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

Report on a female patient suffering from cold urticaria and cold purpura in cryoglobulinemia. The process of diagnosis and further clinical investigation (bithermotest) are described.
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PMID:[Cold urticaria and purpura in cryoglobulinemia]. 329 8

During the last few years, the structure and function of human C1-inhibitor have been elucidated. Chromogenic substrate assays for determination of C1-inhibitor activity in plasma are available, and have proved to be of value not only for the diagnosis of hereditary angioedema but also in acquired diseases involving C1-inhibitor, such as cold urticaria and autoimmune disorders as well as acute-phase types of disease states.
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PMID:Aspects of C1-inhibitor biochemistry and pathophysiology. 332 41

Four patients with aquagenic pruritus (AP), one patient with polycythemia rubra vera, one patient with cold urticaria, and three normal control volunteers were studied to better understand the pathophysiology of water-induced itching. Punch biopsy specimens were taken before and after water contact; the specimens were immediately frozen, sectioned, and stained histochemically for acetylcholinesterase (AChE) activity. This was localized in the nerve fibers surrounding eccrine sweat glands and was quantified by microspectrophotometry. In AP and polycythemia rubra vera after water exposure a significantly increased AChE activity suggesting acetylcholine release was observed, whereas in the patient with cold urticaria and the controls, a significant decrease was noted. Two related patients with AP had an inherited abnormality of serum cholinesterase, which, however, had no obvious correlation with their particular disease. The proof of AChE activation might support the clinical diagnosis and indicate a hypothetical involvement of eccrine sweat glands in the pathogenesis of AP.
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PMID:Aquagenic pruritus. Water-induced activation of acetylcholinesterase. 333 47

Thirteen patients with both cold and cholinergic urticaria are reported. There was considerable variability, particularly in the cold urticaria which was of the common cold contact type in seven patients, of the generalized cold induced cholinergic type in two and in four patients the lesions induced by direct contact with ice were morphologically like cholinergic urticaria, but appeared despite prior application of an acetyl choline antagonist. The natural history, laboratory findings and the effects of therapy are discussed.
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PMID:Combined cold urticaria and cholinergic urticaria--clinical characterization and laboratory findings. 339 61

The mechanism(s) by which repeated cold challenge in a patient with idiopathic acquired cold urticaria resulted in the induction of clinical tolerance to cold stimuli was studied. Plasma histamine levels, mast cell ultrastructure, and the cutaneous response to intradermal injections of morphine, histamine, and substance P were examined before and after the induction of tolerance. Plasma histamine levels draining cold-challenged, clinically tolerant skin were markedly diminished compared to histamine levels obtained during cold-induced angioedema. Furthermore, electronmicroscopy of skin samples taken from tolerant skin after cold challenge revealed intact, largely normal appearing mast cells. Intradermal injection of mast cell secretagogues and vasoactive agonists into normal and tolerant skin sites resulted in similar whealing responses. Thus, these studies suggest that the state of clinical tolerance to cold stimuli is due neither to mast cell-mediator depletion or tachyphylaxis of the cutaneous vasculature to vasoactive agonists. It appears likely that tolerance may be due to the induction of a specific state of unresponsiveness of mast cells to cold stimuli or possibly to depletion of a cold-induced cutaneous antigen capable of triggering mast cell degranulation.
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PMID:A case study on the induction of clinical tolerance in cold urticaria. 340 65

We identified two siblings with exercise-induced anaphylaxis who share the HLA haplotype A3-B8-DR3 with their atopic father. The index case, a 16-year-old female, noted initial episodes at age 13. Intense pruritus, urticaria, facial edema, choking sensation, nausea, hypothermia, and collapse followed vigorous running but not swimming, cycling, racquetball, solar exposure, or cold exposure. Neither antihistamine, antiserotonin, anticholinergic nor epinephrine therapy was entirely effective or protective; only modification of running prevented episodes. Three similar episodes were noted at age 15 years by a brother who, now age 25, relates a 4-year history of seasonal rhinitis and exercise-related urticaria without anaphylactoid reaction. The remainder of the family (father, 47; mother, 46; brother, 22 years) does not have exercise intolerance. The father has allergic rhinitis; his nephew suffers exercise-induced urticaria without collapse. HLA typing revealed the father to be A1-B8-DR3, A3-B8-DR3; the symptomatic daughter to be A3-B8-DR3, A30-B5-DR8; and the symptomatic son to be A3-B8-DR3, A30-B5-DR8. The asymptomatic mother was A30-B5-DR8, A2-B7-DR5 and the asymptomatic son A1-B8-DR3, A30-B5-DR8. We describe exercise-induced anaphylaxis in a unique familial setting, perhaps linked to the HLA haplotype A3-B8-DR3.
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PMID:Familial exercise-induced anaphylaxis. 347 Oct 98

