Coeliac disease may initially be confused with other diarrhoeal syndromes such as irritable bowel syndrome. According to Emami et al
, the sensitivity of serologic marker tests for coeliac disease may not be equal to the reference figures, especially of those performed in commercial laboratories.4
However, Malekzade et al
reported that coeliac disease is the most common cause of chronic non-bloody diarrhoea in patients from the country’s capital, Tehran.5
It has been reported that one out of 166 healthy Iranians have coeliac disease.6
Interestingly, because wheat is one of the major components of the regular diet in the Middle East, North Africa, India and Iran, causing some degree of immune tolerance, patients from these countries may therefore present with milder, longer and even more challenging clinical manifestations of the disease. It has been estimated that 3–20% of the population in these areas suffer from some variation of the disease.7
Both genetic and environmental factors are involved in the disease pathogenesis and it is associated with immunologic disorders such as autoimmune thyroiditis. So there is a question still remaining to be answered: is it just the effect of hereditary predisposition or coeliac disease which may trigger autoimmunity per se. It has been shown that autoimmune thyroiditis responds well to a gluten free diet, and transglutaminase 2 autoantibody may be involved in the development of thyroiditis.8
The association of Crohn’s disease and coeliac disease is of tremendous interest to physicians. More commonly Crohn’s disease is discovered after the pre-existing coeliac disease, yet the reverse has also been reported.9
Ig G anti-transglutaminase antibody may be found in patients with inflammatory bowel disease. Consequently, this type of antibody has been considered of low specificity in the diagnosis of coeliac disease.10
On the other hand, ASCA and antineutrophilic antibodies, that are well known markers for discriminating between ulcerative colitis and Crohn’s disease, may become detectable in patients with coeliac disease. Of interest, not only is the degree of seropositivity for ASCA related to the severity of mucosal injury, but also this autoantibody may disappear on a gluten free diet in coeliac disease. It is wondered if there is a surplus of immune response to microbial agents involved in the pathogenesis of such different gastrointestinal disorders as coeliac disease and Crohn’s disease.11–14
Altered permeability hypothesis may justify these observations; there are some gene products such as those produced by MAG12 maintaining intestinal integrity. Gene polymorphism results in disrupting epithelial integrity, unless the relevant protein is fully functional.15
Another explanation for the simultaneous presence of these two disorders may lie in the hypothesis of shared susceptibility loci such as IL23R.16–18
Similarly, reduced expression of paraoxonase in different parts of the intestine results in coeliac disease, Crohn’s disease or ulcerative colitis. Paraoxonase works not only as an antioxidant but also as a local defence system protecting the epithelium from oxidative stress injury. It has been shown that there are significantly reduced levels of mRNA expression of the enzyme in the duodenum and terminal ileum in coeliac or Crohn’s disease, respectively.19
As mentioned above, collagenous colitis is associated with coeliac disease from which inflammatory bowel disease may evolve.4
Whatever causes the development of these two related diseases in the same patient, it needs to be investigated further; however, the commitment of an astute physician is required to detect the second latent disease in advance, before any serious consequences—such as, for example, intestinal lymphoma—can occur.20,21
According to our knowledge, to date there have been very few cases of simultaneous coeliac disease and Crohn’s disease in the same patient. The underlying mechanism of this association is not yet precisely defined. However, it is important to consider the association, especially when the patient’s diarrhoea seem unusual from the point of its poor response to treatment or its odd characteristics,22–28
because establishing an appropriate therapeutic regimen focusing on both diseases may prevent the patient from developing such noticeable repercussions such as severe growth retardation, delayed puberty, social isolation, and so forth.
- Consider Crohn’s disease in those coeliac patients who do not respond well to a gliadin free diet.
- Do not forget the relationship between these two diseases.
- ASCA may become detectable in patients with coeliac disease.
- IgG antiendomysial antibody is not specific for coeliac disease.