REVIEW

CURRENT
OPINION Update on celiac disease
Michele J. Alkalay

Purpose of review
The purpose of this review is to describe current updates in celiac disease.
Recent findings
Recent developments in the understanding of the pathogenesis of celiac disease continue to emerge that
may implicate the role of gluten exposure. Several studies have shown that the amount of gluten consumed
by the infant may affect the age of onset of celiac disease in genetically predisposed individuals. New
guidelines from the European Society of Paediatric Gastroenterology, Hepatology and Nutrition allow
serology-based celiac diagnosis, omitting endoscopic biopsies, in children. Recent data and updated
guidelines in adults no longer support biopsies in all patients who are genetically susceptible with celiac
disease who have been identified by serology with clinical signs and symptoms of celiac disease. A new
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assay was identified in the immune response to epitopes of the tissue transglutaminase–deamidated gliadin
peptide complex. In addition, a recent study shows that serum IL-2 elevations correlate with timing and
severity of symptoms after gluten ingested in celiac disease patients. Measuring gluten immunogenic
peptides (GIPs) in the stool of celiac patients may help monitor adherence to a gluten-free diet (GFD). Of
importance, we should be aware that the quality of life is affected in celiac disease patients. During
adolescence, the education on the importance of long-term follow-up with an adult gastroenterologist is
associated with more successful rates of medical care transition for young adults with celiac disease.
Latiglutenase, an orally administered mixture of two gluten-specific recombinant proteases that degrades
gluten proteins into small physiologically irrelevant fragments, is currently in a phase 2 trial. Latiglutenase
has shown to be safe and effective in reducing symptoms of celiac disease patients upon a GFD with
improvement of quality of life. Lastly, a recent study describes a mouse model that is characteristic of celiac
disease.
Summary
Our knowledge of celiac disease continues to grow with increasing evidence of contributory factors to its
pathogenesis. There is some evidence that the quantity ingested of gluten by the infant effects the age of
onset of celiac disease in genetically susceptible patients. Changes have been made to the guidelines in
the diagnosis of celiac disease proposed by new studies. Recent studies have shown the significant effects
on quality of life for celiac patients. As improved laboratory methods continue to be developed, these tests
can have utility in both diagnosis of celiac disease and monitoring adherence to the GFD. Current
therapeutic trials offer promising nondietary treatment for celiac patients. The development of an animal
model can provide a better understanding of the pathogenesis of celiac disease.
Keywords
celiac disease, enteropathy, gluten-free diet

INTRODUCTION degree relatives of people with celiac disease, Down

Celiac disease is a common autoimmune condition
which causes enteropathy by exposure to gluten in
genetically predisposed individuals. More than 99%
of people with celiac disease have HLA (Human
Leukocyte Antigen) DR3-DQ2 and/or DR4-DQ8,
compared with approximately 40% of the general
population [1]. Celiac disease affects approximately
0.5–1% of the general population with a female
predominance [2]. There are certain groups that
have a higher risk of developing celiac disease,
&
including first-degree relatives [3 ] and second-
syndrome, type 1 diabetes, selective IgA deficiency,
autoimmune thyroiditis, Turner syndrome, Williams
syndrome, and juvenile chronic arthritis [4–6].
Division of Pediatric Gastroenterology, Hepatology and Nutrition, Depart-
ment of Pediatrics, University of Texas Southwestern, Dallas, Texas, USA
Correspondence to Michele J. Alkalay, MD, 5323 Harry Hines Boulevard,
Dallas, TX 75390, USA. E-mail: MicheleJ.Alkalay@UTSouthwestern.edu
Curr Opin Pediatr 2020, 32:654–660
DOI:10.1097/MOP.0000000000000936

www.co-pediatrics.com Volume 32  Number 5  October 2020

Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.


KEY POINTS
 The quantity ingested of gluten by the infant may effect
the age of onset of celiac disease in genetically
susceptible children.
 Changes have been made to the guidelines in the
diagnosis of celiac disease.
 There are significant effects on the quality of life for
celiac patients.
 Current therapeutic trials provide promising nondietary
treatment for celiac patients.
 The development of a new animal model can lead to a
better understanding of the pathogenesis of
celiac disease.
