Cinco reações adversas de medicações para se ter em mente: From the Joint Task Force Guidelines

Information sourced from AHRQ:
Drug allergy: an updated practice parameter
Joint Task Force on Practice Parameters, American Academy of Allergy, Asthma and Immunology, American College of Allergy, Asthma and Immunology, Joint Council of Allergy, Asthma and Immunology. Drug allergy: an updated practice parameter. Ann Allergy Asthma Immunol 2010 Oct;105(4):259-273.e78.
[Free full-text Ann Allergy Asthma Immunol article PDF | PubMed® abstract | National Guideline Clearinghouse version]
[EXCERPTS]
Major Recommendations
Diabetes Medications

• The advent of human recombinant insulin has greatly reduced the incidence of life-threatening allergic reactions to approximately 1%. (C)
• Metformin and sulfonylurea antidiabetic drugs rarely cause immune-mediated reactions, such as leukocytoclastic vasculitis, generalized arteritis, granulomatous hepatitis, and autoimmune pemphigus vulgaris. (C)

Opiates

• Opiates and their analogs are a common cause of pseudoallergic reactions that are generally mild, are not life-threatening, and can be attenuated by preadministration of histamine₁ receptor antihistamines. (C)

Heparin

• Hypersensitivity reactions to unfractionated heparin and low-molecular-weight heparin are uncommon and include thrombocytopenia, various cutaneous eruptions, hypereosinophilia, and anaphylaxis. (C)

Local Anesthetics

• Most adverse reactions to local anesthetics are not due to IgE-mediated mechanisms but are due to nonallergic factors that include vasovagal responses, anxiety, toxic reactions including dysrhythmias, and toxic or idiosyncratic reactions due to inadvertent intravenous epinephrine effects. (C)
• To exclude the rare possibility of an IgE-mediated reaction to local anesthetics, skin testing and graded challenge can be performed in patients who present with a reaction history suggestive of possible IgE-mediated allergy to these drugs. (B)

Angiotensin-Converting Enzyme (ACE) Inhibitors

• ACE inhibitors are associated with 2 major adverse effects—cough and angioedema. (C)
• ACE inhibitor–related cough often begins within the first few weeks of treatment and occurs in up to 20% of patients, particularly women, blacks, and Asians. (C)
• The mechanism of ACE inhibitor–related cough is unclear. The cough resolves with discontinuation of the drug therapy in days to weeks. (D)
• Patients with ACE inhibitor–related cough are able to tolerate angiotensin receptor blockers (ARBs). (A)
• ACE inhibitor–induced angioedema occurs in approximately 0.1% to 0.7% of patients and is most common in blacks. (C)
• ACE inhibitor–induced angioedema frequently involves the face and oropharynx and can be life-threatening or fatal. (C)
• The mechanism of ACE inhibitor–induced angioedema may be related to interference with bradykinin degradation. It may take months or years after initiation of therapy for a reaction to appear and often occurs sporadically despite persistent treatment. (C)
• ACE inhibitor–induced angioedema is treated with discontinuation of the drug therapy and subsequent avoidance of all ACE inhibitors. (D)
• Most patients who experience angioedema during ACE inhibitor treatment are able to tolerate ARBs. (C)
• Patients with a history of angioedema or C1 esterase inhibitor deficiency are at increased risk of more frequent and severe episodes of angioedema with the administration of ACE inhibitors, so they should not receive these drugs. (C)

[Definitions - Strength of the Recommendations available online]
[Link to free full-text guideline: Ann Allergy Asthma Immunol article PDF | NGC version online]
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