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Educational Plan For Celiac Dise

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 Educational Plan For
Celiac Disease Patients
      Amal Al-Mugthem
                ]‫[ اكتب اسم الكاتب‬




     Enjoy your life, without gluten
  ‫استمتع بحياتك .. بدون الجلوتيه‬
                         Table of content
                 Topic                      Page
             Introduction:                    3
    (Definition, Pathophysiology,
 Epidemiology, Causes, Diagnosis,
       Treatment, Prevention
          Goal & Objectives                  13
            Target Group                     13
               Location                      13
                 Time                        13
            Plan Method:                     14
         A) Individual teaching
  (Objectives, Sessions plan, Tools,
Materials, Evaluation, Documentation)
         B)- Group Teaching                  16
  (Objectives, Sessions plan, Tools,
Materials, Evaluation, Documentation)
         Material & resource                 17
             Tools Needed                    18
                Reveral                      18
              Evaluation                     18




                                        2
Introduction:
Definition:
       Celiac disease, or gluten-sensetive enteropathy, is an intestinal
malabsorption disease that damages the mucosa of the small
intestine. It is results from an inappropriate T-Cell-mediate immune
response caused by ingested gluten by people who are genetically
predisposed. The malabsorption is caused by gliadin, the protein
fraction of gluten.
   Gluten refers to specific peptide fractions of proteins found in
wheat, rye and barley. In reality, each type of protein - gliadin in
wheat, hordein in barley, secalin in rye, avenin in oats, zein in corn
and oryzenin in rice - is slightly different from the others. The
"gluten" in wheat, barley, rye, and a much lower amount in oats,
contain particular amino acid sequences that are harmful to persons
with celiac disease. It is important to note that the gluten found in
corn and rice does not cause harm to those with CD.
Pathophysiology:
        Celiac disease is unique from other autoimmune diseases in
that the there is a clearly identified environmental trigger (gluten), a
dominant HLA contribution required for disease to occur (DQ2 or
DQ8), and autoantibodies against TG are detectable in over 95% of
individuals with celiac disease.
There are multiple proposed pathways involved in the pathogenesis
of celiac disease that leads to enterocyte destruction and subsequent
villous atrophy – all which are related to dietary gluten, the major
storage protein of wheat, barley and rye. Gliadin is a glycoprotein
extract from gluten that is felt to be directly toxic to the enterocytes
of individuals with celiac disease, primarily through the
overexpression of IL-15 in the intestine. In addition, gliadin peptides
have been shown to upregulate both the stress molecule MIC-A on
the surface of enterocytes and also the NKG2D receptor on the
infiltrating intraepithelial lymphocytes, to promote a lymphocyte-
mediated cytotoxic response against enterocytes that is also IL-15
dependent. TG is important in the pathogenesis of celiac disease in
that the enzyme crosslinks ingested gliadin and causes specific
deamidation of glutamine into glutamic acid in gliadin peptides.
When such deamidation occurs, the gliadin peptides are able to be
more efficiently presented (in the context of MHC DQ2 molecule) to
                                   3
gliadin-reactive CD-4 T cells, therefore increasing its
immunogenicity. Without TG, it is believed that gliadin is less
immunogenic, and may not stimulate T cells as effectively. Finally,
since gliadin is unusually rich in proline residues, there is an intrinsic
resistance to digestion in the intestines along with a preference for
binding to DQ2 molecules. An example is a 33-amino acid residue of
gliadin identified to be stable despite digestion with gastric,
pancreatic, and intestinal brush-border membrane proteases, with
preserved immunogenicity. It is believed that the absorption of such
larger intact peptides of gliadin allows the immunogenic response to
occur.
     TG appears to play primarily a molecular role of crosslinking
and deamidation of gliadin, with little evidence at this time to
support an immunologic role. TG autoantibodies are proposed to
occur by antigen presenting cells initially targeting the toxic gliadin
peptides ―inadvertently‖ take up TG-gliadin complexes, resulting in
an immune reaction against both gliadin and TG. It has been
proposed that TG autoantibodies play a role in disease pathogenesis,
but lacks sufficient supportive evidence.
Therefore, there is a combination of activity by the innate and
adaptive immune system in the generation of gliadin-reactive T cells,
a cytotoxic response, and autoantibody formation.

