Celiac Disease and Gluten Sensitivity by Jeffrey Dach MD

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Jeffrey Dach MD

Mar 23, 2008, 8:25:09 AM3/23/08
to Jeffrey Dach MD on Vitamin C and Stroke Prevention
Original Article can be found here:


Fifty three year old Sally McCann came to my office with menopausal
symptoms of hot flashes and night sweats. Sally has trouble sleeping,
chronic fatigue, and patchy hair loss. She has taken anti-anxiety
medication (Buspar) for daily anxiety attacks, and Ambien for sleep,
both for the past nine years. Sally is from West Ireland, and has
typical features with red hair, green eyes and a fair complexion. She
mentions GI symptoms of "irritable bowel", i.e. bloating, gas,
alternating constipation and diarrhea. She mentions neurological
symptoms of tingling and numbness in her hands and feet. Sally has
been to many doctors over the years and has tried many different
treatments, and so far nothing has helped her.


Upon examination Sally had a small bald spot on her scalp, loss of
outer third of the eyebrows, and brittle cracking nails.

Image at right shows a typical bald spot, called Alopecia Areata
caused by Celiac Disease (different patient).

Laboratory Findings

Sally's lab studies showed a microcytic anemia. Her blood cells were
smaller and fewer than normal. This usually indicates Iron deficiency
anemia. Her serum Iron, however was not too low because she has been
taking Iron supplements. Sally informs me that her blood count has
always been low and she has been taking Iron supplements for years.

Sally's blood test also showed Hashimoto's thyroiditis with elevated
thyroglobulin and peroxidase antibody levels.

Sally's blood test also showed Celiac Disease; (IgA TTG and EMA) were
both positive indicating that Sally has intolerance of wheat gluten,
also called celiac disease. I explained that many of her symptoms of
peripheral neuropathy (tingling sensations), hair loss, anemia, and
anxiety are caused by her inability to tolerate wheat gluten in her
diet. And that all of her symptoms would be resolved on a gluten free
Sally was also started on bioidentical hormones for her menopausal
symptoms, and natural thyroid for her low thyroid Hashimotos Disease.
Of course, she would need a GI consultation and small bowel biopsy,
and other family members should have genetic screening.

Treatment Program

The major treatment for Celiac Disease is a Gluten Free Diet.

Sally's Salivary Cortisol test showed a reversed pattern with low
cortisol in the morning and high cortisol at night, explaining her
morning fatigue and inability to sleep. The treatment for this is a
nutritional supplement called Seriphos, (phosphorylated serine ) which
resets the biological cortisol clock and the pattern returns to normal
in about 6 weeks.

To address adrenal fatigue, an adrenal vitamin program was also
started which includes Vitamin C, B5, biotin, and adrenal herbs such
as ashwaganda and licorice.

For sleep, Sally was started on melatonin and 5-HTP which replaces the
Ambien. And to increase morning energy, Sally was started on D-
ribose, L-L-Carnitine and Co-enzyme Q-10.

For the peripheral neuropathy, Sally is given B12, R-Alpha Lipoic Acid
and and Benfotiamine, a lipid soluble form of thiamine.

A Successful Outcome

Six weeks after starting a Gluten free diet, Sally says she is much
better. The neuropathy symptoms of tingling and numbness in the hands
and feet have improved, she has more energy, sleeping better, and her
hot flashes and night sweats are gone. The hair loss is better as
well. In short she is a happy camper.

Watch this video on celiac disease from the Mayo Clinic:


Celiac Disease is commonly associated with Hashimoto's Thyroid
Disease, Adrenal disorders, Osteoporosis, Alopecia areata, chronic
abdominal pain, Skin disorder called Dermatifromis Herpetica, Vitamin
K and B12 deficiency, Iron deficiency Anemia, Peripheral Neuropathy,
and other neurological disorders. It tends to run in families and has
a genetic component.

Jeffrey Dach MD
4700 Sheridan Suite T
Hollywood FL 33021

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Video on Celiac Disease

Video from Mayo Clinic on Celiac Disease, Gluten Free Diet

Review Articles

Detecting Celiac Disease in Your Patients. HAROLD T. PRUESSNER, M.D.,
University of Texas Medical School at Houston Am Fam Physician Mar
1998. excellent review in American Academy of Family Physicians.

Celiac disease may be greatly underdiagnosed and is relatively common
in this country. Approximately 95 percent of patients with celiac
disease have a particular type of HLA DQ alpha and beta chain encoded
by two genes, HLA-DQA1 0501 and HLA-DQB1 0201
Viral exposures may trigger an immunologic response in persons
genetically susceptible to celiac disease; this occurs with adenovirus
type 12, which shares a sequence of eight to 12 amino acids with the
toxic gliadin fraction.

Causes of Delay in Diagnosis

Recognizing celiac disease on the basis of the various manifestations
of the disorder is difficult. In a study20 of 228 patients with adult-
onset celiac disease, it was found that 42 were diagnosed at age 60 or
later. Seven patients with dermatitis herpetiformis were excluded,
leaving 35 patients in the analysis. Fifteen of the 35 patients had
been seen--with unexplained symptoms and abnormal blood tests--for an
average of 28 years by their family physicians or in hospital
outpatient departments before the diagnosis of celiac disease was

Symptoms and Prevalence of Celiac Disease

NIH. How common is celiac disease? Data on the prevalence of celiac
disease is spotty.
In Italy about 1 in 250 people, and in Ireland about 1 in 300 people,
have celiac disease.
Recent studies have shown that it may be more common in Africa, South
America, and Asia than previously believed. Until recently, celiac
disease was thought to be uncommon in the United States. However,
studies have shown that celiac disease is very common. Recent findings
estimate about 2 million people in the
United States have celiac disease, or about 1 in 133 people. Among
people who have a first-degree relative diagnosed with celiac disease,
as many as 1 in 22 people may have the disease.

Symptoms of celiac disease may include one or more of the following:

* gas
* recurring abdominal bloating and pain
* chronic diarrhea
* constipation
* pale, foul-smelling, or fatty stool
* weight loss/weight gain
* fatigue
* unexplained anemia (a low count of red blood cells causing fatigue)
* bone or joint pain
* osteoporosis, osteopenia
* behavioral changes
* tingling numbness in the legs (from nerve damage)
* muscle cramps
* seizures
* missed menstrual periods (often because of excessive weight loss)
* infertility, recurrent miscarriage
* delayed growth
* failure to thrive in infants
* pale sores inside the mouth, called aphthous ulcers
* tooth discoloration or loss of enamel
* itchy skin rash called dermatitis herpetiformis

Eur J Gastroenterol Hepatol. 2006 Jul;18(7):747-54. Links
Health-related quality of life in adult coeliac disease in Germany:
results of a national survey.

