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Query: UMLS:C0042109 (urticaria)
6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic urticaria remains one of the major unsolved clinical problems in dermatology. My group has employed an integrated experimental approach in order to shed light on the pathophysiology and treatment of this group of disorders. Using delayed pressure urticaria as a model, evidence has emerged of the role of eosinophil major basic protein (MBP) and of interleukin-6 (IL-6) as important molecular mediators, possibly explaining the poor response to H1 antihistamines. Our recent work in chronic idiopathic urticaria has led to identification of a circulating greater than 100 kD factor which causes wealing following intradermal injection and which releases histamine from normal leukocytes in vitro. Further characterisation confirmed that this skin and histamine releasing reactivity is due mainly to an IgG anti-IgE autoantibody. That this autoantibody is functionally significant is supported not only by its ability to release histamine and cause local wealing, but also by the results of removal by plasmapheresis which we have shown to cause clinical improvement in seven out of eight patients with severe unremitting chronic urticaria. It is concluded that chronic 'idiopathic' urticaria is an autoimmune disease due, in most patients, to a functionally significant IgG anti-IgE autoantibody. Immunotherapy offers the best long-term prospects of relief in severe unremitting cases.
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PMID:Urticaria: new molecular insights and treatments. The Parkes Weber Lecture 1991. 137 92

Multiple sequential biopsy specimens of wheals elicited by a solar simulator in four patients with severe solar urticaria were studied with the use of indirect immunofluorescence for eosinophil granule major basic protein. Examination of control biopsy specimens from normal, unstimulated skin did not show eosinophils or major basic protein deposition. Five minutes after solar simulation, eosinophils were observed in vessels in the dermis, and 2 hours later there was marked tissue eosinophilia. Extracellular major basic protein was extensively deposited in the dermis at 2 and 24 hours, suggesting eosinophil degranulation. Thus evolution of the solar urticaria wheal is accompanied by infiltration of eosinophils and neutrophils and by tissue deposition of the eosinophil major basic protein, suggesting eosinophil degranulation.
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PMID:Evidence for eosinophil degranulation with deposition of granule major basic protein in solar urticaria. 208 77

Utilizing affinity chromatography-purified antibody to the eosinophil granule major basic protein and formalin-fixed paraffin embedded tissue, we investigated the localization of major basic protein by immunofluorescence in twenty-four skin biopsy specimens from ten patients with pressure urticaria. Fourteen of twenty-four biopsy specimens were obtained from spontaneously occurring urticarial lesions of 4 to 48 hours' duration, and ten of the twenty-four specimens were from dermographometer-induced lesions that had been present from 40 minutes to 24 hours. Twenty-one of twenty-four biopsy specimens showed extracellular fluorescence of eosinophil granule major basic protein within the dermis. The extent and intensity of extracellular staining were not related to the presence or degree of tissue eosinophilia. Serial section controls from each block were stained with protein A purified rabbit IgG and were negative. Previous immunofluorescence studies have demonstrated deposition of major basic protein in lesions of chronic idiopathic urticaria, episodic angioedema, and facial edema. Major basic protein causes release of histamine from human basophils and induces wheal-and-flare reactions on intradermal injection. The present observations add further evidence to support a role for eosinophil mediators, particularly major basic protein, in the pathogenesis of cutaneous disease characterized by edema.
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PMID:Extracellular deposition of eosinophil granule major basic protein in pressure urticaria. 354 18

This study presents the clinical and laboratory findings of a novel syndrome associated with eosinophilia. Two young women presented with marked eosinophilia, and large, non-tender compressible articular nodules arising from the tenosynovium of extensor tendons, dermatitis, episodic swelling of the hands and/or feet and pain in adjacent muscles and joints. Tissue specimens were examined by routine haematoxylin and eosin staining, immunofluorescent staining for eosinophil granule major basic protein (MBP) and rhodamine-avidin or tryptase staining for mast cells. Plasma levels of MBP and eosinophil-derived neurotoxin (EDN) were quantitated by immunoassay. The first patient presented in 1967 at the age of 20 and had, in addition to nodules and eosinophilia, dermographism, recurrent episcleritis and axillary urticaria. Biopsy of a nodule showed tenosynovitis with necrotizing granulomas, non-specific vasculitis, eosinophils and eosinophil degranulation as shown by extracellular deposition of eosinophil granule MBP. Her symptoms responded to low-dose, alternate-day prednisone and have remained quiescent over the past 15 yr. The second patient presented in 1990 at the age of 28 with generalized pruritic dermatitis for 15 yr, eosinophilia for 2 yr, subcutaneous nodules and non-limiting pain in several joints. Biopsy of a nodule showed chronic mild tenosynovitis, numerous eosinophils and extracellular deposition of MBP. She remains untreated. Serum IgE values and plasma levels of MBP and EDN were elevated in both patients; mast cells were numerous in their synovial tissue. Based on their clinical courses, these patients reveal the existence of a distinctive, relatively benign eosinophilic disorder with good long-term prognosis.
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PMID:Nodules, eosinophilia, rheumatism, dermatitis and swelling (NERDS): a novel eosinophilic disorder. 822 Dec 54

Urticarial dermographism and delayed pressure urticaria are two forms of physical urticaria which are well defined clinically and histologically. Previous studies have shown eosinophil granule protein deposition in urticarial reactions, including chronic urticaria, solar urticaria and delayed pressure urticaria. To evaluate and compare the involvement of granulated inflammatory cells in urticarial dermographism and delayed pressure urticaria, we studied sequential biopsies of induced lesions of urticarial dermographism and delayed pressure urticaria by indirect immunofluorescence, to detect eosinophil granule major basic protein (MBP) and neutrophil granule elastase. Biopsies from dermographic lesions at time 0, 5 min, 15 min, 2 h and 24 h, showed few infiltrating eosinophils, with minimal extracellular MBP deposition, and a few infiltrating neutrophils, with minimal neutrophil elastase deposition, throughout the evolution of the lesions. Sequential biopsies of delayed pressure urticaria at time 0, 20 min, 6, 12 and 24 h, showed eosinophil infiltration with extensive MBP deposition beginning at 20 min, and neutrophil infiltration with variable elastase deposition beginning at 20 min. Control tissue specimens from normal volunteers showed neutrophil infiltration and slight degranulation, but no eosinophil infiltration or degranulation. Comparison of urticarial dermographism with delayed pressure urticaria showed marked differences in the patterns of infiltration. Delayed pressure urticaria, with eosinophil and neutrophil degranulation, was strikingly similar to the IgE-mediated late phase reaction. In contrast, eosinophil and neutrophil involvement in urticarial dermographism was minimal. Considering the extent of eosinophil granule protein deposition and the biological activities of the eosinophil granule proteins, the findings in delayed pressure urticaria point to an important pathophysiological role of eosinophils in the disease.
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PMID:Immunohistological comparison of granulated cell proteins in induced immediate urticarial dermographism and delayed pressure urticaria lesions. 854 35