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)

1. The mechanism of the flushing, hypotension and tachycardia associated with i.v. administration of desGlyd(CH2)5D-Tyr(Et)VAVP (SK&F 101926; 25 micrograms kg-1) and the selective V2 antidiuretic agonist, desamino-8-D-arginine vasopressin (dDAVP; 3 micrograms kg-1) was studied in ketamine-anaesthetized rhesus monkeys. 2. The flushing associated with SK&F 101926 was reduced by pretreatment with a mast cell stabilizer and by repeated administration of peptide (within 2-4 weeks). A similar desensitization to dDAVP-associated flushing was observed on repeated administration. 3. Treatment with dDAVP also resulted in reduced SK&F 101926-associated flushing. 4. The hypotension associated with SK&F 101926 was not affected by pretreatment with a mast cell stabilizer. A similar degree of hypotension was observed with repeated administration of either SK&F 101926 or dDAVP. 5. The tachycardia associated with SK&F 101926 was reduced by pretreatment with a mast cell stabilizer or repeated administration of SK&F 101926. Repeated administration of dDAVP, however, resulted in an enhanced tachycardia. 6. Indomethacin (5 mg kg-1 i.v.) did not alter the flushing or the hypotension associated with the administration of either SK&F 101926 or dDAVP, but resulted in an enhanced tachycardia to SK&F 101926. 7. Administration of a selective V1 vasopressor antagonist did not result in flushing, hypotension or tachycardia. 8. It was concluded that the flushing response to vasopressin-like peptides in rhesus monkeys may be due to an action on mast cells, whereas the haemodynamic responses are not, but probably involve direct vasodilator actions.
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PMID:Flushing and haemodynamic responses to vasopressin peptides in the rhesus monkey. 317 11

Urticaria pigmentosa, characterized by cutaneous mast cell proliferation, usually occurs sporadically in childhood and resolves over a period. Rarely is the condition seen in two or more members of a family. We encountered a family in which urticaria pigmentosa occurred in four members of two generations. Skin findings were similar in all four. No systemic manifestations other than occasional flushing episodes were noted in any of the affected individuals. HLA typing was performed, but no significant correlation between affected and unaffected individuals was seen. In a review of a number of previously reported cases, we found a slight female preponderance.
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PMID:Familial urticaria pigmentosa. 345 8

An autopsy case of systemic mastocytosis without cutaneous involvement in a 76-year-old woman was described. The patient presented with general malaise, chest and epigastric discomfort, flushing of the face and progressive hepatosplenomegaly, and she terminated in hemorrhagic complications of DIC within 2 months. There was neither rash nor urticaria pigmentosa recognizable in the entire course. The diagnosis was made by the histologic identification of abnormal aggregates of mast cells in a bone marrow aspirate. These mast cell granules were chloroacetate esterase-positive, peroxidase-negative, and electronmicroscopically they were composed of fine granular materials containing variable numbers of lamellar structures. At autopsy, diffuse infiltration of the mast cells was found in the liver, spleen, bone marrow, lymph nodes, lungs, kidneys, stomach, and adrenal glands.
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PMID:Systemic mastocytosis without cutaneous involvement. 355 89

Systemic mastocytosis is a disease characterized by an excessive accumulation of mast cells, and associated with skin lesions, flushing, diarrhea, tachycardia, and psychiatric manifestations. In order to define more clearly the psychiatric manifestations, ten patients with this disorder underwent unstructured psychiatric interviews and a battery of psychologic testing. Both revealed a pattern of cognitive and affective changes in the majority of these patients, best categorized as an atypical or mixed organic brain syndrome. The cognitive changes consisted of diminished attention and memory, and the affective changes of anger, irritability, and, to a lesser extent, depression. These manifestations fluctuated with the level of disease activity, and appeared in some cases to respond to histamine antagonists and disodium cromoglycate, medications used to control the excessive mast cell activity. It is important for psychiatrists to be aware that mental status changes can represent psychiatric manifestations of mastocytosis, a readily treatable medical disorder.
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PMID:Mixed organic brain syndrome as a manifestation of systemic mastocytosis. 374 21

A patient with symptomatic urticaria pigmentosa who responded to nifedipine therapy is reported. Relief from cold-induced urtication and flushing was obtained with 10 mg taken orally three times daily. Calcium influx is an early step in the degranulation of mast cells. We hypothesize that the beneficial effect of nifedipine was due to calcium-channel blockade causing elevation of the mast cell threshold for degranulation.
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PMID:Urticaria pigmentosa responsive to nifedipine. 649 Oct

Mastocytosis gives rise to clinical symptoms such as flushing, itching and diarrhoea. We report a patient with urticaria pigmentosa without evidence of systemic involvement but with recurrent episodes of diarrhoea. The patient had elevated circulating levels of calcitonin, which might have been a mediator of her diarrhoea. We suggest that serum calcitonin level should be checked in patients with mast cell disease and diarrhoea.
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PMID:Hypercalcitoninaemia in a patient with urticaria pigmentosa. A possible cause of diarrhoea. 673 Oct 41

