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 sought to explore immunological factors in patients who died with rapidly fatal fibrosing lung diseases (Hamman-Rich syndrome). A retrospective review of cases of interstitial lung disease showed 12 recent deaths from Hamman-Rich syndrome. The mean age was 62, men outnumbering women 3 : 1. Five patients had proved collagen vascular disease (rheumatoid arthritis three, lupus two). Four others had a history of allergic disorders, syphilis, chronic eosinophilia, or hypersensitivity reactions. One patient showed disappearance of immunofluorescence as fibrosis advanced, which has not previously been reported. The study suggests a possible aetiological link between disorders of immunity and Hamman-Rich syndrome. The evidence also supports the notion that Hamman-Rich syndrome is an accelerated variant of the more indolent interstitial pneumonias.
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PMID:Rapidly fatal pulmonary fibrosis: the accelerated variant of interstitial pneumonitis. 16 92

Strongyloides stercoralis is an intestinal nematode which infects a large portion of the world's population. Individuals with infection confined to the intestinal tract are often asymptomatic but may have abdominal pain, weight loss, diarrhea, and other nonspecific complaints. Enhanced proliferation of the parasite in compromised hosts causes an augmentation of the normal life-cycle. Resultant massive invasion of the gastrointestinal tract and lungs is termed the hyperinfection syndrome. If the worm burden is excessive, parasitic invasion of other tissues occurs and is termed disseminated strongyloidiasis. A variety of underlying conditions appear to predispose to severe infections. These are primarily diseases characterized by immunodeficiency due to defective T-lymphocyte function (Table 1). Individuals with less severe disorders become compromised hosts because of therapeutic regimens consisting of corticosteroids or other immunosuppressive medication. The debilitation of chronic illness or malnutrition also predisposes to systemic stronglyloidiasis. The diagnosis of strongyloidiasis can be readily made by microscopic examination of concentrates of upper small bowel fluid, stool, or sputum. Important clues suggesting this infection include unexplained gram-negative bacillary bacteremia in a compromised host who may have vague abdominal complaints, an ileus pattern on X-ray, and pulmonary infiltrates. Eosinophilia is helpful, if present, but should not be relied upon to exclude the diagnosis. The treatment of systemic infection due to Strongyloides stercoralis with either thiabensazole 25 mg/kg orally twice daily is satisfactory if the diagnosis is made early. Because of several unusual features of this illness in compromised hosts, the standard recommendation for 2 days of therapy should be abandoned in such patients. Immunodeficiency, corticosteroids, and bowel ileus reduce drug efficacy. Thus a longer treatment period of at leuch as blind loops or diverticula necessitate longer treatment. Stool specimens and upper small bowel aspirates should be monitored regularly and treatment continued several days beyond the last evidence of the parasite. In particularly difficult situations where either worm eradication is impossible or reinfection is probable, short monthly courses of antihelminthic therapy seem to be effective in averting recurrent systemic illness. Finally, prevention of hyperinfection or dissemination due to Strongyloides stercoralis can be accomplished by screening immunocompromised hosts with stool and upper small bowel aspirate examinations. These would be especially important prior to initiating chemotherapy, or before giving immunosuppressive medications or corticosteroids to patients with nonneoplastic conditions such as systemic lupus erythematosus, nephrotic syndrome, or renal allografts.
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PMID:Overwhelming strongyloidiasis: an unappreciated opportunistic infection. 36 22

A profound defect in granulocyte chemotaxis was documented in an otherwise healthy 21-yr-old man who failed to localize granulocytes to an area of cellulitis during an allergic reaction to cephalothin. During the period of drug allergy, characterized by urticaria, eosinophilia, and profound hypocomplementemia, in vitro migration of the patient's granulocytes in the Boyden chamber was markedly impaired. Although devoid of hemolytic complement activity, the patient's serum possessed supranormal chemotactic activity, even following heat inactivation, suggesting the presence of chemotactically active complement split products. Chemotactic function improved concomitantly with steroid therapy and normalization of serum complement levels, and was entirely normal following clinical recovery and cessation of steroid therapy. The chemotactic abnormality noted in the patient's cells was reproduced in normal granulocytes by preincubation either with patient serum or with cobra venom-activated fresh (but not heated) normal serum, suggesting that in vivo exposure of granulocytes to activated complement was responsible for the patient's abnormal chemotactic response. This mechanism may contribute to the increased infection propensity noted in other conditions characterized by in vivo complement activation, such as rheumatoid arthritis and systemic lupus erythematosis.
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PMID:Acquired granulocyte abnormality during drug allergic reactions: possible role of complement activation. 83 Mar 75

A child is reported with chorea as the initial presentation of acute lymphoblastic leukemia. Subsequent laboratory studies revealed marked eosinophilia and a lupus anticoagulant. No peripheral or central nervous system lymphoblasts were observed. The chorea, eosinophilia, and lupus anticoagulant all resolved once remission of the acute lymphoblastic leukemia was induced. It is suggested that acute lymphoblastic leukemia be included in the differential diagnosis of chorea and eosinophilia in childhood.
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PMID:Chorea, eosinophilia, and lupus anticoagulant associated with acute lymphoblastic leukemia. 147 78