Even while on a diet, health-related quality of life (HRQOL) may be
decreased in people with coeliac disease. Some have persisting
digestive symptoms or dermatitis herpetiformis, mouth ulcers,
osteoporosis and fractures. Symptoms suggestive of irritable bowel
syndrome may be present, and there is an increased rate of anxiety,
fatigue, dyspepsia and musculoskeletal pain.[55]

Screening for Celiac Disease, In the United Kingdom, the National
Institute for Health and Clinical Excellence (NICE) recommends
screening for coeliac disease in patients with newly diagnosed

1) chronic fatigue syndrome
2) irritable bowel syndrome
3 ) autoimmune thyroid disease. Hashimotos

University of Chicago CeliacDisease Center 773.702.7593 www.CeliacDisease.net.

Screening Test: anti-tissue transglutaminase (tTG-IgA)A screening
test is commonly used when an individual is in a risk group for celiac
disease, whether or not he/she has symptoms. This test is usually the
one offered for celiac screening events, as it is the most sensitive
test available.

Other Tests: * Total Serum IgA to test for IgA deficiency (this health
condition can affect accuracy of antibody test)* Anti-endomysial
antibody test (EMA-IgA) EMA-IgA are very specific for celiac disease
but they are not as sensitive as the tTG-IgA.*

HLA-DQ2 and HLA-DQ8 gene tests for celiac disease The "gene tests" are
not antibodies: they can be used to exclude celiac disease (if
negative) in doubtful cases NOTE: Anti-gliadin Antibodies (AGA-IgG and
AGA-IgA) are no longer used to test for celiac disease due to a low
level of accuracy http://www.celiaccenter.org/faq.asp

What are the recommended blood tests to diagnose CD? There is a
particular series of blood tests called the 'Celiac Panel". These
tests measure your immune system's response to gluten in the food you

tTG-IgA or tissue transglutaminase-IgA
AGA-IgG or Antigliadin IgG
AGA-IgA or Antigliadin IGA
Total IGA

The presence of tTG antibodies is highly suggestive of CD, while AGA
can be elevated also in cases of wheat allergy.

How accurate are the celiac blood tests?

The current diagnostic tests for CD are very accurate, particularly
when tTG and anti-endomysial antibodies are elevated. The isolated
presence of anti-gliadin antibodies does not necessarily imply that
the subject is affected by CD, with the exception of children under
the age 2 in which tTG and EMA may not be present.

Are the villi permanently damaged in a patient with Celiac Disease and
how long does it take for the villi to return to normal?

The villi are not permanently damaged. The intestine is an organ,
which renews itself every three days. Therefore, if the damage is
exclusively due to CD, the villi will be reformed once on a gluten-
free diet. The time for the villa to return to normal varies between

What is the meaning of HLA DQ2/DQ8?

As an autoimmune disease, CD is the consequence of the interplay
between genes and the environment (gluten). We don't know all the
necessary genes to develop CD; however, HLA DQ2 and/or DQ8 are
absolutely necessary to develop the disease. Since 1/3 of the general
population also have these genes, the presence of DQ2 or DQ8 does not
imply that the person will develop CD, rather, that they have a
genetic compatibility with CD. Conversely, the absence of DQ2/DQ8
almost certainly rules out CD.
Fat soluble vitamins malabsorbed : panel A, D, E and K

Pattern of Presentation of Celiac Disease

The changing clinical presentation of coeliac disease M Ravikumara, D
P Tuthill, H R Jenkins Department of Paediatric Gastroenterology,
University Hospital of Wales, Cardiff, UK

Methods: A 21-year review of prospectively recorded data on the mode
of presentation of biopsy confirmed coeliac disease in a single
regional centre. Presenting features over the past 5 years were
compared with those of the previous 16 years. Between 1983 and 1989
(inclusive), no serological testing was undertaken; between 1990 and
1998, antigliadin antibody was used with occasional use of
antiendomysial antibody and antireticulin antibody. From 1999 onwards,
anti-tissue transglutaminase was used.

Patterns of clinical presentation of adult coeliac disease in a rural
setting. Sián Jones , Charles D'Souza and Nadim Y Haboubi Nutrition
Journal 2006, 5:24doi:10.1186/1475-2891-5-24

Anaemia was the most common mode of presentation accounting for 66% of
patients. Less than half of the patients had any of the classical
symptoms of coeliac disease and 25% had none of the classical symptoms
at presentation. Anti-gliadin antibodies, anti-endomysial antibody and
anti-tissue transglutaminase showed 75%, 68% and 90% sensitivity
respectively. In combination, serology results were 100% sensitive as
screening tests for adult coeliac disease. Fifty nine percent patients
had either osteoporosis or osteopenia.

With the introduction of serologic tests for coeliac disease, disease
variants have been recognised which present with atypical features
such as fatigue, asymptomatic iron deficiency, decreased bone density
and dyspepsia without the classic malabsorption syndrome. Other
presentations could include isolated hypoalbuminaemia, elevated
aminotransferase levels (transaminitis), microscopic colitis, symptoms
of irritable bowel syndrome, recurrent aphthous stomatitis,
infertility, neurologic symptoms such as peripheral neuropathy, ataxia
and epilepsy with posterior cerebral calcification. The findings of
this study suggest that patients presenting to their general
practitioner with unexplained iron deficiency anaemia, unexplained
fatigue or generalised abdominal pain should undergo serological
testing for coeliac disease.

Celiac Disease Gluten Free Diets

Gluten Free Diets

Going Gluten-Free: A Primer for Clinicians PRACTICAL GASTROENTEROLOGY,

One Mom's Experence with Celiac Disease
Sorta Crunchy One moms experience with Son having celiac disease,
gluten free diet.

News about Gluten Free Restaurants

Gluten-Free Restaurant Recommendations Double in Less Than 3 Months.
Wednesday February 27, Glutenfreeonthego.com Answers Exploding Demand
from Celiacs / Coeliacs, Gluten-Free Guests & Food Allergic Customers

The challenge of cooking gluten-free, David Hagedorn, L.A. Times-
Washington Post News Service Vail CO, Colorado February 26, 2008

Celiac.com Web Site http://www.celiac.com/ Celiac Com Gluten Free
Diets etc.

How Early Can Celiac Disease Be Diagnosed? Rodney Ford

http://www.doctorgluten.com/cms/ Rodney Ford Web Site Celiac Disease

Rodney Ford. To diagnose coeliac disease (that is when you get gut
tissue damage), the first step is to look for evidence of gut damage
by blood tests. These "tissue damage" tests are called: tissue
transglutaminase (tTG) or endomesial antibodies (EMA). If these are
positive, then you should have an endoscopy (also called a small bowel
biopsy) to confirm the diagnosis. If you do have coeliac disease,
then you are committed to a lifelong gluten-free diet. So it is very
important to make a firm diagnosis.

