The presentation may give you an idea abouth the disease, its pathophysiology, signs, symptoms, diagnosis, treatment....Thanks toall the websites which helped me to make this presentation.

1. CELIAC SPRUE
By,
Devi Priya
Sugathan
MSc

2. CONTENT
 History of Celiac
 Celiac Disease
 Gluten
 Genetic changes
 Molecular mechanisms
 Epidemiology
 Signs and symptoms
 Types of CD
 Diagnosis
 Celiac Iceberg
 Inheritance Pattern
 Treatment

3. HISTORY OF CELIAC
 Aretaeus from Cappadochia (now
Turkey) in the 2nd century AD
described a chronic malabsorptive
condition.
 He named this disorder "koiliakos”
which is Greek for "suffering in the
bowels.”
Booth, CC. History of celiac disease. BMJ 1989; 298:527.

4.  The first clear description of celiac
disease was given by Samuel Gee in
1888.
 He suggested that dietary treatment
might be of benefit.
 In the early 20th century various diets
were tried, with some success, but
without clear recognition of the toxic
components.
 The doctoral thesis of Wim Dicke of
1950 established that exclusion of
Samuel Gee
Wim Dicke

5. DEFINITION
 Celiac disease is a condition caused by
inflammatory injury to the mucosa or
lining of the small intestine.
 This damage is caused by sensitivity to
gluten.
 The damaged intestine does not absorb the
needed components of food (fat, protein,
carbohydrates, vitamins, iron, water).
 Other terms for celiac disease include:
Gluten Sensitive Enteropathy, Non-

7. GLUTEN
 Gluten is a family of proteins found
in grains like wheat, rye ,barley,
oats.
 Of the gluten containing grains,
wheat is by far the most commonly
consumed.
 The two main proteins in gluten are
glutenin and gliadin.
 Gliadin is responsible for most of
the negative health effects .

8.  Gluten is composed of about 75-86%
protein, while the other components
are carbohydrates and lipids.
 Glutenin becomes a tough and rubbery
mass upon hydration, while gliadin
becomes a viscous, fluid mass.
 This is what allows gluten to exhibit
both elastic and viscous properties
in dough and lends to its properties of
extensibility, resistance to stretch,
mixing tolerance, and gas holding

9.  Gliadin and Glutenin are connected
by disulfide bridges.
 In bread and other baked goods,
yeasts consume sugar and produce
carbon dioxide via fermentation.
 The carbon dioxide becomes trapped
in this molecular mesh structure of
gluten, causing bread to “rise.”
 Finally, when the dough is baked, the
gluten hardens , giving the bread its
structure.

10.  When a person with sprue eats
food that contain gluten, the
immune system responds by
damaging villi in the small
intestine.
 Without the action of the villi , a
person can become malnourished
to matter how much the food is
eaten.
 Sprue is an autoimmune
disorder causing the bodys
own immune system to turn
against or damage the body.

11. GENETIC CHANGES
 The risk of developing celiac disease is
increased by certain variants of the HLA-
DQA1 and HLA-DQB1 genes.
 These genes form receptors that bind to
gliadin peptides tightly and intiate the immune
reponse.
 The HLA-DQA1 and HLA-DQB1 genes belong
to a family of genes called the human
leukocyte antigen (HLA) complex.
 The HLA complex helps the immune system
distinguish the body's own proteins from
proteins made by foreign invaders such as
viruses and bacteria.

13.  Almost all people with celiac disease
have specific variants of the HLA-
DQA1 and HLA-DQB1 genes, which
seem to increase the risk of an
inappropriate immune response to
gliadin.
 These variants are also found in 30
percent of the general population,
and only 3 percent of individuals with
the gene variants develop celiac
disease.
 It appears such as environmental
factors and changes in other
genes, also influence the

14. Molecular Mechanism on the toxic effects of Gluten
 Usually food proteins are degraded into small
peptides and aminoacids by peptidases before
they can be transported across the epithelium.
 The high proline content in gliadin and similar
proteins of wheat and related cereals, renders
these proteins resistance to complete
proteolytic digestion in the human intestine.
 Therefore toxic oligopeptides with high
concentration of proline and glutamine are
accumulated in the small intestine and can
exert toxic effects in genetically susceptible
subjects.
 Two groups of gliadin peptides are found: serine
containing and tyrosine containing.
 The serine-containing group of peptides

15. Imunomodulatory Effects of Gluten Peptides
 The “immunogenic” peptides binds to
HLA-DQ2 or DQ8 of antigen presenting
cells and stimulates T-cells.
 The secretion of
cytokines activates the release of enzyme
matrix metalloproteinases that can dama
ge the intestinal mucosa
with a loss of villous structure.
 The cytokines increase epithelial
permeability and increase the passage
of gluten peptides and peptides binding
to DQ2 and DQ8 molecules on APC.

