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)

The authors provide the results of studying the methodologic characteristics and of the clinical trial of the C1q-ELISA for detection of the circulating immune complexes. The C1q-ELISA is shown to have a high sensitivity and to make it possible to identify 3 micrograms/ml and more of aggregated gamma-globulin. The method can use for detection of CIC E (ab')2-fragments of antibodies to IgG of man and protein A labeled with peroxidase. Using the method, the circulating immune complexes were identified in the sera of 50% of patients with systemic lupus erythematosus, of 30% of patients with dilated cardiomyopathy and of 53% of patients with nonspecific aortoarteritis. It is concluded that the C1q-ELISA can be used in clinical practice for detecting the circulating immune complexes in different diseases of man.
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PMID:[Use of solid-phase Clq-ELISA for detecting circulating immune complexes in human diseases]. 247 7

To determine whether or not male (NZWXBXSB)F1 [WXB)F1) mice exhibiting a lupus-like syndrome died of acute myocardial infarction (MI), and whether acute MI is directly related to small coronary artery disease, acute and old MIs were examined histologically in 55 dead (WXB)F1 male mice and 30 age-matched, surviving (WXB)F1 male mice used as a control group. In each heart from the 15 dead mice with MI and the five surviving mice without MI, 300 to 400 5-microns-thick serial sections were made; every fourth section was stained. Acute MI was found in 35 (64%) dead mice and in one (3%) survivors, whereas old MI was found in 50 (91%) dead mice and 17 (57%) survivors: a significant difference between the dead and surviving mice. The MIs were numerous, scattered, and small in most mice. Quantitative analysis revealed that the percentage of acute MI and old MI in the left ventricular (LV) wall was 6% +/- 11% and 3% +/- 3% in the dead group, and 0.4% and 2% +/- 3% in the control group. This indicated that recurrent acute MI is a major factor in the death of the mice. Although all the epicardial major coronary arteries of the (WXB)F1 male mice were intact, significant stenoses were noted in the intramyocardial small arteries. The serial sections in the 15 dead mice with MI revealed 1) segmental occlusive thrombi in the infarct-related small coronary artery in 14 of the 20 foci of acute anemic MIs, two of the 18 foci of acute hemorrhagic MIs, and four of the 58 foci of old MIs; and 2) segmental intimal thickenings in the infarct-related small artery in six of the 20 foci of acute anemic MIs, two of the 18 foci of acute hemorrhagic MIs, and 56 of the 58 foci of old MIs. There was no evidence of small coronary artery disease in the surviving mice without MI. The thrombus would result in thickened intima as MI progresses from the acute to the old stage. Because it was established that acute MI of hemorrhagic type follows reperfusion after transient occlusion of the coronary artery, hemorrhagic acute MI with rare incidence of thrombi in this mouse suggests that thrombolysis occurs after occlusion due to thrombus formation. Thus, the pathogenesis of multiple MIs is occlusive thrombi, recanalization in small coronary arteries or both. Some of the mice had dilated cardiomyopathy (DCM)-like features (marked LV dilatation).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:High frequency of spontaneous acute myocardial infarction due to small coronary artery disease in dead (NZWxBXSB)F1 male mice. 259 79

Twenty-eight patients with malignant ventricular arrhythmias were treated with the automatic implantable cardioverter-defibrillator (AICD) in a 14-month period. Thirteen patients were resuscitated from a ventricular fibrillation (VF) episode. Fifteen patients presented with ventricular tachycardia (VT) refractory to medical therapy. The etiology was coronary artery disease in 23 of 28 patients (82%), dilated cardiomyopathy in 2 of 28 patients (7%), sarcoidosis in 2 of 28 patients, and 1 patient in 28 had lupus erythmatosis. The mean left ventricular ejection fraction was 29%. A total of 27 of 28 patients (96%) patients had inducible ventricular tachycardia using programmed stimulation. The patients considered for AICD implant failed a mean of 3.6 antiarrhythmic drugs. Rate counting and defibrillating leads were inserted through a lateral thoracotomy in 17 patients and a mediansternotomy incision in 11 patients in conjunction with another cardiac procedure in 10 patients. The generators were positioned in a subcutaneous pocket beneath the left costal margin. There were no operative deaths. The mean follow-up was 6.7 months (range 1 to 14) with no VT/VF deaths in patients with defibrillators. The study demonstrated that AICD is an effective device for prevention of sudden cardiac death.
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PMID:Treatment of malignant ventricular arrhythmias with the automatic implantable cardioverter defibrillator. 270 27

