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)

A 41-year-old female was admitted to our hospital with acute renal failure. The renal biopsy showed focal necrotizing crescentic glomerulonephritis, and her serology revealed a high titer of MPO-ANCA. The diagnosis of MPO-ANCA-associated microscopic polyarteritis was made, and her basic illness proved to be systemic lupus erythematosus (SLE) because of renal injury, polyarteritis, pancytopenia, anti-double-strand DNA antibody, and anti-nuclear antibodies. After treatment with prednisolone (PSL) and cyclophosphamide, her renal function improved and her MOP ANCA titer was lowered. After 2 years, she was readmitted due to dyspnea. Chest X-ray and echocardiography revealed pericarditis and bilateral pleural effusion. Renal biopsy was carried out again because of an increase in MPO-ANCA, which showed minor abnormalities. PSL therapy led to remission of pericarditis, resulting in a decrease in MPO-ANCA. In this case, MPO-ANCA is likely to be associated not with the activity of polyarteritis, but with that of SLE, and care should be taken in evaluating the clinical usefulness of MPO-ANCA in cases with SLE.
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PMID:[Renal microscopic polyarteritis replaced by pericarditis with episodic increases in MPO-ANCA in a patient with systemic lupus erythematosus]. 989 59

The authors report an unusual case of acute renal failure occurring in a patient with systemic lupus erythematosus and antiphospholipid antibodies. Kidney biopsy revealed glomerular thrombosis, in the absence of glomerulonephritis. The authors stress the clinical and biological signs that suggest the thrombotic nature of kidney failure in lupus patients.
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PMID:Glomerular thrombosis: an unusual cause of renal failure in systemic lupus erythematosus. 1002 47

The renal vascular involvement of systemic diseases can be of embolic, thrombotic or inflammatory nature. Occlusion of proximal arterial vessels results in a dissociation between the rapid progression of renal failure, and the urinary abnormalities. Urine examination can be nearly normal and non revealing, except for a loss in maximal concentrating ability. In contrast, inflammatory changes of distal vessels are variably transmitted to the glomeruli, resulting in proteinuria, variable hematuria associated to mixed abnormalities of the urinary sediment. In diffuse vascular involvement acute renal failure can supervene, difficult to distinguish from that of diffuse glomerulonephritides. Most systemic vasculitides, mainly those of SLE, microscopic polyangiitis, Henoch-Schoenlein purpura and that of Wegener granulomatosis cause a clinical picture either of acute, rapidly progressive glomerulonephritis, or of a nephritic syndrome. The vasculitides affecting small arteries, capillaries and venules can result in a clinical-histopathologic picture closely mimicking that of acute tubule-interstitial disease. A thorough evaluation of the clinical picture, of the degree and progression of renal failure, of urine analysis, and clinically guided biopsies of the appropriate tissues can lead to differentiation of the different diseases and precocious diagnosis and effective treatment.
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PMID:Clinical assessment of renal vascular involvement and clinical-pathological correlations. 1035 32

A 14-year-old African-American girl was diagnosed with antiphospholipid-positive systemic lupus erythematosus (SLE) in July 1994. The course was complicated by nephrotic syndrome, sepsis, hemolytic anemia, acute renal failure, saphenous vein thrombosis, cutaneous vasculitis, mesenteric vasculitis, appendicitis, hemorrhagic cystitis, and avascular necrosis of the hips. In August 1997, she developed ovarian and fallopian tube complications secondary to SLE. Genitourinary complications of SLE, however, are uncommon, and ovarian vasculitis has not previously been reported as a complication of SLE. This report describes the course of an adolescent patient with SLE and focuses specifically on her genitourinary complications.
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PMID:Genitourinary complications of systemic lupus erythematosus. 1080 72

We present a case of multiple organ dysfunction syndrome with acute respiratory failure due to alveolar haemorrhage associated with antiphospholipid antibodies in a 42-year-old woman with a medical history of antinuclear antibody-negative systemic lupus erythematosus and antiphospholipid syndrome. Severe respiratory failure, circulatory shock and acute renal failure necessitated artificial ventilation, inotropic and vasopressor therapy, and continuous venovenous haemofiltration. A tentative diagnosis of haemorrhagic lupus pneumonitis or pulmonary manifestation of antiphospholipid syndrome was made. Lupus anticoagulant, IgG anticardiolipin and anti-beta2-glycoprotein I antibodies were positive. High-dose glucocorticoid, anticoagulation with heparin, plasmapheresis and cyclophosphamide improved her clinical condition. Despite this, the patient died several days later of spontaneous intracranial haemorrhage. This case illustrates the uncommon manifestation of acute respiratory failure associated with antiphospholipid syndrome.
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PMID:Acute respiratory failure associated with catastrophic antiphospholipid syndrome. 1088 95

Nocardia asteroides infection are unusually observed in systemic Lupus erithematous (SLE) patients. They are generally associated to steroidal and immunosuppressive therapy. We report a 24 years old female with SLE diagnosed in 1994 who developed a severe preeclampsia in her first pregnancy requiring emergency caesarean section. Post partum acute renal failure and type IV lupus nephropathy were treated with hemodialysis, methylprednisolone, cyclophosphamide and prednisone. Three months later, while she was receiving the fourth cyclophosphamide dose, she presented with a pleuro pneumonia and occipital abscess, both caused by Nocardia asteroides. She was treated with cotrimoxazole + cefixime and pleural decortication was required. Five months later, she developed Meningitis caused by Nocardia asteroides and hydrocephalus. She was treated with ceftriaxone, vancomycin, cotrimoxazole and ventricular shunting procedure. Two months later, a retroperitoneal abscess was diagnosed and surgically drained but the patient died, due to a methicillin-resistant Staphylococcus aureus septicemia.
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PMID:[Nocardia asteroides infection in a patient with systemic lupus erythematosus]. 1100 57

