Celiac Disease: Pathogenesis and Novel Therapeutic Strategies
Mariella Baldassarre, Anna Maria Laneve, Roberto Grosso and Nicola Laforgia
Affiliation: Dipartimento di Ginecologia,Ostetricia e Neonatologia, U.O. di Neonatologia e T.I.N., Universita di Bari, Policlinico, P.zza G.Cesare 11- 70124 Bari, Italy.
Keywords: Celiac disease, AT-1001, respondin1, zonulin
Celiac disease is a digestive disease, considered as an autoimmune disorder, that damages the small intestine and interferes with absorption of nutrients. Individuals affected by celiac disease cannot tolerate a protein called gluten, present in wheat, rye, and barley, but also in other common products such as stamp and envelope adhesive, medicines, and vitamins. Celiac disease is a genetic condition that is triggered — or becomes active for the first time — after surgery, pregnancy, childbirth, viral infection, or severe emotional stress. Symptoms may occur in the digestive system, or in other parts of the body. Diagnosis involves blood tests and a biopsy of the small intestine. Recent findings estimate that about 2 million people in the United States have celiac disease, or about 1 in 133 people, as in Europe. Recent studies have shown that it may be more common in Africa, South America, and Asia than previously believed. The only treatment for celiac disease is to follow a gluten-free diet. Various other approaches are being studied that would reduce the need of dieting. One of those promising new approaches involves treating celiac patients with AT-1001, a paracellular permeability inhibitor, and with R-spondin1, a recombinant, secreted protein that early animal studies have shown to act as a highly specific stimulator of the gastrointestinal (GI) epithelial cells .
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