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Subject:
From:
Jim Lyles <[log in to unmask]>
Date:
Mon, 21 Sep 1998 23:50:05 EST
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<<Disclaimer: Verify this information before applying it to your situation.>>

                Nutritional Aspects of Celiac Sprue<3>
                --------------------------------------
                        by Kenneth D. Fine, MD
                       summarized by Jim Lyles

This article contains highlights from an article by Kenneth D. Fine,
MD, Baylor University Medical Center, GI Research, in Dallas, Texas.

The degree of mucosal damage varies from one celiac patient to
another.  Also, the amount of the small intestine that is affected
also varies, with the damage usually progressing from the beginning of
the small intestine and then moving downward toward the end of the
small intestine.  This may explain the variable symptoms in different
patients.  For example, when a significant portion of the small
intestine is involved, diarrhea, malabsorption, and weight loss
result.  When damage is isolated to only the top portion of the small
intestine, the only affect may be iron deficiency.  (Incidentally,
when iron deficiency is not corrected by iron supplements, it is
highly likely that celiac disease is the cause of the deficiency.)

Gluten in a celiac's diet causes the immune system to produce gliadin
antibodies in the intestine.  Some of these leak into the blood
stream, where they can be detected in blood tests.  These blood tests
are useful for screening for celiac disease, though a small intestinal
biopsy remains the gold standard for diagnosing celiac disease (CD).

There are few diseases for which diet and nutritional issues are more
important than for CD.  At this time, the only known treatment of CD
is the removal of wheat, barley, rye, and oats from the celiac's diet.
On the surface this sounds simple, but complete removal of dietary
gluten can be very difficult.  Gluten-containing grains are ubiquitous
in the Western diet.  Also, grain-derived food additives such as
partially hydrolyzed vegetable protein [and modified food starch] are
widely used in processed foods and oral medications.  Content labels
are often vague or incomplete regarding these additives.

What further complicates matters is a lack of significant experience
on the part of physicians and dietitians in the dietary treatment of
CD.  This is mainly because there are so few celiac patients for any
one practitioner.  Therefore the best sources of dietary information
for a new patient are other knowledgeable, more experienced celiacs.

It is very important that the diet be followed with full and strict
compliance.  Celiacs, expecially if they've had active CD for a long
time, are at higher than normal risk for GI malignancies.
(Fortunately, compliance to a good GF diet returns the risk of
malignancy and life expectancy to that of the general population.)
Another complication of long-term untreated CD is bone loss, which may
be irreversible in older patients.

When a large portion of the small intestine is affected by active CD,
the result can be a generalized malabsorption problem, resulting in
deficiencies of water- and fat-soluble vitamins and minerals.  Folic
acid deficiency is particularly common in CD because, like iron, it is
absorbed in the upper small intestine [where the highest concentration
of celiac-related damage generally occurs].  Folic acid is necessary
for DNA replication, which occurs in cell turnover.  So a deficiency
of folic acid can impair the regenerative ability of the small
intestine.  Vitamin B12, also essential to DNA synthesis, is not
malabsorbed as commonly as folic acid.

Magnesium and calcium deficiency are also common in active CD, because
of decreased intestinal absorption AND because these minerals tend to
bind with malabsorbed fat which passes through the system.  It is
particularly important for doctors to assess the magnesium status of
celiacs, because without correction of a magnesium deficiency, low
levels of calcium and potassium in the blood cannot usually be
corrected with supplements.  In severe cases, magnesium
supplementation should be done intravenously because of the tendency
of oral magnesium to cause diarrhea.

Supplemental calcium generally should be provided to celiacs, possibly
with vitamin D, to help restore tissue and bone calcium levels to
normal.  The exact dose of calcium is not known.  Dr. Fine usually
recommends 1500-2000 mg of elemental calcium per day, divided into two
doses, for several years and sometimes indefinitely.<4>,<5>,<6>

Zinc is another mineral that often becomes depleted in patients with
chronic malabsorption.  Zinc supplementation (usually the RDA via
multi-vitamin and mineral supplements) helps avoid skin rashes and
restores normal taste.

Up to 20% of celiacs will continue to experience loose or watery
stools even after going on a GF diet.  Sometimes this is due to
inadvertent gluten in the diet, but a recent study at Dr. Fine's
medical center showed that in these cases other diseases
epidemiologically associated with CD are present.<7>  These include
microscopic colitis, exocrine pancreatic insufficiency, lactose
intolerance, selective IgA deficiency, hypo- or hyperthyroidism, and
Type I diabetes mellitus.  When diarrhea continues after beginning a
GF diet, a search for these associated diseases or others should be
undertaken and treated if found.

The use of corticosteroids has been advocated in celiacs when the
response to the GF diet is sluggish or absent.  This is necessary more
often in older than in younger patients.  However, pancreatic enzyme
supplements (prescribed by a doctor) may be needed to help digestion
and resolve ongoing malabsorption in some patients.

The endomysial antibody blood test is highly accurate and specific for
detecting CD.  However, the current method of detecting these
antibodies involves an operator looking through a microscope and
observing the antibody binding on monkey esophagus or human umbilical
cord tissue substrates.  The correct interpretation of results is
highly dependent on the skill and experience of the technician
interpreting the fluorescence pattern through the microscope.
Moreover, determination of the amount of antibody present relies upon
repeat examinations following dilutions of the blood serum, with the
last positive test being reported as a titer.

A new discovery was reported by a research group in Germany.<8>  The
antigen substrate of the endomysial antibodies has been identified.
This allows the development of a new test that can detect and
quantitate serum endomysial antibodies in one, chemically-based test
run [thus greatly reducing the potential for human error and
significantly reducing the time needed for each test--ed.]  These new
tests should be available for clinical use shortly.

In a recent study, Dr. Fine found that the frequency of positive
stool blood tests was greater in patients with total villous atrophy
relative to partial villous atrophy, and all tests were negative in
treated patients without villous atrophy.<9>  This suggests that fecal
occult blood may be a non-invasive and inexpensive method of following
the response of the damaged intestine to treatment.  Also, it should
be noted that the high frequency of positive tests due to villous
atrophy will decrease the accuracy of the tests when used for cancer
screening in this same patient population (which is how these tests
are normally used by health care providers).

There have been two recent reports touting the lack of deleterious
effects when 50 grams of oats per day are added to the diet of celiac
patients.  Although this finding is exciting for celiacs, both studies
possess certain limitations.  In the first study, published by a
Finnish group, the exclusion criteria for symptoms and histopathology
were somewhat strict, so that patients with more mild forms of CD
seemingly were selected for study.  And though no damage to duodenal
histology occurred after one year of oats consumption, no physiologic
or immunologic parameters of disease activity were measured.
Furthermore, several patients in the treatment group dropped out of
the study for reasons not mentioned in the article.<10>  The second and
more recent study involved only 10 patients, studied for twelve weeks.
The favorable results of this study must be interpreted with caution
because of the small sample size and short study period.<11>  Even the
one-year treatment period in the Finnish study may be too short to
observe a harmful effect, as it is known that small intestinal damage
sometimes will not occur for several years following the
reintroduction of gluten to a treated celiac.  At the worst, an
increase in the incidence of malignancy may result from chronic
ingestion of oats, an effect that could take decades to manifest.
Therefore, this issue will require further study before oats can be
recommended for the celiac diet.

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