Celiac disease: Prevalence, diagnosis, pathogenesis and treatment

Table 9 Key points from recent findings

Cause

Environmental (gluten) and genetic factors (HLA and non-HLA genes)

Prevalence

0.5%-1% worldwide in normal at-risk population

Higher risk in the population with diabetes, autoimmune disorder or relatives of CD individuals

Pathogenesis

Gliadin gains access via trans- and para-cellular routes to the basal surface of the epithelium, and interact directly with the immune system

Types of CD symptoms: “typical” or “atypical”

Diagnosis

Positive serological (TGA or EMA) screening results suggestive of CD, should lead to small bowel biopsy followed by a favourable clinical and serological response to the GFD to confirm the diagnosis

Current treatment

Strict life-long GFD

Alternative future CD treatments strategies

Hydrolysis of toxic gliadin peptide

Prevention of toxic gliadin peptide absorption

Blockage of deamidation of specific glutamine residues by tissue

Restoration of immune tolerance towards gluten

Modulation of immune response to dietary gliadin

Restoration of intestinal architecture

HLA: Human leukocyte antigen; CD: Celiac disease; EMA: Endomysial; TGA: Transglutaminase; GFD: Gluten-free diet.