Currently, the pathogenesis of celiac disease is
not well understood. Studies have shown an associ-
ation between celiac disease and the gut micro-
biome composition and suggest that this may be
causative in its pathogenesis [7–10]. There is evi-
dence that infants who are genetically susceptible to
developing celiac disease have an increased presence
of pathogenic bacteria [11]. However, further large-
scale longitudinal studies are needed to determine if
the gut microbiota composition effects the onset of
celiac disease in genetically susceptible individuals.
In addition, a recent study shows that the exposure
of probiotics during the first year of life is not
associated with celiac disease autoimmunity (posi-
tive autoantibodies) nor celiac disease itself (biopsy
&
confirmed or persistent elevated antibodies) [12 ].
The pathogenesis of celiac disease requires ingestion
of gluten. Previous studies have shown conflicting
results of whether there is a higher risk for children
developing celiac disease who are exposed to higher
levels of gluten [13,14]. There is some evidence that
the amount of gluten consumed by the infant effects
the age of onset of celiac disease in genetically
&& &&
predisposed individuals [15 –17 ].
Small intestinal biopsy historically has been the
gold standard for diagnosis of celiac disease, though
highly sensitive and specific serologic tests are avail-
able for diagnostic screening and work-up. These
tests include tissue transglutaminase (TTG), endo-
mysial, and deamidated gliadin peptide (DGP) anti-
bodies. At present, no antibody test is available with
100% sensitivity and specificity, therefore, an intes-
tinal biopsy has been the gold standard for confir-
mation of the diagnosis [18]. Previously, European
studies have shown accuracy in identifying children
with celiac disease without biopsy by high-TTG
antibody titers, positive antiendomysial antibodies
and HLA-DQ2/HLA-DQ8 positivity with clinical
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Update on celiac disease Alkalay
symptoms, however, there was poor reproducibility
of TTG assays [19–21]. Recent data and updated
guidelines from the European Society of Paediatric
Gastroenterology, Hepatology and Nutrition
(ESPGHAN) allow serology-based diagnosis for
celiac disease omitting endoscopic biopsies in chil-
&&
dren [22 ]. Currently, there is evidence that biop-
sies may not be warranted for diagnosis of celiac
disease in symptomatic adults who are genetically
susceptible and antibody positive [23 ].
&&
The treatment for celiac disease is a gluten-free
diet (GFD). Current serology is not enough for eval-
uating the response to a GFD and the regrowth of
villi [24,25]. There are no studies available to screen
for celiac disease in patients already on a GFD. Most
importantly, the GFD resolves clinical symptoms
and mucosal inflammation in celiac disease
patients, preventing complications like ulcerative
jejunoileitis, small intestinal carcinoma, and lym-
phoma, with an improved quality of life [26,27].
QUANTITY OF GLUTEN
The quantity of gluten in an infant’s diet may
contribute to the risk of, or timing of, developing
celiac disease. A multinational, prospective, obser-
vational study of 6605 children carrying HLA anti-
gen genotype associated with celiac disease showed
that the quantity of gluten exposure during the first
5 years of life was associated with the development
of celiac autoimmunity and celiac disease [15 ].
&&
Among children who consumed the reference
amount of gluten (mean intake 3.7 g/day), 28%
developed celiac autoimmunity (defined as two con-
secutive positive TTG autoantibodies), and 21% had
developed celiac disease (defined by intestinal
biopsy or persistently elevated TTG autoantibody
levels), compared with 34% and 28% for those who
consumed an additional 1 g/day of cooked pasta.
The high prevalence of celiac autoimmunity and
celiac disease in these children suggest the genetic
susceptibility of this study population. Long-term
follow-up of these pediatric patients is required to
determine whether the amount of gluten ingested at
an early age effects the later development of celiac
disease. In addition, similar epidemiological obser-
vations have been reported for other autoimmune
diseases in the Western hemisphere, indicating that
environmental factors (geographical distribution,
pathogenic organisms, and gut commensal bacteria)
may play a role in the pathogenesis of celiac disease
[28].
Another prospective study evaluating early glu-
ten intake included 1875 at-risk children in which
8.6% developed celiac disease autoimmunity and
4.5% developed celiac disease. The risk of celiac
www.co-pediatrics.com 655
Gastroenterology and nutrition
disease autoimmunity increased by 5% for each
gram of gluten consumed between the ages of 1
and 2. The risk for developing celiac autoimmunity
and celiac disease was the strongest for increased
gluten at 1 year of age. However, these results were
based upon a small subset of a larger sample and the
results may not be representative of the broader
population by focusing only upon genetically at-
&&
risk children [16 ].
