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)

Anaphylaxis is an often severe, potentially life-threatening symptom complex. Urticaria, airway edema, vascular collapse, asthma, abdominal pain, and diarrhea are common clinical signs. Recently recognized syndromes of anaphylaxis include reactions due to exercise, food preservatives, aspirin, steroids, dialysis, various serums, and human seminal fluid. Initial therapy is directed at maintaining an effective airway and circulatory system. Administration of aqueous epinephrine is always indicated. Other measures may include oxygen delivery by controlled flow, administration of an aerosolized beta agonist, slow infusion of aminophylline, and rapid infusion of intravenous fluid. Patients with severe acute reactions should be monitored in-hospital.
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PMID:Anaphylaxis. Why it happens and what to do about it. 289 Jan 45

Patients with cold urticaria can after exposure to cold air or infusions react with hypotension and cardiovascular collapse. We here report on a patient having a severe cold urticaria who because of angina required myocardial revascularization: She was successfully operated in normothermic cardiopulmonary bypass with cardioplegia.
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PMID:Aortocoronary bypass surgery with normothermia in a patient with severe cold urticaria. 325 34

Human C5a anaphylatoxin is a potent bioactive molecule that possesses both spasmogenic and leukocyte-related properties. As such, it normally serves as a local mediator of the acute inflammatory response. Additionally, C5a, through its actions of mononuclear phagocytes, may act to bridge the gap in the acute-chronic inflammatory continuum. While these properties are critical to normal host defense mechanisms, it is now apparent that this anaphylatoxin and/or its des-Arg74 derivative, may exert significant systemic effects that are manifest as cardiopulmonary abnormalities and intravascular activation of granulocytes. Knowledge of these properties is critically important for understanding the clinical sequelae exhibited by patients undergoing extracorporeal circulation since we now know that both hemodialysis and cardiopulmonary bypass [28-30] procedures promote intravascular complement activation and C5a formation. Viewed in this context, it seems reasonable to postulate that many of the immediate and delayed responses to extracorporeal circulation might be mediated by C5a formed in the extracorporeal circuit (table IV). For example, it is now recognized that a few particularly susceptible patients display adverse reactions during the initial phases of hemodialysis. The symptoms of this so-called 'first-use syndrome' may range from severe urticaria and angioedema to life-threatening bronchospasm, hypotension, and cardiopulmonary collapse. Some investigators have presented data which suggest that complement-derived products may be causative of these symptoms in some patients [31]. While this hypothesis remains to be confirmed, present evidence clearly demonstrates that C5a alone may produce many of the observed phenomena. In addition to the acute effects produced by C5a, both our own basic studies and the clinical investigations presented by others at this conference suggest that the long-term effects of repeated C5a exposure in the dialyzed patient may be considerable. Thus, there has been a great deal of interest in the role of complement-derived mediators as initiators of leukocyte degranulation and toxic oxygen radical production and an exploration of the significance of these events in the eventual development of chronic pulmonary fibrosis in the dialyzed patient. Similarly, the effects of repeated exposure to IL-1 that has been postulated to occur as a result of C5a triggering of monocytes during dialysis is currently an active area of investigation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The properties of human C5a anaphylatoxin. The significance of C5a formation during hemodialysis. 332 50

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

The syndrome of exercise induced anaphylaxis represents a distinct form of physical allergy. This syndrome and the features which distinguish it from other forms of physical allergy are discussed in the context of 10 case reports. The symptoms usually start after 5-30 minutes' exercise with cutaneous pruritus, warmth and progress to urticaria and angioedema. In 3 cases signs of laryngeal edema were present; additional manifestations included upper respiratory distress, gastrointestinal tract symptoms and collapse. The syndrome is distinct from exercise induced asthma or cholinergic urticaria. One patient had both cholinergic urticaria induced by stress, heat and exercise, and anaphylactoid symptoms induced by exercise alone. While the symptoms of cholinergic urticaria subsided after 2-4 hours, the anaphylactoid symptoms lasted up to 48 hours. The symptoms are elicited irregularly, which suggests a multifactorial trigger mechanism. The intake of particular foods or acetylsalicylic acid, and certain weather conditions, are possible cofactors. In 8 of 10 patients an atopic diathesis was found but no exposition to a specific allergen, which could explain the symptoms, was observed. Therapy consists of avoidance of cofactors, change of training habits and cessation of exercise as soon as prodromal symptoms develop. If attacks are frequent, antihistamines or ketotifen can be tried. The acute attack should, like other anaphylactoid reactions, be treated by antihistamines, injection of epinephrine (s.c.) and infusions (colloidal solutions).
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PMID:[Exertion-induced anaphylaxis]. 381 Jan 6