To diagnose gluten-sensitivity (reactions to gluten without the gut
damage). The blood tests that you need are the IgG-gliadin and the
IgA-gliadin tests. A positive test shows that you are experiencing an
immune reaction to gluten. Most gluten-sensitive people have a high
IgG-gliadin test.
We prefer the test kits form Inova Diagnostics

Incidence of Celiac Disease, Epidemiology

Slide show of Celiac Disease epidemiology

Doctor Gluten. When Dr Alessio Fasano (Medical Director, University
Of Maryland, Center for Celiac Research, http://www.celiaccenter.org/mission.asp
) was asked how many of the population were just gluten intolerant.
His reported to reply a staggering "35%.(1 in 3)" This is in line
with Ken Fine who also has data to show that about a third of all
people react in some way to gluten.

I have been more cautious, claiming that at least 10% (one in ten) of
the population is gluten-sensitive. For a fact, about 1% (one in a
hundred) of the population has celiac disease.So how common is the
gluten problem? Very common!

Research article, Secretion of celiac disease autoantibodies after in
vitro gliadin challenge is dependent on small-bowel mucosal
transglutaminase 2-specific IgA deposits. Satumarja M Stenman , Katri
Lindfors , Ilma R Korponay-Szabo , Olli Lohi , Paivi Saavalainen ,
Jukka Partanen , Katri Haimila , Herbert Wieser , Markku Maki and
Katri Kaukinen BMC Immunology 2008, 9:6doi:10.1186/1471-2172-9-6.
Published: 29 February 2008

Review Articles on Celiac Disease

American Journal of Clinical Nutrition, Vol. 69, No. 3, 354-365, March
Review Article The widening spectrum of celiac disease1,2 Joseph A

Deficiencies of the fat-soluble vitamins D, E, A, and K; iron; folic
acid; and calcium are also common. The deleterious proteins are
gliadins (wheat), hordeins (barley), secalins (rye), and possibly
avidins (oats)

These atypical modes of presentation include deficiencies of single
micronutrients; nonspecific gastrointestinal complaints such as
bloating, abdominal pain, diarrhea, constipation, flatulence,
secondary lactose intolerance, and dyspepsia; and nongastrointestinal
complaints such as fatigue, depression, arthralgia, milk intolerance,
osteomalacia or osteoporosis, and iron deficiency anemia (11, 48-50).
Iron deficiency anemia can occur with or without heme-positive stool

Psychiatric referral is also common before diagnosis; often, patients
require a great degree of determination to persist in seeking an
organic cause for their symptoms

Celiac disease is particularly common in patients with type 1
diabetes, thyroid disease, Addison disease, osteopenic bone, Down
syndrome, and rheumatologic complaints

Celiac disease should be considered in anyone with conditions
associated with a high risk of the disease, such as type 1 diabetes,
autoimmune thyroid disease, T cell lymphoma, osteoporosis, and
infertility, and in those with a family history of celiac disease or
dermatitis herpetiformis

Dermatitis herpetiformis is an extremely itchy, bullous skin rash that
affects the extensor surfaces of the limbs, trunk, and scalp.

Several noninvasive tests of malabsorption are used to decide whether
a biopsy should be performed. These include tests of deficiency
states, such as measurements of hemoglobin and red cell indexes,
carotene, vitamin D, prothrombin time, and iron and folate
concentrations; tests of absorption, including the D-xylose test;
qualitative or quantitative fecal fat tests; and contrast radiography.
These tests may be important for identifying malabsorption but have
variable sensitivity for celiac disease. For example, fecal fat
measurements may be normal in 30% of persons with celiac disease. Many
patients with celiac disease also have normal concentrations of
hemoglobin and vitamins, which may be due to the widespread use of

Gluten-Sensitive Enteropathy (Celiac Disease): More Common Than You
DAVID A. NELSEN, JR., M.D., M.S., University of Arkansas for Medical
Sciences, Little Rock, Arkansas 1: Am Fam Physician. 2002 Dec
15;66(12):2259-66 Excellent review clinical

Volume 120, Issue 6, Pages 1522-1525 (May 2001)
American Gastroenterological Association medical position statement:
Celiac sprue. Official recommendations of the American
Gastroenterological Association (AGA) on Celiac Sprue.

1: NIH Consens State Sci Statements. 2004 Jun 28-30;21(1):1-23.
NIH Consensus Development Conference on Celiac Disease.

Alopecia Areata

Gastroenterology. 1995 Oct;109(4):1333-7. Links
Celiac disease and alopecia areata: report of a new association.
Corazza GR, Andreani ML, Venturo N, Bernardi M, Tosti A, Gasbarrini G.
Department of Internal Medicine, University of L'Aquila, Italy.

Celiac disease is frequently associated with other autoimmune
disorders but has never been reported in association with alopecia
areata. In a routine clinical practice, 3 patients with such an
association were observed. In one of the patients, celiac disease was
diagnosed after the occurrence of malabsorption symptoms. In the
youngest patient, a 14-year-old boy, gluten-free diet resulted in
complete regrowth of scalp and body hair. A prospective screening
program for celiac disease using antigliadin and antiendomysial
antibodies was therefore set up in 256 consecutive outpatients with
alopecia areata. Three patients, all completely asymptomatic for
intestinal diseases, were found to be positive and underwent biopsy.
Histological analysis showed a flat intestinal mucosa consistent with
the diagnosis of celiac disease. The results show that alopecia areata
may constitute the only clinical manifestation of celiac disease and
that the association between these two conditions is a real one
because the observed frequency of association is much greater than can
be expected by chance. It is suggested that antigliadin and
antiendomysial antibodies should be included in the work-up of
patients with alopecia areata.

Celiac Disease and Osteoporosis

Increased Prevalence of Celiac Disease and Need for Routine Screening
Among Patients With Osteoporosis

William F. Stenson, MD; Rodney Newberry, MD; Robin Lorenz, MD, PhD;
Christine Baldus, RN, BSN; Roberto Civitelli, MD Arch Intern Med.

Individuals also received serologic testing for IgG antigliadin, IgA
antigliadin, IgA antitissue transglutaminase (anti-TTG), and IgA
antiendomysial antibody (anti-EMA). Reagents for the antigliadin and
anti-TTG tests were from INOVA Diagnostics, Inc (San Diego, Calif);
reagents for anti-EMA were from Binding Site (Birmingham, England).

