Prevalence of peanut and tree nut allergy in the US determined by a random digit dial telephone survey

Background: Allergy to peanuts and tree nuts (TNs) is one of the leading causes of fatal and near-fatal food-induced allergic reactions. These allergies can be lifelong and appear to be increasing in prevalence. Despite the seriousness of these allergies, the prevalence of peanut and TN allergy in the general population is unknown. Objective: We sought to determine the prevalence of peanut and TN allergy among the general population of the United States. Methods: We used a nationwide, cross-sectional, random digit dial telephone survey with a standardized questionnaire. Results: A total of 4374 households contacted by telephone participated (participation rate, 67%), representing 12,032 individuals. Peanut or TN allergy was self-reported in 164 individuals (1.4%; 95% confidence interval [CI], 1.2%-1.6%) in 151 households (3.5%; 95% CI, 2.9%-4.0%). The prevalence of reported allergy in adults (1.6%) was higher than that found in children under 18 years of age (0.6%). In 131 individuals, details of the reactions were obtained. When applying criteria requiring reactions to be typical of IgE-mediated reactions (hives, angioedema, wheezing, throat tightness, vomiting, and diarrhea) within an hour of ingestion, 10% of these subjects were excluded. Among the remaining 118 subjects, allergic reactions involved 1 organ system (skin, respiratory, or gastrointestinal systems) in 50 subjects, 2 in 45 subjects, and all 3 in 23 subjects. Forty-five percent of these 118 respondents reported more than 5 lifetime reactions. Only 53% of these 118 subjects ever saw a physician for the allergic reaction, and only 7% had self-injectable epinephrine available at the time of the interview. The prevalence of peanut and TN allergy was adjusted by assuming that 10% of the remaining 33 subjects without a description of their reactions would also be excluded and correcting for a 7% false-positive rate for the survey instrument. A final “corrected” prevalence estimate of 1.1% (95% CI, 1.0%-1.4%) was obtained. Conclusions: Peanut and/or TN allergy affects approximately 1.1% of the general population, or about 3 million Americans, representing a significant health concern. Despite the severity of reactions, about half of the subjects never sought an evaluation by a physician, and only a few had epinephrine available for emergency use

Pancreatic cancer and autoimmune diseases: An association sustained by computational and epidemiological case-control approaches

This is the peer reviewed version of the following article: Gomez‐Rubio, P. , Piñero, J. , Molina‐Montes, E. , Gutiérrez‐Sacristán, A. , Marquez, M. , Rava, M. , Michalski, C. W., Farré, A. , Molero, X. , Löhr, M. , Perea, J. , Greenhalf, W. , O'Rorke, M. , Tardón, A. , Gress, T. , Barberá, V. M., Crnogorac‐Jurcevic, T. , Muñoz‐Bellvís, L. , Domínguez‐Muñoz, E. , Balsells, J. , Costello, E. , Yu, J. , Iglesias, M. , Ilzarbe, L. , Kleeff, J. , Kong, B. , Mora, J. , Murray, L. , O'Driscoll, D. , Poves, I. , Lawlor, R. T., Ye, W. , Hidalgo, M. , Scarpa, A. , Sharp, L. , Carrato, A. , Real, F. X., Furlong, L. I., Malats, N. and , (2019), Pancreatic cancer and autoimmune diseases: An association sustained by computational and epidemiological case–control approaches. Int. J. Cancer. doi:10.1002/ijc.31866, which has been published in final form at https://doi.org/10.1002/ijc.31866. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.Acción Especial de Genómica, Spain. Grant Number: #GEN2001‐4748‐c05‐03 Swedish ALF. Grant Number: #SLL20130022 Cancer Focus Northern Ireland and Department for Employment and Learning EU H2020 Programme 2014‐2020. Grant Number: 634143 MedBioinformatics676559 Elixir‐Excelerate EU‐6FP Integrated Project. Grant Number: #018771‐MOLDIAG‐PACA EU‐FP7‐HEALTH. Grant Number: #256974‐EPC‐TM‐Net#259737‐CANCERALIA#602783‐ Cam‐Pac Italian Foundation for Cancer Research (FIRC) Italian Ministry of Health. Grant Number: FIMPCUP_J33G13000210001 Red Temática de Investigación Cooperativa en Cáncer, Spain. Grant Number: #RD12/0036/0050#RD12/0036/ 0073(#RD12/0036/0034 The work was partially supported by Fondo de Investigaciones Sanitarias (FIS), Instituto de Salud Carlos III‐FEDER, Spain. Grant Number: #PI0902102#PI11/01542#PI12/ 00815#PI12/01635#PI13/ 00082CP10/00524PI15/01573 World Cancer Research Fund. Grant Number: WCR #15‐039

