Disease relevance of Anaphylaxis

• Cold urticaria: release into the circulation of histamine and eosinophil chemotactic factor of anaphylaxis during cold challenge [1].
• Tryptase levels as an indicator of mast-cell activation in systemic anaphylaxis and mastocytosis [2].
• During a type I allergic reaction histamine, slow-reacting substance of anaphylaxis (SRS-A) and other mediator substances are elaborated from specific tissue sites [3].
• Leukotriene D4 (LTD4), a component of slow reacting substance of anaphylaxis (SRS-A)1, produces marked hypotension in laboratory animals2,3, implicating it as a potential mediator of anaphylactic shock [4].
• Impaired IgG-dependent anaphylaxis and Arthus reaction in Fc gamma RIII (CD16) deficient mice [5].

Psychiatry related information on Anaphylaxis

• The clinical outcome--the intensity of the reaction--is not only influenced by the degree of sensitization, but also by concomitant other factors: sometimes, individuals only develop anaphylaxis after simultaneous exposure to the allergen and an infection, physical exercise, psychological stress or concomitant medication (e.g. beta blockers) [6].
• Knowledge and perceived self-efficacy of participants were measured before and after the training program to determine if a theory-based anaphylaxis recognition and epinephrine auto-injector training program would increase participants' knowledge and self-efficacy in responding to an anaphylactic emergency [7].

High impact information on Anaphylaxis

• Anaphylaxis from the carboxymethylcellulose component of barium sulfate suspension [8].
• Anaphylactic reaction to latex gloves [9].
• Mast cells and basophils, which are activated by immunoglobulin E (IgE) and allergen, play a prominent role in anaphylaxis [10].
• Anaphylactic reaction to gonadotropin-releasing hormone [11].
• The relative contribution of these IgE receptors, and possibly other receptors such as Fc epsilon RII/CD23 and Mac-2, to the genesis of in vivo anaphylaxis is still unclear [10].

Chemical compound and disease context of Anaphylaxis

• Blood specimens were obtained from each arm serially over a one-hour interval, and serum speciments were assessed for histamine, eosinophil chemotactic factor of anaphylaxis, and complement components [1].
• Kunitz soybean trypsin inhibitor: a specific allergen in food anaphylaxis [12].
• Apparent anaphylactic reaction to zomepirac (Zomax) [13].
• Anaphylactic reaction to intravenous cyclosporine [14].
• Anaphylaxis from tolmetin [15].

Biological context of Anaphylaxis

• Similar disappearance kinetics were observed for two subjects presenting in the emergency room with immediate type reactions, one with severe asthma after indomethacin ingestion, the other with systemic anaphylaxis after a bee sting [16].
• Immunisation of sensitised rats with the same peptide reduced IgE antibody formation and serum histamine concentration, and abolished systemic anaphylactic reactions in response to allergen challenge [17].
• The data demonstrate that parenteral administration of myeloma IgE inhibits the PCA reaction only when given before passive sensitization and does not prevent cutaneous anaphylaxis in actively immunized rats [18].
• Platelet-activating factor (PAF) is a potent proinflammatory phospholipid mediator that causes hypotension, increases vascular permeability, and has been implicated in anaphylaxis, septic shock and several other inflammatory responses [19].
• A high affinity binding site for leukotriene C4 (LTC4), one component of slow reacting substance of anaphylaxis, has been identified in a membrane preparation from rat lung [20].

Anatomical context of Anaphylaxis

• In addition, a factor chemotactic for human eosinophils with the size and charge characteristics of the eosinophil chemotactic factor of anaphylaxis was identified in blullous fluid [21].
• Effects of chronic treatment with the c-kit ligand, stem cell factor, on immunoglobulin E-dependent anaphylaxis in mice. Genetically mast cell-deficient Sl/Sld mice acquire anaphylactic responsiveness, but the congenic normal mice do not exhibit augmented responses [22].
• Histamine, slow reacting substance of anaphylaxis (S.R.S.-A), IgE, eosinophils, and an eosinophil-associated enzyme, arylsulphatase IIB, were measured in sputum from 11 chronic bronchitics at weekly intervals for 6 weeks [23].
• By using anti-IgE antibody treatments and mice with targeted mutations of the FcgammaRIII alpha-chain or the common gamma-chain of FcepsilonRI and FcgammaRI/III, we demonstrate that IgE crosslinking of FcepsilonRI appears to be necessary and sufficient for myelin peptide-induced anaphylaxis [24].
• Release of slow reacting substance of anaphylaxis (SRS-A) from human leukocytes by the calcium ionophore A23187 [25].

Gene context of Anaphylaxis

• As has been shown with conventional antibodies, monoclonal IgG1 and IgE are the two classes capable of sensitizing the mouse for anaphylactic reactions, IgE sensitizes the rat, and IgG2a sensitizes the guinea pig [26].
• These 5LO(-/-) mice were unable to synthesize detectable levels of leukotrienes and were more resistant to lethal anaphylaxis induced by platelet-activating factor [27].
• Vav1-deficient mice contain normal numbers of mast cells but respond more weakly than their normal counterparts to a passive systemic anaphylaxis challenge [28].
• IL-4 exacerbates anaphylaxis [29].
• Pretreatment of mice with IL-4 or the related cytokine, IL-13, rapidly and dramatically increased the severity of anaphylaxis induced by cross-linking Fc(epsilon)RI or FcgammaRIII [29].

Analytical, diagnostic and therapeutic context of Anaphylaxis

• There were no hospitalizations for acute renal failure or anaphylaxis; the upper 95% confidence bound for the risk of either of these outcomes was 5.4 per 100,000 ibuprofen-treated children [30].
• These observations demonstrate the value of ECG monitoring of patients during anaphylaxis and emphasize the potential hazards of administering epinephrine by the IV route in this clinical setting [31].
• We have studied active and passive immunization models in mice to approach these issues and to determine whether any inhibition of anaphylaxis observed was a direct effect of allergen neutralization by IgG Ab or an indirect effect of cross-linking of Fc epsilonRI to the inhibitory IgG receptor Fc gammaRIIb [32].
• Using an animal model of intestinal anaphylaxis, we have correlated alterations in water and electrolyte transport, associated with intraluminal challenge, with specific intestinal mucosal mast cell degranulation by following systemic as well as local release of rat mast cell protease II [33].
• A major problem with allergen-specific immunotherapy involving repeated injection of allergens is the risk of an anaphylactic reaction [34].

References