<<Disclaimer: Verify this information before applying it to your situation.>>

Here are the responses to my request for information and experiences
with anemia and elevated liver enzymes as related to CD.
Most of the people who responded had anemia and/or elevated liver
functions that resolved after some time on a GF diet.  Following are
excerpts of those people who said *other* things.  The section on gall
bladder disease is plagiarized with permission from Ronald Hoggan.
More information is available at Don Wiss' home page:
http://www.panix.com/~donwiss/hoggan/
Ron Hoggan also kindly provided the journal articles.

It bears repeating:  CD is as individual as each person who has it!
Please remember these are accounts of individual experiences.
I hope it's helpful.  Thanks to all who took time to reply!

--Stephanie (Colorado)


        I'd tell ya what I think of doctors and their blood evaluations,
but I should be polite.  I was diagnosed as anemic for 20 years.
The last few years before I was diagnosed, my blood chemistry also showed
elevated liver functions.  My doctor told me not to worry. It didn't
mean a thing! And I was anemic (according to him) because of my
ITALIAN background!  (How do ya like THAT one?)
        Well, after being diagnosed by biopsy and being GF for 6 months
(and after switching to another witch-doctor) my new blood test came back
with normal results on the liver function and - Guess what -I was
(and still am)  no longer anemic.  Amazing!
        If I sound angry - It's because I am every time I think about it.
It astounds me how doctors tend to take the easy answers, rather than
do some thinking.

You may need to be tested for Gaucher's disease:  it usually has liver or
spleen complications, but goes with symptoms like nose bleeds, bruising,
anemia..  This is not medical advice.  I was anemic for years before the GF
diagnosis and now although I still take iron supplements my iron now is
within normal range.  Hope this helps.

Is it the SGOT test that is elevated?  If so (and I believe
that is a liver function test) mine has been elevated ever since the celiac
disease kicked in.  It's not terribly high - in the 75 range, and always
higher in the summer.  I recall one doctor saying it was nothing to worry
about. I think he may have meant that he didn't know what on earth was
causing it...

I am not a doc, nor a patient, but a spouse.  My husband's chronic anemia
cleared up like a charm after he went GF.  I seem to remember that he also
had slightly elevated liver function tests, and that our doc (a sprue guru)
said that was not uncommon in untreated CD.

I had numerous tests before being refered to her and
one of them showed elevated liver 'enzymes' (can't remember the acutal
thing that was high) and also many small gall stones.  I have speculated
that they could be related to the high amount of undigested fat that was
going through my system as a result of CD.  My body was trying to deal
with the fat and the liver was getting a bit overworked, so to say.  The
liver does deal with fat, by the way.

Now that I am gluten free,my
anemia is cured,last test showed hemoglobin 15.2%,and hematocrit level
49.9!.......The worry now is that my liver enzymes are high..728....the high
norm is 500.Cholesterol is also up at 220,before diagnosis it was184....and
have also had a pos ANA,..

I was diagnosed w/ CD five and half months ago.  Before I was diagnosed,
I was having A LOT of pain under my ribs (right side).  (This, of course,
was one of many symptoms)   I had many tests on my gallbladder and liver,
and the resulting diagnosis from my GI doctor was "Gilbert's syndrome"
(pronounced shell-bayers).  This diagnosis was the result of elevated
liver bilirubin.  (Blood test, although my urologist also picked it up in
my urine)  After going gluten free, my symptoms have subsided.
Gilbert's Syndrome is genetic.  As it was explained to me, my liver uses
a different enzyme and it doesn't work as well as the enzyme used by most
people. (that's a brief synopsis) The CD caused a lot of stress on my
liver by creating a heavy toxic load, hence the liver pathology.
**Bilirubin levels DO fluctuate, however, so your tests may not always
come out the same, especially if you have changed your diet.
Sometimes they will be elevated, and sometimes they will be normal.**
        From my GI's standpoint, there is nothing that can be done about
Gilbert's syndrome.  He told me to make sure I informed the hospital
staff if I was ever admitted to the hospital, because they may think I
have liver disease.

xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
Gall Bladder Disease
Ronald Hoggan

Gall bladder disease or malfunction is often associated with celiac disease.
It can cause pain in the upper right quadrant of the abdomen, just at the
lowest rib on the right side. In one study of 1300 celiacs in Canada, 9%
indicated that gall stones were the earliest presentation, sometimes
followed by many years prior to correct diagnosis of their celiac disease.
In another report, Dr. Kozlowska indicated that 13 of the 41 newly diagnosed
celiacs she investigated were suffering from atresia, a condition which is a
partial or complete blockage of the bile duct.