Epidemiology:
    The prevelance of the disease may have been underestimated in
the past and now is considered to be about 1 in 133 persons in United
States. Prevalence is higher in relatives of persons with celia disease.
Onset is usually from infancy to young adulthood, but about 20% of
cases occur in adults over 60 years of age.The study by Mayo Clinic
researchers also linked undiagnosed and untreated celiac disease
with an increased risk for earlier death. Even with increased
awareness about gluten-free diets and celiac, the disease remains
underdiagnosed, experts say. "We believe that only about 5% of
people with celiac disease know they have it," University of Chicago
Celiac Disease Center Director Stefano Guandalini, MD, tells
WebMD. "Many of these people have no symptoms, but many do
have symptoms that are not recognized for what they are."

     The risk of death for celiac disease patients has been known, less
is known about those with a less severe form of the disease. "We

                                    4
studied the early stage of celiac disease as well, inflammation and
latent celiac disease," Ludvigsson says. Ludvigsson and his colleagues
looked at data reports on intestinal tissue studied at the microscopic
level, collected from biopsies that had been taken from Swedish
patients from the years 1969 to 2008.

     They divided the biopsy data from more than 46,000 patients into
three groups: those with celiac disease, defined by the presence of
villous atrophy (intestinal damage); those with a less severe form, in
which there is inflammation without villous atrophy of the intestinal
lining; and those with latent disease. Patients with latent disease have
positive blood tests but no physical findings of intestinal damage or
inflammation, and doctors typically take a wait-and-see approach
with them before treating.

    The researchers compared all patients with a comparison group
from the general population and followed them for a median of about
seven to nine years (half were followed longer, half less). Among
those with celiac disease, there were 3,049 deaths; among those with
inflammation, 2,967 died and among the latent group, 183 died.

   The increased risk of death, the researchers found, differed by
group:

      Those with inflammation had a 72% increased risk of death.
      Those with celiac disease had a 39% increased risk of death.
      Those with latent disease had a 35% increased risk of death.

    Given the background prevalence of celiac disease of 1:100, there
are populations that are at an increased risk for disease, including
patients with type 1 diabetes, autoimmune thyroid disease (both
hyper- and hypothyroidism), relatives of patients with celiac disease
and type 1 diabetes and patients with Turner and Down syndromes.
Rates of celiac disease in these populations range from 5–10%.
Increase risk of disease:

     Celiac disease is an immune system disorder in genetically
predisposed people that results in damage to the lining of the small
intestine when foods with gluten are eaten. The risk for the disease
may be inherited, since about 10% of first-degree relatives (mother,
father, brother, sister, son, or daughter) of people who have celiac
disease also develop the condition. In people who are genetically


                                   5
predisposed, celiac disease may be triggered by environmental
factors, including viral and bacterial infections.

People who have celiac disease are also more likely than others to
have:

      Dermatitis herpetiformis (more common in adults but can
       occur in children).
      Osteoporosis.
      Type 1 diabetes (insulin-dependent diabetes).
      Autoimmune thyroid disease.
      Down syndrome.
      Sjögren's syndrome.
      Selective antibody deficiency (immunoglobulin A [IgA]
       deficiency).
      Iron deficiency anemia or folic acid deficiency anemia.
      Abnormal liver function tests that are not caused by any other
       disease.

Causes:

      Although the exact cause of celiac disease is not known, having
certain genes increases your risk. You are more likely to have these
genes and may get celiac disease if you have a first-degree relative
(mother, father, brother, sister, son, or daughter) with the condition.
Environmental factors, such as viral or bacterial infections, may
trigger changes in the small intestine of a person with these genes.
Then, eating foods that contain gluten can trigger an abnormal
immune system response. Eventually, digestion and absorption
problems may result. Research continues on how genetic,
environmental, and immune factors interact and affect a person's
symptoms, at what age they begin, and whether long-term health
problems develop.

Symptoms:

     Symptoms of celiac disease occur after eating foods containing
gluten. These foods trigger an abnormal immune system response
that damages the intestine. Symptoms vary widely: they may be very
mild and go completely unnoticed, or they may be severe and impact
daily life.

