Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Splenomegaly confirmed by surgery or necropsy in 100 dogs was diagnosed histologically as benign neoplasia (n = 1), primary splenic malignancy (n = 59), neoplastic metastases (n = 6), and nonneoplastic disease (n = 34). Dogs with known systemic disease, such as lymphoma and mast cell tumor, that caused splenomegaly were not included in the study. Hemangiosarcoma was the most common splenic disease (43 cases). Overall mean age of the dogs was 10.7 years, the most common breed was German Shepherd dog, and 72 of the dogs weighed more than 21 kg. Dogs with anemia, nucleated red blood cells, abnormal red blood cell morphology, or splenic rupture had a significantly greater chance of having splenic neoplasia (P less than 0.002). A multivariable logistic regression analysis found that the presence of anemia and splenic rupture in dogs with splenomegaly was up to 69% accurate in predicting presence of splenic neoplasia. After splenectomy, the median survival time of dogs with splenic neoplasia was 13 weeks. For dogs with nonneoplastic splenomegaly it was at least 36 weeks.
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PMID:Splenomegaly in dogs. Predictors of neoplasia and survival after splenectomy. 277 49

The objective of the present investigation was to establish the frequency of systemic spreading of urticaria pigmentosa by means of bone and bone marrow scintigraphy as a noninvasive imaging technique with a low radiation exposure. Bone scintigraphy: Seven of nine patients investigated showed diffuse and focal nuclide accumulation. After exclusion of other causes by reference to the case history and the clinical and chemical laboratory findings, these nuclide accumulations were regarded as mastocytosis-specific in accordance with the atypical localization. Bone-marrow scintigraphy: All the patient investigated showed a peripheral expansion of the bone marrow. This must be interpreted as an expansion of the macrophages of the bone marrow on the basis of the method used. Since the mast cell is regarded as a more highly differentiated form of the same cell-type as macrophages/monocytes, on the basis of the scintigraphic results presented, urticaria pigmentosa can be regarded pathogenetically as a hyperplasia of the macrophages of the bone marrow organ, with increased differentiation in mast cells. The extent of this differentiation and its pathological quality then determine the clinical signs and symptoms (cutaneous, systemic, or malignant mastocytosis). Urticaria pigmentosa thus has the character of a systemic disease.
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PMID:[Urticaria pigmentosa--an obligate systemic disease? Results of nuclear medicine studies and etiopathogenetic significance]. 367 11

Mast cells are connective tissue elements likened to unicellular endocrine organs because of the wide diversity of physiologic and pathologic events associated with the secretion of biologically active compounds. Using an immunoperoxidase method (PAP), we studied tissue from patients with benign and malignant systemic mastocytosis and with a variety of reactive conditions. The following immunoreactive antigens were identified in mast cells: a heparinlike compound or compounds (HLC), prostaglandin, serotonin, and fibronectin. HLC is constantly present, staining mast cells in a granular fashion from most lesions. Serotonin and prostaglandin stain in a diffuse cytoplasmic manner in occasional lesions. Fibronectin is found in a surface location in selected cases. We found no clear association between the immunoreactivity of one compound in mast cells and one clinical symptom, e.g., HCL with bleeding, prostaglandin, or serotonin with systemic vasomotor activity or fibronectin with increased tissue fibrosis. However, patients with localized and systemic disease had symptoms that might have been attributed to more than one compound. Only occasional patients with reactive conditions showed such symptoms. The presence of these compounds, either alone or in combination, did not separate benign from malignant conditions. Other cells within selected tissues also stained with the antibodies tested. Despite the lack of exclusivity, these antibodies are useful in identifying mast cells within tissue sections and may have a role in the study of mast cell constituents.
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PMID:Immunohistochemical characterization of reactive and neoplastic mast cells. 641 52

