Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of type I disorders, particularly allergic asthma and urticaria, requires a critical review in the light of recent findings which indicate a second pathway for the release of granulocyte mediators. The isolation of enzyme activity of some of these released mediator establishes a direct link between the immunological system and bradykinin, as well as a system of self modulation of kinin activity. These findings open the door for a broader understanding of the asthmatic process and lay the foundation for integrating extrinsic and intrinsic asthma.
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PMID:A new look at type I immediate hypersensitivity immune reactions. 5 57

A profound defect in granulocyte chemotaxis was documented in an otherwise healthy 21-yr-old man who failed to localize granulocytes to an area of cellulitis during an allergic reaction to cephalothin. During the period of drug allergy, characterized by urticaria, eosinophilia, and profound hypocomplementemia, in vitro migration of the patient's granulocytes in the Boyden chamber was markedly impaired. Although devoid of hemolytic complement activity, the patient's serum possessed supranormal chemotactic activity, even following heat inactivation, suggesting the presence of chemotactically active complement split products. Chemotactic function improved concomitantly with steroid therapy and normalization of serum complement levels, and was entirely normal following clinical recovery and cessation of steroid therapy. The chemotactic abnormality noted in the patient's cells was reproduced in normal granulocytes by preincubation either with patient serum or with cobra venom-activated fresh (but not heated) normal serum, suggesting that in vivo exposure of granulocytes to activated complement was responsible for the patient's abnormal chemotactic response. This mechanism may contribute to the increased infection propensity noted in other conditions characterized by in vivo complement activation, such as rheumatoid arthritis and systemic lupus erythematosis.
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PMID:Acquired granulocyte abnormality during drug allergic reactions: possible role of complement activation. 83 Mar 75

Neutrophil granulocyte function was determined in three patients with systemic staphylococcal infection, clinical manifestations of generalized allergic disease, and hyperimmunoglobulinemia E. Each of the patients had urticarial skin rashes before or at the time of development of staphylococcal suppurative lymphadenitis, pneumonia, or sepsis. Neutrophil chemotaxis, random migration, phagocytosis, and bactericidal capacity were assessed to determine if an abnormality in these functions might have contributed to the development of severe staphylococcal infections. Each of the three patients with generalized urticaria was found to have a marked defect in neutrophil chemotaxis. The mean chemotactic index of the patients was 12 +/- 4, whereas that of 20 controls was 72 +/- 11. Neutrophil random migration, phagocytosis, and bactericidal capacity were normal in each patient. The serum or plasma of the patients did not inhibit chemotaxis of control neutrophils and did not contain an increased concentration of the chemotactic-factor inactivator found in normal serum. Treatment of the neutrophils of these three patients with the competitive histamine H2 receptor blocking agent, burimamide, produced a significant increase in chemotactic responsiveness. These studies suggest the possibility of pharmacologic modification of neutrophil granulocyte function.
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PMID:Severe staphylococcal disease associated with allergic manifestations, hyperimmunoglobulinemia E, and defective neutrophil chemotaxis. 97 42

Eosinophil diamine oxidase, histaminase, activity was assayed in acute inflammatory states and correlated to disease activity. Correlation to serum and urine histamine, metabolites of histamine and granulocyte histamine metabolizing enzymes was also studied. Using a radiochromatagraphic assay, diamine oxidase, histaminase, activity was determined in human peripheral blood eosinophils from patients with acute inflammatory states including active asthma, cold-induced urticaria and parasitic infestation; eosinophils from non-active asthmatic patients and normals were used as controls. Eosinophils were purified over a metrizamide discontinuous (16-30%) gradient. Total eosinophils were purified over a metrizamide discontinuous (16-30%) gradient. Total eosinophil histaminase activity was increased two- to three-fold in patients with active disease and returned to lower levels in eosinophils from patients without active disease or with treated disease. Thus, the induction of eosinophil histaminase might be a control mechanism for the inflammation induced by histamine during these acute inflammatory states.
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PMID:Eosinophil diamine oxidase activity in acute inflammation in humans. 680 65

The Authors report the results obtained with the histamine radioenzymatic test in the evaluation of the histamine content of granulocytes of 91 subjects, suffering from urticaria and urticaria-angioedema syndrome. The laboratory investigation was also integrated, according to the clinical implications, by other in vitro tests such as: kallikrein, RAST, PRIST, secretory IgA, precipitins assays. In urticaria-angioedema syndrome the quantitative and functional evaluation of C1-esterase inhibitor was also performed, to exclude the heredity of these pathologic forms. Basing on the results obtained, the authors expect that the granulocyte histamine radioenzymatic assay is highly reliable from the diagnostic viewpoint in the urticaria and angioedema forms.
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PMID:[Diagnostic use of a radioenzyme test in urticaria-like disorders and in urticaria-angioedematous syndromes]. 734 23

