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PubMed1989

Cerebrovascular disease and antiphospholipid antibodies in systemic lupus erythematosus, lupus-like disease, and the primary antiphospholipid syndrome.

PURPOSE AND PATIENTS AND METHODS: Antiphospholipid antibodies, lupus anticoagulant antibodies to cardiolipin, and a false-positive result on testing for syphilis have been linked to thrombotic vascular occlusions, particularly in patients with systemic lupus erythematosus (SLE) or lupus-like disease, i.e., patients not fulfilling four American Rheumatism Association criteria for the classification of SLE. The clinical and serologic features of 35 patients with cerebrovascular disease (strokes/transient ischemic attacks) who demonstrated antibodies to phospholipids are presented. Complete histories were obtained from all 35 patients, and all underwent routine physical examinations, radiography, electrocardiography, computed tomographic brain scanning, and immunologic studies. Psychometric tests were performed in nine patients. RESULTS: The strokes were often multiple and were followed by multi-infarct dementia in nine patients. Of particular interest were 10 patients in whom the presence of antiphospholipid antibodies was the major and often the sole immunologic disturbance present. Several of these patients were antinuclear antibody-negative, and the antinuclear antibodies, when present, were usually of a low titer (1:40 to 1:160). These patients conform to a group classified as having a primary antiphospholipid syndrome. CONCLUSION: Antiphospholipid antibodies are strongly associated with cerebrovascular occlusions in patients with SLE as well as in those with lupus-like disease and the primary antiphospholipid syndrome. All patients with any of these conditions who present with vascular events should be screened for these antibodies, as their occurrence may have a bearing on future therapy.

Adult↗
PubMed1993

Disseminated intravascular coagulation in a patient with systemic lupus erythematosus with lupus anticoagulant.

A 19-year-old female patient with systemic lupus erythematosus (SLE) who had lupus anticoagulant (LA) and concurrently developed disseminated intravascular coagulation (DIC) during an exacerbation of "central nervous system (CNS) lupus". Since no other indications or causes for DIC could be demonstrated, she was treated with prednisolone and anticoagulants, which rapidly alleviated her DIC condition as well as "CNS lupus". Although abnormalities of coagulation are frequently reported in SLE patients, DIC rarely occurs in patients with SLE without associated complications. A review of the pathogenesis of DIC in patients with SLE is discussed.

Adolescent↗
PubMed1988

Renal disease in systemic lupus erythematosus.

Lupus nephritis is the archetype of diseases caused by the deposition of immune complexes. The characteristics which render only a portion of circulating immune complexes nephritogenic are not well delineated, but cat-ionic charge of antigen and/or antibody may contribute. Lupus nephritis is characterized by extreme diversity of clinical manifestations and pathologic features. Scrupulous monitoring of urinary sediment and renal function tests is necessary to identify renal involvement in a phase which is amenable to therapeutic intervention. Evaluation of renal biopsies also assists in development of indications for therapy. The pathology of lupus nephritis is classified primarily as mesangial, focal proliferative, diffuse proliferative, and membranous nephropathy. Indexes of activity and of chronicity provide a succinet description of the balance of reversible and irreversible disease. The activity index incorporates glomerular hypercellularity, karyorrhexis/fibrinoid necrosis, leucocyte exudation, hyaline thrombi, cellular crescents, and interstitial inflammation. The chronicity index incorporates glomerular sclerosis, fibrous crescents, tubular atrophy, and interstitial fibrosis. Delineation of the activity and chronicity indexes also facilitates the assessment of prognosis and the ordering of indications for therapy.

Humans↗
PubMed1993

Neonatal lupus erythematosus and maternal lupus erythematosus mimicking HELLP syndrome.

A 4-month-old boy had a faint, confluent, macular erythema involving the forehead, nose, and philtrum, and matlike telangiectases over the forehead and eyelids. The clinical features, course, and laboratory studies were characteristic of neonatal lupus erythematosus. He was otherwise healthy and the product of a preterm twin pregnancy complicated by the development of maternal HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome. The patient had elevated Ro(SSA) and La(SSB) antibody titers, and studies performed on maternal blood disclosed positive antinuclear antibodies and elevated Ro and La antibody titers.

Adult↗
PubMedDate not supplied

Discoid lupus erythematosus and lupus profundus in childhood: a report of two cases.

