by cultured aortic endothelial cells was noted in lupus patients with the anticoagulant, but inhibition was present in the two patients with recent thrombosis. These results indicate that although patients with the lupus anticoagulant are not always in a hypercoagulable state, haemostatic abnormalities found in some patients with the anticoagulant may be predictive of thrombotic events.

6-Ketoprostaglandin F1 alpha↗
PubMed2005

Anti-ribosomal P-protein and its role in psychiatric manifestations of systemic lupus erythematosus: myth or reality?

Systemic lupus erythematosus (SLE) is an autoimmune disease that may involve the central nervous system (CNS) resulting in neuropsychiatric manifestations. The associated psychiatric disorders include depression, psychosis, mood disorders, anxiety, cognitive dysfunction, and delirium/ encephalopathy. Several autoantibodies may play a role in the pathogenesis of psychiatric complications of SLE, particularly antibodies against ribosomal P-proteins (anti-P) and possibly antibodies against endothelial cells (AECA). The reported prevalence of anti-P is highly variable in SLE patients and is dependent on different ethnic backgrounds, sensitivity and specificity of the assays employed for autoantibody detection, and the time at which sera were analysed in relation to the clinical event. Controversial data exist on the association of anti-P with psychiatric manifestations of SLE. These autoantibodies have been suggested to be specific markers of the psychiatric manifestations of SLE, particularly of the psychosis and depression, and the antibody level varied with the clinical activity of the disease. Some studies have confirmed the hypothesis of an association of anti-P antibodies with psychiatric manifestations of neuropsychiatric SLE (NPSLE) while others have disputed this relationship. This review summarizes the recent studies about relationship between anti-P antibodies and psychiatric manifestation of SLE.

Autoantibodies↗
PubMed1982

Influence of oral contraceptive therapy on the activity of systemic lupus erythematosus.

Since harmful effects of estrogens in murine lupus are well established, we studied the influence of oral contraceptive therapy on systemic lupus erythematosus activity in 26 female patients with lupus nephropathy. Combined preparations containing either 50 micrograms (14 patients) or 30 micrograms (7 patients) of ethinyl-estradiol were used in 21 courses in 20 patients. Initial manifestations or exacerbations of systemic lupus activity appeared within 3 months of beginning hormonal therapy in 9 patients, an overall incidence of lupus flare-up of 43%; there was major renal involvement in 4 patients. Conversely, evidence of lupus exacerbation did not develop in any of 11 patients who received pure progestogen oral contraceptive therapy with either continuous low-dose norsteroids (6 patients) or discontinuous progestogens at normal dosage (5 patients). These patients were followed for 5--30 months. Our data indicated that oral contraceptive therapy that used estrogens, even at low doses, often induced exacerbation of systemic lupus erythematosus activity. Pure progestogens, which were effective and devoid of such unfavorable effects, may be preferred in these patients.

Adolescent↗
PubMed1990

Idiotypic characteristics of immunoglobulins associated with human systemic lupus erythematosus. Association of high serum levels of IdGN2 with nephritis but not with HLA class II genes predisposing to nephritis.

Serum levels of IdGN2 (an idiotype enriched in nephritogenic antibodies), IdX (an idiotype not enriched in nephritogenic antibodies), IgG, and anti-DNA were measured in 23 Caucasian patients with lupus nephritis, in age- and sex-matched lupus patients without nephritis, and in similarly matched healthy individuals. Serum levels of IdGN2 were significantly higher in the patients with lupus nephritis than in those without, and they were higher in all lupus patients compared with the healthy control subjects. However, the same observations were true for serum levels of IdX. There were significant positive correlations between the serum levels of IgG, IdGN2, IdX, and anti-DNA. HLA typing at the DR and DQ loci was performed in 105 lupus patients of different races (Caucasian, black, and Asian/Polynesian/Filipino). Serum levels of IdGN2 in 83 of these individuals did not correlate with any of the HLA class II haplotypes currently known to predispose to lupus nephritis. We conclude that the high serum levels of IdGN2, which are characteristic of some patients with lupus nephritis, may often result from polyclonal B cell activation rather than from idiotype-specific upregulation associated with one or more of the class II genes that predispose to nephritis in this disease.

Genes, MHC Class II↗