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 studied 28 patients with SLE, five of whom had had thrombotic episodes. Platelet function and coagulation and fibrinolytic studies were performed to determine whether any of these factors may predispose to thrombosis in SLE. An inhibitor of blood coagulation was detected in 12 patients, and von Willebrand's syndrome was observed in two others. The most striking findings which could be correlated with thromboembolic phenomena were the increase in VII R:WF and the absence of plasminogen activator release after venous occlusion. Both proteins are synthesized by the endothelial cell, and the abnormalities observed are possibly related to damage of the vascular endothelium by immune complexes observed in SLE.
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PMID:Predisposing factors to thrombosis in systemic lupus erythematosus: possible relation to endothelial cell damage. 45 49

It is uncommon for ascites secondary to severe peritoneal inflammation to be the major manifestation of systemic lupus erythematosus. Chronic nonspecific inflammation with a granular type immunofluorescent staining along the mesothelial layer of the peritoneum and peritoneal blood vessels was demonstrated in peritoneal tissue obtained at laparotomy. Paramyxovirus-like structures were seen within vascular endothelium. The ascites diminished with high-dose prednisone and cyclophosphamide therapy.
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PMID:Arthritis Rounds: Ascites as the major manifestation of systemic lupus erythematosus. 94 8

Antiphospholipid antibodies can be detected by three methods; agglutination reactions with a cardiolipid antigen (VDRL, Kline, Kolmer) as observed in false positive syphilitic serologies; secondly coagulation reactions using thromboplastin (activated cephalin time, diluted thromboplastin time, Stipven time...). These cases are called lupus-like or, better, antiprothrombinase circulating antibody; finally, solid phase immunological tests (ELISA, RIA) with purified phospholipids, usually cardiolipin. The antiphospholipid antibodies detected by this method are not the same and the percentage of concordance between the two tests does not exceed 50 per cent. These antibodies are present in 30 to 60 per cent of patients with disseminated lupus erythematosus and also, less frequently, in other connective tissue disorders. They are always found in the so-called primary antiphospholipid syndrome, featuring recurrent venous or arterial thrombosis, repeated abortion, thrombocytopenia, and often a livedo reticularis and leg ulceration. Arterial thrombosis may occur in any part of the body (eye, central nervous syste, visceral or peripheral arteries). Mortality is related to neurological or coronary complications. The pathogenicity of antiphospholipid antibodies has not been formally demonstrated, but they could interact with membrane phospholipids of the vascular endothelium and/or platelets. Immuno-suppressor therapy is not very effective and long-term anticoagulant and/or platelet antiaggregant therapy is usually required.
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PMID:[Anticardiolipin antibody in peripheral arterial diseases]. 176 82

A 45-year-old woman with a 4-year history of systemic lupus erythematosus (SLE) developed fever, decreased visual acuity and skin ulceration. A biopsy of a cutaneous ulcer demonstrated small vessel vasculitis with characteristic cytomegalovirus (CMV) inclusions in the vascular endothelium. The presence of CMV was confirmed by DNA hybridization immuno-histochemistry. Retinal artery vasculitis, previously associated with flares of her SLE, was also noted on ophthalmologic examination. Our case demonstrates that CMV infection can mimic the cutaneous manifestations of collagen vascular disease and that early identification can be made by biopsy of suspicious skin lesions.
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PMID:Systemic lupus erythematosus and concurrent cytomegalovirus vasculitis: diagnosis by antemortem skin biopsy. 254 61

Fibrinolysis was evaluated in 16 women with SLE, who were divided into three groups of increasing disease severity according to their past history, and in 10 normal subjects. Fibrinolysis parameters assessed were tissue-type plasminogen activator (t-PA) activity in plasma and in euglobulin fractions and rapid plasminogen activator inhibitor activity. All parameters were evaluated before and after venous occlusion to assess endothelial cell t-PA release in response to localized anoxia. Markers of deficient fibrinolysis were persistently undetectable t-PA activity and increased rapid plasminogen activator inhibitor activity after venous occlusion. Defective fibrinolysis was correlated with disease severity; it was noted only in patients with severe or moderate disease and in no patients with mild disease or in controls. Fibrinolysis abnormalities were independent of disease activity, suggesting that vascular endothelium injuries occurring during flare-ups persist during inactive phases of the disease. No correlation was found between fibrinolysis abnormalities and disease duration, corticosteroid administration, or the presence of lupus anticoagulant or anticardiolipin antibodies. These data support the hypothesis of parallelism between the severity of vascular injuries, suggested by deficient fibrinolysis, and the severity of clinical manifestations in SLE.
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PMID:Fibrinolysis abnormalities in systemic lupus erythematosus and their relation to vasculitis. 312 85