Discoid lupus erythematosus (DLE) is a rare disorder in childhood, with 22 cases reported in the English-language literature. Less than 2% of patients with DLE have an onset before 10 years of age. We describe two children with DLE and lupus profundus with an onset of the disease at the ages of 11 and 15 years and focus on likely histopathologic differences between DLE in children and in adults. Histopathologic characteristics for childhood DLE might be an intense periadnexal and perivascular infiltrate extending into the interstitium and subcutaneous tissue consisting of lymphocytes, histiocytes, eosinophilic granulocytes, and plasma cells and lacking epidermal atrophy. The diagnosis of DLE in our two patients was established by clinicopathologic correlation based on clinical presentation, histologic and immunofluorescent findings in skin biopsy specimens, and the absence of clinical and laboratory evidence of systemic involvement. Therapy with antimalarials resulted in reduction of the skin lesions, but in one patient severe lipoatrophy occurred.

Adolescent↗
PubMed2025

Uncovering potential biomarkers and metabolic pathways in systemic lupus erythematosus and lupus nephritis through integrated microbiome and metabolome analysis.

OBJECTIVE: This study aims to explore the relationship between gut microbiota and fecal metabolomic profiles in patients with systemic lupus erythematosus (SLE), with and without lupus nephritis (LN), in order to identify potentially relevant biomarkers and better understand their association with disease progression. METHODS: Fecal samples from 15 healthy controls (HC) and 36 SLE patients (18 SLE-nonLN and 18 SLE-LN) were analyzed using 16S rRNA gene sequencing and untargeted metabolomics. Differential microbial taxa and metabolites were identified using Linear Discriminant Analysis Effect Size (LEfSe) and Orthogonal Partial Least Squares Discriminant Analysis (OPLS-DA). Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and Receiver Operating Characteristic (ROC) curve analyses were used to assess the potential clinical relevance of selected metabolites. RESULTS: Beta diversity analysis demonstrated distinct microbial clustering between groups (p&#x2009;<&#x2009;0.05). SLE-LN samples showed an increased relative abundance of Proteobacteria and decreased Firmicutes compared to SLE-nonLN. Metabolomic profiling identified multiple differentially abundant metabolites, with notable enrichment in primary bile acid biosynthesis pathways (e.g., Glycocholic acid, AUC&#x2009;=&#x2009;0.951). In the SLE-nonLN group, increased Glycoursodeoxycholic acid levels (AUC&#x2009;=&#x2009;0.922) were observed in pathways related to taurine and hypotaurine metabolism. Correlation analysis indicated a negative association between Escherichia-Shigella and bile acid levels (p&#x2009;<&#x2009;0.01). CONCLUSION: This integrative analysis suggests that patients with SLE and LN harbor distinct gut microbiota and metabolomic profiles. The identified microbial taxa and metabolites may have potential as non-invasive biomarkers and could contribute to a better understanding of SLE pathogenesis and progression.

Humans↗
PubMed2005

Transplantation and 6-month follow-up of renal transplantation from a donor with systemic lupus erythematosus and lupus nephritis.

Transplantation of kidneys with pre-existing glomerulonephritis (GN) has rarely been reported. Little is known of the subsequent evolution of donor pathology in the recipient. We report a transplant using a donor with systemic lupus erythematosus (SLE) and a history of remote acute renal failure but normal renal function at death. Although the screening harvest biopsy was unremarkable, time zero post-implantation renal biopsy showed evidence of lupus nephritis (LN). Sequential protocol biopsies demonstrated gradual resolution of the donor pathology, and renal function was stable despite severe cardiac disease in the recipient. Studies examining the role of functional and biopsy data on outcomes in expanded criteria renal transplantation are reviewed, and the limits of guidance from use of this data are discussed. Pre-existing mild GN may not be an absolute donor exclusion for candidates willing to accept expanded criteria donors. Use of expanded pool kidneys should be guided by functional, biopsy and demographic information, as no single factor alone predicts outcome.

Acute Kidney Injury↗
PubMed2006

Anti-dsDNA antibody subtypes and anti-C1q antibodies: toward a more reliable diagnosis and monitoring of systemic lupus erythematosus and lupus nephritis.

