2. It is estimated to affect 1
in 100 people worldwide.
http://celiac.org/
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3. • 2.5 million Americans are undiagnosed
and are at risk for long-term health
complications.
• 1 in 250 Americans
estimated rate
• Actual diagnosis
rate is 1 in 4,700
Americans
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4. 1 in 250 in Italy
1 in 300 in Ireland
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5. 0.3% in Germany
2.4% in Finland
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6. • 1:100-1:310 in India
• 1:80-1:251 in Australia
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7. • 1:87- 1:166 in Middle east
• 1:18 - 1:355 in Africa
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8. • 1:88 -1:262 in Europe
• 1:100- 1:200
in North America
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9. • 1:67 – 1:681 in South America
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10. Potbelly and muscle
wasting in an affected
child
http://emedicine.medscape.com
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11. People with a first-
degree relative with
this disease (parent,
child, sibling) have a
1 in 10 risk of
developing the same
disease.
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12. Their risk of
gastrointestinal cancer
increases by a factor of 40
to 100 times over the
general population.
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13. Gastrointestinal carcinoma or
lymphoma develops in up to 15
percent of patients with untreated or
refractory disease.
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14. Prof. Dr. Saad S Al Ani
Senior Pediatric Consultant
Head of Pediatric department
Khorfakkan Hospital
Sharjah ,UAE
saadsalani@aol.com
A Glance on Celiac
Disease
15. Q1.Gluten is
A. An additive to many foods
B. A preservative
C. A protein found naturally in certain
foods
D. A flavoring
http://www.webmd.com/digestive-disorders/rm-quiz-live-gluten-free
Pretest
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16. Q2.Which is a symptom of gluten intolerance?
A. Poor circulation
B. Sore throat
C. Diarrhea
D. Ringing in the ears
http://www.webmd.com/digestive-disorders/rm-quiz-live-gluten-free
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17. Celiac Disease Timeline:
A Glutinous History
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18. 10,000 years ago
The Neolithic agricultural revolution introduced
wheat and other cultivated grains to the human
diet.
Chris Stein/Getty Images
http://protomag.com/assets/celiac-disease-timeline-a-glutinous-history
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19. Wellcome Library
Second century A.D.
Aretaeus of Cappadocia described a
condition called koiliakos (derived from
koelia, Greek for abdomen) that caused
abdominal pain and diarrhea, referring to
patients with the malady as celiacs.
http://protomag.com/assets/celiac-disease-timeline-a-glutinous-history
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20. 1888
British physician Samuel Gee published the
first modern description of this ancient
affliction, suggesting it was associated with
diet. To relieve symptoms, in the 1920s
many diets (including all-banana and all-
carbohydrate) were introduced.
Justin Lightley/Getty Images
http://protomag.com/assets/celiac-disease-timeline-a-glutinous-history
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21. 1940s
Dutch physician Willem Karel Dicker's
recommendation of a wheat-free diet was
supported by the discovery that celiac disease
declined during the bread shortages of the Second
World War but climbed again after the war.
1952
By studying fecal content, Dicke and his
colleagues identified gluten as the trigger for
celiac disease, and the gluten-free diet became
standard treatment.Pulse Picture Library/CMP Images/ Phototake
http://protomag.com/assets/celiac-disease-timeline-a-glutinous-history
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22. 1956
In London, gastroenterologist Margot Shiner
developed the definitive way to diagnose
celiac disease: a biopsy based on a specific
pattern of damage to the fingerlike villi in the
small intestine.
ISM/ Phototake
http://protomag.com/assets/celiac-disease-timeline-a-glutinous-history
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23. 1989
Immunologist Ludvig Solid's group from Oslo
narrowed down the major genetic risk for celiac
disease to two versions of the histocompatibility
leukocyte antigen (HLA) molecule.
