Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present the unusual case of 16-year-old girl who developed intractable convulsions five days after the onset of a cold. Meningeal signs, lymphopenia, proteinuria, and lupus anticoagulant were also present. Treatment with anticonvulsants, antituberculous agents, and adenine arabinoside were ineffective. The initiation of methylprednisolone pulse therapy immediately resolved convulsions and fever. The diagnosis, suggested by the clinical course and the marked improvement of the meningoencephalitis by pulse therapy, was an encephalitic form of acute disseminated encephalomyelitis. Clinical and laboratory findings indicated that an immune disorder may have triggered an abnormal response to a viral infection leading to this patient's neurologic disorder.
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PMID:Patient with both lupus anticoagulant and acute disseminated encephalomyelitis. 889 67

A 31 year-old man treated with sulfasalazine for ulcerative colitis, developed nephrotic syndrome, photosensitivity, alopecia, lymphopenia and hypocomplementemia. Anti-nuclear antibody (speckled) and antibodies to single-stranded DNA and SS-A were positive, while those against native DNA and histon were negative. Renal biopsy revealed diffuse proliferative lupus nephritis. His nephrotic syndrome partially improved with corticosteroid therapy combined with cessation of sulfasalazine. His complement level became normal, however it decreased again during the gradual reduction of corticosteroid dosage. In conclusion, we diagnosed the patient's illness as an idiopathic syntemic lupus erythematosus rather than sulfasalazine-induced lupus.
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PMID:[Diffuse proliferative lupus nephritis in a patient with ulcerative colitis]. 891 Oct 83

CD28 on T cells provides a potent costimulatory signal for T cell activation. Down-regulation of CD28 on peripheral T cells has been reported in certain clinical conditions, but full studies on the mechanism and biological significance have not been performed. Our extensive phenotype analysis of peripheral blood lymphocytes (PBL) from SLE patients revealed that the absolute number of CD28+ T cells of both CD4 and CD8 phenotypes was selectively decreased, while that of CD28- T cells was maintained. CD28+ T cells from SLE patients exhibited mostly normal proliferative responses to both CD28-dependent and -independent stimulations. In contrast, CD28- T cells were hyporesponsive to anti-CD3 stimulation in both SLE and normal controls. These results implied that the selective decrease of CD28+ T cells in SLE does not result from a hyporesponsiveness of CD28+ T cells. To investigate the reason for the selective loss of CD28+ T cells, we determined the appearance of apoptotic cells in culture with or without anti-CD3 stimulation. Apoptotic cells defined by merocyanine (MC)540 were gradually increased from 12 h to 24 h. Anti-CD3-induced apoptosis of CD28+ T cells was significantly accelerated in SLE, whereas apoptosis of CD28- T cells was hardly detected in both SLE and normal controls. Comparative analysis between CD28+ and CD28- T cells on CD95 (Fas) and Bcl-2 expression, which are related to activation-induced cell death (AICD), did not show a major difference, although CTLA4, which has been demonstrated to transmit an apoptosis-inducing signal, was expressed only on CD28+ T cells. Our results suggest that CD28-mediated costimulation influences T cell susceptibility to AICD and may be involved in T cell lymphopenia in SLE.
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PMID:Preferential elimination of CD28+ T cells in systemic lupus erythematosus (SLE) and the relation with activation-induced apoptosis. 891 66

