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)

IgE antibodies are usually thought to induce only immediate skin reactions. We have shown that the intradermal injection of a number of different allergens can produce a prolonged inflammatory reaction after the immediate wheal and flare in most sensitive subjects. This late inflammatory response occurs 6-12 h after challenge and is characterized by diffuse edema, erythema, pruritus, and heat. Both immediate and late responses can also be seen after passive sensitization of skin sites in nonatopic subjects. That IgE is involved in inducing the reaction was shown by the abolition of both immediate and late responses by passive transfer tests in the following experiments: (a) heating atopic serum at 56degreesC for 4 h, (b) removing IgE from the atopic serum by a solid phase anti-IgE immunoabsorbent, and (c) competitively inhibiting the binding of IgE antibodies to cells by an IgE myeloma protein. In addition, both responses were induced by affinity chromatography-purified IgE antibody, followed by antigenic challenge. Very similar lesions could also be induced by intradermal injection of Compound 48/80, thus suggesting a central role in the reaction for the mast cell or basophil. Histologically, the late phase is characterized by edema and a mixed cellular infiltration, predominantly lymphocytic but also containing eosinophils, neutrophils and basophils. Direct immunofluorescent staining did not show deposition of immunoglobulins or complement components, except IgM in 2 of 15 and C3 in 1 of 15 patients. This finding indicates that the late phase does not depend on the deposition of immune complexes. The results of the study suggest that IgE-allergen interaction on the surfaces of mast cells or on infiltrating basophils causes both immediate and late cutaneous responses.
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PMID:The late phase of the immediate wheal and flare skin reaction. Its dependence upon IgE antibodies. 78 99

Sixteen patients with allergic rhinitis were recruited into a double-blind crossover protocol studying the immediate effect of nedocromil sodium (NS) on the pattern of nasal symptoms and secretions after allergen challenge. After pretreatment with placebo or NS, allergen challenge resulted in pruritus, rhinorrhea, nasal congestion, and/or sneezing within 10 minutes in 12 of 16 subjects. Prostaglandin D2 (PGD2), a marker of mast cell degranulation, increased proportionately with symptom scores, remaining above the 95% confidence interval for 120 minutes after both pretreatments. No difference in PGD2 between the NS-treatment and placebo-treatment days was observed. Protein markers extravasated through the vasculature (albumin and IgG) or secreted by mucosal glands (lactoferrin) were assayed. Total protein, albumin, IgG, and lactoferrin all remained greater than 95% confidence interval for 100 minutes after allergen challenge in the placebo-pretreated group and 120 minutes in the NS-pretreated group. Although there appeared to be a trend for lower secretion of PGD2, albumin, and IgG in the NS-treated group, the overall differences did not achieve statistical significance. This protocol revealed that two topical 130 microliter doses of a 1% solution of NS failed to significantly reduce allergen-induced symptoms, PGD2 generation, or secretion of albumin, IgG, or lactoferrin when NS was compared with placebo. The anti-inflammatory and mast cell-stabilizing effects of NS may require more prolonged pretreatment before provocation to be effective.
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PMID:Effects of nedocromil sodium on allergen-induced rhinitis in humans. 131 Oct 8

A double-masked, randomised, placebo-controlled study was conducted to evaluate the effectiveness of nedocromil 2% eyedrops, a mast cell stabilizer, in 20 symptomatic patients with vernal conjunctivitis. A 1-week baseline period was followed by 6 weeks of treatment. Clinical examination and cytological evaluation of tear fluid were performed weekly, and the patients recorded their subjective assessment on a daily diary card. The nedocromil group showed significantly less hyperaemia in the course of treatment than did the placebo group, and significantly less itching at all visits compared with baseline itching. In the nedocromil-treated group, but not in the placebo group, the number of neutrophils, eosinophils and lymphocytes in tears decreased significantly during some treatment weeks when compared with baseline. The overall assessment of treatment efficacy by both clinician and patient was significantly in favour of nedocromil treatment over placebo.
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PMID:Effectiveness of nedocromil sodium 2% eyedrops on clinical symptoms and tear fluid cytology of patients with vernal conjunctivitis. 133 45