Recent evidence suggests that mast cell derived mediators other than histamine are likely to be involved in the pathogenesis of physical urticarias. Much of the work has been performed in idiopathic cold contact urticaria where the presence of neutrophil and eosinophil chemotactic factors, and platelet activating factor-like lipid substances have been previously demonstrated. Now, an increase in prostaglandin D2 measured by GC-MS has been demonstrated in venous blood draining the cold challenged area. This appeared a few minutes later than histamine, but then both substances paralleled the onset, development and subsidence of the urticarial reaction. There appeared to be no quantitative relationship between histamine and PGD2 release. A similar rise in histamine and PGD2 occurred on heat challenge of a subject with the rare localized form of heat urticaria. This rise of both substances was considerably reduced after combined treatment with induction of tolerance and oral indomethacin. The concentrations of PGD2 measured suggested that it plays an indirect role.
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PMID:[New pharmacologic developments in physical urticaria--therapeutic consequences]. 347 18

Purpura is provoked when the affected area is warmed up to 40 degrees C by means of an infrared lamp in cryoglobulinemia after exposition to cold with consecutive urticaria. For this way of causing purpura in two steps, we suggest the designation "bithermo-test".
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PMID:[Purpura following bithermotest in cryoglobulinemia]. 359 Sep 15

The acquired form of cold induced urticarial syndrome can be found associated with serum cryoproteins, in idiopathic form (generally IgE mediated) and transitory forms associated with other factors. The viral infections, specially infectious mononucleosis and hepatitis B can cause urticaria, mostly chronic, although infrequently produces cold urticaria. We present a case of a 13 year old patient with history suggestive of cold urticaria wherein we have found the existence of a mixed polyclonal cryoglobulinemia, IgG-IgA (exceptionally associated) and serologic markers of hepatitis B, HBsAb and HBsAb (the last being suggestive of a recent infection) 3 months from the urticaria, without recent or past history of hepatitis B infection. We also observed an elevated total serum IgE and peripheral blood eosinophilia. The provocation test presented an evolution similar to the cryoglobulinemia and markers of hepatitis B (after 18 months were negative) but serum IgE and eosinophilia remain elevated until the present time. All of this make us think that the patient could have suffered a subclinical form of hepatitis B which triggered off a cryoglobulinemia, presenting as cold urticaria.
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PMID:[Cold urticaria associated with serologic markers of hepatitis B and cryoglobulinemia]. 366 57

To determine whether morphological differences in the response of cutaneous mast cells characterize clinically distinct forms of urticaria, we used ultrastructural techniques to examine skin biopsy specimens from three patients with cold-induced urticaria and four patients with dermographism. Biopsy specimens were obtained before application of the stimulus and at the time of lesion formation. Patients with cold-induced urticaria exhibited morphological alterations only after stimulus application consisting of enlargement and uniform disorganization of some, but not all, granules, fusion of the membranes of adjacent granules, fusion of granule membranes with mast cell membranes, and discharge of electron-lucent and disorganized granule contents into the extracellular space. Mast cells from patients with immediate as well as delayed dermographism exhibited alterations before and after stimulus application consisting of enlargement of most granules, nonuniform (zonal) disorganization or solubilization of granule contents, fusion of granule membranes with mast cell membranes, and extracellular discharge of granule contents. Small cytoplasmic vesicles containing disorganized granular material were associated with the degranulation process. Endothelial cells lining nearby postcapillary venules exhibited prominent perinuclear condensation of contractile microfilaments during degranulation in both groups. Both before and after application of the stimulus, the walls of the superficial dermal vessels of the patients with dermographism were thinner and contained less extracellular matrix material than vessel walls of the patients with cold-induced urticaria. The morphologically distinctive types of mast cell degranulation that characterize these two clinically separable urticarial disorders may indicate different pathogenic mechanisms of lesion formation.
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PMID:Morphologically distinctive forms of cutaneous mast cell degranulation induced by cold and mechanical stimuli: an ultrastructural study. 366 25


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