The extent of eosinophils in skin biopsy and peripheral blood specimens of patients with lupus panniculitis and morphea profunda was determined by studying 37 biopsies from 33 patients with lupus panniculitis and 55 biopsies from 53 patients with morphea profunda. Specimens from 8 (24%) of 33 patients with lupus panniculitis showed eosinophils, and 13 (25%) of 53 patients with morphea profunda had eosinophils in the subcutaneous tissue. In all cases, the diagnosis of lupus panniculitis or morphea profunda was established on the basis of other, more characteristic histologic features; the presence of eosinophils was incidental and not a diagnostic criterion. Occasional cases of lupus panniculitis or morphea profunda had numerous eosinophils. However, in most of the specimens, eosinophils were absent or observed in small numbers. Only 3% of patients with lupus panniculitis showed an increase in the number of eosinophils in the peripheral blood, whereas 47% of patients with morphea profunda had peripheral eosinophilia. The degree of hyaline necrosis in lupus panniculitis or of sclerosis in morphea profunda did not correlate with the number of eosinophils present in the biopsy specimen or peripheral blood.
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PMID:Eosinophils in lupus panniculitis and morphea profunda. 191 6

We experienced a case of idiopathic hypereosinophilic syndrome (HES) associated with pulmonary infarction. The case was a 22-year-old woman with marked eosinophilia (16835/microliters) and peripheral edema and cyanosis. During hospitalization, she suddenly developed lower right chest pain, and infiltrative lesions with pleural effusions in the right lung were prominent. A diagnosis of pulmonary infarction was made after perfusion scan and angiography of the lung. Lupus anticoagulant was found to be positive and a transient increase of anti-cardiolipin antibody slightly in her serum was also observed. Recurrent thrombosis is known to be complicated by HES but its mechanism remains to be clarified. There has also been no study reported in the literature on the role of lupus anticoagulant in this process; its possible role in this patient is discussed.
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PMID:[A case of idiopathic hypereosinophilic syndrome (HES) complicated by pulmonary infarction]. 195 37

A prospective study of pleural fluid eosinophilia (PFE) during initial thoracocentesis in 162 patients of pleural effusion was undertaken to determine its value in establishing an etiological diagnosis. Eighteen of the 162 cases showed pleural fluid eosinophilia (PFE), twelve could not be labelled with any definitive etiology even after extensive investigations, four belonged to the para-pneumonic group and resolved with treatment. Of the 32 patients with malignancy, PFE was seen in a single case of pleural mesothelioma. None of the patients with tuberculosis, empyema, systemic lupus erythematosus or amoebiasis had PFE. These findings suggest that PFE seen at initial thoracocentesis favours a benign diagnosis, with a rare chance of malignancy. Tuberculosis is unlikely in such patients.
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PMID:Diagnostic significance of pleural fluid eosinophilia during initial thoracocentesis. 263 66

The fascia had received little attention until Shulman's delineation of EF. Evidence is now accumulating that in addition to EF and scleroderma, significant fascial inflammation may be seen in polymyositis, dermatomyositis, eosinophilic polymyositis, systemic lupus erythematosus, and mixed connective tissue disease. It is still unclear whether EF represents a variant of scleroderma; however, it is becoming increasingly recognized that scleroderma shares many features in common with EF including eosinophilia, hypergammaglobulinemia, positive ANA and rheumatoid factor, and an association with hematologic disease. The rarity of Raynaud's phenomenon and significant visceral changes help distinguish EF from systemic scleroderma. In this regard, however, EF more closely resembles the localized scleroderma syndromes, especially morphea profunda and pansclerotic morphea. Biopsy in EF, systemic scleroderma, and localized scleroderma will show comparable changes, the essential difference being the levels at which they occur.
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PMID:Eosinophilic fasciitis. 267 38

With the increasing number of drugs, the list of agents which are capable of inducing pulmonary reactions continues to lengthen. This article is a compendium of presently available information on drug induced pulmonary reactions which we have found clinically useful. We have divided the drugs in groups on the basis of two features, pharmacologic actions and type of pulmonary reactions. A total of 109 drugs are cited. Categories of pharmacologic actions include cytotoxic drugs, analgesic and antirheumatic drugs, antimicrobial agents, vasoactive drugs, tranquilizers, anticonvulsants, antidepressants, antiarrhythmics, oral antidiabetics and a group of miscellaneous drugs. Type of pulmonary reactions include pulmonary eosinophilia, bronchoconstriction, acute interstitial pulmonary disease, mediastinic involvement, pleural effusion, pulmonary hypertension, pulmonary calcifications, pulmonary infections and drugs reported to cause drug-induced Systemic Lupus Erythematosus.
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PMID:Pulmonary reactions induced by drugs: a clinical compendium. 289 85

Because no systematic analysis of drug fever has been done, there has been no means for testing the validity of published characterizations of this clinical entity. We reviewed the clinical characteristics of 51 episodes of drug fever in 45 patients hospitalized at two Dallas hospitals between 1959 and 1986, and 97 episodes reported in the English literature between 1966 and 1986. Unlike characterizations found in textbooks and review articles, we found relative bradycardia in a minority of cases reviewed; little risk associated with rechallenge unless underlying cardiovascular disease was present; no characteristic fever pattern; a highly variable lag time between the initiation of the offending agent and the onset of fever; an infrequent association with either rash or eosinophilia; and no apparent association of drug fever with systemic lupus erythematosus, atopy, female sex, or advanced age.
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PMID:Drug fever: a critical appraisal of conventional concepts. An analysis of 51 episodes in two Dallas hospitals and 97 episodes reported in the English literature. 356 71


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