Exercise is a physical cause of allergic reactions, including exercise-induced anaphylaxis (EIAna), exercise-induced urticaria (EIU), exercise-induced asthma (EIA), and exercise-induced rhinitis (EIR). Since its first description in 1979, EIAna has been reported with variable clinical manifestations, with exercise alone, and in combination with food ingestion. Elevated serum histamine levels and cutaneous mast cell degranulation have been noted. Exercise-induced urticaria appears as small, punctate lesions that differ from the classic coalescent type seen with EIAna. Variant forms of EIAna with cholinergic urticarial lesions manifesting systemic collapse and/or respiratory distress have been studied. Exercise-induced urticaria and cold-induced urticaria may cause elevated plasma histamine levels coincident with the onset of pruritus and hives. Theories accounting for EIA include respiratory heat loss, water loss, and mast cell activation. Although some studies have shown increased plasma histamine with EIA, others have not. Recently, bronchoalveolar lavage in atopic subjects with EIA has been evaluated preexercise and postexercise, with no significant differences in histamine or tryptase, suggesting a pathogenesis of EIA independent of the mast cell. Exercise-induced rhinitis, with varying degrees of rhinorrhea, congestion, and sneezing, has been increasingly recognized in athletes who run, cycle, and ski. Cold-air-induced rhinorrhea in laboratory challenges displays a mediator release pattern similar to that produced by allergen-induced nasal challenges. Therapeutically, H1 antihistamines are recommended for EIAna both as pretreatment and acute therapy. H1 antihistamines may be helpful in EIU, but are recommended for EIAna both as pretreatment and acute therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exercise-induced allergies: the role of histamine release. 137 Oct 41

This review of SSc has addressed the clinical features, pathophysiology involving the mast cell, T cell cytokines, and their interaction with other inflammatory cells (Figs 4 and 5). Therapeutic dilemmas and the future use of immunomodulatory therapy is also discussed. The allergist-immunologist may be the first physician to identify this insidious condition, since patients may present with cutaneous changes, swelling, pruritus, dyspnea, and with obstructive and restrictive findings on pulmonary function testing, or gastrointestinal symptoms, mimicking gastrointestinal hypersensitivity.
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PMID:Systemic sclerosis. The role of the mast cell and cytokines. 145 80

The mast cell, equipped with enzymes, chemotactic factors, a vasoactive amine, an anticoagulant, and lipid-derived proinflammatory products, may be essential in tissue modeling as well as in defense. Its primarily perivascular location in skin and the mucosa of the respiratory tract and the gut assures its availability to counter parasites. By the same token, the mast cell is responsible for interactions with inhaled, ingested, and injected antigens that comprise IgE-mediated allergic reactions. Abnormally high numbers of mast cells in the skin, either localized or generalized, result in urticaria pigmentosa or generalized cutaneous mastocytosis, respectively. Tissue infiltration by excessive mast cells, primarily in gut, bone, liver, and spleen, results in systemic mastocytosis; this may be accompanied by myelodysplasia or lymphoma and may eventuate in mast cell leukemia. Until the etiology of mastocytosis is understood, the treatment is symptomatic: histamine antagonism by H1 +/- H2 blockade for flushing, itching, and gastric distress; cyclooxygenase inhibition to prevent prostaglandin D2 (PGD2)-induced hypotension when indicated; and oral cromolyn to prevent gastrointestinal symptoms and bone pain.
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PMID:Mast cell disease. 149 Jun 22

The number of mast cells in the skin was evaluated in 25 patients with end-stage renal failure on different treatment modality (conservative, hemodialysis and peritoneal dialysis). According to the presence of pruritus, uremic patients were divided into two groups: group A, 13 patients with diffuse pruritus, and group B, 12 patients without pruritus. Controls were 6 age- and sex-matched healthy subjects. In comparison with patients without pruritus, patients with pruritus had mainly degranulated, diffusely spread and more numerous mast cells in the skin; significantly higher levels of plasma middle molecular weight substances, serum histamine and PTH and significantly lower serum iron levels. However, no differences were noted in observed parameters between groups on different treatment modalities. Favorable therapeutic effects in patients with pruritus were achieved either with iron supplementation in those with hypoferremia or with antihistamines, mast cell membrane stabilizers and high-permeability membranes.
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PMID:Uremic pruritus and skin mast cells. 152 40