Another pediatric study that diagnosed 738 chil-
dren (1.1%) with celiac disease showed findings
suggestive of a greater risk for developing celiac
associated with increased gluten exposure during
&&
infancy [17 ]. The risk of celiac disease increased
by 3% with each gram of extra gluten intake per day,
with children who were introduced to gluten at
6 months of age or older having a higher risk of
celiac disease than those introduced at 4–6 months
of life. However, a randomized clinical trial of dif-
ferent amounts of gluten during early childhood in
genetically at-risk patients would be necessary to
confirm these findings.
DIAGNOSIS OF CELIAC DISEASE
Autoantibodies, including TTG, endomysial and
DGP antibodies, are useful for diagnostic purposes.
TTG antibody is the most commonly used serologic
test for celiac disease, though the newer DGP anti-
&&
body is increasingly being utilized [29 ]. Children
from birth to 18 years of age with positive DGP IgG
serology were retrospectively studied. Forty patients
with DGP positive serology and TTG negative anti-
body, underwent duodenal biopsies via endoscopy.
Only one patient had celiac disease confirmed via
histology, and this patient was IgA deficient. The
positive predictive value was 2.5% for isolated DGP
IgG-positive antibody.
The gold standard for celiac disease diagnosis,
historically, has been intestinal biopsy. After obtain-
ing positive screening serological autoantibodies
(TTG, endomysial and DGP antibodies), duodenal
biopsies are obtained which show mucosal inflam-
mation with villous atrophy. In a recent large study,
the triple combination of positive TTG antibodies
(over 10 times the cutoff) with positive antiendo-
mysial antibodies and HLA-DQ2/HLA-DQ8 positiv-
ity showed a high accuracy in detecting adult celiac
&&
disease patients [23 ]. Over 5000 subjects were
studied and divided into three groups: adults with
high-risk clinical celiac disease suspicion, moderate-
risk, and low-risk subjects from the general popula-
tion. Serologic and clinical data were collected, and
triple criteria for celiac disease included two positive
TTG antibodies greater than 10 times the upper limit
of normal, positive endomysial antibodies and
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positive genetics (HLA-DQ2/HLA-DQ8) with the
diagnosis based upon biopsy. Out of 5079 subjects,
274 patients were diagnosed with celiac disease with
positive histology, and 33% of these patients could
have avoided biopsy. Therefore, this study suggests
that triple criteria may be an appropriate option in
avoiding biopsy in diagnosis of celiac disease
in adults.
The new American Gastroenterological Associa-
tion guidelines to diagnose and monitor celiac dis-
ease consider serology and histology. TTG IgA
antibody at high levels (>10 times the upper normal
limit) is a reliable and accurate test for diagnosis of
&&
celiac disease [30 ]. The combination of positive
TTG IgA antibody with positive endomysial anti-
body in a second blood sample has a positive pre-
dictive value of approximately 100%.
Recent ESPGHAN guidelines for diagnosing
celiac disease in 2020 recommend serology diagno-
sis, and to forego the histopathology for confirma-
&&
tion of diagnosis in children [22 ]. Literature
databases show that the combination TTG IgA
and IgA serum is more accurate than other test
combinations, such as DGP antibodies. If the total
IgA is low, then an IgG-based antibody is warranted.
If the TTG IgA is greater than or equal to 10 times the
upper limit of normal, and a second blood test is
positive with an antiendomysial antibody, then
endoscopy with biopsies is not necessary for diag-
nosis of celiac disease. However, pediatric patients
with a TTG IgA antibody less than 10 times the
upper limit of normal should undergo biopsies to
avoid the risk of a false positive diagnosis. Those
patients with positive autoimmunity with negative
biopsies should be followed closely for symptoms.
Lastly, as HLA DQ2/DQ8 testing is costly, not uni-
versally available and may not improve the accu-
racy of the no-biopsy diagnosis, HLA is not
obligatory to determine serology-based celiac dis-
ease diagnosis.
