Aspirin and nonsteroidal anti-inflammatory drug hypersensitivity.

Acetylsalicylic acid (ASA) or aspirin and nonsteroidal anti-inflammatory drug (NSAID) sensitivities encompass a diverse group of both pharmacological and hypersensitivity reactions. Conventionally, hypersensitivities include aspirin-exacerbated respiratory disease (AERD), ASA-induced urticaria, and anaphylaxis. With an increasing prevalence of coronary artery disease in an aging population, aspirin continues to play a significant role in cardiac prophylaxis in a large patient population. Invariably, the clinician will encounter patients with clear indications for aspirin therapy but a history of aspirin sensitivity. Although protocols have been established for aspirin challenge and desensitization, it is not always an efficacious or safe procedure. This article reviews the different classifications of ASA/NSAIDs hypersensitivities to better guide the clinician in dealing with this patient population. History of crossrelativities between multiple NSAIDs implies a non-IgE-mediated process. Similarly, a history of monosensitivity to one NSAID implies an IgE-mediated process, although specific antibodies are often elusive. Despite the name, AERD can potentially be exacerbated by all cyclooxygenase (COX) inhibitors based on dose-dependent inhibition of COX-1. Aspirin desensitization can be achieved to improve both upper and lower respiratory symptoms for most patient with AERD. Aspirin desensitization can usually be achieved for those in need of the antiplatelet effects of aspirin, with the exception of those with aspirin-induced urticaria and baseline chronic urticaria. However, desensitization should only be attempted in those with stable coronary artery disease because the process of desensitization carries the inherent risk of anaphylaxis/anaphylactoid reaction, which may further increase cardiac demand and bring about ischemic injury. Therefore, desensitization is reserved until coronary artery disease is stabilized.

Potential adverse events with biologic response modifiers.

In recent years, an explosion of biologic response modifiers has entered the market to combat a variety of immune-mediated diseases. These can be in the form of recombinant cytokines, as in the case of interferon beta in the treatment of multiple sclerosis, or novel engineered antibodies constructed by combining non-human determinants with a human immunoglobulin scaffold, as in the case of omalizumab in the treatment of allergic asthma. More recently, completely human monoclonal antibodies have also been constructed. Adverse reactions related to these agents can be classified as expected or unexpected events. A number of case studies and a handful of randomized trials have demonstrated the potential toxicities with the use of biologic response modifiers. This article aims to review adverse event profiles of select biologic response modifiers for which the most data is available and are common to a rheumatology, allergy/immunology, and dermatology patient population.

Mastocytosis: the great masquerader.

Variants of mastocytosis can present with puzzling cutaneous and systemic symptoms and signs that can result in an erroneous diagnosis of idiopathic urticaria or idiopathic anayphylaxis. The molecular basis of mastocytosis is now better understood, with updated classification based on distinct growth factor and oncogene abnormalities. Elicitation of a full history and careful attention to the skin examination will usually provide the clinician enough information to deduce that the condition is not simply chronic idiopathic urticaria.