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)

This study tested the hypothesis that the rate of antigen entry into the circulation in systemic lupus erythematosus (SLE), a naturally occurring immune complex glomerulonephritis (IC-GN), is slow compared with that of traditional experimental models of IC-GN, in which the antigen is delivered rapidly as a daily iv bolus. This hypothesis was tested by comparing rates of decline of the third component of complement (C3) and of circulating neutrophils (PMN) in SLE patients with active disease with those of cynomolgus monkeys (CYN) undergoing induction of experimental IC-GN by means of a daily bolus infusion of antigen. It has previously been shown that, as antigen enters the circulation and forms circulating IC, C3 levels and circulating PMN decline acutely. Thus, acute changes in these parameters can be surrogates for the rate of antigen entry into the circulation. In the CYN undergoing induction of IC-GN (N = 11), infusion of the antigen (bovine gamma-globulin) over 10 min resulted in acute declines in C3 levels (25 +/- 6.6%; P = 0.0018 and PMN counts (59 +/- 9%; P < 0.0002). In addition, the CYN experienced the onset of acute respiratory distress and hypotension. By contrast, in patients with active SLE (N = 9), C3 and white blood cell counts measured at 24-h intervals did not change significantly, and episodes of acute hypotension or respiratory distress were not observed. In the CYN, the onset of visible vasculitic lesions in the omentum were also documented within minutes of the infusion of bovine gamma-globulin. The rapidity of onset of these vascular lesions suggests that the tempo at which lesions develop in experimental models of IC disease is faster than that of naturally occurring IC diseases. It was concluded that, in naturally occurring IC diseases, antigen probably enters the circulation slowly over prolonged periods of time, rather than as large boluses over short periods of time, as in traditional experimental models of IC-GN. Thus, models of IC-GN involving a daily bolus infusion of antigen may not be clinically relevant, particularly when IC clearing mechanisms are tested, because the efficiency of these mechanisms may be markedly influenced by the rate at which IC form in the circulation.
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PMID:Rate of antigen entry into the circulation in experimental versus naturally occurring immune complex glomerulonephritis. 753 10

We report a case of hypocomplementemic urticarial vasculitis syndrome (HUVS) with membranous glomerulopathy in a 62-year-old man who had a 2-month history of secondary iritis. He was transferred to our hospital because of uncontrollable edema and respiratory dysfunction. Physical examination revealed anasarca, pulmonary edema, hypertension and urticaria-like eruption on his arms. Urinalysis, blood chemistry and serological studies showed massive proteinuria (10.5g/day) with numerous granular casts, hypoalbuminemia (1.5g/dl), renal dysfunction (creatinine; 1.6mg/dl, BUN; 86mg/dl), hypercholesterolemia (total cholesterol; 455mg/dl), positive results for antinuclear factor, microsome test, thyroid test, lupus anticoaglant, antithyroglobulin test and rheumatoid factor, but LE cell or double-strand anti DNA antibody was negative. Serum complement levels were persistently low as CH50 of 13 U/ml and Clq of 6.0 micrograms/dl. The patient serum precipitated with normal human Clq by immunodiffusion analysis, indicating the presence of anti-Clq antibody. Renal biopsy revealed membranous glomerulopathy with prominent fine granular deposition of Clq along the glomerular basement membrane by immunofluorescent study and subepithelial dense deposit by electron microscopy. Corticosteroid treatment was ineffective for hypocomplementemia and nephrotic syndrome. Acute subendocardial infarction occurred on the 25th hospital day and he died of acute respiratory distress syndrome on the 45th hospital day. Autopsy revealed leucocytoclastic vasculitis in the alveolar wall. HUVS was confirmed by clinical symptoms, such as iritis and urticaria-like eruption, serum anti-Clq antibody, the absence of any specific autoantibody for systemic lupus erythematosus (SLE) and leucocytoclastic vasculitis in the alveolar wall.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Nephrotic syndrome due to membranous glomerulopathy in hypocomplementemic urticarial vasculitis syndrome;--a case report]. 807 26