We investigated whether, in systemic lupus erythematosus (SLE), the CD45 isoforms expression on peripheral blood T-lymphocytes (T-PBL) is related to the auto-immune processes and hematological manifestations. The CD45RA/RO patterns of CD4+ and CD8 bright+ T-PBL were determined by three-colour flow cytometry. The serum levels of anti-nuclear (ANA), anti-double stranded DNA (ds DNA) and anti-cardiolipin (CL) autoantibodies were quantified by ELISA. The hematological parameters were routinely assessed. 72% of SLE patients (n = 29) had reduced lymphocyte counts, which correlated with more severe physician's assessment of disease activity, increased ANA and anti-ds DNA auto-antibodies. The lymphopenia preferentially affected the CD4+ T-PBL and, among them, the "naive" CD45RA+, RO- cells. Thus, compared with healthy women (n = 29), SLE patients had less naive and more "transient" CD45RA+, RO+ cells among CD4+ T-PBL. Meanwhile, on average, the CD45 isoforms expression on CD8+ T-PBL was unchanged. Interestingly, in 3 patients who were repeatedly evaluated, increases of transient CD8+ T-PBL paralleled the elevation of anti-ds DNA. In addition, high anti-CL was associated with more transient CD4+ and CD8+ T-PBL. The loss of naive and increase of transient CD8+ T-PBL was associated with increased disease activity and possibly hemolytic anemia. Thus, in SLE, the enhanced phenotypic switch from naive CD45RA+, RO- to "memory" CD45RO+ T-PBL patterns paralleled the auto-immune processes characteristic of this disease.
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PMID:CD45 isoforms expression on CD4+ and CD8+ peripheral blood T-lymphocytes is related to auto-immune processes and hematological manifestations in systemic lupus erythematosus. 894 97

We studied the frequency, location, clinical and histopathological features, associated manifestations, and prognosis of vasculitides in a cohort of 667 SLE patients. Exclusion of patients with previous vasculitis or insufficient information left 540 patients, 194 of whom has vasculitis (incidence density: 0.053 new cases/person/year, cumulative incidence of 0.051 at one year, 0.232 at 5 years and 0.411 at 10 years). Vasculitis was confirmed by biopsy in 46 cases, by arteriography in five, and by both in three. A single episode of vasculitis occurred in 119 and two or more in 75 patients. Vasculitis was cutaneous in 160, visceral in 24, both in 10. In the first episode of cutaneous vasculitides, 111 had punctuate lesions, 32 palpable purpura, 6 urticaria, 6 ulcers, 8 papules, 5 erythematous plaques or macules confirmed with biopsy, 2 erythema with necrosis, and 1 panniculitis (plus small vessel vasculitis). Of 29 with visceral vasculitis in the first episode, 19 had mononeuritis multiplex, 5 digital necrosis, 3 large artery vasculitis of limbs, one mesenteric, and one coronary, more than one type could appear simultaneously or in subsequent episodes. Patients with vasculitis had longer disease duration and followup, younger age of onset of SLE, and were more frequently males than those without. Lupus manifestations associated with vasculitis in univariate logistic regression included myocarditis, psychosis, Raynaud's phenomenon, serositis, leukopenia, lymphopenia and pleuritis. Vasculitis also associated with the antiphospholipid syndrome. The strength of this association increased when patients with vasculitis confirmed by biopsy and/or arteriography were considered separately. Visceral vasculitis associated with increased mortality when controlled for age of onset and nephropathy.
Lupus 1997
PMID:Vasculitis in systemic lupus erythematosus. 910 29

Patients with systemic lupus erythematosus (SLE) frequently have anti-lymphocyte autoantibodies, some of which also bind to surfaces of neurons. Since anti-ribosomal P protein autoantibodies (anti-P) from SLE patients also bind to surfaces of neurons, we hypothesized that anti-P are anti-lymphocyte antibodies. A panel of human T lymphocytes was evaluated for anti-P binding by indirect immunofluorescence. Affinity-purified anti-ribosomal antibodies were used as a source of anti-P. These autoantibodies bound to the surfaces of all transformed T cell lines tested. This binding was not mediated by Fc receptors. It was inhibitable by ribosomes. Anti-P bound to circulating T lymphocytes from healthy adults and children. They also bound to thymocytes and cord blood T cells from normal neonates. Circulating T cells from SLE patients with anti-P bound less anti-P than cells from healthy controls. Two patients were studied on multiple occasions. The capacity of their T cells to bind anti-P correlated inversely with titres of anti-ribosomal antibodies. Anti-ribosomal antibodies, other than anti-P, also appear to bind to T cells. The surface of T cells contains a protein with the size and antigenicity of the ribosomal P protein, P0. We conclude that anti-ribosomal antibodies are a subset of anti-lymphocyte autoantibodies. Their possible role in the pathogenesis of lymphopenia or lymphocyte dysfunction in SLE has to be defined in further studies.
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PMID:Anti-ribosomal and 'P-peptide'-specific autoantibodies bind to T lymphocytes. 921 16