1997
Gastroenterologist Deltlef Schuppan then at the
Free University of Berlin, discovered that the
autoantibodies of celiac patients are directed
against tissue transglutaminase (an enzyme
released from the intestine’s cells when gluten
passes into the mucosal layer). He introduced a
simple blood-screening test for initial diagnosis.
http://protomag.com/assets/celiac-disease-timeline-a-glutinous-history
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24. 2000
At the University of Maryland, Alessio
Fasano discovered zonulin, a molecule he
believes increases intestinal permeability
and vulnerability to celiac disease.
Courtesy of Center for Celiac Research, University of Maryland
http://protomag.com/assets/celiac-disease-timeline-a-glutinous-history
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25. 2010
Clinical trials testing new nondietary
therapies for celiac disease are under
way, including one to reduce
intestinal permeability.
http://protomag.com/assets/celiac-disease-timeline-a-glutinous-history
Larazotide Acetate
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26. What is Celiac Disease?
Celiac disease is an autoimmune disorder
that can occur in genetically predisposed
people where the ingestion of gluten leads to
damage in the small intestine.
http://celiac.org/
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27. What is gluten
Gluten is a specific type of protein that is found
in wheat, rye, and barley.
http://www.webmd.com/diet/ss/slideshow-gluten-free-diet
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28. The Gluten types:
• Gliadin (found in wheat gluten)
• Secalin (found in rye gluten)
• Horedin (found in barley gluten).
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www.waterwereld.nu
29. Causative factors in Celiac Disease
Genetic
Predisposition
Immune Mediated
Disorder
Gluten
Exposure/
Intolerance
Inflammatory Injury of
the small Intestine
Reduced Absorption
of Calcium ,Iron,
Vitamin A,D,E,K
and Folate
Celiac
Disease
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30. Genetic susceptibility to celiac disease
The genetic susceptibility to celiac disease
is conferred by well-identified haplotypes
in the human leukocyte antigen (HLA)
class II region (i.e. DR3 or DR5/DR7 or
HLA DR4).
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[Best Evidence] Rubio-Tapia A, Kyle RA, Kaplan EL, et al. Increased prevalence and
mortality in undiagnosed celiac disease. Gastroenterology. Jul 2009;137(1):88-93.
33. The Clinical presentations
Celiac disease (CD) :
May occur without any symptoms
Minimally symptomatic celiac disease
is probably the most common form of
the disease, especially in older
children and adults
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36. GI signs and symptoms
of Celiac disease
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37. GI signs and symptoms of Celiac disease in
Infants and young children
Infants and young children typically
present with:
Chronic diarrhea
Anorexia
Abdominal distension
Abdominal pain
Poor weight gain or weight loss
Vomiting
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38. Celiac crisis
Severely affected infants present with a celiac
crisis, which is characterized by:
Explosive watery diarrhea
Marked abdominal distension
Dehydration
Hypotension
Lethargy, often with profound electrolyte
abnormalities, including severe hypokalemia
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39. GI signs and symptoms of Celiac disease in
older children
GI symptoms in older children are
typically less evident and include:
Nausea
Recurrent abdominal pain
Bloating
Constipation
Intermittent diarrhea.
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50. Psychiatric disorders
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Some people with celiac experience:
• Depression
• Irritability
• Poor memory
• Trouble concentrating.
63. 1.Autoimmune conditions
Type 1 diabetes mellitus
Approximately 10% of patients
have typical findings of celiac
disease on duodenal biopsy samples.
Thyroiditis
Alopecia
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64. 2. Genetic syndromes
Down syndrome
The prevalence of Down syndrome in
celiac disease is 8-12%.
Most patients with Down syndrome who have
celiac disease have some GI symptoms
About one third of these patients do not have
GI symptoms
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65. 5/20/2014
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2. Genetic syndromes (Cont.)
Turner syndrome
Williams syndrome
66. Diagnosis
• Serologic tests
IgA anti-TTG2
(Sensitivity :61-100% ,
Specificity :86-100%)
Some 10% of patients whose disease is
diagnosed earlier than 2 yr of age show
absence of IgA anti-TTG2.
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67. Cont.