Physical exercise is a stimulus capable of provoking urticaria and anaphylaxis in certain individuals. The cutaneous manifestations of EIA include erythema, pruritus, and urticarial whealing. Symptoms may also progress to angioedema, laryngeal edema, bronchospasm, and hypotension. Attacks are consistently associated with increases in serum histamine levels, and atopic individuals are more commonly affected. At least two distinct diseases cause EIA, including CU and classic EIA. A variant form of EIA may also exist. CU episodes are induced by increases in body temperature occurring secondary to physical exercise or passive body warming. Classic EIA episodes are induced only by exercise. Further differences between these two disorders include the size of skin lesions and the high frequency of progression to upper airway distress and shock in classic EIA. The manifestations of EIA occur as a result of mast cell degranulation that releases histamine and other mediators into the circulation. An exaggerated cholinergic response to body warming seems to provoke mast cell degranulation in individuals with CU. In classic EIA, exercise acts as a physical stimulus, which through an unknown mechanism provokes mast cell degranulation. The treatment of acute episodes of EIA includes administration of epinephrine and antihistamines, airway maintenance, and cardiovascular support. Prophylactic treatment includes exercise avoidance, abstention from coprecipitating foods and medications, pretreatment with antihistamines and cromolyn, and the induction of tolerance through regular exercise.
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PMID:Exercise-induced anaphylaxis and urticaria. 159 87

Mast cells may be more abundant in the tissues of uremic patients and may contribute to itching via mediator release. Because mast cell (MC) granule release may be inhibited by ultraviolet B (UVB) radiation, we investigated skin MC in the superficial dermis by quantitative histomorphometry before and after whole body UVB for uremic itching. Toluidine blue-stained 3.5 mm punch biopsy specimens were examined with a micrometer grid after separate coding. Upon entry to the study, itching dialysis patients indicated their itching intensity on a visual analog scale (0 to 10). Concurrent study of living, related kidney donors (controls, n = 11) and their recipients (n = 11) showed no differences in MC number per unit area. Compared to controls, skin MC number was not greater in itching dialysis patients (n = 20). MC number decreased after 2 months of UVB from 1.6 +/- 0.6 (standard deviation) to 1.0 +/- 0.7 (n = 11, p = 0.025). Pre-UVB total plasma calcium correlated directly with itching intensity, but not with MC number. Plasma phosphate and intact parathyrin level were not statistically related to itching or MC number. Of the 14 subjects that completed UVB, 8 had objective benefit, and mean itching intensity declined from 7.1/10 to 5.2/10 in the 14 subjects. The conclusion is that although skin MC number may decline with chronic UVB, MC number is not related to uremic itching, and hypercalcemia, but not elevation of parathyrin or plasma phosphate, relates statistically to severe uremic itching.
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PMID:Mast cells and calcium in severe uremic itching. 160 64

The focus of this study on coital allergy is on discussing the basis for and clinical implications of the immunological reactions that mediate allergic reactions to semen. Allergic reactions to antigens in seminal plasma occur in the case of acute systemic hypersensitivity (ACH), localized postcoital allergic seminal vulvovaginitis, and/or hypersensitivity to exogenous allergens in semen. In the few cases (30 cases at present), ACH may manifest itself in generalized urticaria, orbital and vulval edema, vulval and generalized pruritus, bronchospasm, lower abdominal pain, hypotension, and loss of consciousness. There may be a family history of atopy. Symptoms may appear over months or years before reaching a severe level. The usual case is the appearance after the 1st coital act or after a change in coital, genital, or reproductive occasions. It is not specific to a particular male partner. It may be self-limiting. Condom usage or abstinence may lead to abatement. Localized vulvovaginitis may occur simultaneously with ACH or exist alone. The symptoms are local pruritus, burning, swelling, erythema, and urticaria in varying degrees for up to a week and occur during or after coitus. Douching or vulval irrigations may ameliorate symptoms. Misdiagnosis as genital herpes or infective vulvovaginitis may occur in mild cases. Exogenous allergens derived from drugs, food, and other sources presenting in the semen may contribute to hypersensitivity. This is different from reactions to intrinsic components of seminal plasma. Vaginal exposure to chemical products such as soaps or to airborne particles such as pollen may produce allergic responses. Another possibility is that genital candidiasis may produce local Ige antibodies, and PGE2 induced suppression of cell-mediated immunity. The immunological mechanisms are described as type I hypersensitivity reactions with the antigen reacting with reaginic antibodies of the Ige class which are bound to mast cell or circulating basophils. The antigens and the immune reactions are specified. In the clinical diagnosis, the rare acute systemic form is obvious, but the atypical, recurrent, and intractable forms of vulvovaginitis require investigation with skin tests. Treatment may involve artificial insemination for those seeking pregnancy, immunotherapy, or antihistamines, rather than use of a condom or abstinence.
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PMID:Allergy to coitus. 168


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