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In March 2015, the Australian Competition and Consumer Commission (ACCC) launched proceedings against Reckitt Benckiser; for misleading advertising for its targeted pain range. In December 2015, the Federal Court of Australia found that Reckitt Benckiser, which makes Nurofen, had misled consumers with its "Nurofen Specific pain range", and ordered that all Nurofen specific pain products be removed from retail sale within three months. [30] A spokeswoman for Reckitt Benckiser argued that, "[This] specific-pain range" was intended "to help consumers navigate their pain relief options, particularly within the grocery environment where there is no healthcare professional to assist decision making". [31] The ACCC said that the products were found to be "no more effective at treating the type of pain described on its packaging than any of the other Nurofen specific pain products", and sold for almost twice the price. [32] Specific pain range painkillers include Nurofen Back Pain, Nurofen Period Pain, Nurofen Migraine Pain and Nurofen Tension; and all contain the "same active ingredient, 342 milligrams of ibuprofen lysine". [31]

A variety of allergic or allergic-like NSAID hypersensitivity reactions follow the ingestion of NSAIDs. These hypersensitivity reactions differ from the other adverse reactions listed here which are toxicity reactions, . unwanted reactions that result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual; hypersensitivity reactions are idiosyncratic reactions to a drug. [67] Some NSAID hypersensitivity reactions are truly allergic in origin: 1) repetitive IgE -mediated urticarial skin eruptions, angioedema , and anaphylaxis following immediately to hours after ingesting one structural type of NSAID but not after ingesting structurally unrelated NSAIDs; and 2) Comparatively mild to moderately severe T cell -mediated delayed onset (usually more than 24 hour), skin reactions such as maculopapular rash , fixed drug eruptions , photosensitivity reactions , delayed urticaria , and contact dermatitis ; or 3) far more severe and potentially life-threatening t-cell-mediated delayed systemic reactions such as the DRESS syndrome , acute generalized exanthematous pustulosis , the Stevens–Johnson syndrome , and toxic epidermal necrolysis . Other NSAID hypersensitivity reactions are allergy-like symptoms but do not involve true allergic mechanisms; rather, they appear due to the ability of NSAIDs to alter the metabolism of arachidonic acid in favor of forming metabolites that promote allergic symptoms. Afflicted individuals may be abnormally sensitive to these provocative metabolites or overproduce them and typically are susceptible to a wide range of structurally dissimilar NSAIDs, particularly those that inhibit COX1. Symptoms, which develop immediately to hours after ingesting any of various NSAIDs that inhibit COX-1, are: 1) exacerbations of asthmatic and rhinitis (see aspirin-induced asthma ) symptoms in individuals with a history of asthma or rhinitis and 2) exacerbation or first-time development of wheals or angioedema in individuals with or without a history of chronic urticarial lesions or angioedema. [26]

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