Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

MRL/MpJ-lpr/lpr mice spontaneously develop a lupus-like autoimmune disorder characterized by massive proliferation of T cells and rapidly fatal immune complex glomerulonephritis. We evaluated the therapeutic effect of 5-azacytidine (5AC), a cytidine analogue known as an inhibitor of DNA methylation, in MRL/MpJ-lpr/lpr mice. Intraperitoneal injection of 5AC (50 micrograms, twice a week) starting from 6 weeks of age retarded the development of lymphadenopathy and autoimmune syndrome. Its beneficial effects included: (a) increased life-span, (b) diminution of lymphadenopathy and splenomegaly, (c) reduction in circulating levels of autoantibodies such as anti-DNA and rheumatoid factors, and (d) suppression of lupus glomerulonephritis. However, similar treatment in BALB/c mice did not affect the development of IgG anti-human IgG antibody responses. These results suggest that the protective effect of 5AC is related to the inhibition of the lpr gene-induced T cell proliferation, thereby suppressing the autoimmunity-accelerating effect mediated by the lpr gene.
Eur J Immunol 1990 Sep
PMID:5-Azacytidine inhibits the lpr gene-induced lymphadenopathy and acceleration of lupus-like syndrome in MRL/MpJ-lpr/lpr mice. 169 37

The authors analyze the course and outcomes of 33 pregnancies in 26 women suffering from systemic lupus erythematosus (SLE). In patients with active SLE the incidence of gestoses and abnormalities of the newborns is significantly higher than in those with inactive SLE, whose gestational and neonatal complication rate is almost the same as in healthy women. Pregnancy course and outcomes are particularly unfavorable in cases with lupus glomerulonephritis.
Akush Ginekol (Mosk) 1991 Sep
PMID:[Systemic lupus erythematosus and pregnancy: specific features of gestation and course of the disease]. 174 89

We describe a 35-year-old man with a history of previous deep vein thrombosis who presented with hypertension. Renal investigations revealed failure to excrete contrast medium by the right kidney on intravenous pyelography. Digital subtraction angiography showed an 80% stenosis of the left renal artery. He was antinuclear antibody negative, as well as negative for antibodies to double stranded deoxyribonucleic acid and extractable nuclear antigens. The lupus anticoagulant test and antibodies to cardiolipin were positive. He conforms to a diagnosis of "primary" antiphospholipid syndrome.
J Rheumatol 1991 Sep
PMID:Hypertension, renal artery stenosis and the "primary" antiphospholipid syndrome. 175 47

Genetic studies of experimental models of autoimmune diseases, including systemic lupus-like syndromes and organ-specific autoimmunity, provide major information on genetic control of autoimmune diseases. In addition to genes known to be linked to the major histocompatibility complex (MHC), these studies point to multiple genes located outside the MHC that influence the onset and the progression of autoimmune diseases. Identification of these genes and of their interrelationships is now a major task that will be facilitated by recent progress in molecular biology and gene mapping. Among candidate genes, antigen-receptor genes (i.e., immunoglobulin- and T-cell receptor genes) most likely contribute an important part of the autoimmune susceptibility in several of these animal models. Available linkage data suggest a similar involvement of these antigen-receptor genes in several human autoimmune diseases. In addition to a better understanding of pathogenic mechanisms associated with autoimmunity, the knowledge of these disease-predisposing genes is expected to permit a better classification of often complex syndromes as well as the design of new treatments.
Hum Immunol 1991 Sep
PMID:The contribution of non-MHC genes to susceptibility to autoimmune diseases. 177 93

Based on current evidence from the literature the authors outline the concept, epidemiology and pathogenesis of lupus erythematosus as well as the histopathological, immunopathological and clinical diagnosis of the disease. An original iconography of the latter aspects is given.
Av Odontoestomatol 1991 Sep
PMID:[Lupus erythematosus. 1. Etiopathology, pathology and clinical findings with special reference to the oral mucosa]. 177 85

Based on current evidence from the literature, the prognosis, treatment and outcome of lupus erythematosus are presented with special reference to difficulties encountered in the management of patients with involvement of the oral cavity. Original iconography of illustrative treated cases is included.
Av Odontoestomatol 1991 Sep
PMID:[Lupus erythematosus. 2. Prognosis, treatment, outcome and stomatological management]. 177 86

