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 rare case of sarcoidosis-lymphoma syndrome with vertebral bone destruction. A 63-year-old woman was previously diagnosed as sarcoidosis by supraclavicular lymph node biopsy, and came to our hospital complaining of back pain. Both serum angiotensin-converting enzyme and lysozyme level had been continuously elevated. Magnetic resonance imaging revealed lumbar vertebral bone destruction. Histopathologic examination of lumbar vertebral tumor obtained by CT-guided biopsy revealed non-caseating epithelioid granuloma with CD 68 (+), AE1/AE3 (-), and no malignant cells. She was admitted to our hospital again for dyspnea and pancytopenia. We diagnosed active sarcoidosis and administered oral 30mg prednisolone daily. One month later, prednisolone became ineffective. Flow cytometry of tumor cells obtained from the gastric ulcer floor showed CD 5 (+), CD 20 (+), K chain monoclonality and we diagnosed B-cell non Hodgkin's lymphoma. She was treated by eight cycles of CHOP plus rituximab chemotherapy and achieved complete response. FDG uptake of the entire body decreased, whereas MRI revealed residual mass in the vertebrae. Sarcoidosis had been diagnosed for two and half years before lymphoma developed. Bone destruction is very rare and sarcoidosis is rarely the cause. This is quite an unusual case presenting histologically proved epithelioid granuloma and vertebral destruction in sarcoidosis-lymphoma syndrome.
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PMID:[Sarcoidosis-lymphoma syndrome with vertebral bone destruction]. 1999 5

A 70-year-old male was admitted because of back pain due to peri-vertebral tumors. The histologic picture of a needle-biopsied tumor specimen showed pleomorphic large cell infiltration into the collagen fibers. On immunohistochemistry, these abnormal cells were positive for CD68, CD163 and lysozyme but negative for CD1a, 21, 30, and S100. Flow cytometric analysis also demonstrated that these cells were positive for CD13, 14, 38, 45, 56, and HLA-DR. A bone marrow aspirate showed the marked infiltration of abnormal large cells with the same surface antigens as described above. A diagnosis of HS was made. He showed monocytosis in the peripheral blood of more than 1.0 x 10(9)/L from presentation. The karyotype of bone marrow cells was 46,XY,+8. Fluorescent in situ hybridization (FISH) analysis with a probe for chromosome no. 8 showed that all these monocytes carried +8, indicating that he had another disorder of chronic myelomonocytic leukemia (CMML). FISH analysis with a probe for chromosome no. 12 demonstrated that the abnormal large cells in the bone marrow were all tetraploid, while analysis with the chromosome no. 8 probe showed more than 8 signals per cell, indicating that HS cells carried octasomy to decasomy of chromosome no. 8. These findings strongly suggest that HS in the present patient originated from underlying CMML.
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PMID:Histiocytic sarcoma and underlying chronic myelomonocytic leukemia: a proposal for the developmental classification of histiocytic sarcoma. 2053 95