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 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

Twenty-seven patients with systemic lupus erythematosus (SLE) were investigated for the presence of allergic reactivity, and serum IgE levels were measured by immunoassay. Compared to controls, SLE patients had significant increases of only allergic rhinitis and drug allergy. Despite the usual hyperimmunoglobulinemia in SLE, IgE levels were not elevated (mean: 251 IU). Because recent reports have noted elevated IgE in rheumatoid arthritis, this finding may suggest basic immunologic differences between rheumatoid arthritis and SLE.
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PMID:Allergy in systemic lupus erythematosus. IgE levels and reaginic phenomenon. 94 98

Hydralazine is associated with a lupus-like syndrome. There is evidence that many drug hypersensitivity reactions are due to reactive metabolites. Incubation of hydralazine with activated neutrophils or monocytes led to the production of phthalazinone, phthalazine and 3 unidentified metabolites. Formation of the metabolites, with the exception of phthalazine, required activation of the leukocytes. Using radiolabelled hydralazine, covalent binding to activated neutrophils was observed. Oxidation of hydralazine catalyzed by myeloperoxidase (MPO) produced the same metabolites and covalent binding to protein. We conclude that hydralazine is metabolized by activated leukocytes to a reactive metabolite which may be associated with hydralazine induced lupus.
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PMID:Metabolism of hydralazine by activated leukocytes: implications for hydralazine induced lupus. 166 57

Although interview information is usually the sole source of data in case-control studies, the accuracy of such data is infrequently assessed. We compared interview data on selected medical conditions and surgical procedures with medical records of subjects with chronic lymphocytic leukemia. We examined agreement by type of respondent (self or surrogate), age, sex, race, and type of hospital. The strength of agreement between the two data sources (as measured by kappa statistics) was substantial kappa greater than 0.6) for splenectomy, appendectomy, asthma, and systemic lupus erythematosus; moderate kappa greater than 0.4) for tonsillectomy/adenoidectomy, tuberculosis, diverticulitis, hepatitis, rheumatic fever, and drug allergy; and poor kappa less than 0.3) for chronic bronchitis, chronic sinusitis, psoriasis, rheumatoid arthritis, and most other types of allergy. In general, self respondents had more accurate recall than surrogate respondents. Among self respondents the strength of agreement tended to be greater for males than females, for whites than blacks, and for subjects from referral hospitals than for community hospitals. No consistent patterns were apparent by age. Despite a number of limitations, the findings of the study provide an addition to the scant epidemiologic literature on this topic, and suggest that for certain conditions medical record data collection may be needed to supplement interview information.
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PMID:A comparison of interview data and medical records for previous medical conditions and surgery. 258 11

Hypersensitivity drug reactions are a major source of serious adverse drug reactions, yet very little is known about their mechanism. Several drugs are oxidized by activated neutrophils and mononuclear cells to reactive metabolites. Jack Uetrecht explains that the pattern of hypersensitivity reactions associated with these drugs - drug-induced lupus, agranulocytosis, and generalized hypersensitivity reactions - fits a mechanism in which leukocyte-generated reactive metabolites initiate the hypersensitivity reaction. Because activation of the leukocyte is necessary for reactive metabolite formation, one risk factor for a drug hypersensitivity reaction may be an infection or other inflammatory condition.
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PMID:Mechanism of hypersensitivity reactions: proposed involvement of reactive metabolites generated by activated leukocytes. 269 59

Cats receiving propylthiouracil (PTU) develop antinuclear antibodies (ANA) and an immune-mediated disease syndrome characterized by anorexia, lymphadenopathy, weight loss, and Coombs-positive hemolytic anemia. Investigation of the ANA specificity indicated that the predominant ANA activity consistent of anti-native DNA (nDNA) antibodies. The formation of anti-nDNA antibodies and immune-mediated disease syndrome appeared to be dose-dependent, even in cats in which a response had been induced on 4 prior occasions. These results supply further evidence that PTU-induced autoimmunity is not the result of a simple drug allergy. Rather, it appears that PTU induces a lupus-like syndrome, including the hallmark sign of systemic lupus erythematosus, anti-nDNA antibodies.
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PMID:Dose-dependent induction of anti-native DNA antibodies in cats by propylthiouracil. 325 86