• Ultimate diagnosis via biopsy that
demonstrates specific, though not
pathognomonic, histopathologic
abnormalities in the small bowel mucosa
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68. Different grades of small intestinal
damage in Celiac disease
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69. Treatment
• Lifelong strict adherence to a gluten-free diet
is the only treatment yet
• Wheat-, barley-, and rye-free diet.
• All celiac disease patients should be treated
with a gluten-free diet regardless of the
presence of symptoms
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71. Complication
• Lymphoma is the most common GI
malignancy in the pediatric population
• Predisposing conditions include:
- HIV/AIDS
- Agammaglobulinemia
- Long-standing celiac disease
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72. Some of the researches
concerning celiac disease during
the early2014
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73. BMC Gastroenterol. 2014 Feb 13;14:28.
Follow-up of pediatric celiac disease: value of antibodies
in predicting mucosal healing, a prospective cohort study.
Vécsei E, Steinwendner S, Kogler H, Innerhofer A, Hammer K, Haas
OA, Amann G, Chott A, Vogelsang H, Schoenlechner R, Huf W,
Vécsei A1.
BMC Gastroenterol. 2014 Feb 13;14:28. doi: 10.1186/1471-230X-14-28.
Follow-up of pediatric celiac disease: value of antibodies in predicting mucosal healing, a prospective cohort study.
Vécsei E, Steinwendner S, Kogler H, Innerhofer A, Hammer K, Haas OA, Amann G, Chott A, Vogelsang H, Schoenlechner R, Huf W, Vécsei A1.
Abstract
BACKGROUND:
In diagnosing celiac disease (CD), serological tests are highly valuable. However, their role in following up children with CD after prescription of a gluten-free
diet is unclear. This study aimed to compare the performance of antibody tests in predicting small-intestinal mucosal status in diagnosis vs. follow-up of
pediatric CD.
METHODS:
We conducted a prospective cohort study at a tertiary-care center. 148 children underwent esophohagogastroduodenoscopy with biopsies either for
symptoms ± positive CD antibodies (group A; n = 95) or following up CD diagnosed ≥ 1 year before study enrollment (group B; n = 53). Using biopsy (Marsh ≥
2) as the criterion standard, areas under ROC curves (AUCs) and likelihood-ratios were calculated to estimate the performance of antibody tests against
tissue transglutaminase (TG2), deamidated gliadin peptide (DGP) and endomysium (EMA).
RESULTS:
AUCs were higher when tests were used for CD diagnosis vs. follow-up: 1 vs. 0.86 (P = 0.100) for TG2-IgA, 0.85 vs. 0.74 (P = 0.421) for TG2-IgG, 0.97 vs. 0.61
(P = 0.004) for DPG-IgA, and 0.99 vs. 0.88 (P = 0.053) for DPG-IgG, respectively. Empirical power was 85% for the DPG-IgA comparison, and on average 33%
(range 13-43) for the non-significant comparisons. Among group B children, 88.7% showed mucosal healing (median 2.2 years after primary diagnosis). Only
the negative likelihood-ratio of EMA was low enough (0.097) to effectively rule out persistent mucosal injury. However, out of 12 EMA-positive children
with mucosal healing, 9 subsequently turned EMA-negative.
CONCLUSIONS:
Among the CD antibodies examined, negative EMA most reliably predict mucosal healing. In general, however, antibody tests, especially DPG-IgA, are of
limited value in predicting the mucosal status in the early years post-diagnosis but may be sufficient after a longer period of time.
CONCLUSIONS:
Negative endomysium (EMA) antibodies most reliably predict
mucosal healing
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74. Childs Nerv Syst. 2014 Feb 25.
Prevalence of resistant occipital lobe epilepsy associated
with celiac disease in children.
Dai AI1, Akcali A, Varan C, Demiryürek AT.
Childs Nerv Syst. 2014 Feb 25. [Epub ahead of print]
Prevalence of resistant occipital lobe epilepsy associated with celiac disease in children.
Dai AI1, Akcali A, Varan C, Demiryürek AT.
