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)

Pneumatosis intestinalis in association with connective tissue diseases is an unusual combination whose pathogenesis is not yet understood. Furthermore, steroid medication, often used to treat these diseases, may itself cause pneumatosis. Three cases of scleroderma, systemic lupus erythematosus, and amyloidosis in association with pneumatosis and without prior steroid therapy are presented. The small vessel occlusive pathologic processes in these diseases may cause focal areas of mucosal ischemia resulting in small, perhaps transient ulcerations that allow gas to enter the gut wall from the lumen.
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PMID:Pneumatosis intestinalis in association with connective tissue disease. 101 66

Quinidine, procainamide and disopyramide are antiarrhythmic drugs in the class 1A category. These drugs have a low toxic to therapeutic ratio, and their use is associated with a number of serious adverse effects during long term therapy and life-threatening sequelae following acute overdose. Class 1A agents inhibit the fast inward sodium current and decrease the maximum rate of rise and amplitude of the cardiac action potential. Prolonged Q-T interval and, to a lesser extent, QRS duration may be observed at therapeutic concentrations of quinidine. With increasing plasma concentrations, progressive depression of automaticity and conduction velocity occur. 'Quinidine syncope' (a transient loss of consciousness due to paroxysmal ventricular tachycardia, frequently of the torsade de pointes type) occurs with therapeutic dosing, often in the first few days of therapy. Extracardiac adverse effects of quinidine include potentially intolerable gastrointestinal effects and hypersensitivity reactions such as fever, rash, blood dyscrasias and hepatitis. Procainamide produces electrophysiological changes that are similar to those of quinidine, although Q-T interval prolongation with the former is less pronounced at therapeutic concentrations. Hypersensitivity reactions including fever, rash and (more seriously) agranulocytosis are associated with procainamide, and a frequent adverse effect requiring cessation of therapy is the development of systemic lupus erythematosus. Of the 3 drugs, disopyramide has the most pronounced negative inotropic effects, which are especially significant in patients with pre-existing left ventricular dysfunction. As with quinidine, unexpected 'disopyramide syncope' at therapeutic concentrations has been described. Anticholinergic side effects are common with this drug and may require cessation of therapy. Disopyramide therapy may unpredictably induce severe hypoglycaemia. Severe intoxication with the class 1A agents may result from acute accidental or intentional overdose, or from accumulation of the drugs during long term therapy. Acute overdose can result in severe disturbances of cardiac conduction and hypotension, frequently accompanied by central nervous system toxicity. Decreased renal function can cause significant accumulation of procainamide and its active metabolite acecainide (N-acetyl-procainamide), resulting in severe intoxication. Mild to moderate renal dysfunction is less likely to lead to quinidine or disopyramide intoxication, unless renal failure is severe or concurrent hepatic dysfunction is present. Management of acute intoxication with class 1A drugs includes gut decontamination with provision of respiratory support and treatment of seizures as needed. Hypertonic sodium bicarbonate, by antagonising the inhibitory effect of quinidine on sodium conductance, may reverse many or all manifestations of cardiovascular toxicity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Poisoning due to class IA antiarrhythmic drugs. Quinidine, procainamide and disopyramide. 228 95

Sera from 82 patients with chronic inflammatory liver diseases and from patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and Hashimoto's thyroiditis were studied by immunoblotting against purified liver plasma membranes (LPM) and soluble liver protein (SLP) fractions from different species after previous separation by SDS-PAGE. Eighteen of 19 sera with LMA of IgG type in immunofluorescence assay and six LMA-negative sera (three sera from patients with RA) showed antibodies of the IgG or IgM classes against a protein with a molecular weight of 26 kD which was present in LPM and SLP fractions from rats, rabbits, pigs and humans. The reaction with 26-kD liver protein did not correlate with other known autoantibody-antigen systems. All sera were negative in the 26-kD region with liver mitochondria, liver microsomes and soluble proteins of kidney (with one exception), heart and gut from the rat. The 26-kD protein was purified by affinity chromatography on immobilized anti-26-kD protein antibodies from patients, eluted from the 26-kD band of immunoblots. Studies with purified 26-kD liver protein and with SLP as antigens after separation in two-dimensional electrophoresis confirmed that patient serum and experimental rabbit antiserum react with the same protein. Eluted patient antibodies and rabbit antisera showed a linear fluorescence pattern on isolated hepatocytes from rat and rabbit. The data indicate that one of the target antigens of LMA is a species-nonspecific 26-kD protein located on the hepatocellular surface.
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PMID:Liver membrane antibodies (LMA) recognize a 26-kD protein on the hepatocellular surface. 230 35

