Celiac disease future or investigational therapies

Celiac disease Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Celiac disease from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
X-ray
Echocardiography and Ultrasound
CT scan
MRI
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy Life Style Modifications Pharmacotherapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Celiac disease future or investigational therapies On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Celiac disease future or investigational therapies All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
National Guidelines Clearinghouse
NICE Guidance
FDA on Celiac disease future or investigational therapies
CDC on Celiac disease future or investigational therapies
Celiac disease future or investigational therapies in the news
Blogs onCeliac disease future or investigational therapies
Directions to Hospitals Treating Celiac disease
Risk calculators and risk factors for Celiac disease future or investigational therapies

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Investigational Therapies

Various other approaches are being studied that would reduce the need of dieting. All are still under development, and are not expected to be available to the general public for a while:

• Genetically engineered wheat species, or wheat species that have been selectively bred to be minimally immunogenic. This, however, could interfere with the effects that gliadin has on the quality of dough.
• A combination of enzymes (prolyl endopeptidase and a barley glutamine-specific cysteine endopeptidase (EP-B2)) that degrade the putative 33-mer peptide in the duodenum. This combination would enable coeliac disease patients to consume gluten-containing products.
• Inhibition of zonulin, an endogenous signaling protein linked to increased permeability of the bowel wall and hence increased presentation of gliadin to the immune system.
• Other treatments aimed at other well-understood steps in the pathogenesis of coeliac disease, such as the action of HLA-DQ2 or tissue transglutaminase and the MICA/NKG2D interaction that may be involved in the killing of enterocytes (bowel lining cells).