Livija Wells

NTR 417
Journal Article Summary
April 7th, 2016

In August, 2014 Usta, Merve, MD and Urganci, Nafiye, MD created the article
titled, Does Gluten-Free Diet Protect Children with Celiac Disease from Low Bone
Density?, published in the Iranian Journal of Pediatrics. This article illustrates the
relationship between bone mineral density and a gluten-free diet within children from the
ages 8 to 18 years old. Celiac disease as described by Krauses Food and the Nutrition
Care Process, is a combination of four factors: genetic susceptibility, exposure to gluten,
an environmental trigger and an autoimmune response. Celiac is defined as an
autoimmune disorder that results in poor absorption in the small intestine due to
damaging of the lining from gluten hypersensitivity. When absorption is compromised,
key vitamins and minerals such as vitamin D and calcium can become deficient, which
can lead to serious disorders such as rickets, osteomalacia and osteoporosis. Celiac
disease is prevalent among children and adults today causing malabsorption, and a lifelong commitment to abstaining from gluten in the diet is the only treatment so far.
In this study, the main focus is how a gluten-free diet affects bone health in
children with celiac disease. The subjects included 128 children with (53 boys, 75 girls,
between the ages 8-18) diagnosed with Celiac disease. The participants criteria included
patients who had been on gluten-free diet for at least two years, had no evidence of height
and weight less than 3rd or more than 97th percentile, and had no evidence of precocious
or delayed puberty. Exclusions from the study included children with other diseases that
affect bone mineral density such as chronic inflammatory diseases, endocrine
disturbances, cancer, and chronic liver or kidney disease. The children participating in the
study were assessed every 3-6 months through physical examination to monitor
compliance with a gluten-free diet. During the study, dietary compliance to gluten-free
diet was assessed twice. The methods and tools for each assessment include antiendomysium antibodies and a three-day diet history for patients compliance with a
gluten-free diet. Other tools used in this study include dual-energy x-ray absorptiometry
to measure bone mineral density. After the dietary assessment, the children were divided
into two study groups according to their compliance with a gluten-free diet during a sixmonth period. Group 1 consisted of the patients who were diligent with their gluten-free
diet, and group 2 included to patients with poor compliance to a gluten-free diet. The
patients of group 2 had positive anti-endomysium antibodies and did not strictly follow a

gluten-free diet based on their diet history. For each group, bone mineral measurements
were taken at lumbar 2-4 vertebrae and femoral neck and were measured by dual-energy
x-ray absorptiometry. Bone mineral density was illustrated in grams per square
centimeter (gr/cm2). Biochemical measurements that were included in this study include
serum calcium, phosphate, alkaline phosphatase and magnesium, measured by
radioimmunoassay. These methods were used in determining the affect gluten-free diet
has on bone mineral density, and the results are as followed.
The first assessment with dual-energy x-ray absorptiometry was performed at two
years of a gluten-free diet. 79.4 % of patients were discovered to have low bone density,
while 20.6% were normal based on their dual-energy x-ray absorptiometry. Among
normal dual-energy x-ray absorptiometry, anti-endomysium antibodies and a three-day
diet history were used and compliance to gluten-free diet was good in 12% of patients
and poor in 1%. Bone mineral density was low in 42% patients whose dietary compliance
was good, and 38% patients whose dietary compliance was poor. The correlation between
low bone density and poor dietary compliance was found to be statistically significant
(P<0.01). The second dual-energy x-ray absorptiometry was performed 3 years later and
results showed that the bone mineral density had increased 0.120.15 and 0.100.14
units. These increases found in the study were also statistically significant (P<0.01).
Based on the findings of this article, bone mineral density was normal at the end of the
study. After 3-7 months, some patients illustrated bone mass recovery while others
showed recovery after years of therapy. In conclusion of the study, throughout the two
subgroups, the patients who did not strictly follow a gluten free diet had significantly
lower measurements of bone mineral density.
When comparing the article to Krauses Food and the Nutrition Care Process, the
information regarding Celiac disease is justified. As stated in the article, patients with
Celiac disease have difficulties absorbing vitamins and minerals. Krause further supports
this statement by describing the status of the intestinal mucosa when damaged leads to
impaired secretory, digestion and absorption functions, causing malabsorption of
nutrients. However, Krause does not discuss in-depth the relationship between calcium
and vitamin D with Celiac disease during the malabsorption process compared to the

article. The authors of the article, Does Gluten-Free Diet Protect Children with Celiac
Disease from Low Bone Density?, discusses how defective absorption of calcium and
vitamin D secondary to small intestinal mucosal damage, lactose malabsorption, and
impaired vitamin D absorption along with pro-inflammatory cytokines may prompt
imbalances of bone and mineral metabolism in patients with Celiac Disease. The
malabsorption can also lead to rickets, osteomalacia, and osteoporosis. The evidence that
supports this statement from Krause describes how patients may present with one or more
conditions associated with Celiac Disease including anemias, generalized fatigue, weight
loss or failure to thrive, osteoporosis, and vitamin or mineral deficiencies. The correlation
of the two pieces of literature suggests that Celiac Disease can cause growth failure and
also vitamin and mineral deficiencies. The authors of the article wanted to dive further
into hypothesis by conducting an experiment among children and their bone growth.
This article is significant in our world today because Celiac disease is becoming
more prevalent as the number of incidences has increased throughout the years. The only
treatment currently for Celiac disease is a life-long elimination of gluten in the diet.
While for some eliminating gluten may be simple, its quite difficult for most people
especially without nutrition education. Most of our processed foods found in the grocery
store contain gluten; even in foods you wouldnt think due to its binding characteristics.
This may lead to more consumers being non-compliant of a gluten-free diet, which can
lead to serious health complications. When left untreated, Celiac disease often causes
digestive issues and keeps your body from getting all its needed nutrients. Celiac disease
can eventually lead to serious disorders such as anemia, infertility, weak and brittle
bones, dermatitis and other health problems.
Celiac disease is an immune disorder in which individuals cannot tolerate gluten
because it damages the inner lining of their small intestine and prevents it from absorbing
nutrients, leading to malabsorption of essential vitamins and minerals. Celiac disease is
prevalent among children and adults today and the numbers of incidences are increasing.
A life-long commitment to abstaining from gluten in the diet is the only treatment so far.
Research is ongoing for the treatment of Celiac disease, but in the meantime its crucial to
maintain a gluten-free diet to prevent risks for serious illnesses.

References
Usta, M., M.D., & Urganci, N., M.D. (2014). Does gluten-free diet protect children with
celiac disease from low bone density? Iranian Journal of Pediatrics, 24(4), 429434. Retrieved from http://library.sage.edu:2048/login?
url=http://search.proquest.com/docview/1558481086?accountid=13645
Mahan, L. K., Escott-Stump, S., Raymond, J. L., & Krause, M. V. (2012). Krause's Food
and the Nutrition Care Process. St. Louis, MO: Elsevier/Saunders.