Commentary: Transient coeliac disease back on stage again?

Coeliac disease is an immune-mediated destructive disorder of the small intestinal mucosa that has many clinical manifestations. Only some of these are directly understandable as a consequence of villous damage, and extraintestinal clinical signs are prevalent. Some investigators prefer to call this disorder an autoimmune disease, but all agree that it is triggered by an exogenous antigen: wheat gluten and similar proteins from related cereals. Coeliac disease is readily diagnosed once the clinical suspicion has been evoked. The diagnosis may be formally supported by the presence of serum IgA antibodies to tissue transglutaminase (IgA-TG2). However, the final diagnosis is made by histological demonstration of immune pathology in the small intestine and clinical response to a gluten-free diet. The presence of elevated IgA-TG2 is a typical feature of untreated coeliac disease [1,2]. One theory suggests that elevated IgA-TG2 is a consequence of gluten-specific T cells in the mucosa; these T cells may help TG2-specific B cells [3,4]. The specificity of the easy-to-perform serological test is considered to be in the range 90 to 100% [5]. False-positive tests have been seen in patients with inflammatory bowel disease but most individuals with elevated IgA-TG2 but normal small intestinal mucosa are said to have ‘‘latent coeliac disease’’. Current thinking suggests that within months or years these persons will proceed to a status of intestinal inflammation with definite villous changes [6,7]. A report, however, in the present issue of the Scandinavian Journal of Gastroenterology challenges this view and brings ‘‘transient coeliac disease’’ back on stage again [8]. The term ‘‘transient coeliac disease’’ is not new. The previous criteria for diagnosis of coeliac disease demanded that there should be a damaged mucosa, recovery on a gluten-free diet and then a challenge to precipitate the disease again. Usually, overt coeliac disease develops within months or even years. It has never been fully understood why some individuals relapse later than others. Surprisingly, some children with a definite diagnosis do not develop either symptoms or histological deterioration even after prolonged challenge [9 /11]. In one study, 6.6% of the children had no relapse over a period of 2 /7 years [12]. In these cases, it was believed that the children had transient coeliac disease and had developed a tolerance to gluten. Most investigators now agree that there is no such thing as transient coeliac disease, although the question is continuously debated [13,14]. A childhood diagnosis of coeliac disease followed by a normal diet in adulthood is a strong predictor of osteoporosis and malabsorption [15]. In one case it has been shown beyond doubt that it can take as much as 14 years with challenge before a relapse of coeliac disease is demonstrated [16]. Recently, however, it was found that 11 of 47 adult coeliac disease patients with a childhood diagnosis did not relapse even during prolonged challenge [17]. In the present study, serum originally collected to study type 1 diabetes was used. Finland is a wellknown hot-spot for diabetes and considerable effort has been invested in the detection of prognostic factors. The population is well characterized, being genetically homogeneous and stable, so the stage is set for a detailed analysis of diabetes risk and development and a number of excellent papers have emerged. Both type 1 diabetes and coeliac disease are associated with more or less the same genes. How-