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)

Anti-lymphocyte monoclonal antibodies have shown promise in trials for therapy of lymphocyte malignancies but are associated with a high frequency of immediate-type anaphylactoid reactions. We have previously demonstrated that these immediate-type anaphylactoid reactions are not mediated by immunoglobulin E to anti-lymphocyte monoclonal antibodies. To gain insight into the mechanisms of these immediate-type anaphylactoid reactions, we measured plasma levels of histamine and anaphylatoxins (C3a, C4a, C5a) during 11 infusions in eight patients who received anti-lymphocyte monoclonal antibodies (T101 and Lym-1). Three patients experienced generalized urticaria (two with severe angioedema); a fourth patient had three isolated hives but without generalized manifestations of an immediate-type anaphylactoid reaction. Plasma histamine levels after infusions that were associated with generalized urticaria were significantly higher than those during infusions that were not associated with generalized urticaria (mean, 3.47 vs 0.18 ng/ml, p less than 0.001). Increases in C3a and C4a levels were observed after some infusions, but these did not correlate with generalized urticaria. Measurable rises in plasma C5a levels after infusions were not detected. Although these data should be viewed as preliminary considering the limited number of patients studied, the observed histamine release demonstrates that mast cell or basophil activation that is not mediated by immunoglobulin E to anti-lymphocyte monoclonal antibodies occurs in the pathogenesis of immediate-type anaphylactoid reactions from anti-lymphocyte monoclonal antibodies. Although activation of the classical complement pathway may occur in some anti-lymphocyte monoclonal antibody infusions, this does not appear to explain immediate-type anaphylactoid reactions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma histamine but not anaphylatoxin levels correlate with generalized urticaria from infusions of anti-lymphocyte monoclonal antibodies. 150 Aug 27

Thirty two cases of the association of mastocytosis and bone lesions were collected in a multicentre study. Five cases involved osteocondensation forms. However, most often (27 cases), there was osteoporosis (OP). The diagnosis was made in the absence of obvious risk factors, and thus often in men (2/3 of patients), when there was the association of pigmented urticaria and an excess of mast cells in bone biopsies. Laboratory, radiological and isotope scan findings are often non-specific, being identical to those encountered in common OP. The histomorphometric profile involves an association of decreased cancellous bone volume, increased area of resorption and decreased bone formation parameters. Progression to malignant mastocytosis occurs essentially in diffuse osteocondensation forms and is rare in OP types. Emphasis must be placed on the importance of qualitative study of bone marrow, using specific stains, since the diagnosis may be missed in the absence of typical skin lesions. Conversely, since a simple increase in mast cell count is possible during common OP, a search for mast cell nodules is important in order to establish the diagnosis with certitude.
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PMID:[Mastocytosis and bone manifestations. Results of the survey of the bone and phosphorus-calcium metabolism section of the French Society of Rheumatology]. 157 47

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

Urticaria and angioedema are usually the clinical consequence of vasoactive mediators derived from mast cells in the skin or mucosal tissues. Efforts to classify mast cell-mediated causes of urticaria and angioedema have generally been frustrated by their diverse pathogenesis and clinical course. The term acute is typically used to describe fleeting lesions whose recurrence does not extend beyond 6 weeks. Chronic is the term used to describe lesions that persist for more than a few hours but usually less than a day, and recurrences extend for more than 6 weeks. These definitions do not take histology into account. Skin biopsies of fleeting lesions demonstrate a paucity of inflammatory cells, whereas more persistent lesions display a spectrum of perivascular cuffing by predominantly T cells and monocytes. The presence of leukocytoclastic vasculitis in persistent lesions indicates an underlying immune complex disease. Many of the physical urticarias have fleeting lesions that can be induced with the appropriate stimulus for years. This review article has emphasized the clinical course and histology of urticaria and angioedema lesions in an effort to provide a more complete understanding of the pathogenesis and appropriate treatment. Clearly, avoidance of an identifiable inciting stimulus is optimum management, although most patients have no etiology defined or the cause is not realistically avoidable. At present, treatment options for these patients rely on antihistamines to control the immediate consequence of mast cell degranulation. Corticosteroids are reserved for the treatment of patients whose urticaria or angioedema lesions persist, reflecting the increasing involvement of mononuclear cells in the disease process. For leukocytoclastic vasculitis, corticosteroids are indicated, and cytotoxic drugs may be required for adequate treatment. Future treatments of urticaria and angioedema will evolve based on elucidation of the relevant cells and soluble mediators and will include counterregulatory or antagonistic peptides and drugs. C1 esterase inhibitor deficiency is a relatively uncommon cause of angioedema but is important to understand because of its ability to clinically mimic mast cell-mediated angioedemas and its unique pathogenesis and treatment. HAE can be divided into two serologic subtypes that simply reflect the location of the defect in one of the codominantly expressed C1-INH genes on chromosome 11. AAE can be divided into two serologic subtypes. AAE type I is due to massive consumption of C1-INH, presumably by tumor-related immune complexes. AAE type II is due to an anti-C1-INH autoantibody.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Urticaria and angioedema. 161 35