Cardiomyopathy and Celiac Disease

Mayo Clin Proc. 2005 May;80(5):674-6. Cardiomyopathy associated with
celiac disease.Goel NK, McBane RD, Kamath PS.Department of Internal
Medicine, Mayo Clinic College of Medicine, Rochester, Minn 55905, USA.

Celiac disease or celiac sprue is predominantly a disease of the small
intestine characterized by chronic malabsorption in genetically
susceptible individuals who ingest grains containing gluten, such as
wheat, barley, and rye. Although previously believed to be uncommon,
celiac disease may be present in up to 1% of the general population.
Celiac disease is associated frequently with iron deficiency anemia,
dermatitis herpetiformis, selective IgA deficiency, thyroid disorders,
diabetes mellitus, and various connective tissue disorders but is
rarely associated with cardiomyopathy. We describe a patient with
celiac disease associated with cardiomyopathy whose cardiac function
improved substantially after treatment with a gluten-free diet.
Cardiomyopathy associated with celiac disease is a serious and
potentially lethal condition. However, with early diagnosis and
treatment with a gluten-free diet, cardiomyopathy in patients with
celiac disease may be completely reversible.

Myopathy and Celiac Disease

Muscle Nerve. 2007 Jan;35(1):49-54,
Celiac disease and antibodies associated with celiac disease in
patients with inflammatory myopathy. Selva-O'Callaghan A, Casellas F,
de Torres I, Palou E, Grau-Junyent JM, Vilardell-Tarrés M.

Celiac disease is usually associated with autoimmune disorders and has
occasionally been reported in patients with inflammatory myopathies.
Our aim was to determine the presence of celiac disease and antibodies
associated with celiac disease in patients with inflammatory
myopathies and to investigate their relationship. Serum antigliadin,
anti-tissue transglutaminase, and antiendomysial antibodies were
determined in 51 patients with inflammatory myopathies. HLA-DQ2 and -
DQ8 alleles were studied to assess their complementary diagnostic
value. Jejunal biopsy was performed in patients with moderate to high
levels of antigliadin antibodies. Patients with jejunal histology
consistent with celiac disease initiated a gluten-free diet. Seventeen
patients (31%) were positive for antigliadin antibodies, which were
significantly more frequent in patients with inclusion-body myositis
than dermatomyositis (P < 0.001). Positive status to HLA-DQ2 and/or -
DQ8 did not differ between antigliadin-positive (75% and 12.5%) or -
negative (60% and 15%) patients. Three of five jejunal biopsies were
diagnostic for celiac disease with histological normalization after a
gluten-free diet. Thus, celiac disease is more prevalent in patients
with inflammatory myopathies than in the general population. Positive
status to HLA-DQ2 allele, which is known to be more frequent in
patients with inflammatory myopathies, could explain the high
prevalence of antigliadin antibodies in this population. The
diagnostic value of HLA-DQ2 or -DQ8 haplotypes to detect celiac
disease in patients with inflammatory myopathy is limited.

Sarcoidosis and Celiac Disease


Issue 8393, 7 July 1984, Pages 13-15. J. G. Douglas, R. F. A. Logan1,
J. Gillon, I. W. B. Grant and G. K.

An association between sarcoidosis and coeliac disease is suggested by
the occurrence of both diseases in 5 patients. In 3 cases the
gastrointestinal symptoms of coeliac disease preceded those of
sarcoidosis and in the other 2 patients symptoms of both diseases
appeared at the same time.


Dig Dis Sci. 2007 Oct 13 Sarcoidosis in Patients with Celiac
Disease.Hwang E, McBride R, Neugut AI, Green PH.Department of
Medicine, Columbia University Medical Center, 180 Fort Washington
Avenue, Room 956, New York, NY, 10032, USA,

Purpose Several case reports and European studies have suggested an
association between sarcoidosis and celiac disease; however, they have
been inconsistent. We therefore analyzed a large cohort of celiac-
disease patients to assess this association. Methods An anonymized
database of patients with celiac disease was reviewed to determine the
number of patients with sarcoidosis. Age- and gender-adjusted
standardized morbidity ratios with corresponding 95% confidence
intervals (CI) were calculated by comparing results to US-population-
derived prevalence data. Results Ten patients were found to have a
comorbid diagnosis of sarcoidosis, representing an age- and gender-
adjusted standardized morbidity ratio of 36.8 (95% CI 26.7-50.9).
Conclusions In this cohort of patients with celiac disease, there was
a significantly increased risk of sarcoidosis when compared with the
American white population. This further strengthens prior associations
that have been made suggesting a shared mechanism behind the
etiologies of celiac disease and sarcoidosis.

Prevalence and Epidemiology of Celiac Disease

High prevalence of coeliac disease in apparently healthy Iranian blood
donors. European Journal of Gastroenterology & Hepatology. 15(5):
475-478, May 2003. Shahbazkhani, Bijan a; Malekzadeh, Reza a;
Sotoudeh, Masoud a; Moghadam, Ketaion Fayaz a; Farhadi, Mohammad a;
Ansari, Reza a; Elahyfar, Amin a; Rostami, Kamran b

Abstract: Background/objective: Studies about the prevalence of
coeliac disease in countries in western Asia are scarce and there is
no study on the prevalence of coeliac disease in Iran. The aim of this
study was to determine the prevalence of coeliac in healthy, Iranian,
blood donors.

Study design and methods: Blood samples were obtained from 2000
apparently healthy blood donors (1580 males, 420 females; mean age
35.5 years, range 18-65 years) at the Tehran Blood Donation Centre
during a 4 month period from November 1998 through February 1999.
Total serum IgA was measured in all donors, and IgA deficient cases
were excluded. All cases were analysed for IgA anti-gliadin (AGA) by
an ELISA test and those with positive results were tested for IgA anti-
endomysium antibody (EMA) using immunofluorescence. All donors who had
a positive serology for both AGA and EMA underwent small intestinal
biopsy. The biopsy samples were classified according to revised Marsh
criteria (UEGW 2001).

Results: Forty-nine cases showed positive IgA AGA (38 males and 11
females, mean age 38.6 years). Of the 49 AGA positive cases 12 were
EMA positive. All subjects with positive serology (both AGA and EMA)
were found to have small bowel biopsies compatible with gluten
sensitive enteropathy. Three of 12 had Marsh I, 4/12 Marsh II and 5/12
showed a Marsh IIIa lesion.

Conclusion: The minimum prevalence of gluten sensitivity among
apparently healthy urban Iranian blood donors is 1/166. Further
epidemiological studies in adults from the general population and in
high risk groups seems indicated.

Screening and Detection, LAb Testing of Celiac Disease



INOVA Diagnostics, Inc., Interpretation of Celiac Disease Blood Test
Results. The following detailed explanation of serological tests for
celiac disease was written by Tom Ryan, Technical Service Specialist,
INOVA Diagnostics, Inc.

