PMID- 23155333
OWN - NLM
STAT- MEDLINE
DCOM- 20131112
LR  - 20240317
IS  - 2219-2840 (Electronic)
IS  - 1007-9327 (Print)
IS  - 1007-9327 (Linking)
VI  - 18
IP  - 42
DP  - 2012 Nov 14
TI  - Celiac disease: prevalence, diagnosis, pathogenesis and treatment.
PG  - 6036-59
LID - 10.3748/wjg.v18.i42.6036 [doi]
AB  - Celiac disease (CD) is one of the most common diseases, resulting from both 
      environmental (gluten) and genetic factors [human leukocyte antigen (HLA) and 
      non-HLA genes]. The prevalence of CD has been estimated to approximate 0.5%-1% in 
      different parts of the world. However, the population with diabetes, autoimmune 
      disorder or relatives of CD individuals have even higher risk for the development 
      of CD, at least in part, because of shared HLA typing. Gliadin gains access to 
      the basal surface of the epithelium, and interact directly with the immune 
      system, via both trans- and para-cellular routes. From a diagnostic perspective, 
      symptoms may be viewed as either "typical" or "atypical". In both positive 
      serological screening results suggestive of CD, should lead to small bowel biopsy 
      followed by a favourable clinical and serological response to the gluten-free 
      diet (GFD) to confirm the diagnosis. Positive anti-tissue transglutaminase 
      antibody or anti-endomysial antibody during the clinical course helps to confirm 
      the diagnosis of CD because of their over 99% specificities when small bowel 
      villous atrophy is present on biopsy. Currently, the only treatment available for 
      CD individuals is a strict life-long GFD. A greater understanding of the 
      pathogenesis of CD allows alternative future CD treatments to hydrolyse toxic 
      gliadin peptide, prevent toxic gliadin peptide absorption, blockage of selective 
      deamidation of specific glutamine residues by tissue, restore immune tolerance 
      towards gluten, modulation of immune response to dietary gliadin, and restoration 
      of intestinal architecture.
FAU - Gujral, Naiyana
AU  - Gujral N
AD  - Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, 
      AB T6G 2E1, Canada.
FAU - Freeman, Hugh J
AU  - Freeman HJ
FAU - Thomson, Alan B R
AU  - Thomson AB
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - World J Gastroenterol
JT  - World journal of gastroenterology
JID - 100883448
RN  - 9007-90-3 (Gliadin)
SB  - IM
MH  - Animals
MH  - Autoimmunity
MH  - *Celiac Disease/diagnosis/ethnology/genetics/immunology/therapy
MH  - Diet, Gluten-Free
MH  - Gene-Environment Interaction
MH  - Genetic Predisposition to Disease
MH  - Gliadin/immunology
MH  - Humans
MH  - Intestine, Small/immunology
MH  - Prevalence
MH  - Risk Factors
MH  - Treatment Outcome
PMC - PMC3496881
OTO - NOTNLM
OT  - Celiac disease
OT  - Demography
OT  - Diagnosis
OT  - Pathogenesis
OT  - Treatment
EDAT- 2012/11/17 06:00
MHDA- 2013/11/13 06:00
PMCR- 2012/11/14
CRDT- 2012/11/17 06:00
PHST- 2012/05/22 00:00 [received]
PHST- 2012/07/27 00:00 [revised]
PHST- 2012/08/03 00:00 [accepted]
PHST- 2012/11/17 06:00 [entrez]
PHST- 2012/11/17 06:00 [pubmed]
PHST- 2013/11/13 06:00 [medline]
PHST- 2012/11/14 00:00 [pmc-release]
AID - 10.3748/wjg.v18.i42.6036 [doi]
PST - ppublish
SO  - World J Gastroenterol. 2012 Nov 14;18(42):6036-59. doi: 10.3748/wjg.v18.i42.6036.