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Genetics and genomics
Protocol
Study protocol to investigate the environmental and genetic aetiology of atopic dermatitis: the Indonesian Prospective Study of Atopic Dermatitis in Infants (ISADI)
  1. Conny Tanjung1,2,
  2. Peter Rzehak3,
  3. Muchtaruddin Mansyur4,
  4. Zakiudin Munasir5,
  5. Herawati Sudoyo6,7,
  6. Suzanna Immanuel8,
  7. Roedi Irawan9,
  8. Eva Reischl10,
  9. Hans Demmelmair3,
  10. Berthold Koletzko3,
  11. Sri Rezeki Hadinegoro5,
  12. Damayanti Rusli Sjarif5
  1. 1Postgraduate Program, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia
  2. 2Pantai Indah Kapuk Hospital, Jakarta, Indonesia
  3. 3Division of Metabolic and Nutritional Medicine, Ludwig-Maximilians-Universität München, Dr von Hauner Children's Hospital, University of Munich Medical Centre, Munich, Germany
  4. 4Faculty of Community Medicine, Universitas Indonesia, Jakarta, Indonesia
  5. 5Department of Paediatrics, Faculty of Medicine, Universitas Indonesia, Dr Cipto Mangunkusumo National Referral Hospital, Jakarta, Indonesia
  6. 6Faculty of Medicine, Sydney University, Sydney, Australia
  7. 7Department of Medical Biology, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia
  8. 8Department of Clinical Pathology, Faculty of Medicine, Universitas Indonesia, Dr Cipto Mangunkusumo National Referral Hospital, Jakarta, Indonesia
  9. 9Department of Paediatrics, Faculty of Medicine, Universitas Airlangga, Dr Sutomo General Hospital, Surabaya, Indonesia
  10. 10Research Unit of Molecular Epidemiology, Institute of Epidemiology II, Helmholtz Zentrum Muenchen, Munich, Germany
  1. Correspondence to Dr Conny Tanjung; mfconnytanjung{at}yahoo.com

Abstract

Introduction Atopic dermatitis (AD) is the most common skin disorder in young children worldwide, with a high impact on morbidity and quality of life. To date, no prospective study has been published on the incidence and potential predictors of AD in South East Asian populations. The Indonesian Prospective Study of Atopic Dermatitis in Infants (ISADI) will address the genetic, metabolic and dietary characteristics of mothers and their offspring, as well as potential determinants of AD within the first year of infant life.

Methods and analysis This prospective study will be undertaken in about 400 infants to investigate the direct and indirect effects of filaggrin (FLG) gene mutations, the genetic variants of FADS1, FADS2 and FADS3 and the role of long-chain polyunsaturated fatty acids (LCPUFA) on the development of AD. We will use standardised protocols for subject recruitment, umbilical artery plasma analysis, buccal cell sampling for genotyping, fatty acid analysis, physical exams, 3-day food-intake recall of mothers and children, as well as comprehensive questionnaires on environmental, socioeconomic and AD-related factors, including family history. Monthly monitoring by telephone and physical exams every 3 months will be carried out to assess participants' anthropometry, medical history and incidence of AD diagnosis during the first year of life. Hypotheses-driven analyses of quality-controlled dietary, genetic and metabolic data will be performed with state-of-the-art statistical methods (eg, AD-event history, haplotype, dietary or metabolic factor analysis). Direct and indirect effects of genetics and LCPUFA in buccal cell and cord plasma glycerophospholipids as potential mediators of inflammation on AD development will be evaluated by path analysis.

Ethics and dissemination The Permanent Medical Research Ethics Committee in Medicine and Health/Faculty of Medicine Universitas Indonesia/Dr Cipto Mangunkusumo Hospital (No. 47/H2.F1/ETIK/2014) approved the study protocol (extended by the letter no. 148/UN2.F1/ETIK/2015). We aim to disseminate our findings via publication in an international journal with high impact factor.

  • Atopic dermatitis
  • FADS gene polymorphism
  • Filaggrin gene mutation
  • Long chain poly unsaturated fatty acid composition

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

https://doi.org/10.1136/bmjopen-2016-012475

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    Footnotes

    • Contributors CT, PR, ZM, HS, SI, RI, SRH, BK and DRS conceived and designed the experiments. CT, PR, MM, SRH, BK and DRS analysed the data. ER involved in genotyping. HD contributed to PUFA examination. CT, PR, SRH, BK and DRS wrote the paper. All authors read and approved the final manuscript.

    • Funding The Mead Johnson Pediatric Nutrition Institute (grant number 8670) and in part by the Commission of the European Research Council Advanced Grant META-GROWTH (ERC-2012-AdG – no 322605). The funders have no influence on the study design and the interpretation of the datas.

    • Competing interests CT received a grant from Mead Johnson Nutritionals that contributed to funding of this study. All other authors state no conflict of interest regarding this research study.

    • Patient consent Obtained.

    • Provenance and peer review Not commissioned; externally peer reviewed.