Anaphylaxis anaphylactic reactions

Table 2. Prevalence of symptoms in anaphylactic reactions according to Przybilla and Rueff [see 18]. A meta-analysis of 1,865 cases from 14 publications (Liebermann) and 865 own patients with insect venom anaphylaxis... 

Fatal anaphylaxis occurs mostly due to bronchial obstruction or cardiac arrest, but also disseminated intervascular coagulation as well as adrenalin overdose [2, 7, 21, 31]. When anaphylactic reactions are survived, long-lasting sequels are rare. However,... 

Regarding the management of anaphylaxis, differentiation should be made between the acute treatment of an anaphylactic reaction [see chapter by Ring et al, section Treatment and Prevention, p. 201] and the management of a patient who has undergone an anaphylactic episode. 

Another way to classify anaphylactic reactions regards the eliciting agents the most common elicitors of anaphylaxis are drugs, insect venoms, foods, additives,... 

Finally, patients suffering from mastocytosis have a higher risk of developing severe anaphylaxis after an insect sting [34]. In venom-allergic patients with mastocytosis, elevated baseline serum tryptase levels were foimd to be associated with severe anaphylactic reactions to stings [35]. 

Systemic anaphylaxis in man is frequently accompanied by electrocardiographic alterations ischemic ST waves, arrhythmias and atrial fibrillation [6-11]. Anaphylactic reactions after insect stings can lead to coronary spasm or acute myocardial infarction [12, 13]. Myocardial infarction can also occur as a consequence of idiopathic... 

Studies have now started to clarify the role of histamine Hi and H2 receptors in the cardiovascular manifestations of anaphylaxis. However, histamine can activate H3 and H4 receptors [56, 57]. Levi and coworkers [58-60] identified H3 receptors as inhibitory heteroreceptors in cardiac adrenergic nerve endings. This suggests a mechanism by which endogenous histamine can activate norepinephrine release in normal and ischemic conditions [61,62]. The functional identification ofH3 receptors in the human heart [59] means that these receptors might be directly and/or indirectly involved in the cardiovascular manifestations of anaphylactic reactions. 

In one study, 26% of anaphylactic reactions were reported to have developed after a combination of elicitors [4]. In other patients with mastocytosis, anaphylaxis remains idiopathic despite an extensive search for an allergic basis. 

The application and development of new in vitro diagnostic techniques aims to enable physicians to reach an allergy diagnosis with no risk for the patient. This is particularly desirable in the case of serious reactions such as anaphylaxis, by confirming the existence of an anaphylactic reaction and differentiating between individuals which present with sensitization but no cUnical symptoms following exposure to the allergen from those that show a serious clinical reaction. 

Histamine is a critical mediator in anaphylactic reactions. It is a diamine produced by decarboxylation of the amino acid histidine in the Golgi apparatus of mast cells and basophils. Once secreted, it is rapidly metabolized by histamine methyltransferase [2]. Plasma histamine levels are elevated in anaphylaxis, reaching a concentration peak at 5 min and declining to baseline by 30-60 min [3]. Therefore, histamine samples for assessing an anaphylactic reaction should be obtained within 15 min of the onset of the reaction. Urinary metabolites of histamine may be found for up to 24 h. 

Finally, it is worth mentioning that tryptase levels do not differentiate between immunologic and non-immimological mast cell activation and do not contribute to the identification of the cause of the anaphylactic reaction. To date, very few mediators [10] apart from histamine and tryptase have been investigated as markers for anaphylaxis. Recent studies also include other mediators that we will only examine briefly. A more extensive review can be found elsewhere [2,11]. 

Finally, other mediators such as leukotrienes and prostaglandins may also play a role. Denzlinger et al. [17] first reported an increase in urinary leukotriene E4 in anaphylactic reactions. This has been recently confirmed [18], along with an increase in 9a,l iP PGFj concentrations during anaphylaxis. 

Ebo DG, Ahrazem O, Lopez-Torrejon G, Bridts CH, Salcedo G, Stevens WJ Anaphylaxis from mandarin (Citrus reticulata) identification of responsible allergens. Int Arch Allergy Appl Immunol 2007 144 39-43. Raap U, Schaefer T, Kapp A, Wedi B Exotic food allergy anaphylactic reaction to lychee. J Invest Allergol Clin Immunol 2007 17 199-201. 

