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American Journal of Public Health Research
DOI: 10.12691/ajphr-1-1-3

The Implementation of a Tele-Homecare System with Service Oriented Architecture and HL7 Message Transmission Standard
Ching-Sung Wang

American Journal of Medical and Biological Research
DOI: 10.12691/ajmbr-1-1-2

The Influence of Ethanol on Pyruvate Kinases Activity in Vivo, in Vitro, in Silico
Lelevich Sergey Vladimirovich, Khrustalev Vladislav Victorovich, Barkovsky Eugene Victorovich, Shedogubova Tatyana Aleksandrovna

American Journal of Medical Sciences and Medicine
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Clinical and Histological Features in Wegener Granulomatosis
Li Cavoli Gioacchino, Passantino Rita, Bono Luisa, Tortorici Calogera, Ferrantelli Angelo, Giammarresi Carlo, Rotolo Ugo

American Journal of Infectious Diseases and Microbiology
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The Curse of Lymphatic Filariasis: Would the Continual Use of Diethylcarbamazine Eliminate this Scourge in Papua New Guinea?
Anne Lanham, Lillian Mwanri

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Triggering Agents for Transient Celiac Disease

Hakim Rahmoune*, Nada Boutrid, Mounira Amrane, Belkacem Bioud

Department of Pediatrics, University Hospital of Setif, Setif 1 University, Algeria

Abstract: Celiac disease is a genetically determined gluten-sensitive auto-immune condition, mainly an enteropathy resulting in nutrient malabsorption. Its intestinal damages, with lymphocytic gastroduodenitis, can also be due to a myriad of gastro-intestinal infections that act as true "triggering agents". We present two pediatric patients with infectious associations leading to a transient positive celiac disease serology, with various agents and different genetic suscpetibility.

Keywords: celiac disease, intra-epithelial lymphoctosis, HLA, Giardia, helicobacter pylori

Citation: Hakim Rahmoune, Nada Boutrid, Mounira Amrane, Belkacem Bioud, Triggering Agents for Transient Celiac Disease. International Journal of Celiac Disease, 5 (3). 127-128. January 2017. doi:10.12691/ijcd-5-3-5

1. Introduction

Celiac disease (CD) is a genetically determined gluten-sensitive auto-immune condition, mainly an enteropathy resulting in nutrient malabsorption. This latter enteropathy (with its histological lymphocytic gastroduodenitis) can also be due to a myriad of gastro-intestinal infections.

We present two pediatric patients with infectious associations leading to a transient positive CD serology.

2. Case Presentations

First Patient

A 3 years old girl is consulting for positive CD serology after family screening. Duodenal biopsy found a Helicobacter pylori duodenitis without CD stigma on histopathology. She is put on triple therapy and monitored clinically and immunologically every 3 months.

After 1 year of follow up, her primary serology (weakly positive IgA anti-Transglutaminase, 15 IU) returned negative, along with anti- IgG and IgA deamidated gliadin made at 12 months, also negative. She remained free of clinical signs.

Positive genetic test (presence of the haplotype HLA DQ2) made the close clinical/serological follow-up mandatory.

Second Patient

A boy of 13 years followed during 4 years in private practice for failure to thrive that would be due to CD (positive IgA anti-Transglutaminase = 18 IU, partial villous atrophy, grade: March 2).

Repeted endoscopy with histology confirmed the presence of giardiasis; and three courses of metronidazole were prescribed.

The subsequent negativity CD serology and the absence of HLA DQ2 or DQ8 allow free diet.

3. Discussion

CD is an inflammatory disease of the small intestine with a prevalence of roughly 0.5%-1% and occurs in genetically predisposed population (with Human Leukocyte Antigens HLA-DQ2 or HLA DQ8 haplotypes). It can present with both intestinal or extra-intestinal manifestations. [1]

CD can, by itself, induce lymphocytosis along the digestive tract; but duodenal lymphocytosis are more than 80% of cases due to other etiologies than true gluten intolerance; [2,3] while during the silent forms of CD (including serology positive without any clinical signs), several "triggering infectious agents" are implicated like Giardia and H. pylori:

Giardia lamblia is a worldwide protozoan parasite, with variable seroprevalence from 2% in developed countries to up to 30% in developing world [3]. Giardiasis may cause a clinical disease which mimics CD in both symptomatology and histopathology [4,5,6].

On the other hand, H. pylori is more frequently reported (and thus studied) during CD. Its controversial relationship ranges from proactive to passive infectious agent [7,8].

Particular emphasis should be given to such conditions that may induce intraepithelial lymphocytosis with preserved villosity like eosinophilic gastroenteritis, drugs, autoimmune enteropathies, different immune deficiencies, and, mostly, enteric infections. Most authors do not advocate gluten-free diet at first, but any confounding risk (i.e. HLA genetic risk) would require a tight monitoring [9,10].

Acknowledgements

We would thank the patients families for their kind collaboration.

References

[1]   | AK, Lebwohl B, Snyder CL, et al. Celiac Disease. 2008 Jul 3 [Updated 2015 Sep 17]. In: Pagon RA, Adam MP, Ardinger HH, et al., editors. GeneReviews® [Internet]. Seattle (WA): of , ; 1993-2017. Available from: https://www.ncbi.nlm.nih.gov/books/NBK1727/.
[2]   | Pai RK. A practical approach to small bowel biopsy interpretation: celiac disease and its mimics. InSeminars in diagnostic pathology 2014 Mar 31 (Vol. 31, No. 2, pp. 124-136). WB Saunders.
[3]   | Hammer ST, Greenson JK. The clinical significance of duodenal lymphocytosis with normal villus architecture. Archives of Pathology and Laboratory Medicine. 2013 Sep; 137(9):1216-9.
[4]   | Ortega YR, Adam RD. Giardia: overview and update. Clinical infectious diseases. 1997 Sep 1; 25(3): 545-9.
[5]   | Carroccio A, Cavataio F, Montalto G, Paparo F, Troncone R, Iacono G. Treatment of giardiasis reverses "active" coeliac disease to "latent" coeliac disease. European Journal of Gastroenterology and Hepatology. 2001 Sep; 13(9): 1101-5.
[6]   | Granito A, Muratori L, Muratori P, Petrolini N, Bianchi FB, Volta U. Antitransglutaminase antibodies and giardiasis. The American journal of gastroenterology. 2004 Dec 1; 99(12): 2505.

[7]  
Simondi D, Ribaldone DG, Bonagura GA, Foi S, Sapone N, Garavagno M, Villanacci V, Bernardi D, Pellicano R, Rizzetto M, Astegiano M. Helicobacter pylori in celiac disease and in duodenal intraepithelial lymphocytosis: Active protagonist or innocent bystander?. Clinics and research in hepatology and gastroenterology. 2015 Dec 31; 39(6): 740-5.

[8]   | Basyigit S, Unsal O, Uzman M, Sapmaz F, Dogan OC, Kefeli A, Asilturk Z, Yeniova AO, Nazligul Y. Relationship between Helicobacter pylori infection and celiac disease: a cross-sectional study and a brief review of the literature. Przeglad gastroenterologiczny. 2017; 12(1): 49.
[9]   | Tchidjou HK, De Matteis A, Di Iorio L, Finocchi A. Celiac Disease in an Adoptive Child with Recurrent Giardia Infection. International journal of health sciences. 2015 Apr; 9(2): 193.
[10]   | Edling L, Rathsman S, Eriksson S, Bohr J. Celiac disease and giardiasis: a case report. European journal of gastroenterology and hepatology. 2012 Aug 1; 24(8): 984-7.