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Celiac Disease

Celiac Disease
also known as gluten-sensitive enteropathy, spruce, or coeliac is an autoimmune
disease where the individuals impacted are allergic to gluten which is a
protein that is found in foods such as wheat, barley, rye. When someone has
Celiac Disease, the individual must abide by a strict gluten-free diet. The
intolerance to gluten causes damage to the individuals small intestine which
causes malabsorption of nutrients. The damage to the small intestine causes diarrhea,
fatigue, anorexia, stomach bloating and anemia.

Etiology

Celiac disease occurs when there is
an interaction between the individual’s genes, when the individual eats foods
with gluten. The cause is that the immune system reacts with the gluten causes
damage to the small intestine which can start as an infection in the
gastrointestinal system but also has hereditary components (VanMeter and
Hubert, 2014). The immune response to the infection or genetic issue is damage
to the villi or small hair like projections within the small intestine which
help absorb vitamins and nutrients. When these villi are damaged, the
individual cannot receive all the nutrients regardless of their diet or
lifestyle (VanMeter and Hubert, 2014). Risk factors for celiac disease are
having a family member with the disease, being a Type 1 Diabetic, having
chromosomal abnormalities such as Down Syndrome, having thyroid problems,
colitis, Addison’s disease or Rheumatoid Arthritis. Almost all of the individuals diagnosed with Celiac disease have
the gene HLA-DQ2 or HLA-DQ8, in order to determine if these are the causes a
genetic test would need to be performed (Rubio-Tapia
et al., 2013). As noted prior, having one autoimmune disease such as
Rheumatoid Arthritis increases the individual’s chances of developing another. There
is no age range for celiac disease, as many people wait several years to be
diagnosed or are misdiagnosed with other gastrointestinal disorders first. Men
and women are both affected by celiac disease. Individuals diagnosed with
celiac disease must adhere to a strict gluten-free diet.

Pathophysiological Processes

            Individuals
with Celiac Disease have a sensitivity to various proteins known as prolamines.
These individuals are unable to tolerate the alcohol-soluble component of
gluten which is the protein found in wheat, barley, rye and oats. The grains that
these individuals are sensitive to are known as wheat (gliadin), rye (secalin),
barley (hordein), and oats (avenalin) (Rubio-Tapia
et al., 2013). The genes HLA-DQ2 or HLA-DQ8 are often tied to CD4 T cells
in the small intestine causing the destruction and inflammation of the lining
tissue (Bai et al., 2016). Also,
many individuals are deficient in IgA. The immunological response to the
ingestion of gluten often leads to damage in the small intestine leading to
malnutrition and malabsorption. This autoimmune disease frequently affects individuals
in northern and western European decent. Due to this, patients having shortened
villi in their small intestine due to the damage caused by gluten these individuals
often have an enzyme known as Tissue transglutaminase which is released from
the cells that can cause the destruction (Rubio-Tapia et al., 2013).

Clinical Manifestations and Complications

            Celiac disease can manifest in many different
ways and can occur in childhood and adulthood. A major indicator of a gluten
sensitivity is when infants are given cereal between ages 4-6 months (VanMeter
and Hubert, 2014). Due to having so many gastrointestinal symptoms, many people
go misdiagnosed for years or undiagnosed. When left untreated, individuals with
celiac disease can have extensive damage to the small intestine. Some of the
complications of celiac disease are other autoimmune diseases, osteoporosis due
to malabsorption of calcium, thyroid disorders and cancer. Some of the most
common signs and symptoms are anemia, bloating in the abdominal region, delayed
growth, anorexia, depression, diarrhea, teeth discoloration, fatigue, infertility
and an itchy skin rash known as dermatitis herpetiformis and fragile bones (VanMeter
and Hubert, 2014).

Diagnostics

   Although Celiac disease often goes
misdiagnosed, individuals can receive screenings such as the blood test known
as the celiac panel or tTG-IgA test which tests for celiac disease antibodies (Rubio-Tapia et al., 2013). Individuals who should be screened are children less
than 5 years old who experience the symptoms, first-degree relatives which
means that the parents have the autoimmune disease or individuals with pre-exisitng
autoimmune disorders such as Type 1 Diabetes. Also, the individuals can be
tested for HLA-DQ2 or HLA-DQ8 gene (Bai et al., 2016). The diagnosis of celiac disease is confirmed by
performing an endoscopic biopsy of the lining of the small intestine (VanMeter
and Hubert, 2014). The biopsy of the small intestinal lining will show and increase
in intra-epithelial lymphocytes which is a type of white blood cell found in
the intestines (Bai et al., 2016).
The biopsy will also show the shortened villi. The biopsy is then classified
using the Marsh Classification varying the severity of the damage in the small
intestine showing damage to the folds in the duodenum or small intestine and
fissures within the mucosa. The small intestine biopsy is the only positive
confirmation of Celiac Disease, the blood tests will show a possibility but
will not confirm the diagnosis (VanMeter and Hubert, 2014). The doctor will
also monitor dietary compliance with a strict gluten free diet.

References
Bai, J. C., Ciacci, C.,
Corazza, G. R., Fried, M., Olano, C., Rostami-Nejad, M., &
 
LeMair, A. (2016, July). Retrieved March 11,
2017, from 
 
www.worldgastroenterology.org/UserFiles/file/guidelines/celiac-disease-english-2016.pdf
 
Rubio-Tapia, A., Hill, I.
D., Kelly, C. P., Calderwood, A. H., Murray, J. A., & American
 
College of Gastroeneterology. (2013). ACG
clinical guidelines: Diagnosis and management of
 
celiac disease. American Journal of Gastroenterology,
108(5), 656-676. doi:10.1038/ajg.2013.79
 

  VanMeter, K. and Hubert, R. (2014). Gould’s
Pathophysiology for Health Professionals. 5th ed.

 

St. Louis, Missouri:
Elsevier.