We report here an old male patient with anti-nuclear antibody (ANA) negative systemic lupus erythematosus (SLE) with active renal disease and penile ulcer. He revealed nephrotic syndrome, malar rash and oral ulcer. SLE was discussed, however both ANA and anti-DNA antibody were persistently negative. A penile ulcer was also observed. He died of acute respiratory distress. Autopsy findings including onion skin lesion in the spleen and haematoxylin body in the kidney resulted in the final diagnosis of SLE. To our knowledge, association of penile ulcer with SLE has not yet been reported. Therefore, the present case is thought to be extremely unusual.
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PMID:A case of anti-nuclear antibody negative systemic lupus erythematosus associated with penile ulcer. 825 45

A 22-year-old female patient with an 8-year history of mixed connective tissue disease (systemic sclerosis overlapping with systemic lupus erythematosus) presented with marked respiratory distress, sinus tachycardia (135 bpm), and pulsus paradoxus. The chest x-ray showed an enlargement of the cardiac silhouette, which was due to a 3-cm-wide, circular pericardial effusion, as demonstrated by two-dimensional echocardiography. Pericardiocentesis performed to decompress cardiac tamponade did not lead to clinical improvement. The increase in dyspnea was caused by a rise in pulmonary wedge pressure from 21 to 40 mm Hg following an acute increase of mitral valve regurgitation. In the presence of global hypokinesia of the left ventricle, cardiac output decreased from 3.25 to 2.63 l/min. Intensive care including hemodialysis and plasmapheresis as well as high-dose application of cyclophosphamide and steroids led to a stabilization of the hemodynamic situation over a period of days. The case report presented here supports the general recommendation to perform pericardiocentesis in a stepwise manner under hemodynamic monitoring. This holds true primarily for patients with mitral valve regurgitation and/or cardiac involvement in connection with an underlying disease.
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PMID:[Pulmonary edema as a complication during pericardial puncture in "mixed connective tissue disease"]. 835 45

The effects of high dose iv-immunoglobulin on antiphospholipid antibody levels and on pregnancy outcome was studied in one patient with secondary (SLE) and two patients with primary antiphospholipid syndrome during their four pregnancies. These three women had had two pulmonary embolies related to pregnancy and estrogen containing pills, 13 miscarriages and only one liveborn after pre-eclamptic pregnancy. During the four pregnancies the patients also received 75 mg of aspirin per day. Progressive depression of IgG-anticardiolipin antibody titer was observed after repetitive high dose iv-immunoglobulin (1 g/kg body-weight) infusions. The effects on lupus anticoagulant were variable. Three pregnancies ended in a delivery of healthy child after 36-38 weeks of gestation and one preterm child (34 weeks), with slight respiratory distress syndrome, was born. Our results support the idea that the addition of iv-immunoglobulin to aspirin prophylaxis is worth considering when the patient has a severe antiphospholipid syndrome and/or is refractory to usual treatments.
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PMID:Intravenous immunoglobulin treatment of pregnant patients with recurrent pregnancy losses associated with antiphospholipid antibodies. 838 39

Experience of using an SLE 2000 neonatal trigger ventilator as the sole means of ventilation in 68 infants with respiratory distress syndrome was reviewed. No death or complication was seen in 22 infants with a birth weight above 1500 g. Forty five infants under 1500 g birth weight including 18 infants between 23 and 28 weeks' gestation were trigger ventilated throughout. Six infants died, four of whom were under 28 weeks' gestation. Two infants under 1500 g birth weight sustained a pneumothorax while being ventilated. Nine of 61 infants (15%) had radiological evidence of pulmonary interstitial emphysema, which was mild in seven infants. Intraventricular haemorrhage occurred in 10 babies under 1500 g, four of these being grade III or IV. Twenty two (48%) of the babies under 1500 g required added oxygen at 28 days. The preliminary clinical experience of this trigger ventilator suggests that it is capable of providing respiratory support from birth to extubation in even the most immature infants with respiratory distress syndrome. A controlled clinical trial is now required to compare the safety and efficacy of patient triggered ventilation with conventional neonatal ventilation.
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PMID:Long term trigger ventilation in neonatal respiratory distress syndrome. 846 68