My personal feeling is that the minimum is 2 slices of bread per day
for 6 weeks to get an accurate test IgG anti-gliadin antibodies are
more sensitive but are less specific markers for disease compared with
IgA class antibodies. IgA anti-gliadin antibodies are less sensitive
but are more specific. A sensitive testing protocol includes testing
for both IgA and IgG anti-gliadin antibodies since a significant
portion of celiac patients (approx. 2-5%) are IgA deficient. This
combined IgA and IgG anti-gliadin antibody assay has an overall
sensitivity of 95% with a specificity of 90%. The type of test used to
detect the anti-gliadin antibodies is called an ELISA.

Endomysial Antibodies: IgA class anti-endomysial antibodies (AEA) are
very specific, occurring only in celiac disease and DH (Dermatiformis
Herpeticus). In summary, the tTG ELISA is measuring the same thing
that the endomysial IFA is measuring but with a method that is more
sensitive and specific and not subject to interpretation.

Quest Lab test Panel for Celiac Disease.

Screening for adult coeliac disease - which serological marker(s) to
use? J Intern Med 2001; 250: 241-248.

Design. In a population-based cross-sectional study we compared the
use of antigliadin antibodies (AGA) of isotypes IgA and IgG,
antiendomysial antibodies (AEA) of isotype IgA and
antitransglutaminase antibodies (ATGA) of isotype IgA for detecting
coeliac disease amongst adults.

Setting. Northern Sweden. Subjects. A total of 1850 of 2500 (74%)
invited adults (aged 25-74 years) who were randomly selected from the
population register after stratification for age and sex. Main outcome
measures. The sensitivity, specificity and predictive values of the
AGA, ATGA and AEA tests.

Results. Nine cases of biopsy proven, previously undiagnosed coeliac
disease were detected by screening. The sensitivity of both ATGA and
AEA was 100% whilst AGA IgA and IgG both had a sensitivity of 89%. The
AEA test had a specificity of 100% whereas the specificities of the
ATGA, AGA IgA and IgG tests were 97, 96 and 78%, respectively. The
positive predictive value for the AEA test was 100%, whereas it was
considerably lower for the other tests (ATGA > AGA IgA > AGA IgG),
with further decreases for all tests when shifting from a clinical to
a screening situation.

Conclusions. When screening for coeliac disease we suggest a serial
testing approach, i.e. an initial ATGA test and, when positive,
followed by an AEA test, provided that IgA deficiency has been
excluded. However, assessment of the small intestinal mucosal
morphology is still required to ascertain the diagnosis.

ATGA : antitransglutaminase antibodies (ATGA) of isotype IgA for
detecting coeliac disease amongst adults.

Identification of a new coeliac disease subgroup: antiendomysial and
anti-transglutaminase antibodies of IgG class in the absence of
selective IgA deficiency. J Intern Med 2001; 249: 181-188. Picarelli
A, Di Tola M, Sabbatella L, Mastracchio A, Trecca A, Gabrielli F, Di
Cello T, Anania MC, Torsoli A

Conclusions. In this study, we observed a group of CD patients who
were EMA IgG1-positive even in the absence of EMA IgA positivity and
IgA deficiency. The diagnosis was based on the finding of the gluten-
dependent clinical and histological features typical of CD. Data
emerging from the present investigation thus suggest that the
prevalence of CD should be reassessed and that the determination of
EMA IgG1 could offer a new tool in the diagnostic armamentarium of CD.

Radioimmunoassay to detect antitransglutaminase autoantibodies is the
most sensitive and specific screening method for celiac disease

Objective: The aim of this study was to establish the most sensitive
and specific screening method for celiac disease. We tested three
methods based on different principles, which all detect autoantibodies
against the same antigen (tissue transglutaminase).

Methods: Sixty-two celiac children at the first biopsy (group 1), 78
celiac children on a gluten-free diet (group 2), 14 celiac children on
a gluten-challenge (group 3), and 56 controls with a normal duodenal
mucosa (group 4) were studied. The methods used were: 1)
radioimmunoprecipitation assay using recombinant tissue
transglutaminase (RIA); 2) commercial enzyme immunoassay using guinea
pig tissue transglutaminase (ELISA); and 3) indirect
immunofluorescence method for detection of antiendomysium antibodies

Results: RIA antitransglutaminase autoantibodies were detected in 100%
of group 1, 43.6% of group 2, 100% of group 3, and none of the control
subjects. ELISA antitransglutaminase autoantibodies were detected in
90.3% of group 1, 9% of group 2, 78.6% of group 3, and in none of the
control subjects. IF-EMA were detected in 95.2% of group 1, 11.5% of
group 2, 92.3% of group 3, and 1.8% of the controls.

Conclusions: Our results demonstrate a very high sensitivity and
specificity of the RIA method to detect antitransglutaminase
autoantibodies in comparison to ELISA and IF-EMA assays. We can
explain this finding with the use of human recombinant antigen and the
increased capacity of the RIA method to detect low titers of
autoantibodies. If our data are confirmed by studies on larger series,
tissue transglutaminase RIA could be proposed as the best screening
method for celiac patients.

Am J Gastroenterol. 2007 Jul;102(7):1454-60. Detection of Celiac
disease in primary care: a multicenter case-finding study in North
America. Catassi C, Kryszak D, Louis-Jacques O, Duerksen DR, Hill I,
Crowe SE, Brown AR, Procaccini NJ, Wonderly BA, Hartley P, Moreci J,
Bennett N, Horvath K, Burk M, Fasano A. Mucosal Biology Research
Center and Division of Pediatric Gastroenterology and Nutrition,
University of Maryland School of Medicine, Baltimore, Maryland 21201,

BACKGROUND: Celiac disease (CD) is one of the most common lifelong
disorders in western countries. However, most cases remain currently
undiagnosed in North America, mostly due to poor awareness of CD by
primary care physicians. OBJECTIVES: The aims of this study were (a)
to determine whether an active case-finding strategy in primary care
could increase the frequency of CD diagnosis and (b) to determine the
most common clinical presentations of the condition. METHODS:This was
a multicenter, prospective study involving adult subjects during the
years 2002-2004, attending one of the participating practices. All
individuals with symptoms or conditions known to be associated with CD
were tested for immunoglobulin A anti-transglutaminase (tTG)
antibodies, and those with elevated anti-tTG were subsequently tested
for IgA antiendomysial antibodies (EMA). All subjects who were
positive for EMA were advised to undergo an intestinal biopsy and HLA

RESULTS: The study group included 737 women and 239 men, with a median
age of 54.3 yr. A positive anti-tTG test was found in 30 out of 976
investigated subjects (3.07%, 95% CI 1.98-4.16). CD was diagnosed in
22 patients (18 women, 4 men). The most frequent reasons for CD
screening in these 22 cases were bloating (12/22), thyroid disease
(11/22), irritable bowel syndrome (7/22), unexplained chronic diarrhea
(6/22), chronic fatigue (5/22), and constipation (4/22).