Common symptoms related to celiac disease may come and go. They
include:
                                   6
      Gas, abdominal swelling, and bloating. These symptoms result
       from a failure of the small intestine  to absorb nutrients from
       food. You may also have mild stomach pain, but it is usually
       not severe.
      Abnormal stools. Diarrhea or bulky, loose (or watery), pale,
       frothy, and foul-smelling stools often occur. The stools may
       contain a large amount of fat and may stick to the sides of the
       toilet bowl, making them hard to flush. Although children and
       adults often experience the same types of symptoms, intestinal
       problems, such as constipation, are more likely to occur in
       children.
      Weight loss. Adults and children may have unexplained weight
       loss despite having a normal appetite. Younger children may
       fail to gain weight and grow as expected, a condition known as
       failure to thrive.
      Fatigue and weakness. Celiac disease can result in a general
       lack of energy and strength. Sometimes poor nutrient
       absorption causes fatigue and weakness.
      Vomiting. Some people may get sick after eating gluten.
       Children are more likely than adults to have this reaction.

Celiac disease may also lead to:

      Osteoporosis and other bone problems related to a lack of
       calcium absorption.
      Anemia caused by iron deficiency and/or folic acid deficiency.
      Infertility or having more than one miscarriage.
      Delayed onset of puberty.
      Frequent respiratory infections.
      Problems with memory and concentration.
      Irritability in children. And adults may show signs of
       depression.

Symptoms of celiac disease also occur with a variety of other
conditions, which can delay the initial diagnosis.

Celiac disease in children

In some children, symptoms begin shortly after introducing cereal
into the diet, usually after 6 months of age.

     A child who has celiac disease may not grow and gain weight
normally because the child's body is not absorbing needed vitamins
and other nutrients. Children who have untreated celiac disease can
                                   7
become very ill. They may need hospitalization for treatment with
fluids and medicine to restore nutrients. These treatments are usually
short-term, and most children recover completely.

      As children who have celiac disease grow into adulthood, they
may be at a slightly increased risk for developing cancer (lymphoma)
in the small intestine, the mouth, or esophagus, although the evidence
for this is not clear. But studies have found that following a gluten-
free diet lowers the risk for lymphoma. 1 Even if a child with celiac
disease does not have symptoms after eating gluten, it is critical that
he or she stay on a lifelong gluten-free diet to avoid intestinal
damage. You can help your teenager follow a gluten-free diet by
recognizing his or her need for independence. For example, you can
let your teenager plan meals and choose gluten-free foods.

    Although a gluten-free diet relieves symptoms and promotes the
health of the intestines, children may not reach their full height if
prolonged lack of nutrient absorption stunted their growth before
treatment began.

Celiac disease in adults

    Many adults who have celiac disease do not have any symptoms,
or they have only mild symptoms. Symptoms may occur at any age
but most commonly develop during the 20s, 30s, and 40s.

   Adults who have celiac disease have a slightly higher-than-average
risk of lymphoma, which usually develops in the intestine. They also
may have a slightly increased risk of developing cancer of the
esophagus. Following a gluten-free diet can reduce this risk.

       You are likely to get better if you consistently and permanently
follow a gluten-free diet. About 70% of people find their symptoms
improve within 2 weeks of beginning a gluten-free diet.2 After the
villi return to normal, which usually takes several months to several
years, the body can absorb nutrients properly. Maintaining a gluten-
free diet even when symptoms disappear is very important. Doing so
usually prevents symptoms from returning and reduces the risk for
complications of celiac disease, which may include lymphoma.

     Symptoms usually return any time foods with gluten are eaten.
Although some people who have celiac disease may be able to eat
foods that contain gluten without developing symptoms, this does not
mean that the body is absorbing all nutrients normally. Even without

                                   8
symptoms, if the small intestine is injured from gluten, the lack of
absorption of nutrients may cause complications such as iron
deficiency anemia and osteoporosis.

     In rare cases, people who appear to have celiac disease do not get
better on a gluten-free diet. This condition is called refractory sprue.
In these cases, corticosteroids or other medicines that change the
immune system response may be used to control symptoms. People
who do not improve on a gluten-free diet should be tested for other
conditions, including T-cell lymphoma.

