* Ibuprofen is representative of all nonsteroidal anti-inflammatory drugs (NSAIDs). In breastfeeding patients, avoid cyclooxygenase (COX-2) selective inhibitors such as celecoxib because of scarcity of data, and avoid dose of aspirin >100 mg because of risk of platelet dysfunction and Reye’s syndrome. ** In the case of combination products (such as oxycodone with acetaminophen), the safety with respect to either pregnancy or breastfeeding is dependent on the highest risk moiety. For example, the combination of oxycodone and acetaminophen would be used with caution, since the oxycodone moiety carries the higher risk. *** Oral steroids should not be withheld in acute severe asthma. Note . Adapted from “Pregnancy, Breast-Feeding and Drugs Used in Dentistry,” by M. Donaldson and J. H. Goodchild, 2012, Journal of the American Dental Association, 143 (8), 858-871. Allergy status
The various NSAIDs inhibit COX-1 and COX-2 to different degrees. Aspirin (acetylsalicylic acid, or ASA) is a stronger inhibitor of COX-1 than COX-2, and NSAIDs that similarly inhibit
COX-1 over COX-2 are said to be cross-reactive with ASA (Table 10; Kowalski et al., 2013).
Table 10: NSAIDs and Aspirin Cross-Reactivity (Strength of COX-1 and COX-2 Inhibition) NSAIDs that preferentially inhibit COX-1 and cross-react with aspirin: • Diclofenac • Etodolac • Meclofenamate • Mefenamic acid
• Ibuprofen • Indomethacin • Ketoprofen • Ketorolac
• Piroxicam • Sulindac • Tolmetin
• Fenoprofen • Flurbiprofen
• Naproxen • Oxaprozin
Nonopioid analgesics and nonacetylated salicylates that are poor inhibitors of COX-1, work only with higher concentrations of the drug, and cross-react with aspirin when prescribed in higher doses : • Acetaminophen. • Choline magnesium trisalicylate. • Salsalate. • Diflunisal. NSAIDs that preferentially inhibit COX-2 but also inhibit COX-1 and cross-react with aspirin at higher doses : • Meloxicam. • Nabumetone. Highly selective COX-2 inhibitor that does not inhibit COX-1; cross-reactions are rare, though they may occur at the highest doses : • Celecoxib. Note . Adapted from “Classification and Practical Approach to the Diagnosis and Management of Hypersensitivity to Nonsteroidal Anti-Inflammatory Drugs,” by E. Mogilnicka, A. Romano, A. Szczeklik, S. Testi, M. J. Torres, S. Wöhrl, & J. Makowska, 2013, Allergy, 68(10), 1219-1232. NSAIDs that inhibit both COX-1 and COX-2 are called
Figure 5: The Spectrum of COX-1 versus COX-2 Selectivity for a Majority of the Commonly Prescribed Analgesics
nonselective , and those that predominantly inhibit COX-2 are called COX-2 selective . Within the group of selective NSAIDs are those that are weakly selective for COX-2 but also inhibit COX-1, such as nabumetone and meloxicam. Other agents, such as celecoxib, are considered highly selective for COX-2. Figure 5 demonstrates the spectrum of COX-1 versus COX-2 selectivity for a majority of the commonly prescribed analgesics. Cyclooxygenase isoenzymes selectivity is important to understand in order to select appropriate treatment options for patients who may report an allergy to NSAIDs. Many patients report an allergic history to certain analgesics, which begins to limit the treatment options in managing their oral health. The prudent practitioner should first validate the allergic status by inquiring into the circumstances and allergic reaction reported by the patient. In every case in which the patient reports a reaction that affected his or her breathing (e.g., tongue or throat swelled up, acutely compromising the airway) or reports having been taken to the hospital because of an allergic reaction to an analgesic, this type of immediate, Type 1 IgE-mediated anaphylactic reaction may be considered a true allergy, and future exposure to this medicine should be avoided. For patients who report an intolerance or delayed- type reaction, re-exposure to the medicine may not necessarily be life-threatening and may in fact be considered if the benefit of treatment outweighs the potential risk of the reaction (e.g., diarrhea, itchiness or other mild cutaneous reactions).
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