Severe congestive cardiomyopathy is an uncommon complication of systemic lupus erythematosus (SLE). We describe a patient with active SLE and a circulating anticoagulant. She presented with a rapidly progressive cardiomyopathy, complicated by an intracavitary thrombus and cerebral infarction. The course of the disease is described, with special emphasis on the usefulness of consecutive echocardiographic studies.
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PMID:Severe congestive lupus cardiomyopathy complicated by an intracavitary thrombus: a clinical and echocardiographic followup. 318 75

This case report documents echocardiographically a thromboembolus actively traversing a patent foramen ovale in a 72-year-old man with a dilated cardiomyopathy and systemic lupus erythematosis complicated by chronic low-grade disseminated intravascular coagulation and multiple lower extremity deep venous thromboses. With intravenous heparin therapy, there was apparent resolution of this thromboembolus without clinical evidence of systemic embolization.
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PMID:Thromboembolus traversing a patent foramen ovale: resolution with anticoagulation. 784 Sep 96

Sera from 29 of 48 patients with idiopathic dilated cardiomyopathy (IDCM) and six of six patients with dilated cardiomyopathy (DCM) secondary to suspected viral myocarditis were shown to react with the branched chain alpha-ketoacid dehydrogenase (BCKD) complex mitochondrial proteins. Whereas sera from only 1 of 26 patients with ischemic heart disease showed reactivity against the BCKD complex protein, 0 of 30 sera from normal human volunteers, 0 of 64 sera from patients with lupus, and 0 of 34 sera from patients with rheumatoid arthritis showed detectable reactivity, denoting an element of specificity for the reactivity of sera from IDCM patients. The major reactivity was localized to the dihydrolipoyl transacylase (E2) component of BCKD complex. By using recombinant techniques, the immunodominant BCKD-E2 epitope recognized by sera from IDCM patients was localized to amino acid (aa) sequences 116 to 134. Each of the IDCM sera that reacted with the native BCKD complex was shown to react with the immunodominant peptide, as defined by a peptide inhibition ELISA and by an ELISA using the reactive peptide conjugated to BSA. Sera from IDCM patients that reacted with the native BCKD complex and the reactive peptide also showed inhibition of BCKD enzyme activity. The possible mechanisms for the induction of the Abs and the implications of these findings for the pathogenesis of IDCM are discussed.
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PMID:Epitope mapping of the branched chain alpha-ketoacid dehydrogenase dihydrolipoyl transacylase (BCKD-E2) protein that reacts with sera from patients with idiopathic dilated cardiomyopathy. 796 42

Our study ellucidates the utility of endomyocardial biopsy (EMB) in various cardiac-muscle disorders seen in a tropical country like India. The procedure has been successfully performed in 501 patients (572 procedures) at our centre from April 1985 to December 1992. This included 60 infants and children. The indications were dilated cardiomyopathy (DCM) in 214, non-specific aortoarteritis in 91, rheumatic heart disease in 75, restrictive cardiomyopathy in 45, constrictive pericarditis in 14 and miscellaneous in 62 patients. There was no mortality, however, one patient developed cardiac tamponade and another sustained ventricular tachycardia requiring cardioversion. There was transient atrial fibrillation in six patients and all these had acute rheumatic heart disease. Transient complete heart block occurred in six patients with underlying left-bundle branch-block. Histological examination of EMB revealed myocarditis in 34/214 (15.4%) patients in DCM group and helped in following up these cases on immunosuppressive treatment. In the presence of restrictive haemodynamics it could identify amyloidosis in four patients. It was also helpful in differentiating between endomyocardial fibrosis and chronic constrictive pericarditis. In patients with non-specific aorto-arteritis significant histological changes of inflammatory myocarditis were observed in patients especially in congestive heart failure. Furthermore, it was helpful in identifying the nature of cardiac tumour in one patient. Its utility has also been evaluated in disorders, including rheumatic heart disease, peripartum cardiomyopathy and systemic disorders like systemic lupus erythematosis. Even in the absence of cardiac-transplant programmes at national level we have found EMB to be a useful investigation in a tropical country like India.
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PMID:Endomyocardial biopsy--technical aspects experience and current status. An Indian perspective. 818 91