A systems approach identifies time-dependent associations of multimorbidities with pancreatic cancer risk

Background Pancreatic ductal adenocarcinoma (PDAC) is usually diagnosed in late adulthood; therefore, many patients suffer or have suffered from other diseases. Identifying disease patterns associated with PDAC risk may enable a better characterization of high-risk patients. Methods Multimorbidity patterns (MPs) were assessed from 17 self-reported conditions using hierarchical clustering, principal component, and factor analyses in 1705 PDAC cases and 1084 controls from a European population. Their association with PDAC was evaluated using adjusted logistic regression models. Time since diagnosis of morbidities to PDAC diagnosis/recruitment was stratified into recent (<3 years) and long term (≥3 years). The MPs and PDAC genetic networks were explored with DisGeNET bioinformatics-tool which focuses on gene-diseases associations available in curated databases. Results Three MPs were observed: gastric (heartburn, acid regurgitation, Helicobacter pylori infection, and ulcer), metabolic syndrome (obesity, type-2 diabetes, hypercholesterolemia, and hypertension), and atopic (nasal allergies, skin allergies, and asthma). Strong associations with PDAC were observed for ≥2 recently diagnosed gastric conditions [odds ratio (OR), 6.13; 95% confidence interval CI 3.01–12.5)] and for ≥3 recently diagnosed metabolic syndrome conditions (OR, 1.61; 95% CI 1.11–2.35). Atopic conditions were negatively associated with PDAC (high adherence score OR for tertile III, 0.45; 95% CI, 0.36–0.55). Combining type-2 diabetes with gastric MP resulted in higher PDAC risk for recent (OR, 7.89; 95% CI 3.9–16.1) and long-term diagnosed conditions (OR, 1.86; 95% CI 1.29–2.67). A common genetic basis between MPs and PDAC was observed in the bioinformatics analysis. Conclusions Specific multimorbidities aggregate and associate with PDAC in a time-dependent manner. A better characterization of a high-risk population for PDAC may help in the early diagnosis of this cancer. The common genetic basis between MP and PDAC points to a mechanistic link between these conditions

Altered TMPRSS2 usage by SARS-CoV-2 Omicron impacts infectivity and fusogenicity

The SARS-CoV-2 Omicron BA.1 variant emerged in 20211 and has multiple mutations in its spike protein2. Here we show that the spike protein of Omicron has a higher affinity for ACE2 compared with Delta, and a marked change in its antigenicity increases Omicron’s evasion of therapeutic monoclonal and vaccine-elicited polyclonal neutralizing antibodies after two doses. mRNA vaccination as a third vaccine dose rescues and broadens neutralization. Importantly, the antiviral drugs remdesivir and molnupiravir retain efficacy against Omicron BA.1. Replication was similar for Omicron and Delta virus isolates in human nasal epithelial cultures. However,&nbsp;in lung cells and gut cells, Omicron demonstrated lower replication. Omicron spike protein was less efficiently cleaved compared with Delta. The differences in replication were mapped to the entry efficiency of the virus on the basis&nbsp;of spike-pseudotyped&nbsp;virus assays. The defect in entry of Omicron pseudotyped virus to specific cell types effectively correlated with higher cellular RNA expression of TMPRSS2, and deletion of TMPRSS2 affected Delta entry to a greater extent than Omicron. Furthermore, drug inhibitors targeting specific entry pathways3 demonstrated that the Omicron spike inefficiently uses the cellular protease TMPRSS2, which promotes cell entry through plasma membrane fusion, with greater dependency on cell entry through the endocytic pathway. Consistent with suboptimal S1/S2 cleavage and inability to use TMPRSS2, syncytium formation by the Omicron spike was substantially impaired compared with the Delta spike. The less efficient spike cleavage of Omicron at S1/S2 is associated with a shift in cellular tropism away from TMPRSS2-expressing cells, with implications for altered pathogenesis