The lysozyme (muramidase) activity was measured in the sera of 84 dogs with neoplastic disease. Neoplasms included 32 lymphomas, 13 primary bone neoplasms, 5 melanomas, 5 thyroid neoplasms, 9 soft tissue sarcomas, 5 mast cell sarcomas, and 15 carcinomas. The sera from 21 healthy dogs served as control. Dogs with neoplastic disease had significantly (P less than 0.005) higher serum lysozyme activity than did the healthy controls. For lymphosarcoma, dogs with clinical signs of systemic disease had significantly higher serum lysozyme activity than did dogs without clinical signs. For bone neoplasms, dogs with metastatic disease had higher serum lysozyme activity than did dogs without metastasis. Increased lysozyme activity may be a useful marker of macrophage-mediated host responses to neoplasms in dogs.
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PMID:Serum lysozyme (muramidase) activity in dogs with neoplastic disease. 679 92

Eight patients received PUVA for mastocytosis. Five women had typical adult-onset urticaria pigmentosa, without evidence of systemic disease. Another woman had suspected hepatic involvement while the remaining female had early-onset familial urticaria pigmentosa with morphologically atypical mast cells. The only male patient had cirrhosis with hepatic deposits of mast cells in addition to polycythaemia rubra vera. In all patients, except the man with systemic disease, there was reduced pruritus and wealing and partial to almost complete fading of the macules. The manifestations of urticaria pigmentosa recurred after treatment was discontinued. In both lesional and uninvolved skin there was no significant change in either the mean mast cell counts or mast cell ultrastructure after an average of twenty-seven PUVA exposures. In addition, PUVA did not cause a significant alteration in the histamine content of the skin. The beneficial effect of PUVA in urticaria pigmentosa therefore does not appear to be directly related to a change in mast cell numbers or morphology, or to the histamine concentration in the skin.
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PMID:Photochemotherapy (PUVA) in the treatment of urticaria pigmentosa. 686 May 73

Mastocytosis is a disease in which the mast cell population is increased in various tissues. Although the mechanism for the increased density of mast cells is not understood, recent research into mast cell structure and function has improved our understanding of the symptomatology and prompted newer and better approaches to treatment. To be discussed, and of particular interest to the dermatologist, is the management of, and evaluation for, systemic disease in a patient presenting with cutaneous findings.
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PMID:Mastocytosis and the mast cell. 717 10

Tryptase, a protease produced by all mast cells, was evaluated as a clinical marker of systemic mastocytosis. Two sandwich immunoassays were evaluated, one which used the mAb G5 for capture, the other which used B12 for capture. The B12 capture assay measured both recombinant alpha- and beta-tryptase, whereas the G5 capture assay measured primarily recombinant beta-tryptase. G5 binds with low affinity to both recombinant alpha-tryptase and tryptase in blood from normal and nonacute mastocytosis subjects, and binds with high affinity to recombinant beta-tryptase, tryptase in serum during anaphylaxis, and tryptase stored in mast cell secretory granules. B12 recognizes all of these forms of tryptase with high affinity. As reported previously, during systemic anaphylaxis in patients without known mastocytosis, the ratio of B12- to G5-measured tryptase was always < 5 and approached unity (Schwartz L.B., T.R. Bradford, C. Rouse, A.-M. Irani, G. Rasp, J.K. Van der Zwan and P.-W.G. Van der Linden, J. Clin. Immunol. 14:190-204). In this report, most mastocytosis patients with systemic disease have B12-measured tryptase levels that are elevated (> 20 ng/ml) and are at least 10-fold greater than the corresponding G5-measured tryptase level. Most of those subjects with B12-measured tryptase levels of < 20 ng/ml had only cutaneous manifestations. The B12 assay for alpha-tryptase and beta-tryptase, particularly when performed in conjunction with the G5 assay for beta-tryptase, provides a more precise measure of mast cell involvement than currently available assessments, a promising potential screening test for systemic mastocytosis and may provide an improved means to follow disease progression and response to therapy.
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PMID:The alpha form of human tryptase is the predominant type present in blood at baseline in normal subjects and is elevated in those with systemic mastocytosis. 867 37