Prompted by our impression that microtubuloreticular complexes (MTRC) are frequently observed during electron microscopy at the Red Cross War Memorial Children's Hospital, Cape Town, we reviewed all specimens submitted for routine ultrastructural examination during a 1-year period. Our impression was confirmed. MTRC were present in a high proportion of cases, especially in vascular endothelium of renal biopsies. As all 9 cases of hepatitis B-associated membranous glomerulonephritis were positive for MTRC, we also reviewed the previous 20 cases with this diagnosis and these were also all positive. Hepatitis B-associated membranous glomerulonephritis is common in our region. MTRC are probably induced by a supposedly uncommon heat labile alpha-interferon. Elevated serum levels of this interferon are known to occur in systemic lupus erythematosus and acquired immunodeficiency syndrome. We propose that children with intercurrent infection in our region frequently respond with alpha-interferon, promoting MTRC formation.
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PMID:Frequent occurrence of microtubuloreticular complexes encountered during routine ultrastructural examination at a children's hospital. 323 6

The authors report an autopsied case of systemic lupus erythematosus (SLE) with pulmonary hypertension. The patient was a forty-five-year-old female who had been troubled by obstinate Raynaud's phenomenon for ten years before the definite diagnosis of pulmonary hypertension was made. Microscopic examination of the pulmonary vasculature yielded findings consistent with plexogenic pulmonary arteriopathy. However, the deposition of immune complexes in the pulmonary vascular endothelium was not detected by enzyme antibody study. This case suggests, therefore, that "pulmonary Raynaud's phenomenon" is a possible pathogenesis of pulmonary hypertension in patients with SLE.
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PMID:An autopsied case of systemic lupus erythematosus with pulmonary hypertension--a case report. 334 94

Biopsies from oral lesions of 5 patients with discoid lupus erythematosus (DLE), 5 with lichen planus (LP), 5 with leukoplakia (LEUK) and 3 patients with uncertain diagnoses termed DLE?, LP? were examined in the electron microscope for presence of cytoplasmic tubular structures (CTS) in vascular endothelium. Five vessels were examined in each of two randomly selected sections from each biopsy, without knowledge of the clinical diagnosis. All five DLE biopsies showed presence of CTS in 4-9 out of 10 vessels, as compared with none of 10 vessels in biopsies from LP or LEUK, the difference being significant. Further, CTS occurred in 4 out of 10 vessels in one DLE?, LP? biopsy from a patient with serologic signs of systemic lupus erythematosus. As CTS seem to be absent in oral lesions of LP and LEUK, which are the most important differential diagnoses for oral DLE, the identification of CTS in vascular endothelium sing electron microscopy may be an auxiliary diagnostic procedure in oral DLE.
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PMID:Cytoplasmic tubular structures in the diagnosis of oral discoid lupus erythematosus. 617 35

In a long-term follow-up of 52 patients with oral lesions of discoid lupus erythematosus (DLE) 8 patients showed a gradual transition of the typical DLE lesions to lesions which closely resemble leukoplakia. Histopathologically and immunopathologically the leukoplakia-like lesions generally showed features similar to those in leukoplakias not preceded by DLE. Ultrastructurally, the leukoplakia-like lesions showed the presence of cytoplasmic tubular structures in vascular endothelium in two out of three patients examined. The leukoplakia-like stage is considered to be an inactive or scar-like stage, which may be the mucous membrane counterpart of the atrophic scars following DLE lesions of the skin. A primary examination of a DLE patient presenting oral lesions at the leukoplakia-like stage may result in an incorrect diagnosis. Therefore, when investigating patients with leukoplakias, they should be questioned on previous or present skin lesions as well as symptoms of systemic lupus erythematosus.
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PMID:Leukoplakia-like lesions developing in patients with oral discoid lupus erythematosus. 703 48

Immune complexes (ICs) in the serum of 43 patients with chronic idiopathic thrombocytopenic purpura (ITP) were measured by the C1q deviation assay during the active and inactive phases of the disease. An inverse relationship between platelet count and levels of ICs was demonstrated in all but one patient. To test whether this phenomenon was specific for chronic ITP, ICs were assayed in sera from two groups of control patients with thrombocytopenia. Goup 1 had thrombocytopenia due to recognized immune mechanisms while group 2 had thrombocytopenia secondary to non-immune mechanisms. In both these groups the degree of thrombocytopenia proved to be inversely proportional to IC levels, which was similar to the pattern observed in chronic ITP. The specificity of the assay for detection of ICs was confirmed by demonstrating a positivity rate of 65% in sera of patients with systemic lupus erythematosus, a known IC disease. On analysis the ICs were shown to have molecular weights in excess of 500,000 daltons and contain variable immunoglobulin classes. The findings implicate ICs in immune destruction of platelets both in chronic ITP (as has been suggested previously) and also in thrombocytopenia secondary to known immune mechanisms. In addition the association of ICs with non-immune thrombocytopenias is consistent with the hypothesis that platelets play an important role in clearance of ICs from the circulation, thereby protecting the vascular endothelium from damage.
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PMID:Immune complexes in thrombocytopenic patients: cause or effect? 718 63


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