The Indian Council of Medical Research (ICMR) has issued draft guidelines on diagnosis and management of celiac disease, which is a chronic immune-mediated enteropathy that is caused in genetically susceptible individuals by ingestion of gluten proteins present in wheat, barley and oats.
Celiac disease (CeD) was originally described as a disease causing chronic diarrhoea and malabsorption. Flattening of the villi, inflammatory cell infiltration in the mucosa and loss of surface area were the major reasons for the clinical manifestations. The understanding that this is an immune process in which the intestinal epithelium is damaged is now well accepted. Following from the original descriptions by Dicke relating wheat consumption to CeD, a large number of studies have now established the central role played by proteins from wheat, and to a lesser extent barley or oats. The disease occurs only in individuals with a certain genetic predisposition, but at the same time it does not necessarily occur in all such individuals.
Earlier, the ICMR had created a Task Force on CeD in 2008, recognizing the need to focus on a disease that was beginning to be reported in sizeable sections of the population in several states of northern India. As recommended by the Task Force, data were collected on the prevalence of celiac disease in three regions of India through a population-based study carried out in three regions of the country. The Task Force also recommended that ICMR develop guidelines for the diagnosis and management of celiac disease in India.
While several international groups have generated guidelines for the diagnosis and management of celiac disease, these were largely rooted in the experience of western countries. There has been considerable skepticism over the applicability of these guidelines in a country like India where tropical enteropathy or environmental enteropathy is so widely prevalent, and where the incidence of parasitic and other infections of the small intestine is significant.
Celiac disease classically presents with symptoms of diarrhea and nutritional deficiencies secondary to nutrient malabsorption. This indicates that the small intestine is the target organ most commonly affected in patients with CeD. Small intestinal changes, primarily an increase in intraepithelial lymphocytes associated with varying degrees of crypt elongation and villous blunting, form the primary histological hallmark of CeD. Studies have shown that the intestinal epithelium was the target of autoantibody deposition in CeD. In the bowel, the proximal small intestine appears to be the site of greatest mucosal damage as indicated by the fact that deficiency of iron and folate, which are absorbed preferentially from the proximal small bowel, are the most common nutrient deficiencies clinically manifest in CeD. The infrequency of vitamin B12 malabsorption in CeD shows that involvement of the distal small intestine is relatively infrequent in CeD.