A concept of the pathogenesis of tubular interstitial nephritis (TIN) is presented, based on histologic, immunohistologic and electromicroscopic investigations on 61 patients with glomerulonephritis, lupus erythematodes and rheumatoid arthritis. The pathogenic model is a hypersensitivity reaction which leads to alterations in the tubular basement membrane (TBM) and results in changes in the TBM and secondary damage to stroma, vessels and tubular cells. The findings change depending on the stage, reflecting the transition from an acute to a chronic process. In acute TIN which is generally a drug allergy, the dominant characteristic of the inflammatory process allows the reaction to be categorized in edematous (72%), cellular (23%) and tubular necrotic (5%) types. The cellular types show 4 subdivisions: plasma cellular, eosinophil-granulocytic, lymphohistiocytic and granulomatous. Chronic TIN is in particular characterized through the destruction of the TBM, dystrophy and atrophy of the tubules as well as their degeneration, lymphohistiocytic infiltrates and sclerotic stroma reactions. A distinction is made between cellular destructive and atrophic-sclerotic types. At view of the etiology and pathogenesis a distinction should be made between an infectious and non-infectious TIN and further by the character of the immunoreaction, into a primary and secondary form. If there glomerular changes are present and there is evidence of an immune phenomenon in the glomeruli and TBM we recommend the use of the term glomerulo-tubulo-interstitial nephritis.
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PMID:[Tubulointerstitial nephritis]. 356 28

Diphenylhydantoin (DFH) treatment for epileptic patients has shown adverse effects such as malignant lymphadenopathy, systemic lupus erithematosus, periarteritis nodosa and recently immunological alterations such as a decreased lymphocytic response to fitohemaglutinin and serum IgA concentration, therefore we thought DFH effect on secretory IgA would be an important finding. This phenomenon might imply a defect in resistance local mechanisms for infection. Two groups of patients were studied: a) 25 children with an established diagnosis of epilepsy, "grand mal" type, that received anticonvulsive treatment with DFH for six months and b) 25 children with a diagnosis of infectious meningoencephalitis that required DFH to control convulsive crisis. Patients with a history of recurrent infections, lymphadenopathies, hepatosplenomegaly, drug allergy, collagenopathies and immunodeficiency were ruled out from this study. In all patients T and B lymphocytes, serum IgA, saliva and duodenal fluid and IgA determinations were made. Results show IgA concentration decrease in saliva and duodenal fluid of epileptic and meningoencephalitic patients (p less than 0.05), as well as lymphocyte T depression in epileptic and non epileptic patients treated with DFH (p less than 0.001).
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PMID:Effect of diphenylhydantoin in serum and secretory IgA concentrations. 677 21

Liver disease in 193 patients (17 male and 176 female) with systemic lupus erythematosus (SLE) at Kawasaki Municipal Hospital were analyzed. Abnormal transaminase levels were found in 78 case (40.4%). Among them, there were 35 patients whose liver disease were identified. There were 12 patients whom no cause could be found other than SLE. Other liver disease were as follows: fatty liver in 9 cases, virus infection in 5 cases, gall stone and/or cholecystitis in 3 cases, drug allergy in 2 cases, autoimmune hepatitis 2 cases, primary biliary cirrhoses in 1 case. Liver disease with systemic lupus erythematosus was frequent, but there was no severe case.
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PMID:[Liver disease in systemic lupus erythematosus]. 755 39

A 52-year-old woman was admitted to our hospital because of a skin rash, high fever and myalgia. She had been diagnosed ten years ago by a dermatologist as having MCTD (mixed connective tissue disease). At the time of admission a diagnosis of active SLE was made by fulfilling four of the 1982 ARA criteria together with increasing levels of anti-DNA antibody and low levels of complements. Prednisolone (PSL) given orally in an initial dosage of 60 mg/day was effective during the first 6 weeks. Then a high fever, skin rash and pancytopenia appeared without active findings of SLE. Infection caused by bacteria, fungus or virus was suspected, but no infectious agent was present in cultures derived from blood or other sources. Antimicrobic drugs used were not effective at all. The clinical picture was suggestive of a drug allergy, but no causative drug was found. A diagnosis of hemophagocytic syndrome (HPS) was made because of the increased number of unusual hemophagocytic cells in the bone marrow. High levels of serum ferritin and neopterin, which are known to reflect macrophage activation, supported the diagnosis of HPS. HPS is characterized by activated phagocytosis presumably induced by hypersecretion of cytokines. Malignant lymphoma and infection are the two representative diseases which may cause HPS. Recently, an acute lupus HPS was reported in patients with active SLE. Here we reported a case of reactive HPS observed in a patient with SLE who had been receiving high dose PSL. Symptoms and findings of the patient gradually disappeared in several weeks after rapid reduction of the PSL dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemophagocytic syndrome observed in a patient with systemic lupus erythematosus]. 797 30


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