MONITORING CELIAC DISEASE
Strict compliance with a GFD in most celiac disease
patients leads to the decrease of antibodies within
12–24 months with intestinal villi regrowth. TTG
IgA antibody is the most common test to monitor
follow-up of celiac disease patients [31]. A recent
study demonstrated a very high specificity and sen-
sitivity of a new assay directed to identify the serum
immune response to epitopes of the TTG–DGP
&&
complex [32 ]. These markers can be useful for
diagnosis of celiac disease and follow-up purposes
for compliance of a patient upon a GFD. However,
further studies are required for the validation of
this assay.
Volume 32  Number 5  October 2020

Currently, celiac disease cannot be screened nor
diagnosed in someone already on a GFD, thus sus-
pected patients must be placed on a gluten contain-
ing diet for 2–8 weeks followed by endoscopy with
duodenal biopsy and serology [33]. A new study
discovered that a single-dose gluten reintroduction
combined with IL-2 measurements may be helpful
in diagnosing and monitoring celiac disease for
&&
patients already on a GFD [34 ]. In this study, 25
celiac disease patients on a GFD and 25 healthy
volunteers consumed a standardized 6-g gluten
challenge. Celiac Disease Patient-Reported Outcome
surveys and global digestive symptom assessments
were completed hourly up to 6 h after gluten inges-
tion. Adverse events over 48 h were recorded, and
serum IL-2 was measured at baseline, then 2, 4, and
6 h. Results showed that serum IL-2 was undetect-
able in healthy controls and elevated (>0.5 pg/ml) at
4 h in 92% of celiac disease patients. Celiac disease
patients showed a significant increase in patient-
reported outcome severity scores (P < 0.001 Wil-
coxon signed rank test). Symptoms, mostly nausea
and vomiting, began after 1 h and peaked in the
third hour post gluten ingestion. Furthermore, the
peak IL-2 correlated with symptom severity. Serum
IL-2 elevations correlate with timing and severity of
symptoms after gluten intake in celiac disease
patients. This could provide a valuable clinical test
to diagnose celiac disease in patients already on
a GFD.
QUALITY OF LIFE IN CELIAC DISEASE
PATIENTS
There is limited research on health-related quality of
life (HRQOL) in children with newly diagnosed
celiac disease. Pediatric patients with newly diag-
nosed celiac disease were found to have a lower
quality of life compared with healthy children. In
a large sample of pediatric patients with newly
diagnosed celiac disease of 159 children, over 50%
of patients reported impairment in physical, emo-
tional, school and social functioning. Children with
newly diagnosed celiac disease had similar quality of
HRQOL to that of patients with nonceliac gastroin-
testinal conditions, including both functional dis-
orders (irritable bowel syndrome and recurrent
abdominal pain) and organic gastrointestinal disor-
ders (such as, inflammatory bowel disease, reflux,
&&
gastritis, and fatty liver) [35 ].
The diagnosis of celiac disease can often be
delayed for years from onset of symptoms. Although
there has been a significant increase in the diagnosis
of celiac disease over the last two decades, many
patients remain undiagnosed [36]. In Finland, 332
(54%) of 611 surveyed celiac disease patients
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Update on celiac disease Alkalay
reported a delay in diagnosis of more than 3 years,
and this delay reduced patients’ well being with use
of medications and healthcare services [37]. Atypical
clinical presentation, physician’s lack of awareness,
limited access to specialists, and misdiagnosis con-
tribute to the delayed diagnosis of celiac disease
&
[38 ].
Celiac disease has been associated with mental
health disorders and psychosocial distress. In a
recent systemic review, 26 publications showed an
increased risk for psychological symptoms or con-
&
ditions in pediatric celiac patients [39 ]. Children
with celiac disease had a 1.2–1.8 higher risk of
psychological diagnoses, including, depression,
behavioral problems, attention-deficit hyperactivity
disorder, eating disorders, and autism. However,
many studies were limited by small sample sizes
and inconsistent approaches to measuring psycho-
logical symptoms. In addition, a single-center cross-
sectional study examined psychological comorbid-
ities of children with celiac disease and their parents
&&
[40 ]. Of 73 children, 34% of children had a mental
health disorder, 16% anxiety disorder, and 16%
attention-deficit hyperactivity disorder. Approxi-
mately a quarter of parents reported child psycho-
social distress, and approximately half reported
parental stress with a financial burden on a GFD.
