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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 report on the case of a 25-year-old female with severe systemic lupus erythematosus (SLE) who presented with pancytopenia, fever, arthralgia and abdominal pain. After antibiotic treatment, the patient was afebrile for 3 days before her temperature rose again. Dyspnoea and cough pointed towards pneumonia which was confirmed by X-ray. Different antibiotics and the antimycotic agent fluconazol were given. The lupus flare was treated with high-dose prednisolone. After a couple of days, the dyspnoea increased and mechanical ventilation became necessary. Bronchoscopy and transbronchial biopsy revealed the diagnosis of invasive aspergilloses. Despite of an immediate treatment with amphotericin B, the patient died because of respiratory insufficiency. The literature on aspergillosis in SLE is reviewed and prophylactic, diagnostic and therapeutic options are discussed for this infectious complication which has an 80% mortality in patients with SLE.
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PMID:A fatal case of severe SLE complicated by invasive aspergillosis. 935 8

Pulmonary disorders in systemic lupus erythematosus involve a variety of clinical presentations and pathologic patterns, which can be difficult to diagnose due to systemic dysfunction, infection, or complications of therapy. The causes of dyspnea in systemic lupus erythematosus are multifactorial, and the clinical manifestations of lung disease widely vary. Biopsy is frequently relied on to evaluate and diagnose pulmonary disease in systemic lupus erythematosus. The patient who has systemic lupus erythematosus-associated lung disease is effectively treated with various immunosuppressive drugs, in conjunction with careful evaluation of the patient's systemic involvement, drug-induced complications, and the ever-present threat of infection.
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PMID:Pulmonary involvement in systemic lupus erythematosus. 936 98

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 reviewed the case records of 10 Oriental patients with systemic lupus erythematosus (SLE) who developed pulmonary haemorrhage (PH) between 1987 and 1996 to determine their clinical presentation and outcome. All the patients had clinical evidence of PH including a sudden onset of dyspnoea, tachycardia, fall in haemoglobin (at least 1.5 gm%) and bilateral diffuse alveolar infiltrates on chest radiographs. At the time of PH, nine patients had a disease duration of 2 years or less and all the patients had clinical and/or laboratory evidence of active lupus disease. Fever and lung crepitations were present in 90% of patients while haemoptysis and chest pain occurred in only three and two patients, respectively. All the patients were treated with high dose intravenous corticosteroids and in addition seven had a combination of pulse methylprednisolone and cyclophosphamide, and four had received plasmapheresis. Four patients died as a result of PH. One patient died of pneumonia three years after recovering from PH while the remaining five had no recurrence of PH after a median follow-up of 22 months. Our study suggests that PH in Oriental lupus patients often occurs early in the disease, rarely presents with haemoptysis and has a high mortality despite aggressive immunosuppressive therapy.
Lupus 1997
PMID:Pulmonary haemorrhage in Oriental patients with systemic lupus erythematosus. 941 86

Carbamazepine-induced lupus is uncommon; its frequency is less than 0.001% of the cases of lupus treated. Herein we describe a 52-year-old woman who had development of facial erythema, arthralgia, dyspnea, and multiple pulmonary rounded masses and nodules while she was taking carbamazepine for epilepsy. Pulmonary histologic examination showed bronchiolitis obliterans organizing pneumonia. Antinuclear antibodies and antihistone antibodies were present without antibodies to double-stranded DNA. Thirteen months after carbamazepine had been withdrawn, all symptoms had disappeared without the use of anti-inflammatory drugs. Even though pulmonary involvement is possible during carbamazepine treatment, to our knowledge, bronchiolitis obliterans organizing pneumonia on its own or associated with carbamazepine-induced lupus has not been previously described.
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PMID:Lupus and pulmonary nodules consistent with bronchiolitis obliterans organizing pneumonia induced by carbamazepine. 941 95

