International Journal of Celiac Disease
ISSN (Print): 2334-3427 ISSN (Online): 2334-3486 Website: Editor-in-chief: Samasca Gabriel
Open Access
Journal Browser
International Journal of Celiac Disease. 2016, 4(2), 68-70
DOI: 10.12691/ijcd-4-2-1
Open AccessCritical Review

The Gut-gut Axis: Cohabitation of Celiac, Crohn’s Disease and IgA Deficiency

Aaron Lerner1, , Sandra Neidhöfer2 and Torsten Matthias2

1B. Rappaport School of Medicine, Technion-Israel Institute of Technology, Haifa, Israel

2AESKU.KIPP Institute, Wendelsheim, Germany

Pub. Date: May 28, 2016

Cite this paper:
Aaron Lerner, Sandra Neidhöfer and Torsten Matthias. The Gut-gut Axis: Cohabitation of Celiac, Crohn’s Disease and IgA Deficiency. International Journal of Celiac Disease. 2016; 4(2):68-70. doi: 10.12691/ijcd-4-2-1


An adult patient with IgA deficiency, celiac and Crohn’s disease is described. In addition to the rare association, he developed an unusual proximal Crohn’s disease. Unbalanced microbiome, increased intestinal permeability, susceptibility to infections that might initiate post translational modification of naïve protein and the genetic background, are shared between the three entities. It is speculated that the IgA immune deficiency and its consequences are the early factors that set the stage for the progression of the other two diseases. Based on recent knowledge, special nutritional therapies should be considered, in addition to the gluten free diet.

celiac disease Crohn’s disease IgA deficiency association small bowel case report

Creative CommonsThis work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit


[1]  Ludmila Tankova, Vanya Gerova, Plamen Getsov, Nikolay Penkov, Gergana Taneva, Ivan Terziev, Radislav Nakov.The Association of Crohn’s Disease, Celiac Disease and Selective Ig A Deficiency. International Journal of Celiac Disease, 2016;4:30-33.
[2]  Lerner A, Aminov R, Matthias T. Dysbiosis may trigger autoimmune diseases via inappropriate posttranslational modification of host proteins. Frontiers in Microbiology 2016;7:84.
[3]  Pignata C, Budillon G, Monaco G, Nani E, Cuomo R, Parrilli G, et al. Jejunal bacterial overgrowth and intestinal permeability in children with immunodeficiency syndromes. Gut. 1990; 31: 879-882.
[4]  Lerner A, Matthias T. Changes in intestinal tight junction permeability associated with industrial food additives explain the rising incidence of autoimmune disease. Autoimmun Rev 2015;14:479-489.
[5]  Lerner A, Matthias T. Possible association between celiac disease and bacterial transglutaminase in food processing: a hypothesis. Nutr Rev 2015;73:544-552.
[6]  Lerner A, Reif S. Nonnutritional environmental factors associated with Celiac disease: The Infectome. In: Infections and Autoimmunity. Eds: Shoenfeld Y, Agmon-Levine N, Rose NR. 2nd Ed. Elsevier B.V. Chapter 50. 2015, pages 829-837.
[7]  Cho JH, Brant SR. Recent insights into the genetics of inflammatory bowel disease. Gastroenterology 2011; 140: 1704-1712.
[8]  International MHC and Autoimmunity Genetics Network, Rioux JD, Goyette P, et al. Mapping of multiple susceptibility variants within the MHC region for 7 immune-mediated diseases. Proc Natl Acad Sci U S A. 2009;106:18680-18685.
[9]  Ludvigsson JF, Neovius M, Hammarström L. Association between IgA deficiency & other autoimmune conditions: a population-based matched cohort study. J Clin Immunol. 2014;34:444-451.
[10]  Li YR1, Zhao SD, Li J, Bradfield JP, Mohebnasab M, Steel L, Kobie J, Abrams DJ, Mentch FD, Glessner JT, Guo Y, Wei Z, Connolly JJ, Cardinale CJ, Bakay M, Li D, Maggadottir SM, Thomas KA, Qui H, Chiavacci RM, Kim CE, Wang F, Snyder J, Flatø B, Førre Ø, Denson LA, Thompson SD, Becker ML, Guthery SL, Latiano A, Perez E, Resnick E, Strisciuglio C, Staiano A, Miele E, Silverberg MS, Lie BA, Punaro M, Russell RK, Wilson DC, Dubinsky MC, Monos DS, Annese V, Munro JE, Wise C, Chapel H, Cunningham-Rundles C, Orange JS, Behrens EM, Sullivan KE, Kugathasan S, Griffiths AM, Satsangi J, Grant SF, Sleiman PM, Finkel TH, Polychronakos C, Baldassano RN, Luning Prak ET, Ellis JA, Li H, Keating BJ, Hakonarson H. Genetic sharing and heritability of paediatric age of onset autoimmune diseases. Nat Commun. 2015;6:8442.
[11]  Wang N, Shen N, Vyse TJ, Anand V, Gunnarson I, Sturfelt G, Rantapää-Dahlqvist S, Elvin K, Truedsson L, Andersson BA, Dahle C, Ortqvist E, Gregersen PK, Behrens TW, Hammarström L. Selective IgA deficiency in autoimmune diseases. Mol Med. 2011;17:1383-1396.
[12]  Gutierrez-Achury J, Coutinho de Almeida R, Wijmenga C. Shared genetics in coeliac disease and other immune-mediated diseases. J Intern Med 2011;269:591-603.
[13]  Gommerman JL, Rojas OL, Fritz JH. Re-thinking the functions of IgA(+) plasma cells. Gut Microbes. 2014;5:652-662.
[14]  Diamanti A, Capriati T, Bizzarri C, et al. Autoimmune diseases and celiac disease which came first: genotype or gluten? Expert Rev Clin Immunol 2016;12:67-77.
[15]  Lerner A, Matthias T. Rheumatoid arthritis-celiac disease relationship: joints get that gut feeling. Autoimm Rev 2015: 14:1038-47.
[16]  Lerner A, Matthias T. Food Industrial Microbial Transglutaminase in Celiac Disease: Treat or Trick. International Journal of Celiac Disease 2015;3:1-6.
[17]  Lerner A, Matthias T. Microbial transglutaminase is a potential environmental inducer of celiac disease. In: Autoantigens, autoantibodies, autoimmunity. Volume 10th, Eds: K Conrad, Chan EKL, Andrade LEC, Steiner G, Pruijn GJM, Y Shoenfeld. 12th symposium on autoantibodies, 23-26.9.15, Dresden, Germany. Page 227-233, Pabst Science Publishers, Lengerich, Germany, e-pub.
[18]  Tan J, McKenzie C, Potamitis M, et al. The role of short-chain fatty acids in health and disease. Adv Immunol 2014;121:91-119.