Thirty-six patients with malignant carcinoid tumors were treated with human leukocyte interferon (IFN) im at doses of 3-6 megaunits/day. The origins of the primary tumors were as follows: mid-gut (29 patients); pulmonary (four); rectal (one); ovarian (one); and unknown (one). Nineteen of the 36 patients had previously been treated with cytotoxic agents, streptozocin plus 5-fluorouracil or doxorubicin, but showed progressive disease. With IFN objective tumor responses were seen in 17 of the 36 patients (47%): in 14 of the 29 patients with mid-gut carcinoids (48%) and in three of the four patients with lung carcinoids (75%). The median duration of response was 34 months. Stable disease was noted in 14 of 36 patients (39%), all presenting mid-gut carcinoids. The median duration of stable disease was 25 months. Progressive disease from the start of IFN therapy was seen in five patients (14%). All responders except one had a greater than 50% reduction of urinary 5-hydroxyindoleacetic acid or alpha-human chorionic gonadotropin, whereas four patients also had a significant reduction of tumor size on computerized tomographic scan or at laparotomy. Two patients achieved complete remission. Improvement of clinical manifestations of the carcinoid syndrome was seen in all patients with objective response. Adverse effects including influenza-like syndrome, reduction of blood cells, chemical signs of liver dysfunction, and disturbed lipid metabolism occurred but were reversible or could be circumvented by dose reduction. Autoimmune phenomena were also noted such as development of thyroid autoantibodies with thyroiditis, SLE syndrome with antinuclear factors, and parietal cell antibodies with pernicious anemia. IFN therapy seems to be very effective in controlling tumor-secreted substances and thus giving relief of clinical symptoms. It also arrests tumor growth for extended time periods (median, 2 years). The adverse effects are surmountable and less severe than with cytotoxic therapy.
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PMID:Treatment of malignant carcinoid tumors with human leukocyte interferon: long-term results. 242 64

In the period from 1980-86 we obtained 51 strains of Listeria from meningitis in adults for serotyping and phage-typing. Ten strains were associated with meningitis and 3 with septicaemia of immunocompromised patients. They suffered from leukaemia, diabetes, Hodgkin's disease, alcoholism, lupus erythematodes. The lethality rate in these patients was 70%, in other patients with meningitis 30%. Phage typing has shown that 4b strains were often determined by the phage-code 00010 and similar codes. This phage-pattern might be specific for meningitis strains. The immunocomprised patient is especially endangered in taking up listeriae from the environment, but it must also be in consideration that listeriae may easy gain access from the gut into the vessels.
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PMID:Listeria-meningitis and -septicaemia in immunocompromised patients. 251 62

This study has identified a group of patients with inflammatory chronic, or relapsing acute arthritis who even in the absence of gastrointestinal symptoms have histological evidence of ileocolitis. At colonoscopy simultaneous biopsies of the terminal ileum and colon were taken from 108 patients with reactive arthritis (n = 55) or ankylosing spondylitis (n = 53), 47 patients with other rheumatic diseases and 19 control patients suffering from colonic polyps, adenocarcinoma, or chronic constipation. All control patients and all but one patient with rheumatoid arthritis, juvenile chronic arthritis, systemic lupus erythematosus, lumbar back ache, and psoriatic arthritis did not have histological evidence of acute or chronic inflammatory bowel disease. In contrast, in 30 of 35 (56.6%) patients with ankylosing spondylitis, and in 37 of 55 (67%) patients with reactive arthritis, regardless of HLA B27 phenotype, there was histological evidence of inflammatory bowel disease with features either of acute enterocolitis, or early Crohn's disease. Only 18 of 67 (27%) of the patients with histological gut inflammation, however, had intestinal symptoms.
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PMID:Histopathology of intestinal inflammation related to reactive arthritis. 349 71

