Celiac disease (CD) is an autoimmune pathology, caused by a permanent intolerance to gluten contained in wheat and to similar prolamines present in barley and rye. It is a common disease as its prevalence, in Caucasian populations, is about 1-1.16%. There are several patterns of CD: symptomatic CD and silent CD, both characterized by typical histological lesions in the duodenum mucosa. The classic manifestation is distinguished by gastrointestinal symptoms such as diarrhoea, vomiting, abdominal distension and failure to thrive. On the other hand atypical forms are characterized by extraintestinal symptoms (anemia, low height, delayed puberty, headaches).The gluten-free diet for life is the only therapy currently available for CD. In this way it is ensured to coeliac patient a comparable growth and a state of health to that of a healthy subject. About 70% of the subjects respond with an improvement in symptoms within a few weeks from the start of the gluten-free diet, although histological healing is more delayed and not always complete. The ingestion of gluten in trace amounts can cause the persistence of enteric mucosal lesions. A recent study by Aziz et al. has shown that a large proportion of patients with celiac disease is not satisfied with the gluten-free diet.Considerable progress have been made regarding the biotechnology field, which led to a better understanding of the molecular mechanisms of coeliac disease and the identification of pathogenetic pathways that could be targeted by new drugs. We can distinguish different categories of drugs according to their mechanism of action:• Endopeptidases capable to detoxify gluten in order to decrease its immunogenic power.• Modulation of permeability by the pill AT-1001.• Block of antigen presentation made by inhibitors of TG2 and HLA-DQ2.• Inflammation modulation using monoclonal antibodies directed against inflammatory cytokines.• Block of the recruitment of lymphocytes by molecules that inhibit the migration to the intestinal mucosa.• Immunomodulation and induction of gluten tolerance. © 2013 Nova Science Publishers, Inc. All rights reserved.
Celiac disease: New therapeutic options / Nenna, Raffaella; Matteo, Florio; Pontone, Stefano; Gerarda, Mastrogiorgio; Petrarca, Laura; Pietropaoli, Nicoletta; Bonamico, Margherita. - STAMPA. - (2013), pp. 131-142.
Celiac disease: New therapeutic options
NENNA, RAFFAELLA;PONTONE, Stefano;PETRARCA, LAURA;PIETROPAOLI, NICOLETTA;BONAMICO, Margherita
2013
Abstract
Celiac disease (CD) is an autoimmune pathology, caused by a permanent intolerance to gluten contained in wheat and to similar prolamines present in barley and rye. It is a common disease as its prevalence, in Caucasian populations, is about 1-1.16%. There are several patterns of CD: symptomatic CD and silent CD, both characterized by typical histological lesions in the duodenum mucosa. The classic manifestation is distinguished by gastrointestinal symptoms such as diarrhoea, vomiting, abdominal distension and failure to thrive. On the other hand atypical forms are characterized by extraintestinal symptoms (anemia, low height, delayed puberty, headaches).The gluten-free diet for life is the only therapy currently available for CD. In this way it is ensured to coeliac patient a comparable growth and a state of health to that of a healthy subject. About 70% of the subjects respond with an improvement in symptoms within a few weeks from the start of the gluten-free diet, although histological healing is more delayed and not always complete. The ingestion of gluten in trace amounts can cause the persistence of enteric mucosal lesions. A recent study by Aziz et al. has shown that a large proportion of patients with celiac disease is not satisfied with the gluten-free diet.Considerable progress have been made regarding the biotechnology field, which led to a better understanding of the molecular mechanisms of coeliac disease and the identification of pathogenetic pathways that could be targeted by new drugs. We can distinguish different categories of drugs according to their mechanism of action:• Endopeptidases capable to detoxify gluten in order to decrease its immunogenic power.• Modulation of permeability by the pill AT-1001.• Block of antigen presentation made by inhibitors of TG2 and HLA-DQ2.• Inflammation modulation using monoclonal antibodies directed against inflammatory cytokines.• Block of the recruitment of lymphocytes by molecules that inhibit the migration to the intestinal mucosa.• Immunomodulation and induction of gluten tolerance. © 2013 Nova Science Publishers, Inc. All rights reserved.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.