Not only that but she was also having an allergic reaction to the drug, probably because of the synchronous use of Motrin. She had some raised, red bumps all over her body (very itchy), and a scary swelling around her eyes, lips, hands, feet and genitalia.
Stop it! I can not stand it when people blame doctors for things that can and do happen not because of their fault! My boyfriend is a doctor and he says it's not uncommon for aspirin and other NSAIDs to cause reactions of this kind.
http://img58.imageshack.us/my.php?image=jcr40048f1wj1.gifAspirin and NSAIDs may cause anaphylactic or anaphylactoid reactions. Constitutively-expressed cyclooxygenase (COX-1) inhibition is likely to be responsible for the cross-reactions and side effects associated with these drugs, as well as the anaphylactoid reactions sometimes seen in aspirin-sensitive respiratory disease. Though anaphylactic and anaphylactoid reactions may be clinically indistinguishable, they involve different mechanisms. Anaphylactic reactions are due to immediate hypersensitivity involving cross-linking of drug-specific IgE. Regardless of COX selectivity pattern, NSAIDs may function as haptens capable of inducing allergic sensitization. Unlike anaphylaxis, anaphylactoid reactions are most likely related to inhibition of COX-1 by NSAIDS. Thus, an anaphylactoid reaction caused by a particular COX-1 inhibiting NSAID will occur with a chemically unrelated NSAID which also inhibits COX-1 enzymes. Selective COX-2 inhibitors appear to be safe in patients with a history of NSAID-related anaphylactoid reactions but can function as haptens, with resulting sensitization and anaphylaxis upon next exposure.
http://www.springerlink.com/content/794078kl79727x75Type I: Rhinitis and Asthma Induced by NSAIDs. Respiratory tract reactions to NSAIDs typically consist of rhinorrhea, bronchospasm, and layrngospasm. Patients will usually have a past history of asthma, nasal polyps, and/or rhinosinusitis. These reactions to NSAIDs are termed
aspirin-induced asthma,
aspirin sensitivity,
aspirin intolerance, or more appropriately
aspirin-exacerbated respiratory tract disease (AERD). During NSAID-induced respiratory tract reactions, levels of prostaglandin E2 are rapidly depleted due to COX-1 inhibition. In the absence of the braking effect of prostaglandin E2 on 5-LOX activating protein and 5-lipoxygenase, there is unrestrained synthesis of new leukotrienes and release of histamine from mast cells. Patients with AERD are particularly susceptible to the effects of leukotrienes that are manifested by excessive nasoocular and asthmatic reactions. This airway hyperreactivity may become severe enough to require intubation. Furthermore, patients will cross-react with most other NSAIDs because they also inhibit the COX-1 enzyme. Prior studies have demonstrated that most (or the vast majority of) patients with AERD can successfully undergo acetylsalicylic acid desensitization therapy.
Type II: Urticaria/Angioedema Induced by NSAIDs. Patients with a history of chronic idiopathic urticaria (CIU) will frequently experience an exacerbation of their urticaria/angioedema when challenged with acetylsalicylic acid or other NSAIDs. The prevalence of NSAID-induced urticaria in patients with CIU is between 20% and 30%. The pathogenesis of NSAID-induced urticaria is unknown, but similar to AERD, it appears that patients with CIU are sensitive to COX-1 inhibition by NSAIDs. Thus, these patients will cross-react with all NSAIDs that inhibit COX-1. It is believed that excessive leukotriene production by 5-LOX causes increased vasopermeability and subsequent urticaria. Patients in acetylsalicylic acid desensitization protocols have recurrent flare-ups of urticaria until the NSAID is withdrawn.
Type III: Urticaria/Angioedema Induced by Multiple NSAIDs. Some patients without a history of underlying CIU develop urticaria/angioedema after treatment with more than one NSAID that inhibit COX-1. These patients will usually experience urticaria/angioedema that is limited to the skin and extremities without accompanying anaphylaxis.
Type IV: Urticaria/Angioedema Induced by a Single NSAID. In patients without known risk factors for a NSAID reaction who experience urticaria and/or angioedema to a single NSAID, the presumed mechanism is believed to be secondary to an immunologic phenomenon related to IgE antibody production. A single NSAID acts as a hapten with subsequent production of drug-specific IgE antibodies against the NSAID. On repeat exposure to the same NSAID, patients will experience an immune-mediated phenomenon with histamine release related to drug-specific IgE antibody production against the NSAID. Assays to detect the specific IgE antibodies against NSAID haptens have been difficult to develop, however specific IgE antibodies were identified against acetylsalicylic acid in a patient with single drug-induced angioedema. Because these patients react to a single NSAID, antibodies to specific NSAIDs have been identified, and because these reactions occur after multiple exposures to the NSAID and no satisfying alternative mechanism has been discovered, it has been concluded that these reactions are probably IgE mediated.
Type V: Anaphylaxis Induced by a Single NSAID. Similar to a type IV reaction, a single NSAID can induce anaphylaxis via a presumed IgE-mediated reaction. Patients will not cross-react with other NSAIDs, but are rarely desensitized to the specific drug that caused the reaction given that the reaction is drug-specific to a particular NSAID. Similar to a type IV reaction, no specific data exists regarding efficacy of desensitization therapy, but in our experience desensitization therapy is successful a majority of the time if acetylsalicylic acid is specifically needed.
http://jama.ama-assn.org/cgi/content/full/292/24/3017
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