R24, a murine monoclonal antibody, has been shown to mediate complement- and antibody-dependent cellular cytotoxicity (ADCC) of melanoma tumor targets. We conducted a Phase Ib clinical trial using granulocyte-macrophage colony-stimulating factor (GM-CSF) and R24 in 20 patients with metastatic melanoma. The purpose of this study was to test the hypothesis that treatment with GM-CSF could up-regulate monocyte and granulocyte ADCC and that the combination of GM-CSF plus R24, which mediates ADCC, would lead to enhanced anti-tumor activity in patients with melanoma. GM-CSF was administered by subcutaneous injection daily for 21 days at a dose of 150 micrograms/m2/day. R24 was administered by continuous intravenous infusion on days 8-15 at three dose levels: 0, 10, and 50 mg/m2/day. All 20 patients received one cycle of treatment only. Immune parameters measured were monocyte and granulocyte direct cytotoxicity and ADCC. All patients were evaluable for toxicity. Fifteen patients were evaluable for immune response. Treatment with GM-CSF alone was well tolerated. Toxicity from the combination of GM-CSF plus R24 included diffuse urticaria, nausea and vomiting, hypertension, and hypotension. Hypotension was the dose-limiting toxicity. Two patients on the 50-mg/m2/day dose level of R24 achieved a partial response lasting 2+ and 5+ months. Treatment with GM-CSF led to a statistically significant enhancement of monocyte and granulocyte direct cytotoxicity and ADCC. The maximally tolerated dose of R24 given at this schedule combined with GM-CSF is < 50 mg/m2/day. We conclude that GM-CSF given by subcutaneous injection at 150 micrograms/m2 x 21 days can enhance effector cell ADCC and direct cytotoxicity and that the combination of GM-CSF and R24 can be therapeutic.
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PMID:Phase Ib trial of granulocyte-macrophage colony-stimulating factor combined with murine monoclonal antibody R24 in patients with metastatic melanoma. 780 28

Although copper sulfate can cause systemic contact dermatitis, few such cases have been recorded among copper-releasing IUD users. Reported in this paper is a case of endometritis and urticaria-angioedema syndrome in a 32-year-old user of a copper IUD. Widespread urticaria, as well as angioedema of the eyelids and the labia majora and minora, persisted for about 6 months and were not responsive to corticosteroids and H1-antagonists. Copper sulfate positivity was demonstrated in 72-hour patch test, 48-hour application of the copper spiral to forearm, and in vitro lymphocyte-stimulating test. Histologic examination of the endometrial biopsy revealed vulvovaginitis with hyperplasia of the cervical canal and T-cell and eosinophilic granulocyte infiltration. Removal of the IUD caused complete symptom remission. In experimental animals with a radioactively labeled copper IUD, small amounts of copper sulfate are absorbed through the mucus membrane and carried to the cutis through the blood or lymph. In the cutis, the allergen is intercepted from antigen-presenting cells and recognized by T cells that migrate to the lymph nodes with blastic transformation, proliferation of cytotoxic lymphocytes, and cytokine production.
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PMID:Systemic contact dermatitis to copper-containing IUD. 889 20

Epoxy resin compounds (ERC) include a large number of chemicals, such as epoxy resins (ER), reactive diluents and hardeners. Many hardeners, e.g., aliphatic polyamines, are well-known sensitizers. Another type of ER hardeners are the phthalic anhydrides, such as methylhexahydrophthalic anhydride (MHHPA) and methyltetrahydrophthalic anhydride (MTHPA), which have been reported as causing immunologically-mediated respiratory diseases and contact urticaria, but not allergic contact dermatitis. Here, we present a horizontal boring-machine worker who developed allergic contact dermatitis, as well as allergic rhinitis and an immediate contact skin reaction from MHHPA. Patch testing with a dilution series of MHHPA in pet. elicited the following results: 2%, 1% and 0.5%, +2; 0.25% and 0.125%, + (3- to 6-day readings). An immunohistochemical and electron microscopic study also indicated that the patch test reactions were conventional-delayed allergic reactions. Interleukin 8 was observed in the epidermal cells, whereas interleukin 4 immunoreactivity was detected in the dermal cells. Immunoreactivity to-interleukin 5, granulocyte/macrophage-colophony stimulating factor (GM-CSF) or eosinophil cationic protein was not seen. In conclusion, the patient developed both Type I and Type IV allergy to MHHPA. The clinical data, patch test results, immunohistochemical and electron microscopic observations indicated that the MHHPA allergy detected by the patch test reaction was a conventional delayed-type hypersensitivity reaction. The patient also had an allergic patch test reaction to para-phenylenediamine and diaminodiphenylmethane, possibly representing occupational sensitization.
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PMID:Delayed and immediate allergy caused by methylhexahydrophthalic anhydride. 903 85

Dimethyl sulfoxide (DMSO), depending upon the concentration and mode of application to the skin, can induce either a non-immunological immediate contact urticaria or an irritant reaction. The dermal cellular infiltrate after open application of varying concentrations of DMSO has been studied in an experimental guinea pig model. The composition of the dermal cellular infiltrate showed a spectrum dependent on the concentration and number of applications of DMSO. The immediate reaction infiltrate 3 h after application of 100% DMSO consisted of 50% granulocytes, basophils being predominant. On the other hand, 12% DMSO applied 3 x daily for 3 days (cumulative insult) caused histologically a cellular reaction in which 80% of the infiltrate consisted of mononuclear cells. The present findings are compared to the microscopic findings in 3 other cutaneous reactions previously studied in this animal model, namely, the Type I immediate hypersensitivity reaction, the Type IV delayed hypersensitivity reaction, and the irritant reaction. Differing cellular infiltrate patterns are discernible at the same time points. The study illustrates the spectrum of inflammatory reactions seen in the skin and provides background information for future clinical studies, for instance, on the role of the basophil granulocyte in immediate contact reactions.
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PMID:The spectrum of inflammatory cell response to dimethyl sulfoxide. 1075 Aug 53