Reaction, allergic induced

General Indication Allergic disorders Principal Desired of Glucocorticoids Decreased inflammation Examples of Specific Disorders Anaphylactic reactions, drug-induced allergic reactions, severe hay fever, serum sickness... 

In Finland, from 2000 to 2007, the frequency of cases of severe allergic reactions annually was found to be 0.001%. The reaction was a life-threatening anaphylactic shock in 26% of the mentioned cases, with no deaths reported. Food was the causative agent in 53% of the cases. Out of the foodstuffs, the majority of reactions was induced by nuts and seeds fruit and vegetables in the case of the adult population, and nuts, important allergens, for children along with milk, egg, and wheat (Makinen-Kiljunen and Haahtela, 2008). 

A retrospective analysis of allergic reactions (drug-induced fever and rash) in 90 adults with cystic fibrosis, of whom 26 developed probable allergic reactions to parenteral beta-lactams. There was drug-induced fever in 54 and skin reactions in 28 of 897 treatment courses (6 and 3.1% respectively). There was one case of non-fatal anaphylaxis. The numbers of allergic reactions per number of patients receiving specific antibiotics were carbenicillin 4/56, mezlocillin 7/42, piperacillin 11/31, ticarcUlin 1/20, cefazolin 0/24, ceftazidime 1/35, imipenem + cilastatin 4/16, and nafcillin 3/36 (17). 

Rashes are common in allergic reactions. Photosensitivity induced by quinine has been reported some of the cases occurred in elderly persons taking quinine for night cramps (28). Another form of hypersensitivity to quinine is cutaneous neutrophilic vasculitis, which is a form of photosensitivity (SEDA-16, 305). Local pigmentation has been described after intramuscular injection (SEDA-13, 815). 

Drug-induced liver disease occurs as several different clinical presentations idiosyncratic reactions, allergic hepatitis, toxic hepatitis, chronic active toxic hepatitis, toxic cirrhosis, and liver vascular disorders. 

Allergic contact dermatitis occurs most commonly from nickel-containing objects, plants (such as Rhus)y rubber, adhesives, or dyes in athletic tape, gear, or running shoes, and topical medicaments. Reactions are induced or elicited by the athlete s perspiration, which leaches the chemical allergens from their gear (Cronin 1980). Table 6 lists common contact allergens in the athlete and their recommended patch-test concentrations (Marks and DeLeo 1997). 

C. It is secreted along with noradrenaline by the adrenal medulla, from which it may be obtained. It may be synthesized from catechol. It is used as the acid tartrate in the treatment of allergic reactions and circulatory collapse. It is included in some local anaesthetic injections in order to constrict blood vessels locally and slow the disappearance of anaesthetic from the site of injection. Ultimately it induces cellular activation of phosphorylase which promotes catabolism of glycogen to glucose. 

Intrinsic asthma, also called idiopathic asthma, usually develops in adulthood. In intrinsic asthma allergic factors are not demonstrable. Episodes of intrinsic asthma may be triggered by a variety of stimuli, eg, emotional state, exposure to cold air, or inert dusts. Both intrinsic and extrinsic asthmatics can be prone to exercise-induced attacks. Individuals who experience a combination of extrinsic and intrinsic asthmatic reactions have mixed asthma. Status asthmaticus refers to an especially acute life-threatening asthma attack which is resistant to normal treatments and which may require hospitalization in order to stabilize the patient. 

Prolonged contact with certain chromium compounds may produce allergic reactions and dermatitis in some individuals (114). The initial response is usually caused by exposure to Cr(VI) compounds, but once the allergy is estabUshed, it is extended to the trivalent compounds (111,115). There is also limited evidence of possible chromium associated occupational asthma, but there is insufficient data to estimate a dose for assumed chromium-induced asthma. Reference 116 provides a summary and discussion of chromium hypersensitivity. 

Oral corrosion of metallic restorations does not, per se, generally result in serious damage to the structure. Corrosion can result, however, in various local and systemic effects, notably the hypersensitivity and allergic reactions reported by many workers. Galvanic cells created by mixed metal couples can delay fracture healing and induce oral lesions and cancer. 

In this type of reaction an antigen elicits the generation of cytotoxic T-lymphocytes ( immune defense). Cytotoxic T-lymphocytes (Tc) destroy antigen bearing cells by inducing apoptosis. This reaction can be viewed as the cellular counterpart to the humoral Type II reactions. They play an important physiological role in the defense of viruses, and can become allergic reactions under the same conditions as described for Type II reactions. 

The role of atopy in anaphylaxis has not completely been resolved. On the one hand there is for example no evidence of a higher risk of severe reactions in venom-allergic patients. A recent study by Sturm et al. [38] indicated that patients with high total IgE levels predominantly developed mild to moderate reactions. By contrast, atopy may increase the risk and severity of systemic reactions in beekeepers and their family numbers [39]. On the other hand, atopy and in particular allergic asthma are risk factors for food allergy and therefore are also important risk factors for food-induced anaphylaxis. This is most likely also true for exercise-induced anaphylaxis, but also non-IgE-dependent anaphylaxis induced by NSAIDs or contrast media. 

MH, Townley RG. Mokhtarani M. Seyfert-Margohs V, Asare A. Bateman K. Deniz Y Omalizumab pretreatment decreases acute reactions after rush immunotherapy for ragweed-induced seasonal allergic rhinitis. J Allergy Clin Immunol 2006 117 134-140. 

The most common clinical picture of non-immediate RCM reactions is a macu-lopapular exanthema, which resembles other drug-induced T-cell-mediated hypersensitivity reactions. The reported onset of skin eruptions 2-10 days after the first exposure to a RCM and 1-2 days after re-exposure to the same substance is typical for an allergic drug reaction with a sensitization phase. 

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