The putative distinct diagnostic and pathogenic potential of aDNA-Ab subtypes, differing in their affinity or epitope specificity, was subject of several studies with controversial results. Comparing five assays, characterized by different reaction conditions and nature/source of dsDNA, we investigated the abovementioned problem in a retrospective study on 100 systemic lupus erythematosus (SLE) patients and 100 controls (other CTD, autoimmune hepatopathies). As demonstrated, only assay 3 (Farrzyme, TBS, UK) and 5 (Farr-RIA, Trinity Biotech, Ireland) are really suitable to detect primarily high avidity aDNA-Ab. Both were significantly linked to lupus nephritis (specificity 84%) and highly specific for SLE (95 and 96%). Thereby, assay 3 was found to be the first solid phase ELISA probably suitable to replace the Farr-RIA. Classical ELISAs (assay 1, Orgentec, Germany, and 2, Bindazyme, TBS, UK), detecting aDNA-Ab more or less independent from their avidity, or tests with only intermediate specificity for high avidity Ab (assay 4, ELIAdn, Sweden Diagnostics, Germany), were less specific for SLE (83, 79, 91%, respectively) and not associated with renal involvement (specificity 54-57%). At least in the patients studied here, obvious antigen-related differences could not be observed. With slight differences, all assays were suitable to monitor disease activity and therapy in SLE, agreeing with the ECLAM score in about 70-80% of cases. For lupus nephritis, aC1q-Ab are as specific as high avidity aDNA-Ab and capable to close a diagnostic gap in some cases. Thus, to enhance the specificity (up to 98%) and to consider the distinct diagnostic/pathogenic potential of aDNA-Ab subtypes in SLE, under routine clinical laboratory conditions it should be recommended to combine a sensitive screening test with a more specific second assay.

Adult↗
PubMed2006

Alpha-actinin-binding antibodies in relation to systemic lupus erythematosus and lupus nephritis.

This study investigated the overall clinical impact of anti-alpha-actinin antibodies in patients with pre-selected autoimmune diseases and in a random group of anti-nuclear antibody (ANA)-positive individuals. The relation of anti-alpha-actinin antibodies with lupus nephritis and anti-double-stranded DNA (anti-dsDNA) antibodies represented a particular focus for the study. Using a cross-sectional design, the presence of antibodies to alpha-actinin was studied in selected groups, classified according to the relevant American College of Rheumatology classification criteria for systemic lupus erythematosus (SLE) (n = 99), rheumatoid arthritis (RA) (n = 68), Wegener's granulomatosis (WG) (n = 85), and fibromyalgia (FM) (n = 29), and in a random group of ANA-positive individuals (n = 142). Renal disease was defined as (increased) proteinuria with haematuria or presence of cellular casts. Sera from SLE, RA, and Sjøgren's syndrome (SS) patients had significantly higher levels of anti-alpha-actinin antibodies than the other patient groups. Using the geometric mean (+/- 2 standard deviations) in FM patients as the upper cutoff, 20% of SLE patients, 12% of RA patients, 4% of SS patients, and none of the WG patients were positive for anti-alpha-actinin antibodies. Within the SLE cohort, anti-alpha-actinin antibody levels were higher in patients with renal flares (p = 0.02) and correlated independently with anti-dsDNA antibody levels by enzyme-linked immunosorbent assay (p < 0.007) but not with other disease features. In the random ANA group, 14 individuals had anti-alpha-actinin antibodies. Of these, 36% had SLE, while 64% suffered from other, mostly autoimmune, disorders. Antibodies binding to alpha-actinin were detected in 20% of SLE patients but were not specific for SLE. They correlate with anti-dsDNA antibody levels, implying in vitro cross-reactivity of anti-dsDNA antibodies, which may explain the observed association with renal disease in SLE.

Actinin↗
PubMed1990

IgG subclasses in the serum and skin in subacute cutaneous lupus erythematosus and neonatal lupus erythematosus.

IgG subclasses differ in their biologic and chemical properties, such as complement fixation, protein and cellular binding, and placental transfer. In this study, IgG subclasses of anti-Ro/SSA antibodies in subacute cutaneous lupus (SCLE) and neonatal lupus (NLE) are examined in the serum and in the skin. IgG subclasses in NLE beginning in utero (NLE-heart disease) are compared to subclasses in NLE beginning after birth (NLE-skin disease). Human skin was grafted onto athymic mice, mice were injected with one of eight anti-Ro/SSA maternal NLE sera (four heart block, four skin disease) or seven anti-Ro/SSA SCLE sera, and grafts were examined for IgG subclasses using monoclonal anti-human IgG subclass reagents in an immunofluorescent technique. Lesional skin was examined from four SCLE patients. IgG1 was the only IgG subclass detected in the grafts and skin lesions. IgG1 was the predominant anti-Ro/SSA IgG subclass detected in SCLE and NLE sera in an ELISA using a synthetic Ro/SSA polypeptide. These studies show that the maternal anti-Ro/SSA autoantibodies in NLE-heart disease sera are predominantly IgG1 and are therefore likely to be present in the fetus at the time of gestation, when heart block usually develops. Second, differences in the clinical presentations of NLE (in utero vs. postnatal disease) cannot be attributed to differences in anti-Ro/SSA IgG subclasses. Finally, the subclass bound in the skin in SCLE is IgG1, a subclass capable of mediating tissue injury via complement or cellular effectors.

Animals↗