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)

Cystinosis is a rare autosomal recessive metabolic disorder that results in the widespread accumulation of cystine crystals in ocular tissues as well as in bone marrow, liver, spleen, lymph nodes, and kidneys. We treated a case of pupillary-block glaucoma in a 19-year-old woman caused by cystine accumulation in the iris stroma. Trabeculectomy and iridectomy relieved the pupillary block and decreased the intraocular pressure. Histologic examination disclosed the presence of crystals in the conjunctival and iris stroma and in the iris pigment epithelium. Crystals were also found within conjunctival mast cell granules, confirming the lysosomal nature of cystinosis.
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PMID:Pupillary-block glaucoma associated with childhood cystinosis. 301 11

We have previously shown the presence and localization of mast cells and the intraocular effects of compound 48/80 in the rabbit eye. In the present study we have evaluated the mechanism of action of compound 48/80 using ruthenium red as a blocker of sensory axon reflexes in the rabbit eye and by measuring the intraocular pressure (IOP), the pupil size, the blood pressure, the protein and cAMP content in the aqueous humour. Topical neutral formaldehyde was used as a topical inducer of neuronally mediated response in a separate series of experiment. Intracamerally-injected ruthenium red suppressed the compound 48/80-induced elevation intraocular pressure and prevented miosis, while having little if any effect on the breakdown of the blood-aqueous barrier and on the increase in the cAMP concentration in aqueous humour. Ruthenium red also inhibited the irritative response in eyes treated with topical 1% formaldehyde. As the blood-aqueous barrier in the rabbit is an extremely sensitive system higher doses of ruthenium red causes damage of the barrier in the ruthenium red treated eyes. The results demonstrate that compound 48/80 not only has a mast cell degranulating effect but also a sensory nerve- stimulating effect.
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PMID:Intraocular effects of ruthenium red in responses to compound 48/80 and topical formaldehyde in rabbit. 892 1

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

Allergic conjunctival diseases caused by immediate hypersensitivity are classified into several subtypes, including seasonal or perennial allergic conjunctivitis, vernal keratoconjunctivitis (VKC), atopic karatoconjunctivitis, giant papillary conjunctivitis. The gold standard in treatment of seasonal allergic conjunctivitis, especially Japanese cedar pollinosis, is anti allergic ophthalmic solution, mast cell stabilizer and histamine H1 blocker. During the peak pollen count period, we use an ophthalmic steroid solution. Preseasonal treatment with anti allergic ophthalmic solution is effective to decrease symptoms during the peak pollen count period. Topical steroids are most effective treatment for VKC, but are also frequently associated with increasing intraocular pressure. A recent treatment combining anti allergic ophthalmic solution, steroid ophthalmic solution and topical immunomodulator (cyclosporine 0.1% or tacrolimus 0.1%) proves very effective and safe for severe VKC.
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PMID:[Ophthalmology]. 1989 34

Seasonal allergic conjunctivitis (SAC) is an inflammatory response of the conjunctiva triggered by exposure to seasonal allergens. Treatment options for SAC include artificial tears, antihistamines, decongestants, mast cell stabilizers, nonsteroidal anti-inflammatory drugs, dual antihistamine/mast cell stabilizers, immunotherapy and corticosteroids. Topical, intranasal and systemic formulations of corticosteroids have traditionally provided the most effective relief of the inflammation and signs and symptoms associated with severe, acute exacerbations of SAC. However, steroid-induced ocular and systemic side-effects have limited the prescribing of these agents. This limitation of traditional corticosteroids led to the development of modified corticosteroids that retain the anti-inflammatory mechanism of action of traditional corticosteroids with a much-improved safety profile because of their rapid breakdown to inactive metabolites after exerting their activity. The development of one such novel corticosteroid, loteprednol etabonate (LE), led to the insertion of an ester (instead of a ketone) group at the carbon-20 (C-20) position of the basic corticosteroid structure. Clinical trials assessing this C-20 ester corticosteroid have demonstrated similar efficacy to C-20 ketone corticosteroids in the prevention or treatment of the signs and symptoms of SAC but with a greatly improved safety profile, as the C-20 ester corticosteroid is less likely to elevate intraocular pressure. In addition, the ketone at the C-20 position has been implicated in the formation of cataract, while nonketolic corticosteroids do not form Schiff base intermediates with lens proteins, which is a common first step in cataractogenesis. The clinical relevance of the C-20 ester corticosteroid class, as modelled by LE, is that they provide both effective and safe treatment of the inflammation associated with SAC and relief of its signs and symptoms. Loteprednol etabonate offers a well-tolerated treatment option for patients with debilitating acute exacerbations as well as chronic forms of the disease.
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PMID:Management of seasonal allergic conjunctivitis: guide to therapy. 2206 57

Vernal keratoconjunctivitis (VKC) is a persistent, severe allergic eye disease, mainly occurring in children, that can lead to severe ocular complications including visual loss. The underlying etiology and pathophysiology of VKC remain unclear. Common therapies include topical antihistamines and mast cell stabilizers that are effective in mild-to-moderate forms of VKC but are often ineffective in severe forms that require topical or systemic corticosteroids. Dependence on steroids is common with potential adverse effects both local, as increased intraocular pressure, glaucoma, infection and cataract, as well as systemic ones, as reduction in child growth velocity. Alternative therapies are immunosuppressive drugs, like cyclosporine A and tacrolimus, that usually are effective but may also cause adverse effects. A promising therapeutic option is omalizumab, a recombinant anti-IgE humanized monoclonal antibody, currently used as add-on therapy for moderate to severe uncontrolled allergic asthma and chronic spontaneous urticaria. Here, we report the short-time duration of effective relief of symptoms after the prolonged use of omalizumab in a patient affected by refractory VKC. However, in our case any apparent beneficial effect was short lasting, and we propose that the duration of the disease and the concomitant long-term use of steroids leads to iatrogenic damage; thus, the disease becomes refractory to anti-IgE treatment.
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PMID:Vernal Keratoconjunctivitis: A Case of Anti-IgE Treatment with Short-Lasting Remission. 3277 91