    People with celiac disease have a slightly higher-than-average
death rate, mainly because of the risk of lymphoma. But increasing
evidence suggests that people with celiac disease can decrease their
risk for developing lymphoma by permanently adopting a strict
gluten-free diet.1

Diagnosis:

       Diagnosis of celiac disease is usually first suggested by the
presence of TG autoantibodies, but established by biopsy of the small
intestine by upper intestinal endoscopy. Histology will show some
degree of villous atrophy and crypt hyperplasia. Intraepithelial
lymphocytes are typically seen in celiac disease lesion, but their
presence alone is insufficient to diagnose celiac disease. Histologic
grading is based on the Marsh scoring system. Normal intestinal
histology is scored a Marsh 0. The presence of intraepithelial
lymphocytes alone is a Marsh 1. A biopsy specimen with crypt
hyperplasia and increased numbers of intraepithelial lymphocytes is
a Marsh 2. A specimen with any degree of villous atrophy is a Marsh
3 (38). A Marsh score of 2 or 3 is consistent with celiac disease. Since
other conditions can yield similar histologic findings, the presence of
infiltrative changes alone (Marsh type 1) on intestinal biopsy is not
specific for celiac disease in children. Likewise, positive celiac disease
serology (EMA or TG autoantibodies) increases the likelihood such
an individual has celiac disease. A diagnosis of celiac disease is
considered definitive when there is a complete resolution in
symptoms on a gluten-free diet, or when there is histologic
improvement on a follow-up intestinal biopsy. In addition, a positive
serological test that resolves on a gluten-free diet is helpful in
confirming the diagnosis (37).
Approximately 90% of patients with celiac disease will have HLA
DQ2 (DQA1*0501, DQB1*0201) — which is generally in tight

                                    9
linkage with the DR3 haplotype identified on serologic testing, and
most of the remaining patients (8% to 10%) will have HLA DQ8
(DQA1*0301, DQB1*0302) – associated with the DR4 haplotype by
serologic testing. Therefore, individuals with celiac disease almost
always have the DQ2 or DQ8 molecule, such that the absence of
either of these molecules by genetic testing virtually excludes the
possibility of celiac disease. On the other hand, the presence of either
molecule does not guarantee that an individual will develop celiac
disease, since DQ2 is present in approximately 30% of the general
population, and either DQ2 or DQ8 is present in 40% of the general
population, whereas only about 3% of the general population having
DQ2 will develop celiac autoimmunity. There is not a large role for
genetic testing in celiac disease. Most companies that perform genetic
testing will test specifically for the separate A and B chains that,
when together, comprise a DQ2 or DQ8 molecule. Interpretation of a
genetic test can therefore be very confusing. The high-risk celiac
disease allele, DQ2, requires both A1*0501 and B1*0201 chains,
while DQ8 requires both A1*0301 and B1*0302 chains to form a
complete and functional molecule. It is important to note that the
presence of only one chain of the DQ2 or DQ8 molecule does not
place an individual at increased risk for celiac disease, since the both
chains are needed to form the necessary celiac disease-susceptible
MHC molecule.

Treatment:

The treatment for celiac disease is a strict gluten-free diet, which
means:

      Avoiding all foods with wheat, barley, rye, or oats. Oats may
       later be gradually reintroduced into the diet.
      Not drinking beer, even nonalcoholic versions.
      Eating meals that include rice, corn, millet, and buckwheat.

     Most people with the disease who adopt this diet permanently
and consistently do not develop health problems associated with
celiac disease. If nutritional deficiencies are present, other treatments
may be needed, such as vitamin, iron, and calcium supplements.

      Individuals with active celiac disease are at risk for deficiencies
of zinc, folate and iron, as well as the fat-soluble vitamins A, D, E and
K. Since they are also at risk for decreased bone mineral density,
screening for all of these conditions should be considered. Finally, a
detailed history and exam should be obtained to look for early signs
                                   10
of associated autoimmune conditions such as thyroid disease, type 1
diabetes, or even pernicious anemia in an older individual. We
typically repeat the TG autoantibody and DGP antibodies in 6–12
months to look for a decrease or resolution in the antibodies, and
then yearly.
     There are studies currently underway investigating the utility of
naturally-occurring enzymes to further digest gliadin into smaller,
non-pathogenic peptides. Such drug therapy is aimed at providing
individuals with celiac disease safer thresholds for inadvertent gluten
ingestion. Other targets for treatment include TG inhibitors, which
could potentially reduce the pathogenicity of gliadin that occurs as a
result of enzymatic deamidation.

Treatment if the condition gets worse

     The most common cause of recurrent symptoms of celiac disease
is eating foods containing gluten. In some people, eating even the
smallest amount of gluten can cause symptoms of celiac disease, such
as diarrhea and weight loss. Continuing to eat gluten causes
inflammation and damage to the villi in the small intestine,
regardless of whether symptoms are present. Nutrients may not be
absorbed properly, which can lead to long-term complications, such
as weak bones or growth problems (in children). Prolonged intestinal
damage may increase the risk for developing severe complications,
such as lymphoma.

