2
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Geographic Variability of Childhood Food Allergy in the United States

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The aim of this study was to describe the distribution of childhood food allergy in the United States. A randomized survey was administered electronically from June 2009 to February 2010 to adults in US households with at least 1 child younger than 18 years. Data were analyzed as weighted proportions to estimate prevalence and severity of food allergy by geographic location. Multiple logistic regression models were constructed to estimate the association between geographic location and food allergy. Data were analyzed for 38 465 children. Increasing population density corresponded with increasing prevalence, from 6.2% in rural areas (95% confidence interval [CI] = 5.6-6.8) to 9.8% in urban centers (95% CI = 8.6-11.0). Odds of food allergy were graded, with odds in urban versus rural areas highest (odds ratio [OR] = 1.7, 95% CI = 1.5-2.0), followed by metropolitan versus rural areas (OR = 1.4, 95% CI = 1.2-1.5), and so on. Significance remained after adjusting for race/ethnicity, gender, age, household income, and latitude. An association between urban/rural status and food allergy prevalence was observed.

          Related collections

          Most cited references22

          • Record: found
          • Abstract: found
          • Article: not found

          The prevalence, severity, and distribution of childhood food allergy in the United States.

          The goal of this study was to better estimate the prevalence and severity of childhood food allergy in the United States. A randomized, cross-sectional survey was administered electronically to a representative sample of US households with children from June 2009 to February 2010. Eligible participants included adults (aged 18 years or older) able to complete the survey in Spanish or English who resided in a household with at least 1 child younger than 18 years. Data were adjusted using both base and poststratification weights to account for potential biases from sampling design and nonresponse. Data were analyzed as weighted proportions to estimate prevalence and severity of food allergy. Multiple logistic regression models were constructed to identify characteristics significantly associated with outcomes. Data were collected for 40 104 children; incomplete responses for 1624 children were excluded, which yielded a final sample of 38 480. Food allergy prevalence was 8.0% (95% confidence interval [CI]: 7.6-8.3). Among children with food allergy, 38.7% had a history of severe reactions, and 30.4% had multiple food allergies. Prevalence according to allergen among food-allergic children was highest for peanut (25.2% [95% CI: 23.3-27.1]), followed by milk (21.1% [95% CI: 19.4-22.8]) and shellfish (17.2% [95% CI: 15.6-18.9]). Odds of food allergy were significantly associated with race, age, income, and geographic region. Disparities in food allergy diagnosis according to race and income were observed. Findings suggest that the prevalence and severity of childhood food allergy is greater than previously reported. Data suggest that disparities exist in the clinical diagnosis of disease. Copyright © 2011 by the American Academy of Pediatrics.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Food allergy among children in the United States.

            The goals were to estimate the prevalence of food allergy and to describe trends in food allergy prevalence and health care use among US children. A cross-sectional survey of data on food allergy among children <18 years of age, as reported in the 1997-2007 National Health Interview Survey, 2005-2006 National Health and Nutrition Examination Survey, 1993-2006 National Hospital Ambulatory Medical Care Survey and National Ambulatory Medical Care Survey, and 1998-2006 National Hospital Discharge Survey, was performed. Reported food allergies, serum immunoglobulin E antibody levels for specific foods, ambulatory care visits, and hospitalizations were assessed. In 2007, 3.9% of US children <18 years of age had reported food allergy. The prevalence of reported food allergy increased 18% (z = 3.4; P < .01) from 1997 through 2007. In 2005-2006, serum immunoglobulin E antibodies to peanut were detectable for an estimated 9% of US children. Ambulatory care visits tripled between 1993 and 2006 (P < .01). From 2003 through 2006, an estimated average of 317000 food allergy-related, ambulatory care visits per year (95% confidence interval: 195000-438000 visits per year) to emergency and outpatient departments and physician's offices were reported. Hospitalizations with any recorded diagnoses related to food allergy also increased between 1998-2000 and 2004-2006, from an average of 2600 discharges per year to 9500 discharges per year (z = 3.4; P < .01), possibly because of increased use of food allergy V codes. Several national health surveys indicate that food allergy prevalence and/or awareness has increased among US children in recent years.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The targets of vitamin D depend on the differentiation and activation status of CD4 positive T cells.

              Vitamin D is a potent immune system regulator. The active form of vitamin D (1,25(OH)(2)D(3)) suppresses the development of animal models of human autoimmune diseases. 1,25(OH)(2)D(3) decreased the proliferation of all T helper (h) cells and decreased the production of IFN-gamma, IL-2, and IL-5. In Th2 cells 1,25(OH)(2)D(3) increased the production of IL-4. Quiescent CD4+ T cells express vitamin D receptors but only at a low level, which increased five-fold following activation. 1,25(OH)(2)D(3) treatment of Th0 cells, but not Th1 or Th2 cells, induced the expression of the transcription factor GATA-3. Microarray technology identified over 102 targets of 1,25(OH)(2)D(3) in CD4+ T cells. Of the 102 genes, 57 genes were down-regulated and 45 were up-regulated by 1,25(OH)(2)D(3) treatment of the CD4+ T cells. Two of the identified genes are regulators of NFkB. Other genes of interest included the IL-2Rbeta gene and IgE binding factor. Th2 and Th0 cells produced more IgE binding factor after treatment with 1,25(OH)(2)D(3) while Th1 cell IgE binding factor expression was unaffected by 1,25(OH)(2)D(3) addition. It is unclear why some of the genes identified are expressed in CD4+ T cells and furthermore why 1,25(OH)(2)D(3) regulates the expression of these genes. Clearly CD4+ T cells can be direct targets of vitamin D. The targets of vitamin D in CD4+ T cells depend on the state of activation and differentiation status of the cells. Copyright 2003 Wiley-Liss, Inc.
                Bookmark

                Author and article information

                Journal
                Clinical Pediatrics
                Clin Pediatr (Phila)
                SAGE Publications
                0009-9228
                1938-2707
                December 12 2011
                September 2012
                May 17 2012
                September 2012
                : 51
                : 9
                : 856-861
                Affiliations
                [1 ]Northwestern University Feinberg School of Medicine, Chicago, IL, USA
                [2 ]Children’s Memorial Hospital, Chicago, IL, USA
                [3 ]Loyola Stritch School of Medicine, Maywood, IL, USA
                [4 ]Edward Hines Jr VA Hospital, Hines, IL, USA
                [5 ]Saint Louis University School of Medicine, Saint Louis, MO, USA
                [6 ]Allergy, Asthma and Sinus Care Center, Saint Louis, MO, USA
                Article
                10.1177/0009922812448526
                22605786
                4474eaa1-1248-45a6-a51d-f50c038c25c2
                © 2012

                http://journals.sagepub.com/page/policies/text-and-data-mining-license

                History

                Comments

                Comment on this article