Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of latent cardiac sarcoidosis in reference to differential diagnosis from giant cell myocarditis. A 68-year-old woman succumbed to subarachnoid hemorrhage and acute myocardial infarction within a period of 3 days. Autopsy revealed white fibrotic lesions in the lateral wall of the left ventricle and interventricular septum of the heart in addition to acute myocardial infarction of the anterior wall. Histology showed fibrotic granulomatous lesions with infiltration of lymphocytes and epithelioid cells. Many multinucleated giant cells of Langhans and foreign body types were scattered among these lesions. There was no lesion in the bilateral hilar lymph nodes, but typical epithelioid granuloma was noticed in the lymph node of the carina, liver, and spleen. So we concluded that the heart lesion was a case of cardiac sarcoidosis. Striation could not be seen in the multinucleated giant cells of the cardiac sarcoid lesion, and, using light microscopy, it seemed to us that these cells had no relation to the cardiac muscles. However, by immunohistochemistry (PAP method) some giant cells tested positive for myoglobin, and others tested positive for lysozyme. The fact that giant cells are not always derived from the cardiac muscle can't be used, as a criterion for the diagnosis of cardiac sarcoidosis. Giant cells in the lung and lymph nodes tested positive only for lysozyme. Hence, using only cardiac histology, it is difficult to make a differential diagnosis between cardiac sarcoidosis and giant cell myocarditis, especially in cases where there is multiple organ involvement.
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PMID:[A case of latent cardiac sarcoidosis in reference to differential diagnosis from giant cell myocarditis]. 230 29

Giant-cell myocarditis is a rare inflammatory disorder characterized by degeneration and necrosis of myocardial fibers and presence of chronic inflammatory infiltrates associated with multinucleated giant cells forming a granulomatous inflammatory reaction. The etiology of giant-cell myocarditis is unknown. Many conditions have been reported as associated with this phenomenon such as fungi, virus, sarcoidosis, and hypersensitivity or autoimmune reactions. We are reporting a case of giant-cell myocarditis discovered in a newborn with congenital herpetic sepsis. The myogenic origin of the giant-cells of this case is supported by the positivity for desmin and myoglobin and negativity for muramidase and alpha-1-antichymotrypsin after immunoperoxidase procedure. The presence of Herpes simplex virus type II was confirmed by indirect immunoperoxidase reaction in most of the viscera including the heart, but is not considered a factor in the production of giant cells.
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PMID:Giant-cell myocarditis in a newborn with congenital herpes simplex virus (HSV) infection: an immunohistochemical study on the origin of the giant cells. 329 30

Several aspects of giant cell myocarditis remain controversial, including the natural history of the disease and the nature of the giant cells. We have observed three patients who had long survival with chronic active giant cell myocarditis. The first patient was a 59-yr-old female who had a 10-yr history of complete heart block which was found at autopsy to have been caused by giant cell myocarditis. The second patient is a 36-yr-old female who received a heart transplant 5 yr after a biopsy proven episode of active myocarditis, and examination of the explanted heart revealed giant cell myocarditis. The third patient was a 41-yr-old male who received a heart transplant 2 yr after developing progressive heart failure, and the explanted heart had giant cell myocarditis. On immunohistochemical study of the three hearts, the giant cells stained with the macrophage markers lysozyme and KP-1 (CD-68). Staining of the same cells with desmin and actin was focally positive in a punctate pattern, correlating with the ultrastructural presence of myofibrils within giant cell phagolysosomes. The associated lymphocytic infiltrate stained primarily for the T-cell markers CD-3, CD-45RO, and CD-43 whereas only a few of the lymphocytes stained with the B-cell marker CD-20. The long histories of cardiac dysfunction in the three patients show that giant cell myocarditis may have a protracted course. The morphologic studies show that the giant cells are of histiocytic origin but can contain phagocytosed components of myocytes, observations that may account for the controversy surrounding the nature of the giant cells in giant cell myocarditis.
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PMID:Long survival with giant cell myocarditis. 841 83

A 49-year-old man with cardiac sarcoidosis is presented. He suffered from congestive heart failure, and left ventricular asynergy and reduced function was evident by echocardiogram and left ventriculogram. A light microscopic examination of the endomyocardial biopsy revealed nonspecific myocarditis without giant cells or noncaseating granulomas. Under an electron microscope, however, several epithelioid cells were found in the specimen. The serum level of lysozyme was elevated. The patient had a past history of sarcoidosis of the eyes and lungs 22 years previously. Cardiac diseases presenting epithelioid cells other than sarcoidosis were clinically ruled out. Thus, the diagnosis of cardiac sarcoidosis was made based on both clinical and ultrastructural findings, and corticosteroid therapy was initiated. In the second biopsy, performed 4 months later, a noncaseating granuloma was found. Generally, the incidence of histological diagnosis of cardiac sarcoidosis by light microscopy is relatively low in endomyocardial biopsy specimens. The present case suggests that the addition of an ultrastructural examination may improve the diagnostic usefulness of the endomyocardial biopsy in cardiac sarcoidosis, since electron microscopy can clearly identify the presence of even one epithelioid cell.
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PMID:Usefulness of electron microscopy in the diagnosis of cardiac sarcoidosis. 890 3