Prevention

    Although celiac disease cannot be prevented, symptoms and
damage to the small intestine can be reversed by maintaining a strict
gluten-free diet. At first, you may also have to avoid milk and milk
products. After you stop eating gluten, the intestines begin to heal
and you likely will be able to gradually reintroduce milk products
into your diet without triggering symptoms.

Complications of celiac disease:

    Celiac disease has been associated with increased risk for
fracture and osteoporosis, although the degree of the association
varies from strong with an odds ratio for fractures of 5–7 compared
with control to relatively minor with an odds ratio of 1.9 for fracture
. Bone mineral density is noted to be decreased in patients with celiac
disease and there is at least some improvement in the bone mineral

                                   11
density with institution of a gluten free diet. However, it has been
shown that a gluten free diet instituted late in childhood or
adolescence may not be associated with a normalized bone mineral
density.
       Celiac disease has also been associated with decreased fertility,
miscarriage and infants with intrauterine growth restriction.
However, there are conflicting reports with some studies showing
little to no effect of undiagnosed celiac disease on fertility and
outcomes of pregnancy, while others have shown a significant impact
including pre-term birth, caesarean section, low or very low birth
rate. Therefore, the exact impact of celiac disease on fertility and
pregnancy outcomes is unknown. However, the diagnosis of celiac
disease should be considered in women presenting with recurrent
miscarriage, infertility and/or problems with intra-uterine growth
retardation or small for gestational age babies.
       Gastrointestinal malignancies including adenocarcinoma of the
small intestine and particularly Non-Hodgkins lymphoma are
associated with celiac disease. Adenocarcinoma of the small intestine
is a rare carcinoma and the risk for this carcinoma is increased in
subjects with celiac disease. However, the absolute risk for this
cancer is still quite low given its rarity. Patients may complain of
abdominal pain and/or be found to have occult bleeding and further
evaluation for this carcinoma should be considered in patients with
celiac disease who develop these signs or symptoms after the
resolution of the acute phase of their disease. Non-Hodgkin’s
lymphoma has also been reported to be increased in patients with
celiac disease, although the absolute risk of disease is low, and at this
time would not in itself justify the need for routine screening for
celiac disease in the general population.




                                   12
Goal:
To improve the quality of life of adult celiac disease patient by 25%
among metabolic disorder clinic during 2 years (2010-2012) at DAN
hospital.

Objectives:
At the end of this program, the learner will :

   • Explain what gluten free diet mean.

   • Practices on make and uses gluten free diet.

   • Managing associated symptoms of the condition that can
     substantially reduce quality of life.


Target Group:
Adults (above 18 years old) who have celiac disease.

Location:
Among metabolic disorder clinic at DAN hospital.

Time:
I will start at February 2010 until February 2012.




                                   13
Plan:
I will use two methods to perform my plan:

A)- Individual Teaching:

1- Objectives:

By the end of individual teaching:

    Patient demonstrates what celiac disease mean and what it is
     the symptoms and causes.
    The patient can describe the gluten free diet.
    The patient can identify gluten free diet sources.
    The patient apply to read the food label.

2- Session plan:
Numbers of sessions: 6 sessions (4 educational session and 2 follow up
session).

Sessions plan:

Session 1: (February 2010 – 30 min - metabolic disorder clinic)

    Explain to patient what celiac disease mean and the mechanism
     of it in simple word.
    Lists the symptoms to the patients and told him about the
     causes of this symptoms.
    Summaries the main complications of disease if patient not
     monitor it like increased risk for fracture and osteoporosis and
     explain why it’s associated with the disease.
    Ask the patients about his fairs and feeling and answer any
     question in his mind about the prognosis of the disease.

Session 2: (May 2010 – 30 min - metabolic disorder clinic)

    Describe to patient that importance of gluten free diet and it is
     the only way to treatment.
    Identifies gluten free diet ( avoid wheat, rye and barley).
    Teach patient to use corn, potatoes, rice, and tapioca, bean,
     soybean, and nut flours rather than gluten product.

                                     14
    Manage use of medications by patient and explain to him that
     he cannot use any medication even vitamins without physician
     permission.

