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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urticaria and angioedema are usually the clinical consequence of vasoactive mediators derived from mast cells in the skin or mucosal tissues. Efforts to classify mast cell-mediated causes of urticaria and angioedema have generally been frustrated by their diverse pathogenesis and clinical course. The term acute is typically used to describe fleeting lesions whose recurrence does not extend beyond 6 weeks. Chronic is the term used to describe lesions that persist for more than a few hours but usually less than a day, and recurrences extend for more than 6 weeks. These definitions do not take histology into account. Skin biopsies of fleeting lesions demonstrate a paucity of inflammatory cells, whereas more persistent lesions display a spectrum of perivascular cuffing by predominantly T cells and monocytes. The presence of leukocytoclastic vasculitis in persistent lesions indicates an underlying immune complex disease. Many of the physical urticarias have fleeting lesions that can be induced with the appropriate stimulus for years. This review article has emphasized the clinical course and histology of urticaria and angioedema lesions in an effort to provide a more complete understanding of the pathogenesis and appropriate treatment. Clearly, avoidance of an identifiable inciting stimulus is optimum management, although most patients have no etiology defined or the cause is not realistically avoidable. At present, treatment options for these patients rely on antihistamines to control the immediate consequence of mast cell degranulation. Corticosteroids are reserved for the treatment of patients whose urticaria or angioedema lesions persist, reflecting the increasing involvement of mononuclear cells in the disease process. For leukocytoclastic vasculitis, corticosteroids are indicated, and cytotoxic drugs may be required for adequate treatment. Future treatments of urticaria and angioedema will evolve based on elucidation of the relevant cells and soluble mediators and will include counterregulatory or antagonistic peptides and drugs. C1 esterase inhibitor deficiency is a relatively uncommon cause of angioedema but is important to understand because of its ability to clinically mimic mast cell-mediated angioedemas and its unique pathogenesis and treatment. HAE can be divided into two serologic subtypes that simply reflect the location of the defect in one of the codominantly expressed C1-INH genes on chromosome 11. AAE can be divided into two serologic subtypes. AAE type I is due to massive consumption of C1-INH, presumably by tumor-related immune complexes. AAE type II is due to an anti-C1-INH autoantibody.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Urticaria and angioedema. 161 35

Sympathomimetic bronchodilators relax bronchial smooth muscle via stimulation of the enzyme adenylcyclase. Furthermore, they stabilize the membrane of the bronchial mast cell. Therefore, they are used in the treatment of acute asthma as well as in long-term prophylaxis. A new generation of beta 2-receptor binding derivates of isoproterenol offers increased therapeutic safety because of a reduced risk of cardiovascular side effects. Three routes of medication are available. Parenteral therapy is reserved for the treatment of acute severe asthma. The oral route can be used for long-term medication in smaller children. Mist therapy offers the advantage of topic medication. Efficient handling of a metered-dose aerosol is beyond the capabilities of small children; these patients get their topic treatment by nebulized solutions. The relevant data of clinical pharmacology are summarized for all forms of medication. Focusing on the role of sympathomimetic drugs, a medication strategy for the treatment of acute asthma as well as for long-term prophylaxis is described.
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PMID:[Sympathomimetic drugs in the treatment of childhood asthma]. 714 59

Interstitial cystitis, first described one hundred years ago, is difficult to classify in urological pathology. It essentially affects middle-aged women. Two main theories are currently proposed to explain its pathogenesis: the permeable epithelium theory and the mast cell theory. However, other factors are also involved: vascular, neurological, infectious and immune. This disease has a chronic course with no transformation of the nonulcerative form into the ulcerative form. There are no specific histological criteria, even the presence of mast cells in the bladder wall. However, histology is able to exclude other bladder disease, principally carcinoma in situ. The diagnosis is therefore based on clinical examination and endoscopy, after excluding other diseases. The essential complementary investigations are cystoscopy and cystomanometry which must be performed according to rigorous protocols. Conservative treatment is based on vesical hydrodistension, bladder retraining, bladder instillations (DMSO) and systemic treatments (sodium pentosanpolysulfate). Surgery is required in 1 to 5% of cases due to failure of medical treatment and the severity of the symptoms. Electrical or laser coagulation of the ulcers is effective. Partial cystectomy with cystoplasty is reserved for forms sparing the trigone, while cystourethrectomy and urinary diversion may be indicated in other more advanced and refractory cases.
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PMID:[Interstitial cystitis]. 771 56

