Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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 23-year-old male patient revealed hypercortisolism with stigmata of Cushing's syndrome, and post-operative pathological examination demonstrated primary adrenal nodular dysplasia. Because of the presence of cardiac myxomas and skin pigmentation, the diagnosis of Carney's complex was given. After the control of hypercortisolism by adrenalectomy, the patient experienced iridocyclitis and bilateral hilar lymphadenopathy with elevated levels of serum angiotensin-converting enzyme and lysozyme, all of which indicated the presence of sarcoidosis. Despite the numerous recent descriptions concerning Carney's complex, an association with sarcoidosis has not yet been documented. Moreover, the sequential occurrence of sarcoidosis after adrenalectomy suggests an etiological link between these two rare disorders.
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PMID:Cushing's syndrome due to primary adrenocortical nodular dysplasia, cardiac myxomas, and spotty pigmentation, complicated by sarcoidosis. 129 34

We present an autopsy case of a 29-week-old male fetus with a very unusual set of congenital granular cell tumors, including gingival epulis and granular cell lesions of the kidneys, lung, heart, esophagus, small and large intestine, thyroid, adrenals, spleen, urinary bladder, testis, pituitary, and leptomeninges. The granular cells were distributed mainly through the stroma of the organs, but they also involved the epithelial lining of the seminiferous and renal tubules. Ultrastructurally, the gingival, pulmonary, and renal tumors were basically the same in appearance as membrane-bound heterogeneous bodies. Immunohistochemical studies were negative for S100 protein, lysozyme, alpha 1-antitrypsin, cytokeratin, and vimentin in the gingival mass as well as in other systemic lesions. The immunohistochemical reaction pattern of the granular cells in our case was more like the cells of the congenital granular cell epulis rather than adult granular cell tumor because of its negative reaction to S100 protein. However, the involvement pattern was that of the adult form of granular cell tumor. Several developmentally different cells, such as renal tubular epithelial cells, seminiferous tubular cells, gingival stromal cells, and parenchymal cells of many organs, were involved in this granular cell process. The myofibroblastlike cells seen in the region of segmental dysplasia of the kidney showed the same cytoplasmic material as in typical granular cells. Based on these findings, it is suggested that a histogenesis of multiple cell origin of the granular cell tumor could be strongly supported.
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PMID:Congenital granular cell tumor with systemic involvement. Immunohistochemical and ultrastructural study. 192 90

We examined 12 depressed tubular adenomas of the stomach pathologically and immunohistochemically in order to clarify the difference between the depressed type and the elevated type. Depressed tubular adenomas showed shallow mucosal depression and, of the 12, nine were endoscopically diagnosed as early gastric cancer. Histologically, the adenoma cells showed dysplasia in varying degree and focal adenocarcinoma occurred in two adenomas measuring over 2 cm. The mean height of the adenoma glands was 0.63 +/- 0.31 mm in the 12 depressed adenomas and 1.32 +/- 0.43 mm in 44 elevated adenomas, while the mean heights of the subjacent mucosa were 0.18 +/- 0.19 mm and 1.07 +/- 0.71 mm, respectively. Thus, depressed adenomas resulted from paucity of the mucosa subjacent to the adenoma glands and the height of the adenomatous glands was half that found in the elevated type. Goblet cells, a variety of endocrine cells and lysozyme-containing cells were found in nine, nine and eight depressed adenomas, respectively, in variable numbers. Hyperplasia of these cells was also detected in depressed adenomas showing mild or moderate dysplasia. Immunohistochemical examination revealed no difference in the phenotypic expression of adenoma cells as between the depressed and the elevated type.
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PMID:Depressed tubular adenoma of the stomach: pathological and immunohistochemical features. 198 68