The natural history of Hymenoptera venom anaphylaxis, that is the risk to develop anaphylaxis again when re-stung, has been analyzed in several prospective studies (table 3) [35-37], and in placebo or whole-body extract treated controls of prospective studies on venom immunotherapy [38-40]. It is higher in patients with a history of severe as compared to mild systemic anaphylactic reactions, and in honey bee than in vespid venom-allergic patients - most likely because of the smaller and less constant amoimt of venom applied by vespids [10,41]. A short interval between two stings increases the risk of anaphylaxis [25], but severe anaphylaxis may occur again even after intervals of 10-20 years or more. 

Van der Linden PW, Hack CE, Struyvenberg A, van der Zwan JK Insect sting challenge in 324 subjects with a previous anaphylactic reaction current criteria for insect venom hypersensitivity do not predict the occurrence and severity of anaphylaxis. J Allergy Clin Immunol 1994 94 1512-1519. 

Dyes. Vital dyes have been used for many years in a variety of clinical situations. Patent blue V (also called E131, Acid blue 3, Disulfine blue) and Isosulfan blue (also called Patent blue violet or Lymphazurine), belong to the group of triarylmethane dyes and are the most commonly used [24]. Reports of IgE-dependent anaphylaxis arise. Anaphylactic reactions involving methylene blue seems to be very rare, however, several reports of sensitization to both Patent blue and methylene blue have previously been reported. 

Nybo M, Madsen JS Serious anaphylactic reactions due to protamine sulfate a systematic literature review. Basic Clin Pharmacol Toxicol 2008 103 192. Moneret-Vautrin DA, Kanny G Anaphylaxis to muscle relaxants rational for skin tests. Allerg Immunol (Paris) 2002 34 233. 

Anaphylactic reactions including fatal anaphylaxis other hypersensitivity reactions including dyspnea, urticaria, other rashes, and febrile episodes inflammation at or near injection site, including sterile abscesses (IM) brown skin discoloration at injection site (IM) flushing and hypotension with overly rapid IV administration ... 

Hypersensitivity reactions A few patients receiving the injection have experienced anaphylactic reactions. Although the exact cause of these reactions is not known, other drugs with castor oil derivatives in the formulation have been associated with anaphylaxis in a small percentage of patients. 

It is usual to give a sedating antihistamine, for example chlorphenamine 10 mg by intramuscular or slow intravenous injection, because of the relatively short half-life of epinephrine (adrenaline), and because of the active role of histamine in anaphylaxis. In addition, the inflammatory reaction can be moderated by the administration of a corticosteroid, such as hydrocortisone 200 mg by intramuscular or slow intravenous injection. Corticosteroids may take several hours to act, but can be of some help in so-called biphasic anaphylactic reactions. 

During an anaphylactic reaction, large quantities of inflammatory mediators are rapidly released. The resultant reaction is severe and may threaten the life of the individual. The introduction of a specific antigen— usually in food or in injected material—into a sensitized individual can cause the rapid release of mast cell contents, producing a decrease in blood pressure, impaired respiratory function, abdominal cramps, and urticaria. Extreme and severe anaphylaxis is life threatening and requires prompt medical intervention. 

Acute anaphylaxis occurred in an 18-year-old man after the third course of intradermal injections of triamcinolone suspension ( Kenalog 10 mg per treatment) for alopecia areata (446). Subsequent rechallenge with intradermal triamcinolone 1 ml resulted in the same anaphylactic reaction as before and his serum IgE concentration was increased. 

The probability of occurrence of sudden death due to the food anaphylaxis has been calculated over 10 years retrospective research at 0.06 deaths in 1,000,000 in children aged 0-15 per year based on results of 10 years retrospective studies. The most frequent allergen was cow s milk accounting for approximately 50% of deaths. Also, severe anaphylactic reactions were observed following the consumption of nuts. That estimated probability of death occurrence is 1 in 800,000 children per year, assuming that 5% of the population exhibits symptoms of food allergy (Macdougall et al., 2002). 

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