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)

Passive transfer (PK) tests were performed with a reaginic serum on a recipient reacting with an immediate and a more prolonged reaction when specificity challenged. Both reactions are thought to be mediated by IgE immunology. Ketotifen, a cycloheptathiophene derivative, and clemastine, given to the recipient in maximal clinical doses for 3 days, inhibited the immediate reaction. Ketotifen had a very slight effect also on the prolonged reaction. The results indicate that the in vivo effects of ketotifen in the human system are due not so much to mast cell inhibitory mechanisms, but more to post-release antihistaminic and some anti-inflammatory properties.
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PMID:Effects of ketotifen and clemastine on passive transfer of reaginic reaction. 3 77

Ketotifen, a histamine H1-receptor antagonist and mast cell stabilizer, significantly protected the rat gastric mucosa against lesions induced by necrotizing agents, histamine or compound 48/80. The agent significantly inhibited the basal gastric acid secretion, but had little or no effect on the histamine-stimulated secretion. The mucosal protective effect was observed even at a dose that had little or no effect on gastric acid secretion, suggesting that ketotifen exhibits so-called cytoprotective activity.
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PMID:Effect of ketotifen on acute gastric lesions and gastric secretion in rats. 143 22

The effects of ketotifen, a 'mast cell stabiliser,' on two models of experimental colitis were examined. The inflammatory response elicited by either trinitrobenzene sulphonic acid or acetic acid resulted in increased colonic synthesis of platelet activating factor, prostaglandin E2, thromboxane B2, leukotrienes B4 and C4, and myeloperoxidase activity. Intragastric administration of ketotifen 100 micrograms/100 grams twice daily significantly decreased mucosal damage when given prophylactically 48 hours before the induction of colitis and then throughout the experiment. This effect was consistent in both models and was accompanied by a significant reduction in mucosal generation of platelet activating factor, prostaglandin E2, thromboxane B2, and leukotrienes C4 and B4. Myeloperoxidase activity was reduced as well, reaching significance only in the acetic acid model. This study shows that both trinitrobenzene sulphonic acid and acetic acid colitis can be pharmacologically manipulated by ketotifen. The mechanism of action of ketotifen has not yet been determined. Ketotifen's potential in the treatment of active inflammatory bowel disease or in the prevention of exacertations, or both, remains to be elucidated.
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PMID:Ketotifen effectively prevents mucosal damage in experimental colitis. 145 75

The effect of immunosuppressive drugs, 4-aminosalicylic acid (4-ASA), acetyl 5-aminosalicylic acid (5-ASA), and ketotifen on human colonic eicosanoid accumulation was evaluated in view of enhanced accumulation in patients with active ulcerative colitis. Azathioprine (100 micrograms/ml), cyclosporin (100 micrograms/ml), and methotrexate (100 micrograms/ml) significantly inhibited, by 25-35%, prostaglandin E2 (PGE2) accumulation by organ-cultured colonic mucosa of ulcerative colitis patients. Methotrexate was the only immunosuppressive drug that inhibited leukotriene B4 (LTB4) accumulation (50%), whereas azathioprine inhibited the accumulation of leukotriene C4 (LTC4) (25%). 5-ASA and its metabolite, acetyl 5-ASA, inhibited by 20-70% PGE2, LTB4, and LTC4 accumulation in the culture, supporting the contention that acetyl 5-ASA is as active as 5-ASA in these respects. 4-ASA had no effect on any of the eicosanoids. Ketotifen, a mast cell stabilizer, significantly inhibited the accumulation of PGE2, LTB4, and LTC4 by 33-60%. These results suggest a potential, new, unrecognized mode by which the immunomodulators induce part of their therapeutic effects in inflammatory bowel disease and support the contention that acetyl 5-ASA is as active as 5-ASA. The results obtained also indicate that ketotifen, used effectively in the prevention of bronchial asthma, inhibits the accumulation of colonic eicosanoids and, thus, may be of value in the treatment of inflammatory bowel disease.
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PMID:Effect of drugs on colonic eicosanoid accumulation in active ulcerative colitis. 145 96

Systemic Sclerosis is a multisystemic disease characterized by sclerosis of the skin and visceral organs, vasculopathy (Raynaud's phenomenon) and autoantibodies. The criteria for the classification of the disease requires either proximal scleroderma (major criteria) or the presence of 2 of the 3 minor features namely sclerodactyly, digital pitting scars and bibasilar pulmonary fibrosis. There are 3 subsets of this condition--diffuse variant, limited variant (CREST syndrome) and Overlap Syndrome (where patients have features of other rheumatic diseases). There are localized forms of scleroderma and pseudoscleroderma states. The presenting features of Systemic Sclerosis are usually Raynaud's, skin changes and arthralgia. Systemic complaints like breathlessness, dyspepsia, etc depending on the organ involved may be present. Management starts with patient education regarding the disease, skin care, exercises and regular medical check-up. There is no miracle cure but much can be done to improve the quality of life of the patient. Nifedepine and other drugs may improve Raynaud's phenomenon. Drugs can be used to treat other complications. Various medication have been tested as disease modifying drugs for scleroderma. These include drugs which inhibit collagen like D-penicillamine, colchicine, and immunosupressive drugs like cyclosporin. Ketotifen, a mast cell stabilizer has been reported to be effective in scleroderma. As it is a relatively safe drug, clinical trials are underway.
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PMID:Systemic sclerosis. 162 Nov 27

