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)

Acute massive pulmonary hemorrhage is described as part of the clinical picture of SLE. Seven patients had sudden onset of high fever, dyspnea, tachycardia, and cough with blood-tinged sputum that within hours progressed to massive hemoptysis and death. There were no vasculitis or other inflammatory lung changes found at autopsy. Only one of the seven reported cases survived when treated with 2 g of intravenous hydrocortisone daily. The mechanism of this pulmonary bleeding is unknown but seems to be an immune complex mediated phenomenon.
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PMID:Acute massive pulmonary hemorrhage in systemic lupus erythematosus. 14 42

A 21-year-old woman was admitted to our hospital because of high fever, cough, and headache. Other clinical manifestations included hepatosplenomegaly, anemia, leukopenia, and mild liver dysfunction. As she had been diagnosed to have systemic lupus erythematosus (SLE) previously, we first suspected that this disease had become exacerbated. However, the titers of anti-EB virus (VCA-IgG) and some other viruses were high on admission, and hemophagocytosis by macrophages was observed on bone marrow examination. Therefore, she was diagnosed to have virus-associated hemophagocytic syndrome (VAHS). Prednisolone therapy was then initiated, but the patient responded poorly. We next tried gamma globulin, and the clinical findings and laboratory data were improved. Our patient showed a very favourable clinical course following gamma globulin therapy, suggesting that steroid and gamma globulin should be considered as a treatment even in the early stages of this syndrome in adults.
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PMID:[Steroid and gamma globulin therapy against virus-associated hemophagocytic syndrome]. 127 36

A 60-year-old female was admitted to our hospital because of respiratory failure. She was diagnosed as having systemic lupus erythematosus (SLE) in 1971 and had been treated with low-dose oral corticosteroids for 13 years. She developed cough, fever and anemia several days after oral corticosteroids were tapered. Initially, she had no complications such as congestive heart failure, renal failure or bleeding tendency. Respiratory failure progressed without any response to antibiotic therapy. Chest roentgenogram showed bilateral diffuse infiltrates and air bronchograms. There was no improvement even with steroid pulse therapy, and she died of multiple organ failure. Autopsy revealed massive intra-alveolar hemorrhage and interstitial pneumonitis. Deposition of immunoglobulins in the lung was not seen. To our knowledge, this is the 11th reported case of SLE associated with pulmonary hemorrhage in Japan.
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PMID:[An autopsy case of massive pulmonary hemorrhage in systemic lupus erythematosus]. 143 30

A 27-year-old nonsmoking woman complained of cough and chest oppression for two years since an episode of pneumonia. Clinical tests showed decrease in FEV1.0 during attacks of coughing and evidence of bronchial hypersensitivity. While these events fitted the picture of bronchial asthma, the nonwheezing cough suggested cough variant asthma. Antinuclear antibody and anti-ds DNA antibody were increased and leukopenia was recognized, suggesting the diagnosis of systemic lupus erythematosus (SLE). Bronchoalveolar lavage showed lymphocytic alveolitis and decreased T4/T8. These results were suggestive of collagen lung induced by SLE. Inhalation challenge with capsaicin and rapid intravenous injection of lobelin and alinamin indicated that peripheral c-fiber receptors were involved in the induction of coughing. We conclude that the peripheral lesion of collagen lung stimulates the peripheral c-fiber receptors, leading to cough variant asthma.
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PMID:[Case report of collagen lung in SLE presenting with cough variant asthma: relation between the localization of responsible receptors and cough]. 156 25

Tc-99m DTPA aerosol is often swallowed during inhalation for lung ventilation scans. The authors evaluated a 16-year-old girl with a known history of mixed collagen disorder (positive lupus anticoagulants) for symptoms of cough and acute shortness of breath. Tc-99m DTPA accumulated in the distal esophagus during aerosol inhalation and remained there at the end of the perfusion study, a period of approximately 1 hour. This serendipitous observation antedates clinical signs and symptoms of dysphagia.
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PMID:Esophageal dysmotility as a serendipitous observation on ventilation-perfusion imaging of the lungs. 161 36

Adverse effects of converting enzyme inhibitors are either substance-specific (neutropenia, proteinuria, skin rashes, taste disturbances) or due to the converting enzyme inhibition (hypotension, functional renal insufficiency, hyperkalemia, cough, angioedema). They are rare nowadays because of better knowledge of the pharmacokinetics and -dynamics of the converting enzyme inhibitors, resulting in lower dosage, and because of identifying patients at high risk. The dosage must be adjusted according to renal function, in order to prevent accumulation and toxicity. In addition to patients with renal insufficiency, patients at high risk are those with a stimulated renin-angiotensin-aldosterone system, i.e. patients with renovascular hypertension or heart failure. Patients with collagen vascular disease, for example, systemic lupus erythematosus or scleroderma, should not be considered for long-term therapy with converting enzyme inhibitors because of the increased risk of neutropenia. Life-threatening angioedema may develop, mainly during the first few hours after drug administration.
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PMID:[Angiotensin-converting enzyme inhibition: side effects and risks]. 285 Jun 87