Urticarial vasculitis (UV) is a primary syndrome or a cutaneous vasculitic lesion occurring in the course of a collagen disease, as the systemic lupus erythematosus (LE). UV is a recently recognized disorder which affects most exclusively the female sex and may be differentiated from common (nonvasculitic) urticaria because it is characterized by inflammation and necrosis of blood vessels (vasculitis). UV and common urticaria may be induced by a variety of factors and pathogenetic mechanisms. It seems that a continuum exists, ranging from benign cutaneous lesions of urticaria to vasculitis with strong immunological involvement. On the basis of the clinical evaluation, two major groups of UV have been classified, the normocomplementemic, with a less severe clinical course, and the hypocomplementemic UV, a rare immune complex-mediated disorder related to LE as for as the similar pathogenesis and systemic involvement are concerned. A case of a young female patient with a unique syndrome characterized by crises of urticarial recurrent painful lesions of unknown origin, associated with angioedema of the tongue and soft palate, severe malaise, arthralgias and abdominal pain is reported. Dyspnea and cough were sometimes present, but fever was absent. Symptoms were caused by physical stress, heat or pressure and were little responsive to corticosteroids. Although skin biopsy did not prove with certainty the occurrence of vasculitis, clinical data and laboratory findings (normal levels of complement fractions, raised erythrocyte sedimentation rate, presence of cryoglobulins and ASMA, nDNA and AMA autoantibodies and absence of ANA autoantibodies and LE cells) suggest a normocomplementemic UV, excluding a classic LE. The family doctors and the internist must become familiar with the "lupus-like" syndromes, which include UV. In fact, a correct diagnosis of this syndrome is important because, although prognosis of UV may not be severe, the possibility exists of a systemic involvement (mainly renal) with progression to LE.
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PMID:[Urticarial vasculitis syndrome. A case report and review of the literature]. 945 98

A 22 year-old woman with a seven year history of (SLE) was readmitted because of oliguria, edema, dyspnea and arterial hypertension. She had a previous biopsy diagnosis of focal glomerulonephritis, (WHO III b), and had been treated with immunosuppressors and steroids. Laboratory data showed lupus activity, AHM with thrombocytopenia, nephrotic-range proteinuria and renal failure. A second renal biopsy was performed showing diffuse proliferative nephritis, (WHO IV), in association with noninflammatory necrotizing vasculopathy with luminal obliteration. She started with hemodialysis and was subsequently treated with methylprednisolone pulses, plasmapheresis, cyclophosphamide and oral steroids. During the inpatient period, she had generalized seizures, acute lung injury and pulmonary hemorrhage. These complications, the AHM and the thrombocytopenia receded totally. Renal function was never resumed. We emphasize that this association of diffuse proliferative nephritis with noninflammatory necrotizing vasculopathy is not infrequent and has a poor renal prognosis. The AHM with thrombocytopenia was interpreted as secondary to endothelial cell damage due to vasculopathy.
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PMID:[Renal vascular lesion and microangiopathic hemolytic anemia in systemic lupus erythematosus]. 953 30

A 51-year-old woman was referred to our hospital with dyspnea. Chest roentgenogram on admission showed dilation of the pulmonary arteries and hyperlucency in the lung fields. An ultrasonic cardiographic examination showed that the right atrium and ventricle were dilated. Pulmonary thromboembolism due to left popliteal vein thrombosis was diagnosed by perfusion scintigram of the lung, which showed multiple wedge-shaped defects, and by digital subtraction angiogram, which showed a filing defect in the left popliteal vein. Antiphospholipid syndrome was diagnosed after IgG anticardiolipin antibody was defected. Scleroderma was subsequently diagnosed because the patient exhibited Raynaud's phenomenon and proximal scleroderma. Although closely associated with lupus erythematosus and other lupus variants, antiphospholipid syndrome has not been recognized as a common complication of scleroderma. This is the first report of a patient with pulmonary thromboembolism associated with antiphospholipid syndrome and scleroderma.
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PMID:[Pulmonary thromboembolism associated with antiphospholipid syndrome in scleroderma]. 956 91

A 49 year-old man was admitted for edema and renal impairment due to SLE. Since he did not improve with predonisolone and methylprednisolone pulse therapy, cyclophosphamide pulse therapy (300 mg div.) was administered. The patient subsequently developed a fever, dyspnea and cough, and interstitial regions of the lungs exhibited shadows on X-ray and CT. The patient also suffered hypoxemia and poor lung function. Since several culture tests and viral antibody tests were negative for infection, antibiotics were not effective, and TBLB indicated interstitial pneumonia, which we speculated was induced by cyclophosphamide. However, this was such a severe case of interstitial pneumonia that it could not be cured merely by discontinuing the cyclophosphamide, but it did improve immediately after starting methylprednisolone pulse therapy. The incidence of cyclophosphamide-induced interstitial pneumonia is very low, but the mortality rate is high. Since cyclophosphamide pulse therapy is often used to treat SLE, attention should be focused on the incidence of interstitial pneumonia.
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PMID:[SLE with interstitial pneumonia during cyclophosphamide pulse therapy]. 980 18

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


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