Ileocolonoscopy and microscopic examination of ileum biopsies were performed on 35 patients with reactive arthritis, with asymmetrical pauciarticular arthritis and enthesopathies. Ileocolonoscopy was also performed on 26 patients with ankylosing spondylitis (AS) and on 19 control patients with rheumatoid arthritis, juvenile chronic arthritis, systemic lupus erythematosus and psoriatic arthritis. In the reactive group, ileocolonoscopy showed macroscopic inflammation in 16 cases and abnormal microscopic examination in all but 2 cases, even in patients without gastrointestinal disorders. In the 2 patients with sexually acquired disease, the gut was normal. In the AS group, inflammation was observed in the B27 negative and positive patients with peripheral joint involvement. Occasionally, ileal signs were seen in the HLA-B27 positive patients without peripheral joint involvement. None of the controls showed signs of gut inflammation. Ilecolonoscopy may be of value in detecting subclinical forms of bowel inflammation.
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PMID:HLA-B27 related arthritis and bowel inflammation. Part 2. Ileocolonoscopy and bowel histology in patients with HLA-B27 related arthritis. 387 21

Naturally occurring thymocytotoxic autoantibodies (NTA) have been described in both humans and mice with SLE. To define further the role of anti-thymic autoantibodies in murine lupus, we studied the cellular and molecular specificity of a spontaneous monoclonal NTA, designated TC-17, derived from a 4-mo-old New Zealand Black mouse. TC-17, an IgM autoantibody, has been shown previously to be unreactive with Lyt-1, Lyt-2, and L3T4 (T helper) antigens. We have shown further that it is also unreactive with Thy-1. TC-17 recognizes a new thymic antigen that appears to mark a distinct subpopulation of cortisol-sensitive cortical thymocytes. The antigen consists of a single glycoprotein chain with an apparent m.w. of 88,000. TC-17 shows reduced binding to thymocytes treated with tunicamycin, indicating either that glycosylation of TC-17 antigen is necessary for TC-17 to bind to it or that glycosylation is required for expression of the antigen on the cell surface. TC-17 uniquely reacts with two of 17 murine lymphoid tumor cell lines of intermediate cellular maturity. The thymocytotoxic activity of TC-17 is absorbed by single cell suspensions of murine stomach, small intestine, large intestine, kidney, and thymus. Moreover, the specific binding of TC-17 to gut tissue of normal and germfree mice can be demonstrated by indirect immunofluorescence, suggesting antigenic cross-reactions between thymic and gut tissue. TC-17 reacts with rat thymocytes as well as it does with murine cells, indicating moderate evolutionary conservation of the TC-17 antigen. The expression of this glycoprotein by a discrete thymocyte subset may prove to be a valuable probe for the study of murine T cell differentiation.
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PMID:Tissue localization and biochemical characteristics of a new thymic antigen recognized by a monoclonal thymocytotoxic autoantibody from New Zealand black mice. 392 16

Mannose-rich 90 kD glycoprotein, a constituent of skin and small-bowel mucosa, was identified as antigen in circulating IgG-type immune complexes in dermatitis herpetiformis and coeliac disease by means of an enzyme-linked immunosorbent assay. High levels of 90 kD glycoprotein-IgG complexes were found in 7 out of 12 patients with dermatitis herpetiformis and in 10 out of 20 patients with coeliac disease but in only 2 out of 20 patients with systemic lupus erythematosus. The highest levels of 90 kD antigen-IgG complexes were found in patients with dermatitis herpetiformis. The amount of these complexes did not correlate with the degree of jejunal villous atrophy. The 90 kD glycoprotein-containing immune complexes with targets in skin and gut may be involved in the pathogenesis of dermatitis herpetiformis and coeliac disease.
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PMID:Demonstration of tissue 90 kD glycoprotein as antigen in circulating IgG immune complexes in dermatitis herpetiformis and coeliac disease. 614 20

We have investigated the use of 111Indium granulocyte scanning, which would be expected to identify areas of perivascular or generalized neutrophil infiltration, in patients with collagen-vascular diseases suffering from either gastrointestinal symptoms (diarrhea or abdominal pain in 15 patients) or otherwise unexplained fever (six patients). Among patients with gastrointestinal symptoms, seven of 15 had positive scans suggesting large or small bowel involvement--three of three patients with Behcet's syndrome, four of five with vasculitis, no patient in six with systemic lupus erythematosus, and no patient with Churg-Strauss syndrome. Among patients without gastrointestinal symptoms, only one patient with polyarteritis nodosa had a positive scan, showing both large and small intestinal involvement. White cell scanning offers a noninvasive, readily tolerated technique for identifying inflammatory involvement of the intestine in patients with collagen-vascular disorders. Gastrointestinal involvement is rare in the absence of symptoms; and among symptomatic patients, inflammatory involvement of the gut is more likely to be found in patients with vasculitis or Behcet's.
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PMID:Noninvasive investigation of the gastrointestinal tract in collagen-vascular disease. 650 10


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