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)

Mast cell numbers were quantitated in adult cases of mastocytosis demonstrating non-diffuse perivascular and upper dermal concentrations of mast cells. Using the Leder stain and computerised video image analysis, a mean of 382 (+/- 28 SE) mast cell per mm2 were counted in the superficial dermis in skin biopsies from 30 adult cases of mastocytosis, in contrast to a mean of 43 (+/- 5 SE) mast cells per mm2 in skin biopsies from 50 inflammatory dermatoses represented by subacute dermatitis, pigmented purpuric dermatosis, erythema multiforme, lichen planus and granuloma annulare. Ten skin biopsies showing no significant inflammation had a mean of 54 (+/- 7 SE) mast cells per mm2 in the upper dermis. The mean area of individual mast cells as assessed by image analysis in the mastocytosis group was 47.40 microns 2 (+/- 2.26 microns 2, SE) which was significantly different (P < 0.01) than the mast cell area (32.34 microns 2 +/- 2.22 microns 2, SE) in all other groups combined. Computerised video image analysis represents an alternative technique which is useful in assessing mast cell numbers and particularly mast cell size in adult cases of macular mastocytosis and in other dermatoses.
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PMID:Mast cell quantitation by image analysis in adult mastocytosis and inflammatory skin disorders. 128 34

We compared the number of mast cells in erythema multiforme lesions, in clinically healthy mucosa between the EM attacks and in healthy mucosa from healthy volunteers. The mast cell count in patients with erythema multiforme was numerically higher than in healthy controls, but the differences were not statistically significant. In erythema multiforme lesions the mast cell count was low in the intensely inflamed superficial lamina propria, but high in normal appearing mucosa between the attacks suggesting local mast cell degranulation in the most intensely inflamed areas.
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PMID:Mast cells in oral erythema multiforme. 137 27

Bullous mastocytosis (diffuse cutaneous mastocytosis) is a rare form of mast cell disease that begins during the first month of life and causes extensive blisters that mimic scalded skin syndrome or bullous erythema multiforme. Discrete pigmented macules, papules, and nodules are absent and the characteristic leathery induration of skin may not develop until 6 months of age. Skin biopsy shows a subepidermal blister with mast cells at the base. The most serious complications are gastrointestinal hemorrhage and shock. The symptoms of bullous mastocytosis may be modified by a number of new therapeutic agents.
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PMID:Bullous mastocytosis: diffuse cutaneous mastocytosis with extensive blisters mimicking scalded skin syndrome or erythema multiforme. 638 70

The possible involvement of mast cell tryptase and chymase in subepidermal bullous diseases was studied enzyme-histochemically in specimens from erythematous and vesicular skin and from non-involved skin of patients with dermatitis herpetiformis, bullous pemphigoid, erythema multiforme, infective bullous eruption and linear IgA dermatosis. Patients with pemphigus were biopsied for comparison. The immunoreactivity of chymase inhibitors, alpha1-proteinase inhibitor (alpha1-PI) and alpha1-antichymotrypsin (alpha1-AC), in mast cells was demonstrated using the sequential double staining method. Tryptase-positive mast cells were unchanged or only slightly increased in number in erythematous lesions and slightly decreased in blistering skin compared with healthy-looking skin. Only occasionally were mast cells seen in apparent contact with the basement membrane zone. Chymase-positive mast cells and the chymase/tryptase ratio steadily decreased during the development of the lesions in each subepidermal bullous disease. The percentage of alpha1-PI+ and/or alpha1-AC+ mast cells increased simultaneously, which could explain the disappearance of chymase activity. Similar results were obtained regardless of the bullous disease. The results were also similar in pemphigus, which is an intraepidermal bullous disease. In conclusion, these results show significant alterations in mast cell chymase and protease inhibitors in a range of different bullous diseases, suggesting mast cell involvement. The apparent inactivation of chymase could be due to the action of chymase inhibitors detected in numerous mast cells. However, these alterations probably reflect general inflammation rather than a specific reaction in a certain bullous disease.
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PMID:Mast cells in developing subepidermal bullous diseases: emphasis on tryptase, chymase and protease inhibitors. 1049 9

The need to offer first line therapy for primary and recurrent cancers has spurred the clinical development of rapid desensitizations for chemotherapy and monoclonal antibodies. Rapid desensitizations allow patients to be treated with medications to which they have presented with hypersensitivity reactions (HSRs), including anaphylaxis. Rapid desensitization achieves temporary tolerization to full therapeutic doses by slow administration of incremental doses of the drug inducing the HSR. Protocols are available for most chemotherapy agents, including taxanes, platins, doxorubicin, monoclonal antibodies, and others. Candidate patients include those who present with type I HSRs, mast cell/IgE dependent, including anaphylaxis, and non-IgE mediated HSRs, during the chemotherapy infusion or shortly after. Idiosyncratic reactions, erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis are not amenable to rapid desensitization. The recommendation for rapid desensitization can only be made by allergy and immunology specialists and can only be performed in settings with one-to-one nurse-patient care and where resuscitation personnel and resources are readily available. Repeated desensitizations can be safely performed in outpatient settings with similar conditions, which allow cancer patients to remain in clinical studies. We have generated a universal 12-step protocol that was applied to 413 cases of intravenous and intraperitoneal rapid desensitizations using taxanes, platins, liposomal doxorubicin, doxorubicin, rituximab, and other chemotherapy drugs. Under this protocol all patients were able to complete their target dose, and 94% of the patients had limited or no reactions. No deaths or codes were reported, indicating that the procedure was safe and effective in delivering first line chemotherapy drugs.
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PMID:Hypersensitivity to antineoplastic agents. 1899 7