Kounis syndrome (KS) is a hypersensitivity-associated acute coronary syndrome. Food-associated KS remains poorly characterized, and its clinical presentation may be mimicked by non-immune food-related toxic reactions. To characterize the food exposures, clinical and cardiovascular presentations, allergological assessment, potential cofactors, KS phenotypes, management, and outcomes reported in food-associated KS. PubMed, Scopus, and Web of Science Core Collection were searched from inception to August 22, 2026. Original case reports, case series, and sufficiently informative conference reports describing objective coronary involvement temporally associated with a food or food-derived exposure were included. Patient-level data were synthesized qualitatively. KS diagnostic certainty, coronary phenotype, food causality, and presumed mechanism were assessed separately. Planned sensitivity analyses restricted the synthesis to confirmed or suspected food allergy, definite or probable KS, and cases without epinephrine administration before coronary onset or its first objective documentation. The synthesis included 50 publications or reports describing 53 unique patients. Food-related mechanisms comprised confirmed food allergy in 20 patients, clinically suspected food allergy in 26, scombroid poisoning in six, and a Coprinopsis atramentaria-alcohol interaction in one. The reported coronary spectrum ranged from transient vasospasm and nonobstructive presentations to plaque-related myocardial infarction, native-coronary thrombosis, and stent or graft thrombosis. Type I was the most frequently assigned phenotype. Allergological assessment, paired acute and baseline tryptase measurements, treatment chronology, and long-term follow-up were inconsistently reported. The main cardiovascular patterns remained broadly consistent across the planned sensitivity analyses. Food-associated KS encompasses a heterogeneous spectrum of allergic coronary presentations. Clinically similar non-immune food-related toxic reactions, including scombroid poisoning, should be recognized as differential diagnoses and analyzed separately from true allergic KS. Diagnosis requires integration of exposure chronology, objective cardiovascular findings, coronary substrate, allergological evidence, potential cofactors, and competing exposures. Intramuscular epinephrine remains the first-line treatment for anaphylaxis, and temporal precedence should not be interpreted as evidence that epinephrine caused the coronary event.

Kounis syndrome is an acute coronary syndrome triggered by an allergic or anaphylactic reaction. Diagnosis can be challenging when epinephrine is administered during the same episode because both the allergic reaction and epinephrine may influence coronary vascular tone. We report the case of a 62-year-old man with no previous cardiac history who developed anaphylactic shock after a hornet sting to the upper lip. Acute constrictive chest pain began during the allergic reaction, before epinephrine administration. He was promptly treated with 0.55 mg of epinephrine, methylprednisolone, and dexchlorpheniramine. An electrocardiogram obtained during the acute episode showed ST-segment depression in leads III, aVF, and V3-V6. The chest pain and electrocardiographic abnormalities subsequently resolved. Troponin peaked at 208 ng/L. Transthoracic echocardiography showed preserved left ventricular systolic function without regional wall-motion abnormalities. Coronary angiography revealed only minor non-obstructive coronary irregularities, with no culprit lesion, and follow-up cardiac magnetic resonance imaging was normal. The overall presentation was consistent with type I Kounis syndrome, most likely caused by transient allergy-mediated coronary vasospasm. The onset of chest pain before epinephrine administration was an important element supporting the allergic coronary event as the primary mechanism.

Hypersensitivity reactions to intravenous therapies-including antibiotics, chemotherapeutics, biologics, anesthesia agents, and contrast media-pose significant challenges in acute care settings. These reactions often occur outside the purview of allergy specialists, leading to delays in recognition, suboptimal management, and inconsistent documentation. This article underscores the imperative for proactive, multidisciplinary collaboration to enhance patient safety and treatment continuity. We examine the spectrum of intravenous reactions, including anaphylaxis, highlighting the pivotal role of allergists in both acute intervention and long-term care planning. Emphasis is placed on the development of standardized protocols, the establishment of inpatient allergy consult teams, and the implementation of penicillin allergy delabeling strategies. Supplemental materials provide real-world examples from leading institutions that have successfully integrated multidisciplinary approaches, demonstrating improved outcomes through coordinated care. By proactively engaging in the creation of safety protocols, referral pathways, and joint models of care, allergy specialists can contribute significantly to safer patient environments, even before reactions occur, ensuring timely diagnosis, effective management, and optimal outcomes.