The prevalence of CD in the serologically screened sample was 2.25%
(95% CI 1.32-3.18). The diagnostic rate was low at baseline (0.27
cases per thousand visits, 95% CI 0.13-0.41) and significantly
increased to 11.6 per thousand visits (95% CI 6.8-16.4, P < 0.001)
following active screening implementation. CONCLUSIONS: This study
demonstrates that an active case-finding strategy in the primary care
setting is an effective means to improve the diagnostic rate of CD in
North America.

Townsend Letter

Gluten intolerance: a paradigm of an epidemic Townsend Letter for
Doctors and Patients, Dec, 2002 by Stacy Astor Shaul

Other diagnostic tests which might be helpful in identifying gluten
intolerance, is a urinary peptide for gliadorphin/caseomorphin test
from The Great Plains Laboratory. This test measures the peptides from
incompletely broken down pieces of protein from gluten and casein.

Neuropathy and Neurological Disorders and Celiac Disease


Neurologic presentation of celiac disease. Khalafalla O. Bushara,
Neurology Department, Minneapolis VA Medical Center and University of
Minnesota, Minneapolis, Minnesota Gastroenterology Volume 128, Issue
4, Supplement 1, April 2005, Pages S92-S97

PEDIATRICS Vol. 113 No. 6 June 2004, pp. 1672-1676. Range of
Neurologic Disorders in Patients With Celiac Disease Nathanel Zelnik,
MD, Avi Pacht, MD, Raid Obeid, MD and Aaron Lerner, MD

Small-Fiber Neuropathy/Neuronopathy Associated With Celiac Disease
Skin Biopsy Findings

Thomas H. Brannagan III, MD; Arthur P. Hays, MD; Steven S. Chin, MD,
PhD; Howard W. Sander, MD; Russell L. Chin, MD; Paul Magda, DO; Peter
H. R. Green, MD; Norman Latov, MD, PhD Arch Neurol. 2005;62:1574-1578.

All patients had asymmetric numbness and paresthesias. Three had more
prominent involvement of hands than feet, and 3 had facial numbness.
Celiac disease was diagnosed in 5 after their neuropathy began. The
following serum antibody levels were elevated: tissue transglutaminase
(n = 6), IgA gliadin (n = 4), and IgG gliadin (n = 7). Results of
nerve conduction studies were normal in 7 patients. One patient had
mildly reduced sural amplitudes. The ENF density was reduced in 5
patients. The ENF density was at the low limit of the normal range in
3 additional patients, 2 of whom had morphologic changes in axons.
Three patients had decreased ENF density at the thigh or forearm,
which was more severe than at the distal leg, compatible with a non-
length-dependent process. Four reported improvement with a gluten-free
diet. One had no improvement after 4 months. Symptoms developed in 2
while receiving a gluten-free diet.

Conclusions Patients with CD may have a neuropathy involving small
fibers, demonstrated by results of skin biopsy. The pattern of
symptoms, with frequent facial involvement and a non-length-dependent
pattern on skin biopsy findings, suggests a sensory ganglionopathy or
an immune-mediated neuropathy. Improvement of symptoms in some
patients after initiating a gluten-free diet warrants further study.

Journal of Neurology Neurosurgery and Psychiatry 2005;76:1028-1030
Gluten sensitivity and neuromyelitis optica: two case reports S
Jacob1, M Zarei1, A Kenton2, H Allroggen2

Multiple Sclerosis and Gluten

Acta Neurol Scand. 2004 Oct;110(4):239-41. IgA antibodies against
gliadin and gluten in multiple sclerosis. Reichelt KL, Jensen D.
Institute of Pediatric Research, University of Oslo, Oslo, Norway.

BACKGROUND: Multiple changes in antibodies against various antigens
are found in multiple sclerosis (MS). OBJECTIVE: We wanted to measure
immunoglobulin A (IgA) antibodies to some common food antigens in MS
and also IgG against gliadin and gluten. METHODS: The IgA antibodies
were measured in serum against gluten, gliadin, lactoglobulin,
lactalbumin, casein and ovalbumin in patients with MS and controls
using ELISA technique. IgG was likewise measured for gluten and
gliadin. RESULTS: Highly significant increases compared with controls
were found for IgA and IgG antibodies against gliadin and gluten. IgA
antibodies against casein were significantly increased. Anti-
endomycium and anti-transglutaminase antibodies were negative.
CONCLUSIONS: The data presented indicate that there may be a possible
moderately increased uptake of some specific proteins from the gut in
MS compared with controls.

Clin Neurol Neurosurg. 2007 Oct;109(8):651-3. Epub 2007 May 29.
Multiple sclerosis and gluten sensitivity.Borhani Haghighi A, Ansari
N, Mokhtari M, Geramizadeh B, Lankarani KB.
Department of Neurology, Shiraz University of Medical Sciences,
Shiraz, Islamic Republic of Iran.

OBJECTIVE: To compare the frequency of gluten sensitivity in patients
with multiple sclerosis (MS) and healthy controls. PATIENTS AND
METHODS: The patients were 161 clinically definite MS patients who
referred to neurology outpatient clinic of Nemazee Hospital, Shiraz,
south of Iran from March 2004 to October 2005. IgG and IgA antigliadin
antibodies were measured by enzyme immuno assay (EIA) method. The test
of IgA antitranstissue glutaminase (tTG) and duodenal biopsy were
carried out in patients with either IgA or IgG AGA positive sera.
Antigliadin antibodies were also measured for 166 age and sex matched
control group. RESULTS: Neither IgG nor IgA antigliadin antibodies
showed significant differences between MS patients and controls. Anti-
tTG antibody and histopathologic studies were negative in all patients
with positive IgG or IgA antigliadin antibodies results. Mean values
of IgG and IgA antigliadin antibodies in MS patients with different
sex, age, course, and functional systems involvement were not
significantly different. CONCLUSION: Gluten sensitivity is not
associated with MS in Iran.