Abstract
PURPOSE:
Celiac disease (CD) is a chronic, inflammatory autoimmune disorder caused by intolerance to ingested gluten. Increased
frequency of CD has been reported in occipital lobe epilepsy. The aim of the present study is to investigate the frequency of CD
among children followed up due to epilepsy and diagnosed with epileptic activity in the occipital lobe in at least one
electroencephalography (EEG) test.
METHODS:
For this research, 90 pediatric epilepsy patients with epileptic activity in the occipital lobe were enrolled in the study group, while
the control group comprised of 100 healthy children. In addition to the EEG examination, tissue transglutaminase (tTG) antibody
was determined on duodenal biopsy.
RESULTS:
None of the healthy children in the control group was positive in terms of the tTG antibody test used to scan CD. In the group with
epileptic activity in the occipital lobe, two patients out of 90 were tTG antibody positive. The seroprevalence was 1/45 (2.22 %) in
this group. These two patients were diagnosed with CD based on the endoscopic duodenal biopsy. In these patients, the seizures
were uncontrollable through monotherapy.
CONCLUSIONS:
Our results showed that the prevalence of CD is observed to be higher than the normal population among the patients with
occipital lobe epilepsy. This type of seizure disorder seems to be more resistant to monotherapy, compared with other types of
occipital epilepsy. Therefore, screening for CD is recommended in children with resistant epileptic activity in the occipital lobe.
CONCLUSIONS:
Screening for CD is recommended in children with resistant
epileptic activity in the occipital lobe
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75. Autoimmune Dis. 2014;2014:927190. 2014 Mar 3.
Exploring T cell reactivity to gliadin in young children
with newly diagnosed celiac disease.
Liu E1, McDaniel K1, Case S1, Yu L1, Gerhartz B2,
Ostermann N2, Fankhauser G2, Hungerford V2, Zou C2,
Luyten M2, Seidl KJ2, Michels AW1.
Autoimmune Dis. 2014;2014:927190. 2014 Mar 3.
Exploring T cell reactivity to gliadin in young children with newly diagnosed celiac disease.
Liu E1, McDaniel K1, Case S1, Yu L1, Gerhartz B2, Ostermann N2, Fankhauser G2, Hungerford V2, Zou
C2, Luyten M2, Seidl KJ2, Michels AW1.
Abstract
Class II major histocompatibility molecules confer disease risk in Celiac disease (CD) by presenting gliadin
peptides to CD4 T cells in the small intestine. Deamidation of gliadin peptides by tissue transglutaminase
creates immunogenic peptides presented by HLA-DQ2 and DQ8 molecules to activate proinflammatory CD4
T cells. Detecting gliadin specific T cell responses from the peripheral blood has been challenging due to low
circulating frequencies and heterogeneity in response to gliadin epitopes. We investigated the peripheral T
cell responses to alpha and gamma gliadin epitopes in young children with newly diagnosed and untreated
CD. Using peptide/MHC recombinant protein constructs, we are able to robustly stimulate CD4 T cell clones
previously derived from intestinal biopsies of CD patients. These recombinant proteins and a panel of α- and
γ-gliadin peptides were used to assess T cell responses from the peripheral blood. Proliferation assays using
peripheral blood mononuclear cells revealed more CD4 T cell responses to α-gliadin than γ-gliadin peptides
with a single deamidated α-gliadin peptide able to identify 60% of CD children. We conclude that it is possible
to detect T cell responses without a gluten challenge or in vitro stimulus other than antigen, when measuring
proliferative responses.
Possible to detect T cell responses without a gluten challenge
or in vitro stimulus other than antigen
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76. PLoS One. 2014 Mar 4;9(3):e90552.
Coeliac patients are undiagnosed at routine upper
endoscopy.
Robson K1, Alizart M1, Martin J2, Nagel R3.
PLoS One. 2014 Mar 4;9(3):e90552. doi: 10.1371/journal.pone.0090552. eCollection 2014.