A 25-year-old Caucasian woman developed two areas of tender panniculitis on her left thigh. While one lesion ulcerated, the other showed no overlying cutaneous changes. Histological examination showed lymphocytic perivascular and periappendageal infiltrates, and direct immunofluorescence revealed granular immunoglobulin deposits at the dermal-epidermal junction in the skin overlying the lesions. Laboratory tests revealed lymphopenia, anemia and an increased blood sedimentation rate. The serology for syphilis was false positive. For several months the patient had also been suffering from arthralgia with palpable synovitis of the wrist and several interphalangeal joints. Overall, these clinical findings are consistent with the diagnosis of lupus profundus/panniculitis associated with mild systemic LE.
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PMID:Lupus profundus/panniculitis. 926 58

During an infection with human immunodeficiency virus (HIV) the immune system is deregulated, even before real immunodeficiency, lymphopenia and AIDS occur. The immunologic alterations that have been described are a differentiation of a T-lymphocyte subclass, Th1 to Th0. Immunologic stimulation of these Th0 cells afterwards, makes them mature into Th2 cells. This causes a imbalance between the Th1 and Th2 cells, in favor of the second group. The clinical expression of this imbalance is an elevated risk of HIV-seropositive patients for allergies and for autoimmune disease, specially those autoimmune disease in which the production of autoantibodies prevails. Sometimes of differential diagnosis with systemic lupus erythematosus is difficult. There has been describes a major prevalence of allergic diseases, especially allergic rhinitis, in adult patients infected by HIV. Reports in pediatric patients are still sporadic, and the prevalence of allergies in children infected with HIV-AIDS is unknown. Only after recognizing the allergic nature of some symptoms, the treatment will be complete, reducing morbidity and infectious complications.
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PMID:[Allergic diseases and infection with human immunodeficiency virus (HIV)-AIDS in pediatric patients]. 929 27

A 46-year-old man was admitted to our clinic because of acute heart failure. Six years before admission he was pointed out cardiomegary and hematuria. One year later, he was diagnosed as having jugular foramen syndrome. On admission, he had a fever and dyspnea. Pansystolic blowing murmur was audible at the apex. The chest ratio on his chest X-ray was 52.5%. An electrocardiogram showed left ventricular hypertrophy. An echocardiogram showed marked dilatation and severe dysfunction of left ventricle. Radionuclide scanning with technetium 99 m pyrophosphate identified inflammatory change in the apex. Myocardial biopsy showed fibrotic degeneration and IgG deposits in myocardium. Blood examination showed anemia, lymphopenia. positive anti-nuclear antibody (1000 times, shaggy pattern), positive anti ds-DNA antibody and hypocomplementemia. Furthermore, proteinuria was pointed out. Renal biopsy showed focal segmental glomerulonephritis with active necrotizing lesion (type III nephritis). Lupus myocarditis and nephritis was diagnosed. After prednisolone (80 mg/day) was administered. left ventricular function and hypocomplementemia improved. The ACE inhibitor was also used for proteinuria. In spite of a little amount of blood transfusion, he showed hepatic hemosiderosis. We suspect that the cause of hemosiderosis was related chronic inflammation of active lupus. It was treated with Erythropoietin.
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PMID:[A case of lupus myocarditis and nephritis with transient foramen jugular syndrome]. 939 74

We describe a 22-year-old female with systemic lupus erythematosus and lymphopenia, who developed septic arthritis of the right knee with Listeria monocytogenes type 1/2 A, whilst on low-dose methotrexate (MTX). So far, septic arthritis due to this microorganism has been reported in two other patients treated with low-dose MTX, one having rheumatoid arthritis and the other psoriatic arthritis. No reports exist on patients treated with other cytotoxic antirheumatic therapies.
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PMID:Septic arthritis with Listeria monocytogenes during low-dose methotrexate. 969 30


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