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Purpose of Review: The goal of the paper is to review the epidemiology, pathogenesis, diagnosis, and manifestations of perioperative anaphylaxis (POA). We seek to review the most common culprits of POA and different diagnostic modalities for evaluation. Recent Findings: Specific IgE testing has a limited role in POA evaluation due to lack of widespread availability and low sensitivity. Basophil activation testing is complementary to skin tests and can assist NMBA sensitivity diagnosis in complex cases. In the past years, there has been an exponential increase in suspected teicoplanin allergic reactions in the European Union. Chlorhexidine is also being increasingly implicated as a culprit in POA. Summary: Multiple classes of perioperative medications cause POA. Diagnostic modalities available include skin testing with nonirritating concentrations, basophil activation tests, specific IgE, and drug provocation testing. An accurate record and critical analysis of perioperative events is more important than isolated test results. Future studies evaluating the pathophysiology of these reactions and other therapeutic strategies, such as targeting the MRGPRX2 receptor, are needed. [ABSTRACT FROM AUTHOR]

Vaccination is crucial to curtail the spread of SARS-CoV2; however, reports of adverse reactions including allergic reactions have increased public fears of the vaccine.[1] The incidence of true hypersensitivity including both immediate and delayed reactions is estimated at ~13 cases per million.[2] Delayed allergic reactions are heterogeneous, and there are limited reports regarding delayed reactions to the SARS-CoV2 mRNA vaccines. Patient-reported delayed reactions did not preclude tolerance of subsequent vaccine doses in any of the patients who elected to receive their second vaccine dose. Of the 8 patients, 6 patients received the second vaccine dose following standard protocol and 2 patients received the vaccine via graded-dose challenge, receiving 10% first followed by 90% the following week based on the time course of the index reaction. [Extracted from the article]

The model of asthma as a single entity has now been replaced by a much more complex biological network of distinct and interrelating inflammatory pathways. The term asthma is now considered an umbrella diagnosis for several diseases with distinct mechanistic pathways (endotypes) and variable clinical presentations (phenotypes). The precise definition of these endotypes is central to asthma management due to inherent therapeutic and prognostic implications. This review presents the molecular mechanisms behind the heterogeneity of airway inflammation in asthmatic patients. Asthma endotypes may be broadly regarded as type 2 (T2) high or T2-low. Several biologic agents have been approved for T2-high asthma, with numerous other therapeutics that are incipient and similarly targeted at specific molecular mechanisms. Collectively, these advances have shifted existing paradigms in the approach to asthma to tailor novel therapies. [ABSTRACT FROM AUTHOR]

While peripheral or tissue eosinophilia may certainly characterize drug eruptions, this feature is hardly pathognomonic for a medication-induced etiology. While delayed drug hypersensitivity reactions with prominent eosinophilic recruitment have been typically classified as type IVb reactions, their pathophysiology is now known to be more complex. Eosinophilic drug reactions have a diversity of presentations and may be benign and self-limited to severe and life-threatening. The extent of clinical involvement is also heterogeneous, ranging from isolated peripheral eosinophilia or single organ involvement (most often the skin and lung) to systemic disease affecting multiple organs, classically exemplified by drug-reaction with eosinophilia and systemic symptoms (DRESS). The spectrum of implicated medications in the causation of DRESS is ever expanding, and multiple factors including drug metabolites, specific HLA alleles, herpes viruses, and immune system activation have been implicated in pathogenesis. Due to this complex interplay of various factors, diagnostic workup in terms of skin and laboratory testing has not been validated. Similarly, the lack of controlled trials limits treatment options. This review also describes other localized as well as systemic manifestations of eosinophilic disease induced by various medication classes, including their individual pathophysiology, diagnosis, and management. Given the multitude of clinical patterns associated with eosinophilic drug allergy, the diagnosis can be challenging. Considerable deficits in our knowledge of these presentations remain, but the potential for severe reactions should be borne in mind in order to facilitate diagnosis and institute appropriate management. [ABSTRACT FROM AUTHOR]