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Celiac disease (“CeD”) is a T-cell mediated autoimmune disease of the small bowel, triggered by the ingestion of gluten-containing grains (e.g., wheat, barley, and rye) in genetically susceptible individuals. CeD is one of the few autoimmune disorders in which all the elements of autoimmunity are understood:

  • The triggering environmental factor: glutenin/gliadin, the active fractions of gluten
  • The route of passage into the body: the mucosa of the small intestine
  • A close genetic association: with HLA genes (DQ2 or DQ8), and
  • A highly specific humoral autoimmune response: auto-antibodies to tissue transglutaminase ("anti-tTG"), deamidated gliadin peptides ("DGP"), and endomysium (“EMA”)

While previously thought to be uncommon, the prevalence of celiac disease is approximately 1% of the general population. The 2004 NIH consensus conference on CeD confirmed that the prevalence in the United States alone is approximately 3 million people. The number of diagnosed patients will increase dramatically during the latter half of this decade, driven by broad based educational campaigns, NIH research funding and widely available blood screens for highly specific antibodies (anti-tTG, DGP, EMA).

The disease is highly variable with many non-intestinal manifestations and is frequently characterized by some or all of the following: chronic small bowel inflammation, fatty stools and malabsorption, osteoporosis, anemia, occurrence of other autoimmune diseases, neurological disorders and gastro-intestinal cancers. Symptoms may include chronic diarrhea, abdominal pain, muscle cramps, irritability, and painful skin rashes. Celiac disease patients that do not eliminate dietary gluten increase their chances of other diseases, such as concurrent autoimmune diseases and a 40-100 fold increase in gastrointestinal cancer.  Celiac disease often presents with vague non-gastrointestinal symptoms. During the active phase, characteristic auto-antibodies recognizing tTG, deamidated gliadin peptides and endomysium are produced. Early in the disease, the tight junctions are opened and severe intestinal damage ensues. A biopsy of the small intestine, combined with auto-antibody and anti-tTG blood test, is the most accurate way to confirm the illness.

There is no cure for celiac disease, and complete elimination of dietary gluten with a gluten-free diet is the only management of the disease. For most patients, strict dietary avoidance may heal the small intestine within 3 to 6 months and reduce the markers of autoimmunity (anti-tTG, DGP, and EMA). Several organizations have been formed to help patients meet the challenge of complete gluten avoidance.

It is known that altered intestinal permeability (“leaky gut”) is a hallmark of CeD and tracks the severity of the disease. It is likely that leaky gut is both a cause and a consequence of the disease, facilitating transport of gluten which then triggers an inflammatory process, resulting in tight junction dysfunction ("leak") which can be blocked by tight junction regulation including Alba's lead product candidate, larazotide acetate.