CCK (cholecystokinin) is the hormone responsible for gall bladder
contraction. The bulk of this hormone is produced in the duodenum.

Active celiac disease would be likely, then, to cause a reduction or a
cessation of duodenal production of CCK. A radiologist in Hungary is
currently researching this problem. In private correspondence, one
gastroenterologist reports having found (accidentally) a gallstone in a 12
year old girl who had active celiac disease.

The 30% incidence of atresia among celiac children, as reported by Dr.
Kozlowska, would suggest an even higher number among adults with active
celiac disease. Given the low level of clinical suspicion for celiac disease
in North America, it would not be at all surprising if a large portion of
patients with gall bladder disease were suffering from occult celiac
disease. Future research may reveal that gall stones and atresia are only
symptoms of celiac disease.

I did a Medline search on cck and celiac disease. I got 65 hits. Researchers
repeatedly identified a connection between celiac disease and gall bladder
malfunction with such comments as:
"Thus the already impaired fat absorption in celiac sprue is magnified by
the lack of bile delivery....."; and "We conclude that there is a reversible
defect of gallbladder emptying and cholecystokinin release in celiac
disease." and "Cholecystokinin (cck) release and gall bladder emptying in
response to a fatty meal are completely abolished in coeliac disease." and
"the abnormally decreased gallbladder contraction in coeliac patients is the
result of endogenous cck secretion and not a lack of end-organ
responsiveness to cck."

There just isn't much ambiguity there. If you've got celiac disease, you
have gall bladder malfunction, of the sort that may well develop into
atresia and gallstones.

Upon receiving a diagnosis of gall bladder disease, whether gall stones or
atresia, one might be wise to request a blood test for celiac disease. The
anti-endomysial antibody test is currently the most reliable and available
test.

Now, given the low level of clinical suspicion for celiac disease, I
anticipate the suggestion that absent gall bladder emptying, atresia, and
gall stones might occur in the absence of celiac disease. I did another
Medline search, and I can't find a single study that has tested atresia
patients or gallstone patients for celiac disease. My answer to the
suggestion that gall bladder disease may occur in the absence of celiac
disease is that there is no evidence to support such a contention.
Considerable evidence exists, however, which points to celiac disease as a
likely cause of gall bladder malfunction, atresia, or stones. As for
childhood gallstones, there appears to be only one answer.... it is
associated with celiac disease.

A view that incorporates the association of gall bladder disease, and celiac
disease, but does not preclude the above, has been expressed by Dr. Joseph
Murray, of the University of Iowa, who is a gastroenterologist specializing
in treating celiac disease. He believes there are several "triggers" that
can activate Celiac disease in genetically susceptible people. One of them
is: Surgery, particularly GI (gall bladder, etc.) In any case, the
connection between celiac disease and gall bladder disease is well known.

Title
     Toxicity mechanisms of wheat and other cereals in celiac disease and
     related enteropathies.
Author
     Auricchio S; De Ritis G; De Vincenzi M; Silano V
Source
     J Pediatr Gastroenterol Nutr, 1985 Dec, 4:6, 923-30
Abstract
     This paper is a critical appraisal of current theories on the
     mechanisms of toxicity of wheat and other cereals in celiac disease
     and some related enteropathies. The "peptidase deficiency," "primary
     immune defect," and "gluten-lectin" theories on celiac disease are
     examined and critically discussed on the basis of the relevant data
     available in 88 references. Special attention has been paid in this
     review to the nature of the cereal components triggering the
     appearance of toxic symptoms and signs in celiac disease as well as to
     underlying action mechanisms. The gluten-lectin theory is the one best
     able to explain, in addition to celiac disease, some secondary
     intolerances that may occur in temporarily predisposed individuals as
     a consequence of several causes, including viral hepatitis and
     intestinal infections, as well as the occurrence of intestinal lesions
     in healthy subjects administered very high amounts of gluten.