Multiple sclerosis and occult gluten sensitivity. Connie D.S.N.A.
Pengiran Tengah, MRCP; Robert J. Lock, MPhil; D. Joseph Unsworth, PhD;
and Adrian J. Wills, MD

Abstract--Two atypical patients with a multiple sclerosis (MS)-like
illness and evidence of occult celiac disease (CD) were managed by the
authors. This prompted screening of a further 49 unselected MS cases
for serologic evidence of CD. IgA anti-endomysial antibody was found
in one case (2%). IgG anti-gliadin antibody was found in 12% of
patients and 13% of blood donors. Anti-gliadin antibody (especially
IgG isotype) can be a nonspecific finding. NEUROLOGY 2004;62:2326-2327

Multiple Sclerosis and Celiac Disease


Four serological blood tests exist for coeliac disease. The most
widely used ones detect an antibody of the IgA type against particular
antigens in the small bowel. Older tests detected antibodies against
reticulin (ARA) or gliadin (AGA), but recent evidence supports the use
of the more modern tests, namely those detecting IgA antibodies
against endomysium (EMA) or tissue transglutaminase (TTG). Generally,
serology may be unreliable in young children, with anti-gliadin
performing somewhat better than other tests in children under five.
[25] Serology tests are based on indirect immunofluorescence
(reticulin, gliadin and endomysium) or ELISA (gliadin or tissue

Guidelines recommend that a total serum IgA level is checked in
parallel, as coeliac patients with IgA deficiency may be unable to
produce the antibodies on which these tests depend ("false negative").
In those patients, IgG antibodies against transglutaminase (IgG-TTG)
may be diagnostic.[27]

Genetic Basis for Celiac HLA DQ2

Other tests that may assist in the diagnosis are blood tests for a
full blood count, electrolytes, calcium, renal function, liver
enzymes, vitamin B12 and folic acid levels. Coagulation testing
(prothrombin time and partial thromboplastin time) may be useful to
identify deficiency of vitamin K, which predisposes patients to
hemorrhage. These tests should be repeated on follow-up, as well as
anti-tTG titres.[3]
Some professional guidelines[3] recommend screening of all patients
for osteoporosis by DXA/DEXA scanning.
Almost all coeliac patients have an abnormal HLA DQ2 allele.[1]

Over 95% of coeliac patients have an isoform of DQ2 (encoded by
DQA1*05 and DQB1*02 genes) and DQ8 (encoded by the haplotype
DQA1*03QB1*0302), which is inherited in families. The reason these
genes produce an increase in risk of coeliac disease is that the
receptors formed by these genes bind to gliadin peptides more tightly
than other forms of the antigen-presenting receptor. Therefore, these
forms of the receptor are more likely to activate T lymphocytes and
initiate the autoimmune process.[1]

The frequency of these genes varies geographically. DQ2.5 has high
frequency in peoples of North and Western Europe (Basque Country,
Ireland,[34] with highest frequencies), portions of Africa, and is
associated disease in India,[35] but is not found along portions of
the West Pacific rim. DQ8, spread more globally than DQ2.5, is more
prevalent from South and Central America (up to 90% phenotype

Screening and case finding people with undetected coeliac disease had
(less overweight, lower cholesterol levels). In the United Kingdom,
the National Institute for Health and Clinical Excellence (NICE)
recommends screening for coeliac disease in patients with newly

1) chronic fatigue syndrome
2) irritable bowel syndrome
3) autoimmune thyroid disease. Hashimotos
4) type 1 diabetes,
5) unexplained iron-deficiency anemia
6) Down's syndrome, Turner's syndrome,
7) lupus

Tissue Antigens. 1996 Feb;47(2):127-33. HLA-DR, DQ genotypes of celiac
disease patients and healthy subjects from the West of
Ireland.Michalski JP, McCombs CC, Arai T, Elston RC, Cao T, McCarthy
CF, Stevens FM.

Department of Internal Medicine, University of South Alabama, Mobile,

Celiac disease (CD) has one of the strongest class II HLA associations
of any human illness. We used DNA-RFLP typing to study the class II
HLA genotypes of celiac disease patients from the West of Ireland, the
geographic area with the highest rate of celiac disease in the world.

Nichols DNA Test for Celiac 17135X HLA Typing for Celiac Disease
Assess risk of celiac disease in symptomatic(HLA-DQ2 and -DQ8)
patients and in family members of patients with celiac disease


Vitamin K-deficiency, A small proportion (10%) have abnormal
coagulation due to deficiency of vitamin K, and are slightly at risk
for abnormal bleeding.

Aetna considers testing of anti-gliadin, anti-reticulin, IgA anti-
human tissue transglutimase (TTG), and IgA anti-endomysial antibodies
(EMA) medically necessary for any of the following indications:

As a preliminary diagnostic test for persons with symptoms suggestive
of celiac disease; or To monitor response to a gluten-free diet; or
For screening first-degree relatives of individuals with celiac
disease; or To screen persons with type 1 diabetes for celiac disease.

Aetna considers measurement of total serum IgA, and genetic testing
for HLA-DQ2 and HLA-DQ8 haplotypes medically necessary for members
with symptoms suggestive of celiac disease and indeterminate serology

Aetna considers IgG-TTG and IgG-EMA medically necessary for persons
with symptoms suggestive of celiac disease and a serum IgA deficiency.

On Line Genetic Testing for Celiac Disease

Online genetic testing for 20 diseases From The TimesMarch 1, 2008.
Handle with care: genetic tests are risky, and I've got the proof. A
new online service uses your DNA to assess your risk of developing
disease. Our correspondent paid £500 to learn his fate Mark Henderson.
See www.deCODEme.com and www.23andMe.com

Decodeme. For only $985, we scan over one million variants in your
genome Calculate genetic risk for 20 diseases based on the current
literature Find out where your ancestors came from and compare your
genome with others. Our current list of diseases includes: Age-related
macular degeneration, Alzheimer's disease,
Asthma, Atrial fibrillation, Breast Cancer, Celiac Disease, Colorectal
Cancer, Crohn's disease, Exfoliation Glaucoma XFG, Hemochromatosis,
Lactose Intolerance, Multiple sclerosis, Myocardial Infarction,
Obesity, Prostate cancer,
Psoriasis, Restless legs, Rheumatoid arthritis, Type 1 Diabetes, Type
2 Diabetes .

23 and me online genetic testing.

Adrenal Insufficiency, Adrenal Fatigue

J Clin Endocrinol Metab. 2007 Sep;92(9):3595-8. Epub 2007 Jun 26. Risk
of primary adrenal insufficiency in patients with celiac
disease. .Elfström P, Montgomery SM, Kämpe O, Ekbom A, Ludvigsson JF.

CONCLUSIONS: This study found a highly increased risk of AD (adrenal
insufficnecy) in individuals with CD (celiac disease). We therefore
recommend that individuals with AD should be screened for CD. We also
suggest an increased awareness of AD in individuals with CD.