Acquired antibodies to phospholipids form a heterogeneous group, which may be detected in vitro by the inhibition of phospholipid dependent tests of coagulation (lupus anticoagulant) and also by immunological assays, such that a combined approach is required for their reliable detection. While initially described in sufferers from systemic lupus erythematosus, these antibodies are increasingly recognised in a broad spectrum of disease, most importantly in relation to thromboembolism and recurrent fetal loss; occasionally they may also be found in otherwise healthy individuals. The mechanisms underlying the prethrombotic state associated with these antibodies have not been defined, although interference with the natural anticoagulant systems seems possible. Identification of antiphospholipid in subjects with spontaneous thromboembolism may influence therapeutic decisions, while their presence in women with recurrent fetal loss has lead to attempts to alter the outcome of further pregnancies with anticoagulant and immunosuppressive regimens, however the optimum management has not yet been determined. The recognition of these antibodies and their clinical associations is therefore highly relevant to clinical and laboratory haematology.
Blood Rev 1991 Sep
PMID:Lupus anticoagulant. 177 49

In experimental membranous nephropathy, antibody binding to glomerular epithelial cell membrane antigens results in complement activation and formation of complement C5b-9 membrane attack complexes in glomeruli. During active disease, the C5b-9 complexes are shed into the urine. To test the hypothesis that a similar mechanism might be operative in human membranous nephropathy, we measured urinary excretion of C5b-9 and C5 in 146 proteinuric patients with biopsy-proven glomerular diseases or diabetes mellitus. Urinary excretion of C5b-9 relative to C5 excretion was higher in 40 patients with membranous nephropathy than in 106 patients with proteinuria due to non-membranous glomerulonephritis when analyzed by covariance analysis (P less than 0.0002). Urinary C5b-9 excretion was higher in membranous nephropathy than in membranoproliferative glomerulonephritis (N = 13, P less than 0.05), minimal change-focal sclerosis (N = 33, P less than 0.001), mesangial proliferative glomerulonephritis (N = 9, P less than 0.02) and IgA nephropathy (N = 7, P less than 0.025). Urinary C5b-9 excretion was also higher in patients with lupus nephritis (N = 18, P less than 0.02) compared to those with non-membranous glomerulonephritis. The lupus patients with the highest excretion had clinical or pathological features of membranous nephropathy. Nine patients with membranous nephropathy and elevated urinary C5b-9 excretion had a shorter duration of disease (P less than 0.05), lower serum creatinine levels (P less than 0.05) and more proteinuria (P less than 0.02) than the 31 membranous nephropathy patients with normal values.(ABSTRACT TRUNCATED AT 250 WORDS)
Kidney Int 1991 Sep
PMID:Elevated urinary excretion of the C5b-9 complex in membranous nephropathy. 178 50

In the present study 19 Greek Caucasian children with systemic lupus erythematosus (SLE), onset before the age of 16, were followed up for 1-12 years (mean 5.6 yrs.). Diagnosis was determined early in 14 patients and delayed by 2 to 6 years in 5. The clinical manifestations and laboratory findings did not differ significantly from those reported in adults with lupus. The major organ system involvement at onset and early course were skin and joints (80%) followed by kidneys (42%). During the course of the disease 26% of the children developed central nervous system (CNS) involvement. All the patients were treated with steroids and/or cytotoxic drugs in severe uncontrolled progressive disease. At the mean 5.6 years follow-up most patients were in remission on small doses of steroids; one patient still presents signs of active lupus nephritis and one patient died from sepsis. All the patients with CNS involvement recovered without permanent CNS residue.
Clin Rheumatol 1991 Sep
PMID:Clinical and serological spectrum of systemic lupus erythematosus in Greek children. 179 Jun 34

Pooled normal human IgG for therapeutic use, following depletion of anti-DNA, anti-Fc, and anti-F(ab')2 of normal IgG, expressed antiidiotypic activity against anti-DNA derived from lupus sera. The antiidiotype enriched by elution from anti-DNA affinity columns bound directly to anti-DNA IgG and inhibited the binding of lupus sera to DNA but did not bind to normal IgG or inhibit the binding of anti-tetanus toxoid to tetanus toxoid. Antiidiotypes in pooled normal sera may have a role in the clinical improvement seen in patients with autoimmune diseases receiving intravenous immune globulin.
J Clin Immunol 1991 Sep
PMID:Detection and purification of antiidiotypic antibody against anti-DNA in intravenous immune globulin. 179 44


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>