Title
     Hepatic injury in adult coeliac disease.
Author
     Hagander B; Berg NO; Brandt L; Nord en A; Sj olund K; Stenstam M
Source
     Lancet, 1977 Aug 6, 2:8032, 270-2
Abstract
     In an attempt to determine the frequency of liver injury in adult
     coeliac disease (A.C.D.) the case records of 74 consecutive patients
     were examined. In 13 cases histological sections of the liver were
     available and in 5 of these there were signs of reactive hepatitis.
     Histological signs of distinct hepatic injury with cirrhosis and/or
     chronic active hepatitis were found in 7 other patients. In 5 of these
     serum-IgA was normal, whereas 16 out of 20 control patients with liver
     cirrhosis not associated with A.C.D. had raised serum-IgA.
     Serum-aspartate-aminotransferase and serum-alanine-aminotransferase
     were determined in 53 patients; 29 had raised concentrations. In 19
     patients serum-aminotransferases were repeatedly determined before and
     during the dietary regimen and there was a significant reduction in
     enzyme concentrations during treatment. The median concentration of
     serum-alkaline-phosphatase was also reduced during treatment but not
     significantly. The histological evidence of liver injury in 16% and
     the abnormal liver-function tests in 39% of the patients indicate that
     hepatic injury is common in A.C.D. Since liver-function tests or liver
     biopsy specimens were available for only about two-thirds of the
     patients, liver damage in A.C.D. may be more common than indicated by
     these results. The effect of a gluten-free diet on aminotransferase
     concentrations indicates that the liver injury may be reversible and
     suggests that in some A.C.D. patients progressive liver damage may be
     prevented by suitable treatment. Since A.C.D. is not always
     recognised, the diagnosis should be considered in patients with liver
     disease of unknown aetiology.

Title
     Prevalence of hypertransaminasemia in adult celiac patients and effect
     of gluten-free diet.
Author
     Bardella MT; Fraquelli M; Quatrini M; Molteni N; Bianchi P; Conte D
Address
     Cattedra di Gastroenterologia, Universit a degli Studi di Milano,
     IRCCS Ospedale Maggiore, Italy.
Source
     Hepatology, 1995 Sep, 22:3, 833-6
Abstract
     The prevalence of hypertransaminasemia and the effect of gluten-free
     diet (GFD) were evaluated in 158 consecutive adult celiac patients,
     127 women and 31 men, aged 18 to 68 years (mean, 32). At diagnosis, 67
     patients (42%) had raised aspartate and/or alanine transaminase levels
     (AST and ALT; mean, 47 IU/L, range, 30 to 190; and 61 IU/L, range, 25
     to 470, respectively), whereas 91 patients had normal liver function
     tests (LFT). Patients with and without hypertransaminasemia were
     comparable for epidemiological data, body mass index (18.5 vs. 19.6),
     and severity of intestinal histological involvement. All patients were
     given a strict GFD and were followed for 1 to 10 years (median, 4). At
     1 year, a highly significant improvement in intestinal histology was
     observed in both groups (P < .0001). In the 67 patients with raised
     transaminase levels body mass index (BMI) also increased significantly
     (from 18.5 to 21.0, P < .001), and transaminase levels normalized in
     60 (95%). In the other seven cases liver biopsy showed fatty
     infiltration in two and chronic active hepatitis (CAH) in the other
     five, related to chronic infection with hepatitis B virus in three and
     hepatitis C virus in one, and to autoimmune type in the fifth. We
     conclude that in adult celiac patients elevated serum transaminases
     are a frequent finding and normalize in most cases after GFD. When
     they persist, liver biopsy is mandatory to further investigate hepatic
     involvement, which is our series was mainly attributable to CAH.
Language of Publication
     English