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Nonsteroidal anti-inflammatory drugs are widely prescribed in children. They are the second cause of drug's reactions in pediatrics after beta-lactam antibiotics, however only a part of them are hypersensitivity reactions. The prevalence of these reactions to nonsteroidal anti-inflammatory drugs in children is 0.3 %, increasing to 5 % in asthmatics. The different physiopathological mechanisms involved (inhibition of cyclooxygenase, immunoglobulin E-mediated hypersensitivity, reactive T lymphocytes and/or disturbance of innate immunity) will cause different clinical entities with diverse symptoms. The confusion between the common symptoms of a viral infection and a hypersensitivity reaction, and the variability of the clinical presentations make diagnosis a real challenge. A detailed clinical history, laboratory, skin and controlled provocation tests will provide strategies for each patient, without labeling a child who is not an allergic one, or taking unnecessary risks with those who are sensitized., Competing Interests: The authors report no conflicts of interest in this work., (Sociedad Argentina de Pediatría.)

Background: Nonsteroidal anti-inflammatory drugs (NSAID)-induced hypersensitivity reactions can be clinically apparent with asthma, rhinosinusitis, anaphylaxis or rash. Although natural anti-inflammatory products can have similar components, they are not subjected to rigorous quality control standards., Case Report: The case is presented of a 22-year-old female with NSAID allergy who attended with facial and laryngeal angioedema associated with pruritus in eyelids and pharynx. She developed these symptoms fifteen minutes after taking an over-the-counter (OTC) natural anti-inflammatory product. She received treatment with epinephrine, antihistamines and corticosteroids., Conclusion: Different natural anti-inflammatory products are freely available both OTC and online. Some contain dangerous substances that can cause important, and even lethal. side effects. Allergologists, dermatologists and general practitioners should be able to recognize that the consumption of these products, which is widely spread, can cause angioedema.

Adverse reactions to nonsteroidal antinflammatory drugs are the second cause of reactions to drugs after beta-lactams. Prevalence of these reactions among general population is between 0.1-0.3%, and prevalence of nonsteroidal antinflammatory drug-induced anaphylaxis is 0.01%. Acetylsalicylic acid or nonsteroidal antinflammatory drug sensitivity can be manifested as acute urticaria, angioedema, acute asthma, acetylsalicylic acid exacerbated respiratory disease and anaphylaxis. An updated review based on three cases of patientes with acetylsalicylic acid or nonsteroidal antinflammatory drug intolerance is presented in which, because of their concomitant diseases, permanent treatment with acetylsalicylic acid was required. After undergoing a fast acetylsalicylic acid desentization protocol in an intensive care unit, these patients were able to receive daily acetylsalicylic acid doses without any adverse effects.