A group of 187 asthmatics that had been using corticotherapy for at least a year was studied to ascertain the actual necessity of this treatment as well as the clinical and etiologic forms of bronchial asthma in these patients. Thus 3 categories of patients could be delineated; 112 patients with total (permanent) corticodependence, 25 patients with transient (seasonal) corticodependence and 50 patients with pseudocorticodependence. Generally, the category with total corticodependence consisted of patients with intrinsic asthma or with confirmed polyintricated allergic asthma. The criteria for inclusion in this category were: lack of response to bronchodilating treatment, estimated clinically and by FEV1 and/or Raw (resistance of air ways) determinations, and impossibility to achieve corticotherapy "sevrage" by associating mast cell-degranulation inhibitors (ketotifen and/or disodium chromoglycat--DSCG). In the other two categories corticosteroid sevrage could be achieved either transiently in the case of the second category (corticodependent patients only in the warm season--asthmatics with allergy to pollens, resistant to the usual treatment--or in the cold season--some asthmatics with infectious trigger) or completely in the patients of the third category (with pseudocorticodependence). In these latter subjects (about a quarter of the patients with prolonged corticotherapy), mostly asthmatics with ignored allergic etiology, the etiologic approach of disease and the association of Ketotifen and/or DSCG led to disappearance of corticodependence.
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PMID:Contribution to the study of the etiopathogenic and background peculiarities in patients with corticodependent bronchial asthma. Note I. Concepts of corticodependence and pseudocorticodependence. 194 11

For many years, the mast cell has been considered the principal cell in bronchial asthma. However, there is some evidence to suggest that platelets might be involved in asthma. One of this evidence is the induction by platelet-activating factor or airway hyperreactivity and its inhibition by disodium cromoglycate and ketotifen. Since platelet aggregation is an index of platelet activation, we investigated the effect of these drugs on platelet aggregation induced by ADP, collagen and arachidonate in human platelet-rich plasma. The results obtained show that both drugs inhibit the effect of ADP and collagen. Ketotifen was also shown to inhibit the aggregation induced by arachidonate. The mechanism of the antiasthmatic action of these drugs is at present not clear. If platelet activation as it has been proposed, is involved in asthma, the antiaggregant effect of ketotifen and cromoglycate might be part of its beneficial effect in the treatment of asthma.
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PMID:Effect of ketotifen and disodium cromoglycate on human platelet aggregation. 250 3

3 patients with generalized neurofibromatosis were treated with the mast cell blocking substance Ketotifen. Pruritus and pain could be inhibited significantly and the tumor growth could be prevented.
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PMID:[Ketotifen inhibits urticaria and tumor progression in neurofibromatosis]. 251 Oct 44

Forty-one subjects with dermographia were studied for a 4-week period. Twenty subjects received ketotifen therapy, the other 21 received chlorpheniramine (H1) for 2 weeks, and then chlorpheniramine plus cimetidine (H1 + H2). Both groups had significant suppression of dermographia and skin wheals caused by dextromethorphan and histamine after 2 weeks. The inhibition by ketotifen of dermographia, histamine wheal, and the dextromethorphan wheal increased from week 2 to week 4. During the first 2 weeks, ketotifen's activity was comparable to chlorpheniramine. Ketotifen's activity increased during the second 2 study weeks to match the additional chlorpheniramine. These results suggest that ketotifen may have additional pharmacologic activities besides H1 antagonism, including possible inhibition of mast cell mediator release. As a consequence, cutaneous vascular hyperresponsiveness may decrease. Ketotifen appears promising as treatment for allergic skin disorders.
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PMID:Inhibition of dermographia, histamine, and dextromethorphan skin tests by ketotifen. A possible effect on cutaneous vascular response to mediators. 277 2

Treatment of idiopathic oligo- and asthenozoospermia by the mast cell blocker Ketotifen leads to a very moderate, but statistical significant improvement of sperm count and sperm motility. However, pregnancy rate was within the range of spontaneous conceptions. To evaluate the possible significance of this new treatment approach further research is mandatory to elucidate the relationship between mast cell proliferation and dysfunction of the blood-testis barrier.
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PMID:The use of ketotifen, a mast cell blocker, for treatment of oligo- and asthenozoospermia. 381 45


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