Today, I review and embed StatPearls‘ Celiac Disease. Ewa B. Posner; Muhammad Haseeb. Last Update: August 8, 2023.
All that follows is from the above resource.
Introduction
Celiac disease is an enteropathy of the small intestine. It is triggered by exposure to gluten in the diet of susceptible people. The susceptibility is genetically determined. The condition is chronic, and currently, the only treatment consists of permanent exclusion of gluten from the food intake.[1][2][3]
Patients with celiac disease can present with diarrhea and failure to thrive; some may be asymptomatic.
Etiology
The symptoms of celiac disease are due to the damage of enterocytes in the small intestine. In the full-blown clinical picture, the typical features of the small intestine are chronic inflammation and villi atrophy. [4][5][4]
An individual has to have HLA dominant DQ2 or DQ8 genes. The disease is a result of the immune system reacting adversely to gluten, and one of the important proteins involved is an antibody to tissue transglutaminase. There are however other pathways proposed that contribute to the disease. The glycoprotein gliadin (present in gluten) has a direct toxic effect on enterocytes by the up-regulating production of IL-15.
Some studies indicate that gastrointestinal infections in early childhood are relevant to the development of celiac disease later in life. This is not surprising considering the organ affected, but it is likely that is also directly relevant to the fact that celiac disease is caused by a disorder of immune function.
IgA antibodies to smooth muscle endomysium and tissue transglutaminase are often used to make the diagnosis of celiac disease. However, only about 5% of patients with celiac disease have a deficiency of this immunoglobulin.
Epidemiology
The prevalence of celiac disease in the general population is about 0.5 % to 1%. Both true prevalence, as well as detection and diagnosis, have increased over the past 10 to 20 years. The incidence is greater among people with autoimmune disorders like type 1 diabetes. In first-degree relatives of people affected by celiac disease, the risk is 1 in 10.
Pathophysiology
A peptide derived from gluten called gliadin causes damage to the small intestine. There is local inflammation, and the process leads to the destruction of the small intestinal villi. This destruction, in turn, leads to the decreased functionality of the intestinal surface and malabsorption. The lack of nutrient absorption impacts directly on the digestive system but also indirectly on all the systems of the body. This impact results in generally poor health and is the reason why celiac disease can have signs and symptoms arising from almost any system of the body, not just the gastrointestinal system.[6]
Histopathology
Celiac disease only involves the mucosa of the small bowel. The villi may be absent or atrophic and the crypt hyperplasia is present. An increased proliferation of lymphocytes and plasma cells is seen in the lamina propria.
Toxicokinetics
There has been long-standing doubt about the toxicity of oats for a patient with celiac disease. Recently, studies have shown that oats are not harmful, and any doubts were likely because it is commonly processed together with wheat and therefore, cross-contamination was very high.
