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Subject:
From:
L and N Matsui <[log in to unmask]>
Reply To:
L and N Matsui <[log in to unmask]>
Date:
Thu, 25 Sep 2003 22:52:26 +0000
Content-Type:
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<<Disclaimer: Verify this information before applying it to your situation.>>

Rensch M, 2001.  The Prevalence of Celiac Disease Autoantibodies in Patients
With Systemic Lupus Erythematosus, Amer. Jour. of Gastro 96:  1113-1115.

Recognizing that systemic lupus erythematosus (SLE) patients have false
positive autoantibodies for primary biliary cirrhosis, chronic active
hepatitis, Sjogren’s syndrome, thyroid disorders, rheumatoid arthritis, and
other diseases, this study sought to identify and determine the prevalence
of  CD autoantibodies in SLE patients.  Also, CD and SLE patients share
common (genetic) HLAs, B-8, DR2 and DR3.

Results:  Twenty-four or 23% of SLE patients tested positive for the
anti-gliadin antibody (AGA) but none of them including the remaining 79 SLE
patients tested positive for the anti-endomysial antibody (EmA).  However,
none of the 24 patients positive for AGA had positive biopsies according to
international criteria, assuming characteristic villous atrophy.  Therefore,
the researchers concluded that the false-positive rate of the AGA was 23%,
representing the 24 who tested positive for AGA but not EmA nor biopsy
confirmation (in other words, the specificity of the AGA is 77% for the
diagnosis of CD in SLE patients).  Also, despite the expectation that a
higher prevalence of CD would be found in SLE patients because they share
increased or common HLAs, the data found no specific association with CD
beyond that of the general population prevalence which at the time of this
study was approx. 0.1-0.5%.

Comments:  The drawback to this study is that it does not follow-up the
AGA-positive SLE patients.  That is, negative biopsies do not necessarily
exclude CD as a possible diagnosis.  In recent studies, CD has been been
found in patients without villous atrophy or mild intestinal damage
(subclinical and silent forms of CD) and that patients with milder
intestinal damage often are not detected by blood antibody screenings.  The
expression of gluten-sensitive patients has been found in patients even with
normal intestinal villi.  What may have been the results if the researchers
studied the biopsies for an increased lymphocyte count as an indicator of
gluten-sensitivity?  What about a trial of a gluten-free diet to determine
if there is some symptom remission?  What would be the results of a larger
prevalence study since this study only included a total of 103 patients?
There is no doubt that as the researchers cite- a larger study should be
performed to determine the true prevalence of CD in SLE patients.

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