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Part 2-Celiac Presentations @ national Digestive Disease Conf.: May 19-22,
2002
Dr. MacDonald, a celiac specialist, discussed new insights into the
pathogenesis of  Celiac Disease.  Dr. MacDonald discussed primarily the role
that other factors besides the DQ2 (gene) molecule, control the T-cells in
the gut mucosa which produce the lesion or flat mucosa.  In the genesis of
the lesion, he explained how the T-cell immune response in the gut wall
results in a gut shape of tall villi and short crypts which results in an
increase in mucosa volume with flat mucosa and an increase in mucosa
thickness.
My husband, a PhD immunologist, interpreted this for me;  He said that
imagine the villi are the hill and the crypts are the valley.  The valley is
where things grow.  The oldest cells are at the tip of the hill and as cells
mature, they get transported up the hill.  As damage occurs, the hill gets
chopped down, valleys get deeper making more area for cells to replicate.
Dr. MacDonald assumed “that because the epithelium is turning over so fast
in Celiac Disease that the lamina propria, the shape of the gut itself would
be turning over, but actually the data says otherwise.  The flat mucosa
isn’t turning over at all, … a rather stable shape, it’s not really dynamic,
it’s remodeled.”  He said that putting Celiacs on a gluten free diet may
take them a long time to get better, “because it takes a long time for this
to go back because this is actually stable, it’s remodeled….”

Dr. MacDonald explained that gliadin peptides associate with DQ2 and DQ8
molecules putting themselves into the grooves to be seen by T cells.
However, he gave an instance where a particular gliadin peptide doesn’t fit
well into the pockets of DQ2 to be seen by T cells.  Tissue Transglutaminase
or Ttg deamidates (removes chemical groups on certain amino acids and allows
peptide to bind to DQ2) this peptide in terms of glutamine into glutamic
acid, gives a negative charge, “fits very well into pocket, and binding
increases 100 fold.  Tightness of the binding ... controls the specificity
and strength of the T-cell response”.

MacDonald also described the case of a woman with cancer who was treated
with interferon.  He said that she had the endomysial antibodies, was DQ2
positive, and had Celiac Disease;  However, he cited that the reason why the
Celiac Disease was not found earlier was that interferon alpha/gamma used to
treat the cancer may have “precipitated” clinical Celiac Disease.  He added
that her son was later diagnosed with Celiac Disease as well.
It was also alluded to that a viral infection like a gastrointestinal flu
would stimulate or produce interferon alpha.   Dr. Alessio Fasano from the
Center for Celiac Research at the Univ. of Maryland also explained that it’s
not just the gluten antigen and genes (i.e., HLA DQ2 or DQ8) but an added
element like that alluded to by MacDonald such as a viral infection which
can result in Celiac Disease.
Fasano described a study performed on North African children who were
thought to have symptoms resembling infectious disease with symptoms like
anemia and diarrhea were found to have Celiac Disease at the rate of 1 in
18.  He said because they have a high consumption of grains and seem to
carry a high frequency of the genetic elements, he felt that non-profit
organizations may intervene to help institute a gluten-free diet in this
Celiac population.
Dr. Fasano mentioned a study performed in Southern California which found
Celiac Disease in 2 to 4% of people with symptoms or associated diseases and
5% in family members of Celiacs.
Dr. Fasano stated that the overall prevalence is 1 in 266 which he said “on
a global scale, by far this is the most frequently genetic disease of human
kind.”
Fasano said that in the 1970s, it was thought Celiac Disease was confined to
the pediatric population but that since 1998 there has been a surge in adult
versus child cases.  He believes that the disease may have been overlooked
in adults because adults have more atypical symptoms like anemia,
osteoporosis, abortion that would NOT see a Gastroenterologist but would see
an internist, reproductive OBGyn, endocrinologist, etc.  He said that if the
iceberg idea is diarrhea, weight loss, abdominal symptoms, you will surely
crash into the iceberg , but  he proposed, what about the people who have
joint pain, constipation, fatigue, and so on.  He said that if you are
willing to see the monument of the problems, you have to get down under the
water because in the vast majority of cases, Celiacs will not see a
Gastroenterologist and that doctors must be aware of those under the water.
Dr. Fasano during the question and answer session listened to a doctor in
the audience describe a patient with diarrhea and schizophrenia whose
diarrhea and schizophrenia resolved when put on a gluten-free diet.  The
doctor didn’t know what to do with the patient but explained that the
patients background, being of Irish descent, gave him a “red flag” into the
possibility of Celiac Disease.  Dr. Fasano in response described how there
can be a change in behavior such as attention deficit disorder, depression,
and schizophrenia.  He described a theory that the epitopes of gluten could
cross the intestinal barrier, cut into the bloodstream, and cross the blood
brain barrier.  He believes that there is a clear association between Celiac
Disease and change in behavior.
Laura




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