Based on current data, immediate activation of EMS in all cases of anaphylaxis does not provide significant benefit. Instead, the option for home management or a "watchful-waiting" approach allowing for increased patient autonomy in anaphylaxis management and emphasizing prompt epinephrine use at home. In this model, patients are instructed to quickly administer epinephrine and monitor for resolution of symptoms. The option to escalate care is available, but in 90% of cases, symptoms will resolve after one dose of epinephrine, rendering EMS/ED involvement unnecessary. Thus, patients can immediately treat their anaphylaxis from the comfort of home while avoiding complications from delayed epinephrine use.

Anaphylaxis is an acute, potentially fatal systemic hypersensitivity reaction characterized by striking variability in onset and severity. Although it is traditionally attributed to IgE-mediated activation of mast cells and basophils, multiple IgE-independent pathways are increasingly recognized, including IgG-mediated mechanisms, MRGPRX2-dependent mast-cell activation, and complement-derived anaphylatoxin signaling. Beyond the immune mechanisms, accumulating experimental evidence suggests that neuronal circuits may participate early and contribute to disease severity. In this narrative review, we synthesize mechanistic and translational evidence supporting a receptor-level framework in which mast-cell mediators and proteases activate and sensitize TRPV1/TRPA1-expressing sensory neurons through protease-activated receptor (PAR) signaling. Subsequent neuronal activation can trigger the release of neuropeptides, including substance P and calcitonin gene-related peptide (CGRP), which may contribute to vascular leakage and systemic manifestations while further amplifying mast-cell activation, including through MRGPRX2. Together, these interactions support the concept of a self-reinforcing neuroimmune amplification loop that may help explain the rapid onset and clinical heterogeneity of anaphylaxis. We propose this framework as a conceptual model to integrate current evidence, highlight potential adjunct therapeutic strategies beyond epinephrine, and identify key priorities for future translational and clinical research while acknowledging the current limitations of human evidence.

Perioperative hypersensitivity reactions are uncommon but potentially life-threatening complications of anaesthesia and remain a major concern in clinical practice. This review provides an updated overview of the mechanisms and aetiologies underlying perioperative hypersensitivity and examines contemporary diagnostic strategies for identifying the responsible agent. Emphasis is placed on the integration of clinical assessment with laboratory and functional testing to establish an accurate diagnosis and guide the selection of safe alternatives for subsequent anaesthetic procedures. Current evidence is complemented by the authors' extensive clinical experience in the field.

Different types of Botulinum neurotoxins (BoNTs) cause human botulism. Among them, type F botulism, caused by genetically diverse BoNT/F subtypes, is rare and may be overlooked despite its clinical importance. Toxin-neutralizing human antibodies, which carry the minimum risks of inducing serum sickness or anaphylaxis, are ideal for the treatment of human botulism. In this study, we generated human monoclonal antibodies (mAb) against BoNT/F using trans-chromosomic monoclonal antibody (TC-mAb) mice. A recombinant toxin fragment consisting of the light chain and the heavy chain N-terminal domain (L-HN) of BoNT/F subtype 1 was selected as the antigen because this subtype is used as the reference antigen for currently available antitoxin preparations. Three mAbs (126, 134, and 146) were obtained and reconstructed in a human IgG format. Although the mAbs did not significantly inhibit VAMP2 cleavage in primary cultured neurons, they exhibited partial neutralizing activities in mouse bioassays. In addition, we found that the combinatorial use of 126 and 146 enhanced neutralizing activity. These findings provide important information for the future development of human therapeutic mAbs against BoNT/F.