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Background Anaphylaxis, which is rare, has been reported after COVID‐19 vaccination, but its management is not standardized. Method Members of the European Network for Drug Allergy and the European Academy of Allergy and Clinical Immunology interested in drug allergy participated in an online questionnaire on pre‐vaccination screening and management of allergic reactions to COVID‐19 vaccines, and literature was analysed. Results No death due to anaphylaxis to COVID‐19 vaccines has been confirmed in scientific literature. Potential allergens, polyethylene glycol (PEG), polysorbate and tromethamine are excipients. The authors propose allergy evaluation of persons with the following histories: 1—anaphylaxis to injectable drug or vaccine containing PEG or derivatives; 2—anaphylaxis to oral/topical PEG containing products; 3—recurrent anaphylaxis of unknown cause; 4—suspected or confirmed allergy to any mRNA vaccine; and 5—confirmed allergy to PEG or derivatives. We recommend a prick‐to‐prick skin test with the left‐over solution in the suspected vaccine vial to avoid waste. Prick test panel should include PEG 4000 or 3500, PEG 2000 and polysorbate 80. The value of in vitro test is arguable. Conclusions These recommendations will lead to a better knowledge of the management and mechanisms involved in anaphylaxis to COVID‐19 vaccines and enable more people with history of allergy to be vaccinated.
Accurate assessment of risk factors for nosocomial acquisition of colonization by antibiotic-resistant bacteria (ARB) is often confounded by scarce data on antibiotic use. A 12-month, nested, multicenter cohort study was conducted. Target ARB were methicillin (meticillin)-resistant Staphylococcus aureus (MRSA), vancomycinresistant enterococci (VRE), and ciprofloxacin-resistant Pseudomonas aeruginosa (CR-PA). Nares and rectal swabs were obtained before and after starting antibiotics. Pulsed-field gel electrophoresis was done to define genetic relatedness of the strains. Primary outcomes were (i) the mean time, in days, for acquisition of target ARB colonization in patients previously not colonized; (ii) the rate of acquisition per 1,000 antibiotic-days according to different classes of antibiotics; (iii) the rate of infection caused by the same bacteria as those previously isolated in screening samples; and (iv) the risk factors for ARB acquisition. In total, 6,245 swabs from 864 inpatients were processed. The rate of acquisition was 3%, 2%, and 1% for MRSA, VRE, and CR-PA, respectively. The rate of acquisition of ARB per 1,000 antibiotic-days was 14 for carbapenems, 9 for glycopeptides, and 6 for broad-spectrum cephalosporins and quinolones. The highest rates of acquisition were observed for carbapenems in dialyzed and diabetic patients. Four risk factors were independently associated with acquisition of target ARB: use of carbapenems, age of >70 years, hospitalization for >16 days, and human immunodeficiency virus infection. During the 30-day follow-up, 4 among 42 patients newly colonized by ARB (9%) suffered from an infection due to the same bacteria as those isolated in a previous screening sample. Colonizing and infecting strains from single patients were genotypically identical. Identifying ARB colonization early during antibiotic therapy could target a high-risk hospitalized population that may benefit from intervention to decrease the risk of subsequent nosocomial infections.The control of nosocomial antibiotic-resistant infections is a public health priority worldwide. Meta-analyses have documented that bloodstream infection caused by methicillin (meticillin)-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococci (VRE), extended-spectrum -lactamase-producing Enterobacteriaceae, and multidrug-resistant Acinetobacter baumannii are associated significantly with mortality (7,9,11,24). Numerous papers have demonstrated that prior antimicrobial drug exposure is a strong risk factor for colonization and infection due to a drug-resistant pathogen (2,25,27). However, the association between antibiotic therapy and the acquisition of antibiotic-resistant bacteria (ARB) is still unclear and is often confounded by scarce data on antibiotic usage. In our opinion, two major questions are still unsolved. When does an antibiotic select colonizing ARB in a hospitalized patient? Is there a direct correlation between hospital antibiotic usage, acquisition of ARB colonization, and subsequent bacterial infe...