Treatment of chronic urticaria presents a challenge to both practitioner and patient. Traditional H1 antagonists with good efficacy but substantial side effects are being supplanted in many cases by nonsedating H1 antagonists such as terfenadine and astemizole. Antidepressant medications and combinations of H1 and H2 antagonists offer improved results for selected patients. Further development and investigation of mast cell stabilizers and inhibitors of urticaria mediators other than histamine hold promise. A better understanding of the underlying pathogenesis remains the greatest hope of formulating rational and effective therapy.
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PMID:Pharmacologic therapy for urticaria. 167 97

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

Histamine release from dispersed skin mast cells may be used for functional studies on the mast cell. However, technical difficulties have hampered such studies. In the present study a new fiberglass-based histamine assay was applied to previously described dispersion techniques, using excision biopsies from 7 patients with urticaria pigmentosa, 3 with psoriasis as well as 4 with urticaria. However, sufficient mast cell numbers for performing histamine release could only be obtained from patients with urticaria pigmentosa. The average mast cell yield was 935 +/- 470 cells (mean +/- SD) per mg wet weight of tissue. The skin mast cells from these patients responded with dose-dependent histamine release to anti-IgE, calcium ionophore A23187, and N-formyl-methionyl-leucyl-phenylalanine challenge without previous passive sensitization. The pattern of histamine release of mast cells and corresponding blood basophils did not indicate substantial differences between the two cell types.
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PMID:Histamine release from skin mast cells and basophils in patients with urticaria pigmentosa. 169 Apr 93

Using a combination of avidin-biotin microELISA and solid phase radioimmunoassay, we examined sera from 23 patients with systemic lupus erythematosus (SLE), two patients with established sensitivity to ingested shrimp, and 15 healthy normal subjects. In addition to IgG antibodies, varying amounts of IgE antibodies specific for native DNA (nDNA), denatured or single-stranded DNA (dnDNA), RNA, and tRNA were demonstrable in the sera of SLE patients, but not in the sera of normal subjects. A comparison of the specificity of nucleic acid-specific IgE antibodies present in the sera of shrimp-sensitive patients with those present in the sera of seven SLE patients revealed that the IgE antibodies in the sera of shrimp-sensitive patients specifically recognized shrimp tRNA but not yeast tRNA, calf thymus RNA, or calf thymus DNA, while those present in the sera of patients with SLE recognized all these nucleic acid antigens. The IgE antibodies directed against nDNA, dnDNA, RNA, and tRNA may mediate mast cell and basophil degranulation and thus contribute both to immediate-type hypersensitivity phenomena including hives seen in patients with SLE and to the localization of IgE-nucleic acid complexes in target tissues.
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PMID:Demonstration of IgE antibodies to nucleic acid antigens in patients with SLE. 171 9

Localized heat urticaria is a rare disorder, in which the nature of the mediator is not fully established. We report the case of a 41-year-old woman with the condition, dependent upon mast cell integrity, in which histamine was demonstrated as the dominant, if not sole mediator. Non-sedative antihistamines conferred some therapeutic benefit, but subsequent sequential desensitization has enabled her to lead a full and active life again.
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PMID:Clinical report and investigation of a patient with localized heat urticaria. 172 60

Circulating histamine-releasing factors have been identified in the serum and plasma of chronic-urticaria patients by in vivo skin testing and in vitro histamine release from heterologous mixed leukocytes. Quantitative mast cell studies of serum skin test biopsies and electron microscopy indicate that the serum factors release histamine by mast cell degranulation. Peripheral blood basophils and total cellular blood histamine are reduced in chronic-urticaria patients suggesting that the circulating serum factors cause sustained degranulation. Histamine-releasing activity has been identified by skin testing in ultrafiltered serum fractions less than 30 kDa and greater than 100 kDa. In vitro histamine-releasing activity was confined to ultrafiltered serum fractions greater than 100 kDa and was present in IgG purified from some chronic-urticaria sera by protein G affinity chromatography. The dose-response relationship and kinetics of histamine release in vitro were similar to those of anti-human IgE. 'Desensitisation' of basophils by prior incubation with anti-IgE in the absence of calcium and competitive inhibition studies with myeloma IgE serum indicated that histamine-releasing autoantibodies in chronic-urticaria sera and purified IgG have the properties of anti-IgE. Plasma exchange in 4 patients with active chronic urticaria refractory to antihistamine therapy showing in vivo and in vitro histamine-releasing activity was followed by temporary remission of disease activity in 2 of them. It is possible that chronic urticaria is an autoimmune disease.
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PMID:Histamine-releasing autoantibodies in chronic urticaria. 172 16


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