As young adults with chronic illnesses are vul-
nerable to gaps in medical care with poor disease-
related outcomes, an organized transition of care
from pediatric to adult gastroenterology for celiac
disease patients is recommended. Receiving a refer-
ral to an adult provider during adolescence and the
understanding of the importance of follow-up care
are associated with a more successful transition of
&&
care for young adults with celiac disease [41 ].
However, asymptomatic celiac disease patients
and a young age of diagnosis, less than 13 years of
age, predict poor rates of transition to adult medical
care. Therefore, education of the importance of life-
long follow-up and the pediatric gastroenterolo-
gist’s referral to adult providers may help young
adults with celiac disease continue long-term medi-
cal care with possible avoidance of complications
related to celiac disease. Further studies of celiac
disease young adults diagnosed in childhood with
celiac disease are necessary to evaluate medical out-
comes to better serve them medically as they age.
FUTURE DIRECTIONS FOR MONITORING
AND TREATMENT UPON A GLUTEN-FREE
DIET
As the quality of life of a celiac disease patient is
greatly affected on a lifelong GFD, close monitoring
of compliance is imperative. Strict adherence to the
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Gastroenterology and nutrition
GFD is crucial for reduction of comorbidities and
complications, and until recently, there have been
no direct methods to assess adherence. In this mul-
ticenter prospective study, 64 children with celiac
disease were included, and stool gluten peptides and
celiac disease serology (TTG and DGP autoantibod-
ies) were analyzed at diagnosis, and at 6, 12, and
&&
24 months [42 ]. Gluten consumption was esti-
mated from the stool GIP levels. Most children
(97%) had detectable gluten peptides at diagnosis,
confirming gluten consumption prior to diagnosis.
On a GFD, 87% of the 64 children had no detectable
GIP at 6 months, however, this rate decreased to
75% at 24 months. Furthermore, the mean esti-
mated gluten exposure dropped from 5.5 g of gluten
per day at diagnosis to only 0.14 per day at 6
months. However, gluten exposure later increased
to 0.6 g/day at 24 months. In contrast, DGP anti-
bodies normalized, and only one in five subjects had
elevated TTG by 24 months. However, some chil-
dren had stool GIP levels similar to those of healthy
children on a gluten-containing diet. Measuring GIP
in stool may be helpful for monitoring GFD adher-
ence and may replace the need for additional inva-
sive tests for the follow-up of celiac disease, but
further studies are warranted with good controls.
As the GFD is difficult and the only treatment is
dietary, there is a need for nondietary treatments for
celiac disease. Latiglutenase is an orally adminis-
tered mixture of two gluten-specific recombinant
enzymes that degrade gluten proteins into small
fragments. It is administered as an adjunct to GFD
and is in phase 2 trial testing as an orally adminis-
&&
tered treatment for celiac disease [43 ]. Latiglute-
nase was safe and effective in reducing symptoms of
celiac disease patients on a GFD. There was an
improvement of symptoms and quality of life for
seropositive patients and not for seronegative
patients who exhibited intestinal damage and are
genetically susceptible. The study involved a 12-
week period where 398 patients took an oral dose
of latiglutenase or placebo and documented symp-
toms daily with a quality of life questionnaire at 0, 6,
and 12 weeks. Antibody-positive celiac patients had
a decrease in abdominal pain (58%), bloating (44%),
tiredness (21%), and (54%) constipation. However,
diarrhea and nausea were not improved. As latiglu-
tenase reduced clinical symptoms for seropositive
celiac disease patients on a GFD, this may be a
potential future treatment and further studies are
required to demonstrate evidence that latiglutenase
can lead to mucosal healing.
A recent study describes a mouse model that is
characteristic of celiac disease. IL-15 is overex-
pressed in the gut epithelium and lamina propria,
the HLA-DQ8 molecule is expressed, and the study’s
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mouse develops villous atrophy after ingestion of
gluten. Overexpression of IL-15 in both the epithe-
lium and the lamina propria is required for the
development of villous atrophy, which demon-
strates the significant role of IL-15 in the pathogen-
esis of celiac disease. In addition, CD4þ T cells and
HLA-DQ8 have an important function in activating
cytotoxic T cells to mediate intestinal epithelial cell
lysis. This study also shows a role for the cytokine
IFNg and the enzyme transglutaminase 2 in tissue
destruction. This mouse model provides the possi-
bility in increasing our understanding of the patho-
genesis of celiac disease, and to possibly develop
&&
future therapeutic strategies [44 ].