Coeliac patients are undiagnosed at routine upper endoscopy.
Robson K1, Alizart M1, Martin J2, Nagel R3.
Abstract
BACKGROUND AND AIMS:
Two out of three patients with Coeliac Disease (CD) in Australia are undiagnosed. This prospective clinical audit aimed to determine how many CD patients would be
undiagnosed if duodenal biopsy had only been performed if the mucosa looked abnormal or the patient presented with typical CD symptoms.
METHODS:
All eligible patients presenting for upper gastrointestinal endoscopy (OGD) in a regional center from 2004-2009 underwent prospective analysis of presenting symptoms and
duodenal biopsy. Clinical presentations were defined as either Major (diarrhea, weight loss, iron deficiency, CD family history or positive celiac antibodies- Ab) or Minor Clinical
Indicators (CI) to duodenal biopsy (atypical symptoms). Newly diagnosed CD patients had follow up celiac antibody testing.
RESULTS:
Thirty-five (1.4%) new cases of CD were identified in the 2,559 patients biopsied at upper endoscopy. Almost a quarter (23%) of cases presented with atypical symptoms. There
was an inverse relationship between presentation with Major CI's and increasing age (<16, 16-59 and >60: 100%, 81% and 50% respectively, p = 0.03); 28% of newly diagnosed
CD patients were aged over 60 years. Endoscopic appearance was a useful diagnostic tool in only 51% (18/35) of CD patients. Coeliac antibodies were positive in 34/35 CD
patients (sensitivity 97%).
CONCLUSIONS:
Almost one quarter of new cases of CD presented with atypical symptoms and half of the new cases had unremarkable duodenal mucosa. At least 10% of new cases of celiac
disease are likely to be undiagnosed at routine upper endoscopy, particularly patients over 60 years who more commonly present atypically. All new CD patients could be
identified in this study by performing pre-operative celiac antibody testing on all patients presenting for OGD and proceeding to biopsy only positive antibody patients and those
presenting with either Major CI or abnormal duodenal mucosa for an estimated cost of AUS$4,629 and AUS$3,710 respectively.
CONCLUSIONS:
• One quarter of new cases of CD presented with atypical symptoms
• Half of the new cases had unremarkable duodenal mucosa
• 10% of new cases of celiac disease are likely to be undiagnosed at
routine upper endoscopy
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77. J Pediatr Gastroenterol Nutr. 2014 Mar 31.
Mucosal Healing in Children With Treated Celiac
Disease.
Ghazzawi Y1, Tapia AR, Murray JA, Absah I.
J Pediatr Gastroenterol Nutr. 2014 Mar 31. [Epub ahead of print]
Mucosal Healing in Children With Treated Celiac Disease.
Ghazzawi Y1, Tapia AR, Murray JA, Absah I.
Abstract
OBJECTIVES::
Limited data suggest complete mucosal healing in treated children with celiac disease (CD), but recent data from adult endoscopic biopsies have shown substantial
numbers with persistent mucosal injury. We aimed to assess the rate of mucosal healing and indications for repeat small-bowel (SB) biopsy in children with CD.
METHODS::
We retrospectively reviewed records of children (age 1-18 years) with CD who underwent a second SB biopsy. All were seen at Mayo Clinic (Rochester, Minnesota) from
January 1997 through June 2013.
RESULTS::
Forty children were identified (14 male); average age at diagnosis was 8.5 years. Indications for second small bowel (SB) biopsy were abdominal pain (n = 20), diarrhea
(n = 7), constipation (n = 5), non-celiac-related concern (n = 2), follow-up (n = 5), and persistent serology (n = 1). Average time between biopsies was 24 months (range, 4-120
months). Histology on the second biopsy showed complete healing (n = 25), intraepithelial lymphocytes (n = 9), and persistent villous atrophy (n = 6). Of these 3 patients with
partial villous atrophy, and 3 with complete villous atrophy. Persistent villous atrophy was observed in 2/20 patients with abdominal pain and 1/7 with diarrhea. All patients
with persistent constipation (n = 5) had complete resolution.
