Acute Systemic Anaphylaxis Research Paper

Acute Systemic Anaphylaxis

Anaphylaxis is a systemic allergic reaction involving the respiratory and/or the cardiovascular system; it has a rapid onset with the possibility of causing death. However, less severe reaction may be also defined as “anaphylaxis” if there is a high index of suspicion for allergic reaction in the setting of previously diagnosed allergy (Sanchez et al. 1999; Simons et al. 2007; Tang and Liew, 2008). It was observed by Simons (2006) that anaphylaxis is a disease of modern times; sporadic cases report of anaphylaxis were only published in 17th, 18th and 19th centuries and within the past four decades, the rates of allergic diseases have been increasing dramatically. The most common identifiable triggers of anaphylaxis
The corticosteroids will diffuse across the cell membrane, where they interact with cytoplasmic glucocorticoid receptor, where the activation of these receptors will modulate the transcriptional activity. This will suppress the TH2-cell-mediated inflammation through the inhibition of expression of cytokines, chemokines and adhesion molecules, whose encoding genes are regulated by transcription factors such as nuclear factor – κB and activator protein 1. Β2-adrenoreceptor agonists are usually used for asthma related allergic disease where it will be inhaled (Holgate and Polosa, 2008). These agonists (e.g. epinephrine) bind to the Β2-adrenoreceptors and stimulate the adenylate cyclase through signal-transducing G protein, increasing cyclic adenosine 3’5’-monophosphate (cAMP), activating protein kinase A. This will mediate smooth-muscle relaxation through phosphorylation of myosin light chain kinase and by opening Ca2+- dependent K+¬ (KCa) channels which relieve bronchoconstriction in asthma. Lastly, mediator antagonists such as H1- antihistamines are used to treat allergic reaction by binding to the H1 receptor, thus preventing histamine from binding (Simons, 2004; Holgate and Polosa,