Eighteen consecutive patients, admitted with a diagnosis of dilated cardiomyopathy (DCM), to the Cardiology Section, Department of Internal Medicine, University Hospital, Uppsala, Sweden were enrolled into the study. All patients suffered signs of cardiac incompensation of variable duration. Patients were defined by conventional clinical investigations including chest X-ray, ultrasound, g-camera, catheterization and endomyocardial biopsy with histological evaluation by a specially trained pathologist. Angiography was performed to exclude ischemic heart disease. Several patients were diagnosed as having a specific reason for the cardiac insufficiency, like pheochromocytoma, SLE, ethylism, ischemic heart disease and hypertrophic cardiomyopathy. In this group all 7/7 had negative serology against Coxsackie B viruses. In the other group of idiopathic CM, no other etiology could be found. Serological analysis in this group showed high IgM titres against Coxsackie viruses in 6/8 patients. EDTA-blood was taken for tissue-typing using DNA probe hybridisation. 6/12 patients had DQB1:4 using the newest nomenclature, vs 17% in the control population. The reversed picture was observed for DQB1:2, occurring in 1/12 patients, vs 19% in the normal population, thus indicating a protective value of this genotype, which to our knowledge has not been described before. The results indicate a dual dependence of (host) genotype and (virus) serotype according to the Doherty-Zinkernagel hypothesis. Thus, it would also be in agreement with the virus-immune hypothesis suggested more than 20 years ago to explain the enigmatic pathogenesis of DCM.
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PMID:Genotypic and serotypic profile in dilated cardiomyopathy. 839 Jul 21

Between 1988 and 1994, 23 patients underwent heart transplantation for dilated cardiomyopathy. The age of the 13 boys and 10 girls was from 8 months to 16 years (mean 7.1 years). Selection criteria included failure to thrive despite maximal antifailure treatment and/or intravenous inotrope dependence. The aetiology of cardiomyopathy was idiopathic (n = 13), congenital (n = 3), anthracycline induced (n = 4), Barth's syndrome (n = 1), and maternal systemic lupus erythematosus (n = 2). The waiting period of heart transplantation ranged from one day to 147 days (mean 22 days). Maintenance immunosuppression included cyclosporin, azathioprine, and prednisolone. Follow up after transplantation was from one month to 62 months (median 27 months) with a mean actuarial survival of 95% at one year and 87% at three years. Four patients developed coronary artery disease, one of whom died as a consequence 15 months after heart transplantation. Heart transplantation has emerged as an acceptable therapeutic option, at least in the short term, for patients with dilated cardiomyopathy.
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PMID:Heart transplantation for dilated cardiomyopathy. 855 65

Recurrent fetal loss and pregnancy complications, especially severe early-onset preeclampsia, are frequently associated with anti-phospholipid antibodies. We report a case of post-partum cardiac involvement leading to dilated cardiomyopathy in a woman with a persistent positivity for anti-cardiolipin and anti-nuclear antibodies. Her clinical and obstetric record reported two previous fetal losses but no other signs characteristic of the anti-phospholipid syndrome or diagnostic for a systemic lupus erythematosus. Post-partum cardiomyopathy might be another cardiac presentation of the anti-phospholipid syndrome, in addition to the well known valvular involvement. In patients with persistent positivities for anti-phospholipid antibodies, a prompt identification of such a complication in the post-partum period should be taken into account by physicians. Adequate cardiologic treatment associated with antiaggregant and steroid therapy might be useful to prevent further complications in these patients.
Lupus 1996 Jun
PMID:Post-partum dilated cardiomyopathy in anti-phospholipid positive woman. 880 99


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