Renal disease is a common cause of morbidity and mortality in patients with plasma cell dyscrasia (PCD). We have conducted a systematic study of the formalin-fixed, paraffin-embedded renal tissues from 53 patients with plasma cell dyscrasia, 24 of whom had Bence Jones cast nephropathy (with large casts, often associated with giant cells and polymorphonuclear leukocytes). A battery of 5 immunocytochemical and lectin markers for various segments of the nephron was used [Tetragonolobus lotus, Arachis hypogaea (AH), Tamm-Horsfall protein (THP), epithelial membrane antigen (EMA), and cytokeratin (AE1/AE3)]. In particular, we sought to determine the nature of the intratubular multinucleated giant cells in Bence Jones myeloma cast nephropathy with a variety of epithelial and hematopoietic cell markers. Although tubular epithelial cells stain with their respective markers (whether inflamed, thinned, detached, or adjacent to and lining casts), true intratubular giant cells in PCD were never positive for these tubular markers. In approximately one-third of the cases studied, intratubular and extratubular giant cells stained for several of the seven hematopoietic cell markers employed [i.e., alpha 1-antitrypsin (A1AT), alpha 1-antichymotrypsin (A1ACT), vimentin, and lysozyme], suggesting that giant cells are of hematopoietic origin. The majority of the casts are present in the distal nephron, although some casts were noted in more proximal sites of the nephron. Some larger casts did not stain for THP; smaller casts often showed lamination or stratification of THP staining. Finally, in one-half of the cases, Tamm Horsfall protein (THP) and other distal tubular markers (AH, EMA, AE1/AE3) were found in Bowman's space, almost always in association with interstitial deposits of THP; these markers were virtually never noted in Bowman's spaces of PCD patients without numerous large casts. This suggests that there are communications between distal and proximal nephron, most likely by intraluminal reflux but possibly also through breaks in the tubules and via the interstitium.
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PMID:Myeloma cast nephropathy: immunohistochemical and lectin studies. 246 87

A total of 50 cases of gallbladder dysplasia found adjacent to carcinoma were examined histologically and immunohistochemically for metaplastic changes in order to elucidate the characteristics of the dysplasia of the gallbladder. The incidence of metaplastic changes in the dysplastic mucosa such as the occurrence of endocrine cells, lysozyme-immunoreactive cells, goblet cells, and Paneth cells were 58%, 74%, 32%, and 22%, respectively. Based on the presence or absence of metaplastic changes, these 50 cases of dysplasia were divided into 40 cases (80%) of metaplastic type dysplasia showing at least one marker of metaplasia and 10 cases (20%) of non-metaplastic type dysplasia showing no metaplasia. On the other hand, these 50 cases of carcinoma were divided into 10 cases of non-metaplastic type carcinoma and 40 cases of metaplastic type carcinoma based on the presence or absence of metaplasia in the tumor tissue. The incidence of metaplastic changes in the dysplastic lesions was compared between the dysplasia adjacent to non-metaplastic type carcinoma and that adjacent to metaplastic type carcinoma. The incidence of metaplasia in the dysplastic mucosa adjacent to metaplastic type carcinoma was higher than that adjacent to non-metaplastic type carcinoma with a statistically significant difference. Moreover, the presence or absence of metaplastic changes was also examined in the surrounding dysplasia and non-tumorous mucosa in each case. Most cases of metaplastic type carcinoma were surrounded by dysplasia with metaplastic changes and by metaplastic epithelium, whereas most cases of non-metaplastic type carcinoma were surrounded by dysplasia without metaplasia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dysplasia of the gallbladder. Its histogenesis and correlation to gallbladder adenocarcinoma. 260 18

In a 38-year-old woman, arterial hypertension was diagnosed a few weeks before her death. She died unexpectedly before a diagnostic clarification of the cause was possible. Autopsy revealed an arterial fibromuscular dysplasia with manifestation in both common iliac arteries, both renal arteries, the celiac trunk and the splenic artery. Both renal arteries displayed stenotic dissecant aneurysms which were the cause of the arterial hypertension. As a rare and lethal complication of fibromuscular dysplasia, a ruptured saccular aneurysm was found in the splenic artery. Histologically, the vascular alterations were a combination of medical fibromuscular dysplasia (type II) and periarterial or adventitial fibroplasia (type III). On the basis of the immunohistochemical detection of abundant lysozyme-positive cells, the periarterial fibroplasia appears to be a secondary chronic granulating and cicatricial reaction and not a separate form of fibromuscular dysplasia.
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PMID:[Arterial fibromuscular dysplasia as an unexpected cause of death in adults]. 367 85

