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)

A patient having familiar adenomatosis polyposis and an ileo-rectal anastomosis developed a flat mucosal lesion in the rectum. A punch biopsy revealed a villous adenoma with high-grade dysplasia. The subsequent surgical specimen indicated that the flat villous adenoma was rich in Paneth cells. Special stains included lysozyme muramidase (to visualize Paneth cells), MIB1 proliferation monoclonal antibody and single and multilabel immunohistochemistry for Paneth cells. Other methods included transmission electron microscopy and quantification with an image quantifier (Program Optilab 2.1) of lysozyme-stained Paneth cells. The subjective evaluation of hematoxylin-eosin-stained preparations demonstrated that the Paneth cells were mainly located in the lower half of the villi. Sections labeled with a specific stain (lysozyme muramidase) revealed more Paneth cells in the villi and electron microscopy showed even more in lysozyme-negative areas. Obviously some migrating dysplastic Paneth cells had retained their characteristic granules on their way towards the tip of the villi. Quantitative studies indicated that the lysozyme muramidase-positive material accounted for 41% of the adenomatous tissue. MIB1 revealed intense cell proliferation at the base of the adenoma and in the entire slopes of the villi. Despite the wide distribution of Paneth cells in intestinal metaplasia of the stomach, in the normal small intestine and in the large bowel with chronic inflammatory diseases, it is surprising that tumors arising in Paneth cells are extremely rare. The causes of the apparent natural resistance of Paneth cells to tumor development deserve to be investigated. This is the first case of Paneth cell-rich flat adenoma of the rectum in the literature.
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PMID:Paneth cell-rich flat adenoma of the rectum: report of a case. 860 42

Lysozyme is an innate non-immunologic antibacterial enzyme produced by the Paneth cells of the upper intestinal tract. Lysozyme is not normally secreted in the lower intestinal tract. Previous reports indicate, however, that lysozyme may be secreted by colorectal neoplasias. The aim was to audit lysozyme expression in colorectal diseases including neoplasias. For that purpose, sections were stained with lysozyme (Muramidase), Ki67 (MIB1) and CD 68. Intense lysozyme overexpression (+++) was compared among 177 colorectal tissues: 35 having normal mucosa, 20 regenerative mucosa in inflammatory bowel disease (IBD), 2 inflammatory polyps, 3 collagenous colitis, 2 melanosis coli, 21 hyperplastic polyps, 42 tubular adenomas, 9 serrated adenomas, 30 villous adenomas and 13 invasive carcinomas. Intense lysozyme overexpression (+++) was found in 9.5% of the hyperplastic polyps, in 97.6% of the tubular adenomas, in 88.9% of the serrated adenomas, in 93.3% of the villous adenomas, in 76.9% of the carcinomas, but in none of the other tissues investigated. Neoplastic colorectal cells may acquire the capacity to produce lysozyme. The presence of that enzyme may not be a haphazard, capricious event in mutated colorectal epithelial cells but part of a more elaborate molecular behavior, not necessarily antibacterial. Recently, it was demonstrated that patients having lysozyme-secreting breast carcinomas were associated with a favorable prognosis. Whether lysozyme expression has any bearing on the biological behavior of colorectal carcinomas remains to be elucidated. Lysozyme overexpression (+++) also occurred in 2 of the 21 hyperplastic polyps, suggesting that intense lysozyme production might herald a possible dysplastic evolution in some hyperplastic polyps.
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PMID:Colorectal adenomas produce lysozyme. 1498 84

We present a case of a histiocytic sarcoma incidentally detected in peripheral lung tissue resected for a spontaneous pneumothorax. Furthermore, we discuss the practical approach to pulmonary Langerhans cell histiocytosis, the main differential diagnosis of this lesion in the lung, based on morphological and immunohistochemical features. A 23-year-old male patient presented with recurrent pneumothoraces. The pulmonary tissue showed a single round granuloma-like lesion measuring 4 mm in diameter in close neighbourhood to a bronchial wall. The granuloma consisted of histiocytic cells with enlarged pale nuclei, plasma cells, lymphocytes and scanty eosinophilic granulocytes giving the impression of a granuloma of pulmonary Langerhans cell histiocytosis on haematoxylin and eosin (H&E) stains. Immunohistochemically, the histiocytic cells were negative for CD1a and S-100. They were positive for CD68, HLA-DR, CD14, CD4, CD11c, CD45LCA and lysozyme. MIB1 (Ki67) showed a nuclear staining of approximately 10% of the histiocytic cells. In summary, these findings were in keeping with a histiocytic sarcoma, a rare haematopoetic neoplasm. By demonstrating this particular case, we emphasise the importance of proving the diagnosis of pulmonary Langerhans cell histiocytosis by means of immunohistochemistry. In case of a negative CD1a reaction in a histiocytic lesion, further immunohistochemical studies have to be performed in order not to misdiagnose a malignant haematopoetic lesion.
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PMID:Pulmonary histiocytic sarcoma mimicking pulmonary Langerhans cell histiocytosis in a young adult presenting with spontaneous pneumothorax: a potential diagnostic pitfall. 1956 69