We analyzed the clinical and laboratory characteristics of 50 patients with catastrophic antiphospholipid syndrome (APS) (5 from our clinics and 45 from a MEDLINE computer-assisted review of the literature from 1992 through 1996). Thirty-three (66%) patients were female and 17 (34%) were male. Twenty-eight (56%) patients had primary APS, 15 (30%) had defined systemic lupus erythematosus (SLE), 6 (12%) had "lupus-like" syndrome, and 1 (2%) had rheumatoid arthritis. Mean age of patients in this series was 38 +/- 14 years (range, 11-74 yr). Three (6%) patients developed the clinical picture of catastrophic APS under the age of 15 years, and 11 (22%) were 50 years old or more. In 11 (22%) patients, precipitating factors contributed to the development of catastrophic APS (infections in 3, drugs in 3, minor surgical procedures in 3, anticoagulation withdrawal in 2, and hysterectomy in 1). The presentation of the acute multi-organ failure was usually complex, involving multiple organs simultaneously or in a very short period of time. The majority of patients manifested microangiopathy--that is, occlusive vascular disease affecting predominantly small vessels of organs, particularly kidney, lungs, brain, heart, and liver--with a minority of patients experiencing only large vessel occlusions. Thrombocytopenia was reported in 34 (68%) patients, hemolytic anemia in 13 (26%), disseminated intravascular coagulation in 14 (28%), and schistocytes in 7 (14%). The following antibodies were detected: lupus anticoagulant (94%), anticardiolipin antibodies (94%), anti-dsDNA (87% of patients with SLE), antinuclear antibodies (58%), anti-Ro/SS-A (8%), anti-RNP (8%), and anti-La/SS-B (2%). Anticoagulation was used in 70% of the patients, steroids in 70%, plasmapheresis in 40%, cyclophosphamide in 34%, intravenous gammaglobulins in 16%, and splenectomy in 4%. Most patients, however, received a combination of nonsurgical therapies. Death occurred in 25 of the 50 (50%) patients. In most, cardiac problems seemed to be the major cause of death. In several of these, respiratory failure was also present, usually due to acute respiratory distress syndrome and diffuse alveolar hemorrhage. Among the 20 patients who received the combination of anticoagulation, steroids, and plasmapheresis or intravenous gammaglobulins, recovery occurred in 14 (70%) patients. The use of ancrod and defibrotide appeared to be effective in the 2 respective patients in whom they were used.
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PMID:Catastrophic antiphospholipid syndrome. Clinical and laboratory features of 50 patients. 965 31

Minoeycline, a semisynthetic tetracycline, is often used to treat acne and rheumatoid arthritis. It has been considered an unlikely drug to be associated with systemic lupus erythematosus; however, many cases of drug-induced lupus related to minocycline have been reported. Some of those reports included pulmonary lupus, but none of the patients described developed respiratory distress. We describe a patient treated with minocycline for 2 years who presented with progressive dyspnea, severe hypoxia, and pulmonary infiltrates necessitating hospitalization and oxygen supplementation.
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PMID:Respiratory distress due to minocycline-induced pulmonary lupus. 1033 77

We describe a case of cytomegalovirus (CMV) infection in a 25-year-old woman with a 3-year history of systemic lupus erythematosus (SLE) with persistently high disease activity, who had not received immunosuppressive therapy. Disseminated CMV infection presented with upper gastrointestinal bleeding, high fever, respiratory distress, leukopenia, and thrombocytopenia. The CMV infection was successfully treated with combined antiviral and immunoglobulin therapy, and the SLE activity decreased concomitantly. CMV disease is closely related to host immunosuppression, primarily T-lymphocyte dysfunction. This case should highlight the relationship between clinically significant CMV disease and compromised immunity in patients with active SLE who are not receiving immunosuppressive therapy.
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PMID:Disseminated cytomegalovirus disease in a patient with systemic lupus erythematosus not undergoing immunosuppressive therapy. 1063 27

A 56-year-old woman with rheumatoid arthritis (RA) suddenly developed severe respiratory distress and laryngeal stridor, which required endotracheal intubation. She had had RA for 12 years, which had been controlled well with prednisolone (3 mg/day) at the orthopedic clinic. Laryngoscopy revealed cricoarytenoid arthritis. She was finally diagnosed as having overlap syndrome with RA and systemic lupus erythematosus. She was given high dose corticosteroids that improved her clinical symptoms and laryngoscopic findings. She represents the first patient with overlap syndrome who developed an acute airway obstruction due to cricoarytenoid arthritis.
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PMID:Cricoarytenoid arthritis with rheumatoid arthritis and systemic lupus erythematosus. 1129 70


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