Up to 80% of patients with systemic lupus erythematosus (SLE) are treated with nonsteroidal anti-inflammatory drugs (NSAID) for musculoskeletal symptoms, serositis and headache. This survey reviews the literature on non-selective and selective inhibitors of cyclooxygenases, with an emphasis on the efficacy and safety profile reported in SLE patients. No lupus-specific data on gastro-intestinal side effects of NSAID exist. Both non-selective Cox inhibitors and selective Cox-2 inhibitors induce renal side effects, including sodium retention and reduction of the glomerular filtration rate. Lupus nephritis is a risk factor for NSAID-induced acute renal failure, but not for rare idiosyncratic toxic renal reactions to NSAID. In refractory nephrotic syndrome, NSAID have been used successfully. Cutaneous and allergic reactions to NSAID are increased in SLE patients as well as hepatotoxic effects, particularly with high dose aspirin. Whereas a variety of central nervous system side effects of NSAID are probably no more common in SLE patients than others, aseptic meningitis has been reported more frequently. Ovulation and pregnancy can be adversely affected by Cox inhibitors. The antiplatelet effect of aspirin and non-selective Cox inhibitors has a therapeutic potential in patients with antiphospholipid syndrome (APS). In summary, treatment of SLE with NSAID requires awareness for the increased frequency of some side effects and close monitoring of toxicity.
Lupus 2000
PMID:Nonsteroidal anti-inflammatory drugs in systemic lupus erythematosus. 1103 30

Acute renal failure due to idiopathic tubulo-interstitial nephritis associated with bilateral uveitis (TINU syndrome) is a rare clinical event, contracted mainly by girls or women. Here we report the clinical follow-up regarding a 22-year-old woman with acute renal failure (creat. clearance 13.5 ml/min) due to idiopathic tubulo-interstitial nephritis documented by renal biopsy, after bilateral uveitis which healed with local prednisone. The clinical history and the clinical follow-up of our patient were typical of the TINU syndrome. We were able to exclude all diseases causing acute tubulo-interstitial nephritis such as systemic infection, hypersensitivity to drugs, Behcet's disease, Sjogren syndrome, sarcoidosis, systemic lupus or vasculitides. The patient recovered after systemic prednisone.
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PMID:Acute renal failure due to idiopathic tubulo-intestinal nephritis and uveitis: "TINU syndrome". Case report and review of the literature. 1106 43

Autoimmune thrombocytopenia can be a serious manifestation of systemic lupus erythematosus (SLE) which necessitates treatment with immunosuppressive agents and platelet transfusions. Interleukin-11 (IL-11) is a unique thrombopoietic growth factor which causes proliferation of megakaryocyte progenitors as well as induces megakaryocytic maturation. To our knowledge, this agent has not been used in the treatment of autoimmune thrombocytopenia, since theoretically there is a danger of IL-11 stimulating the immune system by up-regulating the lymphoid stem cells. We describe a 36-year-old splenectomized woman with known SLE who presented with pulmonary hemorrhage, acute renal failure, change in mental status, and severe thrombocytopenia (platelet count 2,000/mm3). Her pulmonary, renal, and central nervous system complications responded to intensive therapy with intravenous (IV) pulse methylprednisone and cyclophosphamide along with hemodialysis. The thrombocytopenia remained refractory to the above treatment plus daily multiple platelet transfusions and IV immunoglobulin. Treatment with recombinant human IL-11 (25 microg/kg/day subcutaneously) was initiated and continued for 5 days. Her platelet count improved to 25,000/mm3 within 48 hours, and she experienced no adverse effects.
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PMID:Treatment of lupus-induced thrombocytopenia with recombinant human interleukin-11. 1121 56

Up to 80% of patients with systemic lupus erythematosus (SLE) are treated with nonsteroidal anti-inflammatory drugs (NSAID) for musculoskeletal symptoms, serositis and headache. This survey reviews the literature on non-selective and selective inhibitors of cyclooxygenases with an emphasis on the efficacy and safety profile reported in SLE patients. No lupus-specific data on gastro-intestinal side effects of NSAID exist. Both non-selective Cox-inhibitors and selective Cox-2 inhibitors induce renal side effects including sodium retention and reduction of the glomerular filtration rate. Lupus nephritis is a risk factor for NSAID-induced acute renal failure, but not for rare idiosyncratic toxic renal reactions to NSAID. In refractory nephrotic syndrome, NSAID have been used successfully. Cutaneous and allergic reactions to NSAID are increased in SLE patients as well as hepatotoxic effects, particularly with high dose aspirin. Whereas a variety of central nervous system side effects of NSAID are probably no more common in SLE patients than in others, aseptic meningitis has been reported more frequently. Ovulation and pregnancy can be adversely affected by Cox-inhibitors. The antiplatelet effect of aspirin and non-selective Cox-inhibitors has a therapeutic potential in patients with the antiphospholipid syndrome (APS). In summary, treatment of SLE with NSAID requires awareness for the increased frequency of some side effects and close monitoring of toxicity.
Lupus 2001
PMID:Nonsteroidal anti-inflammatory drugs in systemic lupus erythematosus. 1131 41


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