A 47-year-old housewife presented with nonproductive cough, progressive breathlessness and intermittent fever during gold treatment, originally prescribed for seropositive polyarthritis, which later fulfilled the criteria for systemic lupus erythematosus (SLE). An open lung biopsy showed abundant interstitial edema with mononuclear inflammatory cells and some eosinophils, and slight bronchiolitis. The picture was nonspecific but suggestive of hypersensitivity pneumonitis. Electron microscopy revealed splitting and local disappearance of the basal laminae of the alveolar capillaries, venules and alveolar epithelium. This injury was confirmed by immunohistochemical staining for type IV collagen and laminin, the major components of basal laminae. In most macrophages there was lysosomal electron dense granular material, i.e. aurosomes, which gave the spectrum of gold in electron microprobe analysis. After the gold treatment was stopped the pulmonary symptoms gradually decreased during several months and no permanent lung disease remained. Whereas the pulmonary manifestation could have been due to her underlying disease we discuss in this study the possibility of its being gold induced.
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PMID:Bronchiolo-alveolitis with pulmonary basal lamina injury in a rheumatoid patient during gold treatment. 312 4

PH is an uncommon manifestation of SLE. The symptoms of PH develop within a few years after the onset of the multisystem disease. The most common presenting complaints of SLE patients with PH are dyspnea on exertion, chest pain, nonproductive cough, edema, and fatigue or weakness. The important physical findings are a loud second pulmonic heart sound and a right ventricular lift. The chest roentgenogram shows a cardiomegaly, a prominent pulmonary segment, and usually clear lung fields. Pulmonary function tests may show evidence of restrictive lung disease; however, the physiologic abnormalities are mild and out of proportion to the severity of the PH. The diagnosis of PH is established by cardiac catheterization showing elevated pulmonary artery pressure, normal capillary wedge pressure, and no evidence of intracardiac or extracardiac shunts. Pathologic examination of the lung demonstrates angiomatoid lesions involving muscular pulmonary arteries. There is a thickening of the media and subintima of the arterioles. Immunoglobulin and complement deposits are found in the walls of pulmonary arteries. Immunoglobulin eluted from the lung contains rheumatoid factor and antinuclear antibody including antibody to DNA activity. DNA antigen is also present in walls of blood vessels. These results suggest an immune complex deposition process as a mechanism in the pathogenesis of PH in SLE. The clinical course of PH in SLE is variable. Symptoms may be mild and the disease follows a stable and protracted course for several years. It can, however, develop a progressive course ending in death in a few years. The clinical response of SLE patients with PH to treatment with high doses of systemic corticosteroids is not consistent or predictable.
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PMID:Immunopathologic and clinical studies in pulmonary hypertension associated with systemic lupus erythematosus. 637

M. pneumoniae is a common cause of pneumonia. The diagnosis is suspected when the patient presents with symptoms suggesting primary atypical pneumonia including cough, fever, chills, headache, and malaise in association with a segmental or subsegmental pulmonary infiltrate(s), the white blood cell count is normal or only slightly elevated, and the Gram stain of the sputum (if any can be obtained) reveals polymorphonuclear leukocytes and few bacteria. The diagnosis is more difficult when the patient presents with symptoms not suggestive of pneumonia including lethargy, dyspnea, and a 1- to 4-week history of shortness of breath without cough or fever in association with diffuse reticulonodular or interstitial pulmonary infiltrates. The disease in the previously healthy host is usually benign and self-limiting. However, the course is shortened by the administration of tetracycline derivatives or erythromycin. M. pneumoniae pneumonia can occur in association with other diseases including sickle cell anemia, sarcoidosis, systemic lupus erythematosus, Hodgkin's disease, and various other immunodeficiency states. In these patients mycoplasma pneumonia can be very serious. Although there is no pathognomonic clinical or radiographic presentation, careful consideration of epidemiologic, clinical, laboratory, and radiographic data are usually sufficient to suggest the diagnosis in most patients.
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PMID:Mycoplasma pneumonia. 676 79

Systemic lupus erythematosus, polymyositis/dermatomyositis, connective tissue disease, and polyarteritis nodosa are the collagen vascular diseases (CVDs) most likely to mimic pneumonia. All can be associated with an acute illness characterized by fever, cough, dyspnea, pleural symptoms, and an abnormal chest roentgenogram. Recognition of the CVD-associated pulmonary process requires sophisticated serological testing and chemical pleural fluid analysis coupled with the exclusion of pulmonary infection and pulmonary embolization. This review emphasizes the clinical characteristics of these CVDs, the diagnostic tests most helpful in recognizing them, and the differential diagnosis of pleuroparenchymal disorders that occur in these patients.
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PMID:Collagen vascular diseases. 756 2


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