CONCLUSION
Our knowledge of the causes and pathogenesis of
celiac disease continues to progress. As we discover
contributing factors in the development of celiac
disease, this will allow more effective screening
measures for earlier celiac diagnosis and for preven-
tion of long-term complications with an improve-
ment in patients’ quality of life. The treatment for
celiac disease is a lifelong GFD, which can have
negative effects on the quality of life of patients.
As new markers are developed for celiac disease,
these may be used in future studies for management
and treatment.
Acknowledgements
None.
Financial support and sponsorship
None.
Conflicts of interest
There are no conflicts of interest.
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Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.
Update on celiac disease Alkalay
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Currently, duodenal biopsy remains the gold standard for the diagnosis of celiac
disease in adult patients. The new American Gastroenterological Association
guidelines to diagnose and monitor celiac disease discuss the combination of
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predictive value of approximately 100%. In these cases, an endoscopy with
biopsies is not warranted.
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The study demonstrates a very high specificity and sensitivity of a new assay
directed to identify the serum immune response to epitopes of the TTG–deami-
dated gliadin peptide complex. These markers can be useful for the diagnosis of
celiac disease and for monitoring patient compliance upon a gluten-free diet.
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The study shows that a single-dose gluten challenge combined with IL-2 may be
helpful in diagnosing and monitoring celiac disease for patients already upon a
gluten-free diet (GFD). Serum IL-2 elevations correlated with timing and severity of
symptoms after gluten ingested in celiac disease patients.
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&& diagnosed pediatric patients with celiac disease. J Pediatr Gastroenterol Nutr
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diagnosed celiac disease. Pediatric patients with newly diagnosed celiac disease
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36. Hujoel IA, Van Dyke CT, Brantner T, et al. Natural history and clinical detection
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& celiac disease. Dig Dis Sci 2019; 64:2095–2106.
Celiac diagnosis is often years delayed from onset of symptoms, which may effect
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& hood celiac disease. A systemic review. J Pediatr Gastroenterol Nutr 2019;
69:25–33.
A review of 26 studies showed an increased prevalence of psychological symp-
toms or diagnoses in pediatric celiac patients.
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&& distress in pediatric celiac disease. J Pediatr Gastroenterol Nutr 2019;
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children with celiac disease and their parents. Approximately a quarter of parents
reported child psychosocial distress.
41. Reilly NR, Hammer ML, Ludvigsson JF, Green PH. Frequency and predictors
&& of successful transition of care for young adults with childhood celiac disease.
J Pediatr Gastroenterol Nutr 2020; 70:190–194.
The study shows that providing referrals to adult gastroenterologists for adoles-
cents with celiac disease is important for successful follow-up health-care transi-
tion for young adults.
42. Comino I, Seguar V, Ortigosa L, et al. Use of Faecal gluten immunogenic
&& peptides to monitor children diagnosed with coeliac disease during transition
to a gluten-free diet. Aliment Pharmacol Ther 2019; 49:1484–1492.
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a direct measure of gluten intake, in stool samples to determine its usefulness in
accurately monitoring GFD adherence.
www.co-pediatrics.com 659
Gastroenterology and nutrition
43. Syage JA, Green PHR, Khosla C, et al. Latiglutenase treatment for celiac
&& disease: symptom and quality of life improvement for seropositive patients on
a gluten-free diet. GastroHep 2019; 1:293–301.
As quality of life is effected with a life-long GFD in celiac patients, latiglutenase is in
phase 2 trial testing, an orally administered treatment for celiac disease. Latiglu-
tenase was safe and effective in reducing symptoms of celiac disease patients on a
GFD.
660 www.co-pediatrics.com
Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.
44. Abadie V, Kim SM, Lejeune T, et al. IL-15, gluten and HLA-DQ8 drive tissue
&& destruction in coeliac disease. Nature 2020; 578:600–604.
A mouse model reproduces the overexpression of IL-15, characteristic of celiac
disease, expresses the predisposing HLA-DQ8 molecule, and develops villous
atrophy after ingestion of gluten. This mouse model provides the opportunity to
both increase our understanding of celiac disease, in hopes to develop new
therapeutic strategies.
Volume 32  Number 5  October 2020