Session 3: (August 2010 – 20 min - metabolic disorder clinic):

    Practice patient to read the food label to know if it content
     gluten or not and read investigated before use.
    Describe the major food additive that use gluten (like ketchup)
     and other commercial (like lipstick, lip balms, and lip gloss).
    Identifies the places that patient could buy gluten free diet (in
     Riyadh: Optimal Health in King Fahad road, Organic food
     company in Ouroba street).

Session 4: (November 2010 – 20 min - metabolic disorder clinic):

    Asks the patient about any difficult he face on gluten free diet
     and solve it with him.
    Lists the symptoms again (gas, abdominal swelling, and
     bloating, abnormal stools, weight loss, fatigue and weakness,
     vomiting) and describe to patient that it connect to eating
     gluten and ask him if he suffer from any of it.

Session 5: (May 2011 – 15 min- metabolic disorder clinic):

    Manage the nutritional status by evaluates weight, and lab
     results.
    Observes for any clinical feature.

Session 6: (Febraury 2012- 15 min- metabolic disorder clinic):

    Manage the nutritional status by evaluates weight, and lab
     results.
    Observes for any clinical feature.

3- Tools:
    Brochure include the basic information about celiac disease
     (the definition, causes, symptoms, and the treatment).
    Table of gluten free diet.



                                  15
      Video explain pathophsiology of celiac disease:
       http://www.youtube.com/watch?v=EmZczwtsbVc
      Gluten free diet sample.
      Products including gluten and not include it to help in label
       reading session.
      Fridge magnets to remind the patient what he can eat and what
       not to eat.

4- Materials:
        Food model.
        Screen.
        Computer.
        Printer.

5-Evaluation:
      By questionnaire to measure understood of gluten free diet and
       how to chose it.
      By lab results and weight.

6-Documentation:

In special form of patient file.

\\

B)- Group teaching:

1- Objectives:

By the end of group teaching:

      Patient could identified the gluten free diet.
      Patient can apply a gluten free diet meal for him.
      Patient demonstrates the complications of celiac disease.

2- Session plan:

Numbers of sessions: 2 sessions .

Session 1: (July 2010- 2 hour- learning kitchen)

      Explain the gluten free diet and where patient could found it.
      Identify the sources of gluten free diet.
                                    16
      Performs a dishes that made from gluten free diet.
      Make the patients participates in gluten free diet cook
       practices.

Session 2: (Oct. 2011- 1 hour- conference room)

      Explain the complication of celiac disease.
      Support the patient morally by a motivate speech.

3- Tools:
      Poster about the complications.
      Video explain the progress of disease if not monitor.

4- Materials:
      Screen.
      Mike.

5-Evaluation:

      By a questionnaire.

6-Documentation:

      In special form of patient file.

\\

Material & resource:
     1. Krause’s Food, Nutrition, and diet therapy.
     2. Celiac Disease Foundation. http://www.celiac.org/.
     3. Celiac Disease and Gluten-free Diet Information Since 1995.
        http://www.celiac.com/
     4. Celiac UK. http://www.coeliac.org.uk/.
     5. Celiac Sprue Association. http://www.csaceliacs.org/.
     6. Celiac Disease Health Center.
        http://www.webmd.com/digestive-disorders/celiac-
        disease/default.htm
     7. Jennifer M. Barker, MD and Edwin Liu, MD. Celiac Disease:
        Pathophysiology, Clinical Manifestations and Associated
        Autoimmune Conditions. Adv Pediatr. 2008; 55: 349–365.

                                     17
Tools needed:
    Brochure include the basic information about celiac disease
     (the definition, causes, symptoms, and the treatment).
    Table of gluten free diet:

    Video explain pathophsiology of celiac disease:
    http://www.youtube.com/watch?v=EmZczwtsbVc
    Gluten free diet sample.
    Products including gluten and not include it to help in label
     reading session.
    Fridge magnets to remind the patient what he can eat and what
     not to eat.
    Poster about the complications.
    Video explain the progress of disease if not monitor.

Reveral:
    Keep connecting with the patient by e-mail if he need any help.
    Rever the patient to social worker if he cannot effort the
     treatment cost.
    Health care team involve:
    Physician.
    Health educator.

Evaluation:
    By questionnaire to measure understood of gluten free diet and
     how to chose it.
    By lab results and weight.

Documentation:
Write report about all program steps, and publish it in scientific
magazine.




                                   18

				
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