CONCLUSION::
Mucosal healing in children with CD may not be complete as previously assumed. Abdominal pain was the most common indication for repeating the SB biopsy.
Persistence of abdominal pain, diarrhea and constipation was poorly associated with persistence of mucosal injury.
CONCLUSION:
Persistence of abdominal pain ,diarrhea and constipation poorly
associated with persistence of mucosal injury
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78. Aliment Pharmacol Ther. 2014 Mar 24
The effects of oats on the function of gut microflora in
children with coeliac disease.
Tjellström B1, Stenhammar L, Sundqvist T, Fälth-Magnusson
K, Hollén E, Magnusson KE, Norin E, Midtvedt T, Högberg L.
Aliment Pharmacol Ther. 2014 Mar 24. doi: 10.1111/apt.12707. [Epub ahead of print]
The effects of oats on the function of gut microflora in children with coeliac disease.
Tjellström B1, Stenhammar L, Sundqvist T, Fälth-Magnusson K, Hollén E, Magnusson KE, Norin E, Midtvedt T, Högberg L.
Abstract
BACKGROUND:
Faecal short chain fatty acids (SCFAs) are produced by the gut microflora. We have previously reported high faecal SCFA levels in children with coeliac disease (CD), indicating alteration in gut microfloral metabolism. Data accumulated
over recent decades by us and others suggest that wheat-free oats can safely be included in a gluten-free diet (GFD). However, concerns have been raised with respect to the safety of oats in a subset of coeliacs.
AIM:
To describe faecal SCFA patterns in children with newly diagnosed CD treated for 1 year with a GFD with or without oats.
METHODS:
This report is part of a randomised, double-blind study on the effect of a GFD containing oats (GFD-oats) vs. a standard GFD (GFD-std). Faecal samples were received from 34 children in the GFD-oats group and 37 in the GFD-std
group at initial diagnosis and/or after 1 year on a GFD. Faecal SCFAs were analysed.
RESULTS:
The GFD-std group had a significantly lower total faecal SCFA concentration at 12 months compared with 0 months (P < 0.05). In contrast, total SCFA in the GFD-oats group remained high after 1 year on the GFD. The children in the
GFD-oats group had significantly higher acetic acid (P < 0.05), n-butyric acid (P < 0.05) and total SCFA concentration (P < 0.01) after 1-year diet treatment compared to the GFD-std group.
CONCLUSIONS:
Our results indicate that oats do affect the gut microflora function, and that some coeliac children receiving oats may develop gut mucosal inflammation, that may present a risk for future complications.
Oats do affect the gut microflora function
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79. Dig Dis Sci. 2014 Apr 6.
Clinical Utility of Celiac Disease-Associated HLA Testing.
Pallav K1, Kabbani T, Tariq S, Vanga R, Kelly CP, Leffler DA.
Dig Dis Sci. 2014 Apr 6.
Clinical Utility of Celiac Disease-Associated HLA Testing.
Pallav K1, Kabbani T, Tariq S, Vanga R, Kelly CP, Leffler DA.
Abstract
BACKGROUND:
Negative predictive value (NPV) of celiac disease (CD)-related human leukocyte antigens (HLA) DQ2 and DQ8 approaches 100 % in individual patients.
However, studies evaluating its exclusionary utility in patient groups are lacking.
AIM:
We aim to assess the performance of HLA testing when applied to patient groups with varying characteristics and propose evidence-based recommendations for its
clinical use.
METHODS:
Demographic and clinical information was recorded in patients undergoing HLA testing. Using predetermined criteria, patients were classified as CD, non-CD, or
indeterminate. Diagnostic yield of HLA testing was defined as the percentage of patients in whom CD could be excluded based on negative HLA test.