Adverse reactions to acetylsalicylic acid (aspirin, ASA) and other non-steroidal anti-inflammatory drugs (NSAIDs) are the second most important cause of adverse drug reactions (ARDs) after beta-lactams. They produce various clinical manifestations and can affect different organs. Gastrointestinal reactions (pyrosis, vomiting, gastralgia), neurological reactions (tinnitus, deafness, vertigo), blood dyscrasias, and nephrotoxic and hepatotoxic reactions are well known.NSAIDs are the drugs of choice in the treatment of chronic arthropathies and other childhood connective-tissue diseases and are also commonly used in the treatment of febrile and acute inflammatory processes. Not all NAIDs are authorized for use in the pediatric population but their spectrum of use varies according to the entity for which they are indicated and the legislation of the country. Published studies on the prevalence of aspirin intolerance in patients with bronchial asthma show a fair amount of disagreement. This may be due to (i) the method of selecting asthmatic patients for the study, which differs according to whether all asthmatic patients are included or only those dependent on corticoids; (ii) the diagnostic method used, whether based on clinical criteria or oral provocation tests, which will affect the number of patients with a diagnosis of intolerance. In children aged less than 10 years, including children with asthma, the prevalence is low, while among children and young adults aged 10-20 years old, the prevalence is estimated at 10 %. Some hypotheses attempt to explain the mechanisms through which adverse reactions to NAIDs take place. One hypothesis attributes the reaction to a reaginic immunological mechanism but this hypothesis has only been confirmed in exceptional cases. The theory of the cyclooxygenase pathway, currently the most widely accepted, is based on the ability of NSAIDs to inhibit the cyclooxygenase pathway of arachidonic acid metabolism, leading to prostaglandin depletion and an increase in leukotrienes. The discovery of two isoforms of the cyclooxygenase enzymes, COX-1 and COX-2, has represented a great advance in our understanding of the mechanism of action of NSAIDs and has also elucidated the problem of cross-reactivities. According to the theory of viral infection, aspirin-induced asthma could be caused by chronic viral infection since, after initial exposure to the virus, cytotoxic lymphocytes are produced. Their activity is inhibited by prostaglandin E2 (PGE2); aspirin and other NSAIDs block PGE2 production and allow cytotoxic lymphocytes to attack and eliminate the respiratory tract cells infected by the virus. During this reaction lysosomal enzymes and mediators are released, which could precipitate an asthmatic crisis.Clinically, five types of reaction have been identified: 1. Respiratory illness with aspirin sensitivity. 2. Aspirin-induced urticarial disease. 3. Allergic reactions to NSAIDs and aspirin. 4 and 5. Aseptic meningitis and pneumonitis due to hypersensitivity. The latter are exceptional and are published as case reports. They have never been associated with aspirin or acetaminophen and usually occur in patients undergoing prolonged treatment. Diagnosis is based on a detailed history. Skin tests are not valid and in vitro tests are not widely used. Provocation tests with aspirin and NSAIDs definitively identify sensitized patients but their indications and limitations should be kept in mind. In children, certain features of adverse reactions to NSAIDs are observed in relation to their incidence and clinical manifestations. Acetaminophen is considered the drug of choice but further studies of other alternatives in children are required.

Forty-two adult patients had been evaluated with a history of Urticaria and Angioedema (U-AE) associated with ingestion of non-steroidal anti-inflammatory drugs (NSAID). None developed attacks of bronchospasm. None had chronic urticaria. The same reaction was repeated in 36 individuals on at least two different occasions following administration of these drugs. Based on patients'history we distinguished three groups: Group A: twenty-three patients who had presented U-AE with the administration of pyrazolone drugs. Thereafter, sixteen of them had taken aspirin without adverse reactions. Group B: Nine patients in whom aspirin caused U-AE, after three of them had taken pyrazolone drugs without intolerance. The remaining six had not taken analgesic drugs since the last reaction. Group C: Ten patients who had developed U-AE with aspirin as well as with pyrazolone drugs. The objective of our study was the following: 1) to observe tolerance level of these patients to other NSAID different from those which had produced the first reactions. 2) To test to see if the patients who had suffered U-AE by noramidopyrine and aminophenazone tolerated other pyrazolone drugs like sulfinpyrazone and phenylbutazone. 3) To see if reactions are produced with tartrazine in patients who had presented U-AE with pyrazolone drugs, given that this colouring (tartrazine) is a pyrazolone derivative. Skin test (prick and intracutaneous test) with noramidopyrine, phenylbutazone and noramidopyrine metasulphonate MG, were carried out on the patients in group A, group C and 30 normal controls. In all the groups oral challenge tests were performed with progressive doses of naproxen, indomethacin, paracetamol, ciclofenac, mefenamic acid, piroxicam and phenylbutazone. Oral challenge tests were accomplished with aspirin in group A and with propiphenazone in group B. Oral challenge tests with sulfinpyrazone and tartrazine were also performed on various patients in group A and group C. The interval between the administration of progressive doses of a drug was 3 and as half hours and were allowed to pass at least 24 hours before testing other different analgesics. The test was considered positive if cutaneous rash, wheals, AE or hypotension were produced. In this case, the test was halted and 7 days were allowed to pass before continuing the study with a new drug. Based on the oral challenge tests performed, three types of patients could be distinguished: 1) individuals sensitive only to the pyrazolone drugs and who can take with impunity other NSAID.(ABSTRACT TRUNCATED AT 400 WORDS)