Thirty-nine patients with cold urticaria seen over a 12-year-period were re-examined. All but 12 still had positive skin tests for cold and only five of these had shown a spontaneous cure. Fourteen patients were prone to collapse on cold exposure. The incidence of atopy in this group was comparable to that in control groups. Cold urticaria is an extremely chronic disease. The mean disease duration was 9.3 years. Serum antibodies to Epstein-Barr virus, measles virus, cytomegalovirus (CMV), varicella-zoster virus (VZV), herpes simplex virus (HSV), Chlamydia psittaci and Mycoplasma pneumoniae were determined in all 39 patients and compared with control groups. The EBV-antibody patterns (heterophile antibodies and different types of EBV-specific antibodies) showed no evidence of current or of recent primary or secondary infection with EBV. Complement fixing antibody titres to measles virus, CMV, HSV and Mycoplasma pneumoniae were significantly higher in cold urticaria patients than in controls. The existence of a basic immuno-regulatory defect responsible for both the cold urticaria and the elevated antibody levels is proposed.
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PMID:Cold urticaria and virus infections: a clinical and serological study in 39 patients. 395 51

Three cases of apparent anaphylactoid reactions to zomepirac sodium (Zomax) are reported. One patient initially appeared to have a dissecting abdominal aortic aneurysm with vascular collapse. The second patient experienced conjunctival pruritus after each of several doses of zomepirac before emergency department presentation with acute dyspnea and urticaria. The third patient had been admitted previously with a diagnosis of rule out myocardial infarction, which in retrospect was probably a zomepirac reaction. All three recovered uneventfully.
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PMID:Anaphylactic reactions to zomepirac. 397 Apr 5

Exercise-induced anaphylaxis (EIA) is a unique and an increasingly recognized syndrome consisting of premonitory symptoms and signs of generalized body warmth, pruritus, and erythema, which progresses on continued exertion to confluent urticaria, laryngeal edema with stridor or hoarseness, and gastrointestinal colic and frequently culminates in vascular collapse. Previous studies of five individuals with this condition have demonstrated significant elevations of serum histamine concurrent with the early clinical manifestations after experimental exercise. To assess relevant morphologic alterations in the skin of these patients, cutaneous mast cells were examined by light and transmission electron microscopy before and during the initial erythema elicited by exertion. The marked alterations observed in mast cells immediately after exercise consisted of (1) loss of electron density and internal substructure of granules, (2) fusion of granule membranes with those of adjacent granules and with mast cell membranes creating conduits to the extracellular space, and (3) an apparent decrease in the number of intact granules per cell. Biopsy specimens obtained before exercise from patients with EIA and from two normal individuals who served as control subjects were identical, and the control subjects had normal mast cell morphology after exercise. Serum histamine levels were significantly elevated in patients with EIA after exercise at the time of biopsy, whereas control subjects had normal levels. These observations provide evidence that EIA is a distinct form of physical allergy associated with mast cell degranulation similar in morphology to that of human pulmonary mast cell IgE-Fc-dependent activation secretion. Characterization of this disorder is important because its prevalence may be underestimated, and its clinical consequences, which may include some morbidity, are not fully known.
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PMID:Exercise-induced anaphylaxis: a serious form of physical allergy associated with mast cell degranulation. 398 Aug 83

The authors studied twenty patients with celery allergy and concomitant hypersensitivity to certain pollens (mugwort, birch). The specific symptoms induced by eating celery were attacks of urticaria and angio oedema (seventeen out of twenty) respiratory complaints (eight out of twenty), systemic anaphylaxis with vascular collapse (three out of twenty). A strong association between clinical reactions to celery and mugwort sensitization, and to a lesser degree between celery allergy and birch pollen sensitization was established. Celery allergy is mediated by IgE antibodies and can be easily diagnosed by cutaneous tests using fresh material and/or by adequate RAST test. RAST inhibitions performed on individual sera suggest the existence of common antigens in celery and mugwort, and in celery and birch pollen. However, the exact nature of these common antigens has not yet been determined.
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PMID:Celery sensitivity: clinical and immunological correlations with pollen allergy. 400 77

Acute allergic reactions range from mild conditions of local tissue swelling and pruritus to severe multisystem syndromes including asthma, urticaria and/or angioedema, gastrointestinal distress, and vascular collapse. Such reactions share a common pathophysiology characterized by vasodilation and postcapillary permeability, resulting in increased extravasation of fluid within minutes after exposure to an eliciting substance. Smooth muscle contraction of the respiratory or gastrointestinal tracts may also be involved. Most of these changes can be explained by the release of chemical mediators from circulating basophilic leukocytes and tissue mast cells. Human basophils and mast cells can be activated to release chemical mediators by several known pathways: crosslinking by allergens of specific immunoglobulin E antibodies attached to basophils and mast cells; anaphylatoxin formation following immune complex activation of the classical complement pathway; anaphylatoxin formed from direct activation of the alternative complement pathway by negatively charged surfaces; non-complement-, non-antibody-mediated direct histamine release; and idiosyncratic mechanisms involving physical exercise, psychological stress, or aspirin intolerance. Any or all of these mechanisms could be operative in patients experiencing acute allergic reactions at the commencement of hemodialysis.
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PMID:Mechanisms of acute allergic reactions. 647 99


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