Vaccines constitute the most effective medications in public health as they control and prevent the spread of infectious diseases and reduce mortality. Similar to other medications, allergic reactions can occur during vaccination. While most reactions are neither frequent nor serious, anaphylactic reactions are potentially life-threatening allergic reactions that are encountered rarely, but can cause serious complications. The allergic responses caused by vaccines can stem from activation of mast cells via Fcε receptor-1 type I reaction, mediated by the interaction between immunoglobulin E (IgE) antibodies against a particular vaccine, and occur within minutes or up to four hours. The type IV allergic reactions initiate 48 h after vaccination and demonstrate their peak between 72 and 96 h. Non-IgE-mediated mast cell degranulation via activation of the complement system and via activation of the Mas-related G protein-coupled receptor X2 can also induce allergic reactions. Reactions are more often caused by inert substances, called excipients, which are added to vaccines to improve stability and absorption, increase solubility, influence palatability, or create a distinctive appearance, and not by the active vaccine itself. Polyethylene glycol, also known as macrogol, in the currently available Pfizer-BioNTech and Moderna COVID-19 mRNA vaccines, and polysorbate 80, also known as Tween 80, in AstraZeneca and Johnson & Johnson COVID-19 vaccines, are excipients mostly incriminated for allergic reactions. This review will summarize the current state of knowledge of immediate and delayed allergic reactions in the currently available vaccines against COVID-19, together with the general and specific therapeutic considerations. These considerations include: The incidence of allergic reactions and deaths under investigation with the available vaccines, application of vaccination in patients with mast cell disease, patients who developed an allergy during the first dose, vasovagal symptoms masquerading as allergic reactions, the COVID-19 vaccination in pregnancy, deaths associated with COVID-19 vaccination, and questions arising in managing of this current ordeal. Careful vaccine-safety surveillance over time, in conjunction with the elucidation of mechanisms of adverse events across different COVID-19 vaccine platforms, will contribute to the development of a safe vaccine strategy. Allergists’ expertise in proper diagnosis and treatment of allergic reactions is vital for the screening of high-risk individuals.

Context: This study was performed to evaluate the effects of genistein on metabolic and cardiovascular risk factors in Caucasian postmenopausal subjects with metabolic syndrome (MetS). Objective: Our objective was to assess the effects of genistein on surrogate endpoints associated with diabetes and cardiovascular disease. Design and Setting: This was a randomized, double-blind, placebo-controlled trial at 3 university medical centers in Italy. Patients: Patients included 120 postmenopausal women with MetS according to modified Third Report of the National Cholesterol Education Program (NCEP), Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) criteria. Intervention: After a 4-week stabilization period, postmenopausal women with MetS were randomly assigned to receive placebo (n = 60) or 54 mg genistein daily (n = 60) for 1 year. Main Outcome Measures: The primary outcome was homeostasis model assessment for insulin resistance (HOMA-IR) at 1 year. Secondary outcomes were fasting glucose, fasting insulin, total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides, visfatin, adiponectin, and homocysteine levels. Data on adverse events were also recorded. Results: At 1 year in genistein recipients, fasting glucose, fasting insulin, and HOMA-IR (mean from 4.5 to 2.7; P < .001) decreased and were unchanged in placebo recipients. Genistein statistically increased HDL-C (mean from 46.4 to 56.8 mg/dL) and adiponectin and decreased total cholesterol, LDL-C (mean from 108.8 to 78.7 mg/dL), triglycerides, visfatin, and homocysteine (mean from 14.3 to 11.7 μmol/L) blood levels. Systolic and diastolic blood pressure was also reduced in genistein recipients. Genistein recipients neither experienced more side adverse effects than placebo nor discontinued the study. Conclusion: One year of treatment with genistein improves surrogate endpoints associated with risk for diabetes and cardiovascular disease in postmenopausal women with MetS.

Background—: Age, estimated glomerular renal function (eGFR), and ejection fraction are preprocedural predictors of contrast-induced acute kidney injury (CI-AKI) after primary percutaneous coronary intervention. The effect of renal function–adjusted contrast volume (CV) remains not totally explored, and a threshold has not yet been established. Methods and Results—: Logistic regression and receiver-operating characteristic curve analyses were used to assess whether CV/eGFR was an independent predictor of CI-AKI. The increased discriminative value of CV/eGFR over the preprocedural model based on age, eGFR, and ejection fraction was examined using the net reclassification improvement analysis. Of 470 patients enrolled, we observed 25 (5.3%) cases of CI-AKI. Patients with CI-AKI had received a higher renal function–adjusted CV (CV/eGFR 3.62 versus 1.96; P <0.001), and CI-AKI incidence was higher (15%; P 2.5; area under the curve, 0.77). At multivariable analysis, CV/eGFR above the cutoff (odds ratio, 5.57; P =0.002) remained an independent predictor of CI-AKI. The model with CV/eGFR demonstrated a statistically significantly net reclassification improvement of 0.23 ( P =0.021) over the baseline preprocedural model, largely driven by a correct decrease in risk estimates for patients not experiencing CI-AKI, with a likelihood ratio χ ² of 5.973 ( P =0.029). Conclusions—: CV remains a key risk factor for CI-AKI after primary percutaneous coronary intervention and our study supports the need for minimizing CV, independently from baseline preprocedural risk. A CV restricted to no more than twice and a half the baseline eGFR might be valuable in reducing the risk of CI-AKI.

Hypertrophic cardiomyopathy (HCM) is a genetic heart disease characterized by the thickening of the heart muscle, which can lead to symptoms such as chest pain, shortness of breath, and an increased risk of sudden cardiac death. However, not all patients with HCM have the same underlying genetic mutations, and some have conditions that resemble HCM but have different genetic or pathophysiological mechanisms, referred to as phenocopies. Cardiac magnetic resonance (CMR) imaging has emerged as a powerful tool for the non-invasive assessment of HCM and its phenocopies. CMR can accurately quantify the extent and distribution of hypertrophy, assess the presence and severity of myocardial fibrosis, and detect associated abnormalities. In the context of phenocopies, CMR can aid in the differentiation between HCM and other diseases that present with HCM-like features, such as cardiac amyloidosis (CA), Anderson–Fabry disease (AFD), and mitochondrial cardiomyopathies. CMR can provide important diagnostic and prognostic information that can guide clinical decision-making and management strategies. This review aims to describe the available evidence of the role of CMR in the assessment of hypertrophic phenotype and its diagnostic and prognostic implications.