Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The endocardial fibroelastosis (EFE) is the most frequent cardiomyopathy. This disease is characterised by endocardial hyperplasia due to proliferation of elastic and collagenous fibres. There are primary and secondary forms. Within the primary form, the infantile form is the most frequent and of greatest importance to the pediatrician. This form is more a syndrom than a distinct disease. It is a reaction of the endocard due to several noxes. Lately a possible viral etiology is being discussed e.g. Parotitis, Coxsackie or other viruses. Clinical criteria for diagnosis are: cardiomegaly, left ventricular hypertrophy seen in 97% in the ECG, the absence of a murmur (or a soft apical mumur) absence of cyanosis and absence of systemic disease. Differential diagnosis is mainly between fibroplastic parietal endocarditis (FPE), cardiovascular collagenosis (CC) and endomyocard fibrosis (EMF). In FPE thrombosis is frequent and typically there is eosinophilia. CC is found in South Africa and is characterised by edema and fibrinoid necrosis. MEF is present mainly in Uganda, Nigeria and South India, characterised by endocardial fibrosis, valve involvement and eosinophilia. The obstructive hypertrophic cardiomyopathy is characterised by a pronounced cardiomegaly, insufficient weight gain as well as dyspnea and cyanosis. Catheterization shows a gradient across one or both of the outflow tracts due to hypertrophic subaortic or subpulmonic stenosis. Therapy of EFE consists in treating the cardiac decompensation and according to the severity of the disease, in steroids.
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PMID:[Endocardial fibroelastosis (E.F.) and its differential diagnosis]. 94 82

Antimyolemmal antibodies can be demonstrated in sera of patients with coxsackie B, influenza, mumps and Q-fever perimyocarditis, in sera of patients with postpericardiotomy and postinfarction syndromes, in part of the sera of patients with endocarditis and in some patients with dilated heart disease most likely due to secondary immunopathogenesis after perimyocarditis. Antimyolemmal antibodies in titres greater than 1: 40 are complement fixing and cytolytic when added to cultures of vital myocytes. In vitro cardiocytolysis indicates that humoral effector mechanisms could also play a pathogenetic role in vivo. In vitro antibody dependent and independent cellular cytotoxicity of patients lymphocytes against isolated cardiocytes could not be observed in perimyocarditis and postmyocarditic cardiomyopathy. It could be demonstrated, however, in patients with postpericardiotomy syndrome and in some patients with dilated cardiomyopathies. Immunological investigations are therefore not only of diagnostic significance but have widened our knowledge of the etiology and pathogenesis of perimyocardial diseases. Furthermore they are helpful in the follow-up and prognosis of patients with protracted perimyocardial affections.
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PMID:[Secondary immunopathogenesis of cardiac diseases]. 637