RESULTS:
Two hundred and fifty-six patients underwent testing for CD-related HLA DQ2 and DQ8. 102 (100 non-CD, 2 CD) patients tested HLA negative for a 98 % NPV and
39 % diagnostic yield. Diagnostic yield was highest (60 %) in patients with intraepithelial lymphocytosis plus normal IgA tissue transglutaminase antibody (IgA-tTG)
and lowest in patients with positive IgA-tTG plus villous atrophy (0 %). CD was diagnosed in two HLA-negative patients, who carried half of DQ2.5 trans genotype.
CONCLUSIONS:
Diagnostic yield of CD-related HLA testing varies widely depending on clinical indication. HLA testing is a practical and valuable test for most patients in whom initial
evaluation for CD is inconclusive. A negative HLA result usually obviates the need for further celiac testing including endoscopy and gluten challenge. Rarely, in
patients reported as HLA negative, half of HLA DQ2.5 (cis or trans) is sufficient for development of CD.
CONCLUSIONS:
A negative HLA result usually obviates the need for
further celiac testing including endoscopy and gluten
challenge
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80. Pediatr Neurol. 2014 May;50(5):479-81.
Prevalence of celiac disease in children with idiopathic
epilepsy in southeast Turkey.
Işıkay S1, Kocamaz H2.
Pediatr Neurol. 2014 May;50(5):479-81. doi: 10.1016/j.pediatrneurol.2014.01.021. Epub 2014 Jan 11.
Prevalence of celiac disease in children with idiopathic epilepsy in southeast Turkey.
Işıkay S1, Kocamaz H2.
Abstract
BACKGROUND:
We examined the prevalence of celiac disease in children with idiopathic epilepsy.
METHODS:
Patients were screened for celiac disease using the immunoglobulin A anti-tissue transglutaminase antibody. Upper
gastrointestinal endoscopy and small intestinal biopsy were offered to all antibody-positive patients. The control group consisted of
400 healthy children.
RESULTS:
A total of 600 patients (332 boys, 268 girls; 8 months-15 years; 9.40 ± 4.09 years) were studied. In 38 patients, the diagnosis was
childhood partial epilepsy with occipital paroxysms. Six of the 38 patients with childhood partial epilepsy with occipital paroxysms
(15.7%) had positive immunoglobulin A anti-tissue transglutaminase antibody. The frequency of biopsy-proven celiac disease was
15.7% (6/38) among children with childhood partial epilepsy with occipital paroxysms. None of the control patients had positive
immunoglobulin A anti-tissue transglutaminase antibody results.
CONCLUSIONS:
These findings suggest that the prevalence of celiac disease in children with partial epilepsy with occipital paroxysms may be
higher than with other types of epilepsies. It may be reasonable to screen individuals with this type of epilepsy for celiac disease.
CONCLUSIONS:
Prevalence of celiac disease in children with partial epilepsy with
occipital paroxysms may be higher than with other types of epilepsies
To screen individuals with this type of epilepsy for celiac disease.
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81. Conclusion
Ratio between patients with diagnosed and
with undiagnosed disease may be as high as
1 : 7
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82. Case finding by liberal use of anti-
endomysium or anti-TTG2 antibodies,
followed by confirmatory jejunal biopsy, is
more cost effective in primary care than
mass screening .
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83. The diagnosis of celiac disease involves:
1. Serologic testing (generally for IgA
anti–tissue transglutaminase antibodies)
2. Upper endoscopy with biopsy for
confirmation in most patients
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84. Patients with celiac disease should follow a
lifelong, strict gluten-free diet.
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85. Monitoring with periodic visits for
assessment of :
- Symptoms
- Growth
- Physical examination
- Adherence to the gluten-free diet.
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86. Q1.Gluten is
A. An additive to many foods
B. A preservative
C. A protein found naturally in certain
foods
D. A flavoring
http://www.webmd.com/digestive-disorders/rm-quiz-live-gluten-free
Pretest
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87. Q2.Which is a symptom of gluten intolerance?
A. Poor circulation
B. Sore throat
C. Diarrhea
D. Ringing in the ears
http://www.webmd.com/digestive-disorders/rm-quiz-live-gluten-free
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