Aliment Pharmacol Ther. 2007 Jun 1;25(11):1317-27. Links

Neurological Disease and Celiac Disease, polyneuropathy

A population-based study of coeliac disease, neurodegenerative and
neuroinflammatory diseases.Ludvigsson JF, Olsson T, Ekbom A,
Montgomery SM.

BACKGROUND: It has been suggested that coeliac disease (CD) is
associated with several neurological diseases. However, the evidence
of such an association is inconclusive as earlier research has often
been based on small numbers with retrospective data collection. AIM:
To use Cox regression to examine the risk of neurological disease in
individuals with CD. METHODS: Through Swedish national registers we
identified some 14 000 individuals with a diagnosis of CD (1964-2003)
and 70 000 reference individuals matched for age, sex, calendar year
and county.

RESULTS: Coeliac disease was associated with later polyneuropathy
[hazard ratio (HR) = 3.4; 95% CI = 2.3-5.1]. We found no statistically
significant association between CD and subsequent multiple sclerosis
(HR = 0.9; 95% CI = 0.3-2.3), Parkinson's disease (HR = 1.2; 95% CI =
0.8-1.9), Alzheimer's disease (HR = 1.5; 95% CI = 0.9-2.6), hereditary
ataxia (HR = 1.3; 95% CI = 0.5-3.6), the symptom ataxia (HR = 1.9; 95%
CI = 0.6-6.2), Huntington's disease (HR = 1.7; 95% CI = 0.3-8.6),
myasthenia gravis (HR = 0.8; 95% CI = 0.2-3.8) or spinal muscular
atrophy (HR = 0.5; 95% CI = 0.1-3.8). Prior polyneuropathy was
associated with subsequent CD (odds ratio = 5.4; 95% CI = 3.6-8.2).

CONCLUSIONS: The association between CD and polyneuropathy indicates
shared risks. We suggest that individuals with polyneuropathy
routinely undergo screening for CD. There is no notable association
between CD and other neurological outcomes investigated in this study.

A case-control study of presentations in general practice before
diagnosis of coeliac disease. Br J Gen Pract. 2007 Aug;57(541):
636-42. BACKGROUND: Delay in the diagnosis of coeliac disease
prolongs morbidity and may increase mortality. Little is known about
presentations in general practice that may predict a subsequent
diagnosis of coeliac disease. AIM: To examine presentations in general
practice during the 5 years prior to diagnosis of coeliac disease.
DESIGN OF STUDY: A case-control study with each biopsy-proven coeliac
disease case matched by age, sex, and general practice to an average
of two controls. SETTING: Thirty-seven general practices in south-east

METHOD: Cases were identified via a secondary care clinic and controls
recruited from the general practices of cases. General practice
clinical records of both cases and controls were analysed to determine
frequency of consultations, presenting symptoms, diagnoses, referrals,
and investigations during the 5 years prior to diagnosis. RESULTS:
Cases (n = 68) had an increased number of consultations compared with
controls (n = 160) during the 5 years prior to diagnosis (mean
difference five consultations, P = 0.001). Three clinical features
were independently associated with subsequent diagnosis of coeliac
disease: depression and/or anxiety (odds ratio [OR] = 2.5, 95%
confidence interval [CI] = 1.1 to 5.7, P = 0.031); diarrhoea (OR =
4.5, 95% CI = 2.0 to 10.0, P <0.001); and anaemia (OR = 26.3, 95% CI =
5.7 to 120.6, P <0.001). Both diarrhoea and anaemia remained
associated even when data for the year prior to diagnosis was excluded
from the analysis.

CONCLUSION: GPs should consider testing for coeliac disease when
patients present often, especially with diarrhoea and/or who are
discovered to be anaemic. Further research is required to clarify the
role of depression and/or anxiety in the diagnosis of coeliac disease.

Celiac and Hashimotos's

Clin Med Res. 2007 Oct;5(3):184-92. Celiac disease and autoimmune
thyroid disease.\Ch'ng CL, Jones MK, Kingham JG. Department of
Gastroenterology, Singleton Hospital, Swansea, United Kingdom.

World J Gastroenterol. 2007 Mar 21;13(11):1715-22.
Coeliac disease in Dutch patients with Hashimoto's thyroiditis and
vice versa. Hadithi M, de Boer H, Meijer JW, Willekens F, Kerckhaert
JA, Heijmans R, Peña AS, Stehouwer CD, Mulder CJ.

AIM: To define the association between Hashimoto's thyroiditis and
coeliac disease in Dutch patients. METHODS: A total of 104 consecutive
patients with Hashimoto's thyroiditis underwent coeliac serological
tests (antigliadins, transglutaminase and endomysium antibodies) and
HLA-DQ typing. Small intestinal biopsy was performed when any of
coeliac serological tests was positive. On the other hand, 184
patients with coeliac disease were subjected to thyroid biochemical
(thyroid stimulating hormone and free thyroxine) and thyroid
serological tests (thyroglobulin and thyroid peroxidase antibodies).

RESULTS: Of 104 patients with Hashimoto's thyroiditis, sixteen (15%)
were positive for coeliac serology and five patients with documented
villous atrophy were diagnosed with coeliac disease (4.8%; 95% CI
0.7-8.9). HLA-DQ2 (and/or -DQ8) was present in all the five and 53
patients with Hashimoto's thyroiditis (50%; 95% CI 43-62). Of 184
patients with coeliac disease, 39 (21%) were positive for thyroid
serology. Based on thyroid biochemistry, the 39 patients were
subclassified into euthyroidism in ten (5%; 95% CI 2-9), subclinical
hypothyroidism in seven (3.8%; 95% CI 1.8-7.6), and overt
hypothyroidism (Hashimoto's thyroiditis) in 22 (12%; 95% CI 8-16).
Moreover, four patients with coeliac disease had Graves' disease (2%;
95% CI 0.8-5) and one patient had post-partum thyroiditis.

CONCLUSION: The data from a Dutch population confirm the association
between Hashimoto's thyroiditis and coeliac disease. Screening
patients with Hashimoto's thyroiditis for coeliac disease and vice
versa is recommended.

Endocr Rev. 2002 Aug;23(4):464-83. Endocrinological disorders and
celiac disease.Collin P, Kaukinen K, Välimäki M, Salmi J. Department
of Medicine, Tampere University Hospital and University of Tampere,
33014 Tampere, Finland.

The American Journal of Gastroenterology Vol. 96 Issue 3 Page 745
March 2001
Vitamin B12 deficiency in untreated celiac disease Anna Dahele
M.R.C.P. (UK), Subrata Ghosh M.D., (Edin)

ICD-9-CM Diagnosis 579.0 Celiac disease

Jeffrey Dach MD www.drdach.com
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