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

We report herein a case of extramedullary myeloid tumor arising bilaterally in the testes of a 66-year-old man, who had previously been diagnosed with myelodysplastic syndrome. Light microscopy of the testicular neoplasm demonstrated a tumor composed of large, slightly polygonal cells with pale blue to weakly eosinophilic cytoplasm. The tumor cells were immunoreactive for CD45, myeloperoxidase, lysozyme, CD43, and MB2. Many of the cells also expressed chloroacetate esterase. Peripheral blood and bone marrow findings were consistent with chronic myelomonocytic leukemia (FAB-CMML), particularly in the most recent material, which showed clear cellular dysplasia and an increase in the percentage of blasts in the bone marrow (15% to 20% of all nucleated cells). This case of extramedullary myeloid tumor is unusual in view of the patient's age and the testicular location. It emphasizes the importance of including extramedullary myeloid tumor in the differential diagnosis of histologically undifferentiated large-cell tumors, as well as a need to use a broad panel of immunohistochemical stains in such cases.
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PMID:Testicular extramedullary myeloid cell tumor in a patient with myelodysplastic syndrome. 861 53

We describe a 70-year-old man with cutaneous granulocytic sarcoma who presented with numerous cutaneous nodules but without any leukaemic involvement of the peripheral blood. The tumour cells were positive for lysozyme, peroxidase, CD11a, CD11c, CD33 and HLA-DR, and weakly positive for CD4 and CD14, suggesting granulocytic differentiation. The bone marrow at admission showed dysplasia of the erythrocytic and granulocytic lineage and complex chromosomal abnormalities in association with an increase in monocytes. The patient was diagnosed as having granulocytic sarcoma of monocytic lineage with concomitant myelodysplastic syndrome. In this case, tumour cells also expressed the neural cell adhesion molecule (CD56), which has been suggested as a possible risk factor for developing granulocytic sarcoma in acute myelogenous leukaemia.
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PMID:A case of CD56+ cutaneous aleukaemic granulocytic sarcoma with myelodysplastic syndrome. 1097 33

The mechanism of progression from gastric endocrine cell hyperplasias (ECHs) to carcinoid tumor (GCT) is still unknown. In these lesions, the distribution of metaplastic Paneth, gastrin and pancreatic acinar cells developing due to consequences of corporal mucosal atrophy has not been investigated in detail. In this study, 33 gastric endoscopic biopsies with endocrine cell lesions were examined. In all cases except 6 with solitary GCT, complete-type (small intestine) intestinal metaplasia (IM) with Paneth cells was observed. The density of lysozyme-positive Paneth cells in IMs in cases with GCTs was less than those in ECH alone. The density of gastrin-positive cells in IMs and average number of micronodules of ECHs were similar. Pancreatic acinar metaplasia (PAM) was observed in 6 cases of GCTs with ECH. The size of GCTs with ECH was smaller than those without ECH. By image analysis, the percentage of Ki67 (MIB-1, proliferation marker) expressing cells of GCTs with ECH was 5.1+/-0.6%, and GCT without ECH 7.8+/-1%. Our results indicate that few Paneth cells and many PAMs in atrophic corporal mucosa are seen more frequently in cases of GCTs with ECH, compared to those in ECH alone. Gastrin-positive cells in the corporal IM may stimulate enterochromaffin-like (ECL) cells, which may induce hyperplasia, dysplasia or neoplasia by augmenting the effects of hypergastrinemia through a paracrine mechanism on local gastrin-sensitive cells.
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PMID:Altered distribution of metaplastic Paneth, gastrin and pancreatic acinar cells in atrophic gastritic mucosa with endocrine cell lesions. 1473 20


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