Background: Hereditary angioedema (HAE) comprises HAE with C1-inhibitor deficiency (C1-INH-HAE) and HAE with normal C1-INH activity (nl-C1-INH-HAE), due to mutations in factor XII (FXII-HAE), plasminogen (PLG-HAE), angiopoietin 1 (ANGPT1-HAE), kininogen 1 genes (KNG1-HAE), or angioedema of unknown origin (U-HAE). The Italian network for C1-INH-HAE (ITACA) created a registry including different forms of angioedema without wheals. Objective: We analyzed clinical and laboratory features of a cohort of Italian subjects with nl-C1-INH-HAE followed by ITACA to identify specific biomarkers. Methods: A total of 105 nl-C1-INH-HAE patients were studied. Plasma concentrations of cleaved high-molecular-weight kininogen (cHK), vascular endothelial growth factors (VEGFs), angiopoietins (Angs), and secreted phospholipase A 2 enzymes (sPLA 2 ) were evaluated. Results:We identified 43 FXII-HAE patients, 58 U-HAE, and 4 ANGPT1-HAE. We assessed a prevalence of 1:1.4 × 10 6 for FXII-HAE and 1:1.0 × 10 6 for U-HAE. cHK levels in U-HAE patients were similar to controls in plasma collected using protease inhibitors cocktail (PIC), but they significantly increased in the absence of PIC. In FXII-HAE patients, cHK levels, in the absence of PIC, were significantly higher than in controls. We found a significant increase of VEGF-A, VEGF-C, and Ang1 levels in U-HAE patients compared to controls. In FXII-HAE, only VEGF-C levels were increased. Ang2 concentrations and sPLA 2 activity were not modified. The levels of these mediators in ANGPT1-HAE patients were not altered. Conclusions:Our results suggest that pathogenesis of FXII-, ANGPT1-, and U-HAE moves through an unbalanced control of kallikrein activity, with bradykinin as most likely mediator. VEGFs and Ang1 participate in the pathophysiology of U-HAE increasing the basal vascular permeability. K E Y W O R D S angioedema, biomarkers, epidemiology, genetic | 1395 BOVA et Al.
Background: Urticaria is a disorder affecting skin and mucosal tissues characterized by the occurrence of wheals, angioedema or both, the latter defining the urticaria-angioedema syndrome. It is estimated that 12-22% of the general population has suffered at least one subtype of urticaria during life, but only a small percentage (estimated at 7.6-16%) has acute urticaria, because it is usually self-limited and resolves spontaneously without requiring medical attention. This makes likely that its incidence is underestimated. The epidemiological data currently available on chronic urticaria in many cases are deeply discordant and not univocal, but a recent Italian study, based on the consultation of a national registry, reports a prevalence of chronic spontaneous urticaria of 0.02% to 0.4% and an incidence of 0.1-1.5 cases/1000 inhabitants/year. Methods: We reviewed the recent international guidelines about urticaria and we described a methodologic approach based on classification, pathophysiology, impact on quality of life, diagnosis and prognosis, differential diagnosis and management of all the types of urticaria. Conclusions: The aim of the present document from the Italian Society of Allergology, Asthma and Clinical Immunology (SIAAIC) and the Italian Society of Allergological, Occupational and Environmental Dermatology (SIDAPA) is to provide updated information to all physicians involved in diagnosis and management of urticaria and angioedema.
Adverse reactions to iodinated contrast media (ICM) are reported in 1%-3% of diagnostic procedures. They represent a relevant problem involving patients' safety as well as relevant costs for healthcare systems. Premedication with antihistamines and corticosteroids is still widely used, but evidence of its efficacy is lacking and there is a risk for underestimation of possible severe adverse reactions to ICM in those who undergo premedication. Data from 98 patients with a previous reaction to ICM that consecutively referred to our unit between 2015 and 2018 were retrospectively analyzed. They underwent an allergologic workup comprehending skin tests and drug provocation tests (DPT) with ICM. The skin test showed a very high negative predictive value (NPV) compared to DPT in patients with a previous immediate adverse reaction, while the NPV in patients with a previous delayed adverse reaction was lower. After completion of the allergologic workup, 94 patients (95.9%) could tolerate a DPT with the culprit or alternative ICM. Subsequently, 90 patients were reached by phone to assess if they had been re-exposed to ICM for radiologic procedure. Thirty-nine patients had been re-exposed, without any premedication in 13 cases: 12 of them had tolerated the ICM, while one reacted again despite a negative DPT with the same ICM. Overall, the NPV of this protocol was elevated (92.3%) for patients undergoing DPT and subsequent exposure to the same ICM in a real-life setting. Collaboration between the prescribing physician, the radiologist and the allergist, and an accurate allergologic workup are essential to ensure maximum safety for the patient.
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