Lymphoreticular neoplasms of the larynx are rare and comprise a heterogeneous group of tumors. A systematic survey of the literature and autoptic evaluation of the larynx in a relatively small number of patients with systemic lymphoreticular malignancies yielded the following findings: Primary tumors of the larynx must be clearly distinguished from laryngeal involvement by systemic or leukemic infiltrations. By far the most common primary hemopoietic tumors of the larynx are extramedullary plasmacytoma (about 90 cases published) and non-Hodgkin's lymphoma (NHL; about 65 cases published). Primary Hodgkin's disease, granulocytic sarcoma and mast cell sarcoma are extremely rare at this site. Plasmacytoma and NHL both preferentially involve the supraglottis. The subglottis is infrequently affected. Laryngeal plasmacytoma and NHL usually present clinically as localized stage IE and IIE tumors that exhibit no significant tendency to recur or generalize. The therapy of choice is local irradiation while chemotherapy should be reserved for recurrent or progressive disease. Prognosis is favourable in most cases of primary laryngeal plasmacytoma and NHL. Secondary involvement of the larynx by systemic lesions or leukemic infiltrations is usually associated with a very poor prognosis. The prognosis of patients with laryngeal involvement in acute or chronic myeloid leukemia is always poor. Although the histopathological diagnoses given in many case reports are often difficult to compare because of differences in terminology, there seems to be a marked preponderance of B-cell tumors of high-grade malignancy (centroblastic or immunoblastic lymphoma in the Kiel classification of NHL) that probably represents lymphomas originating from mucosa-associated lymphoid tissue (MALT).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The larynx in lymphoproliferative and myeloproliferative diseases. Part II: Laryngeal autopsy findings and discussion]. 792 29

Lymphoreticular neoplasms of the larynx are rare and comprise a heterogeneous group of tumors. A systematic survey of the literature and autoptic evaluation of the larynx in a relatively small number of patients with systemic lymphoreticular malignancies yielded the following findings: Primary tumors of the larynx must be clearly distinguished from laryngeal involvement by systemic or leukemic infiltrations. By far the most common primary hemopoietic tumors of the larynx are extramedullary plasmacytoma (about 90 cases published) and non-Hodgkin's lymphoma (NHL; about 65 cases published). Primary Hodgkin's disease, granulocytic sarcoma and mast cell sarcoma are extremely rare at this site. Plasmacytoma and NHL both preferentially involve the supraglottis. The subglottis is infrequently affected. Laryngeal plasmacytoma and NHL usually present clinically as localized stage IE and IIE tumors that exhibit no significant tendency to recur or generalize. The therapy of choice is local irradiation while chemotherapy should be reserved for recurrent or progressive disease. Prognosis is favorable in most cases of primary laryngeal plasmacytoma and NHL. Secondary involvement of the larynx by systemic lesions or leukemic infiltrations is usually associated with a very poor prognosis. The prognosis of patients with laryngeal involvement in acute or chronic myeloid leukemia is always poor. Although the histopathological diagnoses given in many case reports are often difficult to compare because of differences in terminology, there seems to be a marked preponderance of B-cell tumors of high-grade malignancy (centroblastic or immunoblastic lymphoma in the Kiel classification of NHL) that probably represents lymphomas originating from mucosa-associated lymphoid tissue (MALT).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The larynx in lymphoproliferative and myeloproliferative diseases. I: An overview with special reference to primary laryngeal malignant lymphomas and plasmacytomas]. 807 Oct 93

Topical ocular allergy drugs are indicated for the treatment of allergic conjunctivitis after more conservative measures have been employed. Antihistamines, vasoconstrictors, nonsteroidal anti-inflammatory drugs, mast cell stabilizers and corticosteroids are available. Levocabastine and ketorolac tromethamine are new drugs for the treatment of allergic conjunctivitis. Lodoxamide is currently indicated only for the treatment of vernal keratoconjunctivitis, although treatment efficacy has been demonstrated in patients with giant papillary conjunctivitis and atopic keratoconjunctivitis. As a general rule, topical ocular allergy drugs are well tolerated by most patients except for transient stinging and burning on instillation. Ocular steroids should be reserved for severe cases and should be prescribed by an ophthalmologist, who can monitor the patient for possible ocular side effects.
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PMID:A critical look at ocular allergy drugs. 864 76

Eosinophilic esophagitis (EE) is an important esophageal disorder with distinct clinicopathologic features, and the condition is associated with a high prevalence of food allergies and atopy. In the past decade, we have improved our ability to recognize the phenotype of EE, but our ability to treat EE effectively remains limited despite several reports of successful treatment using elemental or elimination diets, and systemic and topical corticosteroids. The limitations for developing effective treatment regimens are due to some still unresolved and ambiguous aspects of the pathogenesis of EE. Neither the predisposing factors for developing EE in a subset of patients with atopy, nor the variable responsiveness to control measures for allergens are fully understood. There also remain questions about the precise role of gastroesophageal reflux, and the natural history of the disorder, contingent on which is the optimal treatment of EE. In devising treatment for a patient with EE, all attempts should be made to identify and control food and other allergies. In patients who have no diagnosed allergies or who are unresponsive to allergy treatment, topical steroids are a safe and effective treatment option. Systemic steroids should be reserved for those patients who are refractory to topical steroids. Beyond the initial phase of induction treatment, it is crucial to develop effective and safe maintenance treatment regimens based on ongoing allergen control and mast cell inhibitors. There are limited but encouraging data to support further exploration of the role of leukotriene and interleukin-5 inhibitors as safe, effective, and steroid-sparing treatment options.
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PMID:Treatment of Eosinophilic Esophagitis in Children. 1220 60