Urticaria pigmentosa is a usually a benign and asymptomatic cutaneous variant of mastocytosis, which is a relatively rare disorder characterized by abnormal aggregates of mast cells in the dermis. These aggregations, if present, can abruptly release vasoactive mediators such as histamine, heparin, and prostaglandins under some physical stresses and may produce flushing, hypotension, syncope, shock, etc. One of the interesting aspects to an anesthesiologist is the effect of drugs administered perioperatively on mast cell degranulation. We report an infant case of urticaria pigmentosa and discuss the anesthetic significance especially of mastocytosis during anesthesia and surgery.
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PMID:[Anesthetic management of a patient with urticaria pigmentosa]. 773 6

Aspirin therapy for patients with systemic mast cell disease (SMCD) decreases the production of prostaglandin D2, which is thought to be a major mediator of flushing. Paradoxically, in 5 to 10% of patients with SMCD, administration of aspirin causes massive mediator release and an anaphylactoid reaction. We attempted aspirin desensitization in a 34-year-old man with SMCD (confirmed by bone marrow biopsy) who was incapacitated by severe flushing episodes and hypotension. His baseline mediator levels of plasma calcitonin, urinary histamine, and urinary N-methyl-imidazoleacetic acid were abnormal. Pentagastrin stimulation increased the plasma level of calcitonin from 47 pg/mL to 130 pg/mL (normal, less than or equal to 110) at 5 minutes. Oral aspirin desensitization was begun; however, after a cumulative dose of 620 mg, an anaphylactoid reaction ensued in conjunction with hypotension, abdominal cramping, and flushing. Coincidentally, 1 hour after the episode, the plasma calcitonin level increased from 37 pg/mL to 540 pg/mL, and the serum tryptase level increased from 1 ng/mL to 3.9 ng/mL. Six hours after the episode, the urine level of histamine increased from 90 micrograms/g creatinine to 337 micrograms/g creatinine, and the urinary N-methylimidazoleacetic acid increased from 32 mg/24 h to 81 mg/24 h. Hence, the patient had increased basal levels of plasma calcitonin that increased substantially during aspirin desensitization and increased to above the upper limit of normal during pentagastrin stimulation. Human mast cells may be capable of producing calcitonin or causing secretion of calcitonin in response to skeletal changes.
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PMID:Increased plasma calcitonin levels in systemic mast cell disease. 793 97

Chronic urticaria can be produced by a number of stimuli that cause mast cell mediator release. Patients with urticaria caused by physical agents account for roughly one-fifth of all cases of chronic urticaria. There are about 20 different types of physical urticaria. Two forms, dermographism and cholinergic urticaria, are quite common and represent more than two-thirds of all cases of physically caused urticaria. More than one agent may precipitate urticaria in a given individual. Urticarial response can be easily reproduced in the sensitive patient and, generally, lasts less than one hour. Systemic features such as flushing, dizziness, headaches, and even hypotension, may occur during severe episodes. Identification of the causative physical agent is necessary for effective therapy.
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PMID:Physical urticarias. 817 38

Morphine and tubocurarine may release histamine by direct mast cell degranulation which may result in systemic effects such as cutaneous flushing, local wheal and flare formation and hypotension. This randomised, double-blind study examined whether preoperative combined oral terfenadine (60 mg) and ranitidine (150 mg) attenuates the reduction in blood pressure and cutaneous flushing after the administration of tubocurarine and morphine in 60 patients undergoing elective gynaecological surgery. In addition, investigation was made of whether tubocurarine and morphine cause a significant decrease in gastric pH in comparison to the nonhistamine-releasing agents fentanyl and vecuronium. Patients were randomly assigned to one of three groups receiving either pre-operative terfenadine and ranitidine and intra-operative tubocurarine and morphine (group A); pre-operative placebo and intra-operative tubocurarine and morphine (group B); pre-operative placebo and intra-operative fentanyl and vecuronium (group C). Compared to group B, group A had less hypotension and tachycardia but no significant decrease in cutaneous flushing immediately following morphine and tubocurarine (p > 0.05). There were no significant differences in haemodynamic changes between the groups A and C. In those patients not pretreated with terfenadine and ranitidine (groups B and C), gastric pH decreased between 5 and 10 min following bolus administration of morphine and tubocurarine (group B), whereas patients receiving fentanyl and vecuronium (group C) had an increase in gastric pH. This suggests that histamine release following administration of morphine and tubocurarine is sufficient to increase gastric acidity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of the H1 and H2 receptor antagonists, terfenadine and ranitidine on the hypotensive and gastric pH effects of the histamine releasing drugs, morphine and tubocurarine. 821 91


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