Serum tryptase was measured with the B12 and G5 antibody-based immunoassays in 25 adult patients with mastocytosis and in 18 controls. Twelve patients had uncomplicated cutaneous mastocytosis (urticaria pigmentosa) and 13 had urticaria pigmentosa with systemic symptoms. Tryptase levels were compared with histamine turnover estimated as urinary excretion of the main histamine metabolite tele-methylimidazoleacetic acid. Elevated B12 tryptase levels (> 20 microg/L) were found in most mastocytosis patients, including five of eight patients with only cutaneous manifestations who had a low urinary histamine metabolite excretion. This indicated a higher sensitivity for diagnosing mild mastocytosis on the basis of levels of serum tryptase as opposed to urinary methylimidazoleacetic acid. However, the serum B12 tryptase assay could not differentiate between urticaria pigmentosa patients with and without systemic disease: the measurement of histamine metabolite excretion probably reflects the mast cell burden more accurately. Serum G5 tryptase levels were generally low in both controls and mastocytosis patients.
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PMID:Serum tryptase measured with B12 and G5 antibody-based immunoassays in mastocytosis patients and its relation to histamine turnover. 989 55

Mastocytosis is characterized by an excessive number of apparently normal mast cells in the skin and, occasionally, in other organs. Characteristic skin lesions, called urticaria pigmentosa, are present in most patients, but clinical presentation can vary from a pruritic rash to unexplained collapse and sudden death. These lesions are typically tan to red-brown macules that appear on the trunk and spread symmetrically. Patients with mastocytosis often have a long history of chronic and acute symptoms that were unrecognized as mastocytosis. Skin lesions may or may not accompany systemic mastocytosis. Systemic disease may involve the gastrointestinal tract, the bone marrow or other organs. Even when the disease is considered as a possibility by the physician, the diagnosis can be difficult because of special technical requirements necessary for biopsy and because of the problems with biochemical testing. Drug therapy is initiated to stabilize mast cell membranes, to reduce the severity of the attacks and to block the action of inflammatory mediators. The mainstay of therapy is histamine H1 and H2 blockers and the avoidance of triggering factors.
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PMID:Cutaneous and systemic manifestations of mastocytosis. 1039 89

Systemic mastocytosis is a disease of mast cell proliferation that may be associated with hematologic disorders. There are no features on examination that allow the diagnosis of systemic disease, and mast cell-derived mediators, which may be elevated in urine or blood, may also be elevated in individuals with severe allergic disorders. Thus, the diagnosis usually depends on results of bone marrow biopsy. To facilitate evaluation, surrogate markers of the extent and severity of the disease are needed. Because of the association of mastocytosis with hematologic disease, plasma levels were measured for soluble KIT (sKIT) and soluble interleukin-2 receptor alpha chain (sCD25), which are known to be cleaved in part from the mast cell surface and are elevated in some hematologic malignancies. Results revealed that levels of both soluble receptors are increased in systemic mastocytosis. Median plasma sKIT concentrations as expressed by AU/mL (1 AU = 1.4 ng/mL) were as follows: controls, 176 (n = 60); urticaria pigmentosa without systemic involvement, 194 (n = 8); systemic indolent mastocytosis, 511 (n = 30); systemic mastocytosis with an associated hematologic disorder, 1320 (n = 7); aggressive mastocytosis, 3390 (n = 3). Plasma sCD25 levels were elevated in systemic mastocytosis; the highest levels were associated with extensive bone marrow involvement. Levels of sKIT correlated with total tryptase levels, sCD25 levels, and bone marrow pathology. These results demonstrate that sKIT and sCD25 are useful surrogate markers of disease severity in patients with mastocytosis and should aid in diagnosis, in the selection of those needing a bone marrow biopsy, and in the documentation of disease progression. (Blood. 2000;96:1267-1273)
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PMID:Soluble stem cell factor receptor (CD117) and IL-2 receptor alpha chain (CD25) levels in the plasma of patients with mastocytosis: relationships to disease severity and bone marrow pathology. 1094 67


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