Ocular allergy is a common condition that usually affects the conjunctiva of the eye and is therefore often referred to as allergic conjunctivitis. The severity of the disease can range from mild itching and redness, as seen in seasonal allergic conjunctivitis, to the more serious vision threatening forms of ocular allergy which affect the cornea, such as atopic keratoconjunctivitis. The pathogenesis of allergic conjunctivitis involves a complex mechanism which centers around IgE-mediated mast cell degranulation and release of multiple preformed and newly formed inflammatory mediators. The diagnosis of allergic conjunctivitis is usually a clinical one which can be made based on a thorough history and careful examination. Treatment of ocular allergy should begin with conservative measures including allergen avoidance, environmental control, ocular irrigation and cold compresses. Pharmacotherapy of allergic conjunctivitis consists of several classes of drugs. Antihistamines are widely used to treat mild conditions such as seasonal and perennial conjunctivitis and potent new agents such as levocabastine and emedastine are now available. Mast cell stabilizers such as sodium cromoglycate are both safe and effective and are commonly used in ocular allergy. More effective mast cell stabilizers such as nedocromil, lodoxamide and olopatadine are now being used. Nonsteroidal antiinflammatory drugs have demonstrated only limited efficacy and, as such, are not widely used. Topical steroids are very effective in treating signs and symptoms but are reserved for only refractory cases due to their serious side effects. Loteprednol and rimexelone are newer corticosteroids which reportedly have less of an effect on intraocular pressure. Cyclosporine has recently been shown to be highly effective in cases of vernal keratoconjunctivitis and atopic keratoconjunctivitis while producing no adverse effects.
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PMID:Ocular allergic disease. 1474 64

Mast cells were described by Erhlich at the end of XIX-th century. Their role was deeply investigated in asthma and allergy. The massive degranulation of mast cells in allergy can lead to anaphylactic shock. Recently, mast cells have been recognized again as a very interesting topic for investigation, due to their possible role in chronic inflammation. Moreover, through adenosine receptors, mast cells can be activated or inactivated. That is why these cells are regarded as a potential target of new drugs. It has been reported, that mast cells generate intracellular reactive oxygen species (ROS) in response to stimulation with divergent physiologically relevant stimulants. The intensification of ROS production may be measured by the level of carbonyl groups, as a marker of protein peroxidation. However, the role of mast cells in other than asthma diseases with chronic inflammation needs further investigation. It was found out that the information about mast cell distribution in colonic mucosa may serve as help in differentiation between inflammatory bowel disease and collagenous colitis. Moreover, its accumulation in focal active gastritis was confirmed in patients with Crohn's disease. An important role in regulation of inflammatory process seems to be reserved for adenosine receptors present on mastocytes. The activation of mast cells through the adenosine receptor is connected with 11-8 release, which stimulate the migration of leukocytes and oxidation reactions. The detection of mast cells in tissues should not be limited only to the simple histologic examination. It should be completed by the detection of products of degranulation, e.g. tryptase. This is the way to find out their actual function and state of activation.
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PMID:[Mast cells, their adenosine receptors and reactive oxygen species in chronic inflammatory pathologies of childhood]. 1720 8

Asthma and nonasthmatic eosinophilic bronchitis are among the most common causes of chronic cough, accounting for about 25 and 10% of cases, respectively. Chronic cough due to asthma may present in isolation in which case it is known as cough-variant asthma. Nonasthmatic eosinophilic bronchitis is characterized by the presence of eosinophilic airway inflammation in the absence of variable airflow obstruction or airway hyperresponsiveness. Both conditions share many immunopathological features with the exceptions to date of mast cell infiltration into the airway smooth muscle, increased IL-13 expression, and narrowing and thickening of the airway wall, which are features reserved to asthma. In most cases the trigger that causes the cough is uncertain. However, removal of potential triggers is important to consider, in particular with respect to occupational exposure to known sensitisers. In both conditions there is subjective and objective improvement following treatment with inhaled corticosteroids, which is associated with the presence of an airway eosinophilia. Whether eosinophilic inflammation is the cause of cough or an epiphenomenon is uncertain, but the failure of anti-IL-5 to modify cough in asthma has questioned a causal association. In asthma, beta-agonist theophylline, leukotriene receptor antagonist, and oral corticosteroid therapy improve cough. In noneosinophilic bronchitis, some patients require oral corticosteroids but the benefit of other additional therapies is unknown. In general, response to therapy in both conditions is very good and the limited long-term data available suggest that both usually have a benign course, although in some cases persistent airflow obstruction may occur.
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PMID:Cough due to asthma and nonasthmatic eosinophilic bronchitis. 1966 8


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