Coeliac disease, also known as coeliac sprue or gluten-sensitive enteropathy, is a permanent intestinal intolerance to gluten – a protein found in wheat, rye, barley, and oats. In these patients, gluten in the small bowel is enzymatically altered by tissue transglutaminase, which causes the immune system to cross react with the small bowel lining, causing inflammatory modification of the digestive barrier, characteristically flattening intestinal villi, alternating mucosal crypts, and recruiting immune cells (lymphocytes). This alteration to gut epitheleal architecture interferes with the absorption of dietary nutrients. Coeliacs malabsorption is also associated with small intestinal bacterial overgrowth (SIBO) and lactose intolerance, contributing to symptoms of fatigue and abdominal bloating and pain. Also, fat malabsorption causes the characteristic steatorrhoea of coeliacs disease, with foul, clay-coloured floating stools, often with diarrhoea.

Full Blood count – Anaemia may result from iron, folate and B12 malabsorption. Low serum iron is common.

Immunoglobulins – Transglutaminase (endomysial) antibodies are more sensitive and specific for coeliac disease than are gliadin antibodies. Immunoglobulins G, A, M.

Small bowel biopsy- Coeliac disease primarily involves the mucosa of the small intestine. The submucosa, muscularis, and serosa are usually not involved. The villi are atrophic or absent, and crypts are elongated. The cellularity of the lamina propria is increased with a proliferation of plasma cells and lymphocytes. The number of intraepithelial lymphocytes per unit length of absorptive epithelium is increased.

Stool sample – The typical bulky, greasy appearance and rancid odour of stools often suggest malabsorption of fat.