coeliac disease

Coeliac disease


The coeliac disease is a diffused enteropathy caused by ingestion of gluten, the protein component of wheat flour, in genetically predisposed individuals. The mucous-membrane lesions start in the duodenus and spread distally, resulting in intestine absorbing surface reduction and in a more or less severe malabsorption syndrome. The occurrence of this pathology is higher than it was thought to be in the past and its rate can reach up to 1:100 / 1:150 individuals in western countries.

Causes and mechanism of damage

The environmental factor causing the coeliac disease is the gluten inside flours derived from wheat, barley, rye and oats (only in some countries, like Italy). Such protein component is absent in corn and rice. Genetic factors are equally important, in fact a more frequent occurrence of coeliac disease can be observed in first-degree relatives (up to 15-20%) with respect to the overall population. A connection between coeliac disease and HLA genes is long-time known even though an analysis of such genes is not enough to make diagnosis bu just to identify a predetermined genetic field. The coalic-disease pathogenesis is associated to a cell-mediated immunity activated by gliadin, a class of protein inside gluten, as it goes through the intestinal barrier; the gliadin gets deaminated by tissue transglutaminasis and is the main antigen of antiendomisial antibodies. After being processed this way, the gliadin is presented to T limphocytes, which get activated and produce a series of cytokines which, in their turn, lead to mucous-membrane damage.


Coeliac disease might appear in any period of life, from childhood to seniority. If symptoms show up for the first time in adult age, they might depend on gastrointestinal infections or pregnancy. The starting symptomatology can vary significantly, depending on the lesion extension in the small intestine. Its classic and most common form arises with a general malbsorption, weight loss, diarrea and steatorrea. Minor forms with less symptoms also exist which show selctive malabsorption of nutrients (e.g. iron). Other signs and symptoms can be sideropenic anaemia, ipertransaminasemia, ipostaturalism, ostheoporosis, infertility, alopecia, recurring aphtha stomatitis, enamel ipoplasy. Finally, a silent and asymptomatic form also exists with lesions confined to the duonenum and asbence of any symptoms whatsoever. Several other diseases have been associated with the coeliac disease: herpes dermatitis, Sjögren syndrome, youth mellitus diabetes, autioimmune epathitis, autoimmune tireopathies, Addison syndrome, IgA nephropathy. Among the non-autoimmune diseases there might be epilessy with brain calcifications, Down syndrome and dilatative cardiomiopathy.


The standard treatment against the coeliac disease e represented by a gluten-free diet which must be strictly followed throughout the entire life. It must be pointed out that wheat flour is not only the basis of our nutrition (bread, pasta etc.) but is also used in the production of salami, packaged sauces and icecreams, canned prodicts, etc. Gluten-free diets must be followed for a lifetime even when few or no symptoms appear but still the coeliac disease has been diagnosed. In recent years, a follow-up for patients has been introduced based on sierologic and clinical response to gluten-free diet (antibody dosage to measure 6-12 months after the beginning of the diet), making it possibile to avoid a new duodenal biopsy, which proves necessary only in case of absent clinical response. The coeliac disease complications to be mostly feared are represented by T-cell intestinal lymphoma, ulcerative digiunoileitis, small-intestine carcinoma, refractory coeliac disease, and the collagenosica sprue. They should be always suspected in all coeliac patients who, despite keeping on following a gluten-free diet, show a new appearance of the symptomatology (abdominal pain, weight loss, fever etc.). Although the mortality of patients diagnosed with coeliac disease in childhood and following a gluten-free diet since then has not risen compared to that of average people, the mortality of those diagnosed with the disease in adult age has nearly doubled.


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