16. This deamidated gliadin
peptides can be strong
activators of the T cells and
also possess more specific
isotopes for the circulating
antibodies.

17. No-Immune Mediated Cytotoxicity of Gluten
OXIDATIVE STRESS
 Some α-gliadin peptides possess the
ability to penetrate cells.
 Therefore they are internalised by
endocytic uptake.
 Peptide accumulation in lysosomes
leads to activation of some signal
transduction pathways and to increased
levels of free radicals.
 The increase in oxidative damage could in
duce alterations of cell morphology,

18. EPIDEMIOLOGY
• Until the 1970s the estimated global prevalence of celiac
disease in the general population was 0.03%.
• The currently estimated prevalence is 1%, with a statistical
range of probability of 0.5–1.26% in the general
population in Europe and the USA.
• Even taking into account that the actual occurrence rate of
celiac disease has been underestimated for many
decades, the prevalence of this disease is increasing.
IN INDIA
• Celiac disease was recognized in northern India,
primarily in children, since the 1960s.
• A community-based study in Ludhiana that involved a step-
wise approach to case detection and diagnosis estimated
that celiac disease prevalence in this city was at least 1 in
310 individuals.
• Celiac disease affecting adults is also now well recognized
in northern India.
• The prevalence of celiac disease in southern India is not

20. SIGNS AND SYMPTOMS
Gastrointestinal symptoms
Gastrointestinal symptoms may include the following:
 Diarrhea 45-85% of patients
 Flatulence 28% of patients
 Weight loss 45% of patients; in infants and
young
children with untreated celiac
disease,
failure to thrive and growth
retardation
are common
 Weakness and fatigue 78-80% of patients; usually related
to
general poor nutrition
 Severe abdominal pain 34-64% of patients

21. Extraintestinal symptoms
Extraintestinal symptoms may include the following:
Anemia 10-15% of patients
Osteopenia and osteoporosis 1-34% of patients
Neurologic symptoms 8-14% of patients
Skin disorders 10-20% of patients
Hormonal disorders Including delayed
menarche, and infertility in
women and
impotence and infertility in men

22. Physical examination
A physical exam may reveal the
following:
 A protuberant and tympanic
abdomen
 Evidence of weight loss
 Peripheral edema
 Hyperkeratosis or dermatitis
herpetiformis
 Cheilosis and glossitis
 Evidence of peripheral neuropathy

24. TYPES OF CELIAC DISEASE
• Classic celiac disease refers to the presence of mild to severe
symptoms of malabsorption such as diarrhea, failure to thrive, and
weight loss .
• Non-classic celiac disease refers to celiac disease without
prominent gastrointestinal symptoms or malabsorption but can have
abdominal pain, bloating, vomiting and constipation.
• Silent celiac disease refers to lack of symptoms in the presence of
a positive celiac-associated antibody screen. Individuals with silent
celiac disease are most often identified through an affected family
member or through screening programs

25. • Refractory celiac disease (RCD) refers to persistence of
symptoms of frank malabsorption with persistent intestinal
inflammation and villous atrophy despite a strict gluten-free diet for
at least six to 12 months. All individuals with refractory sprue are
older than age 20 years.

26. DIAGNOSIS
 In terms of serology, celiac disease is associated
with a variety of autoantibodies, including
endomysial, tissue transglutaminase (tTG), and
deamidated gliadin antibodies.
 Although the IgA isotype of these antibodies usually
predominates in celiac disease, individuals may also
produce IgG isotypes, particularly if the individual is
IgA deficient.
 The most sensitive and specific serologic tests are
tTG and deamidated gliadin antibodies.
 The definitive diagnosis of celiac disease is made by
identification of characteristic histologic changes on
biopsy of the duodenum during upper
gastrointestinal endoscopy.
 Genetic testing

27. CELIAC ICEBERG
 Since only the tip of the
CD iceberg is above the
waterline and a much
large portion remains
under water undetected,
it can be expected that
prevalence of the
disease will increase
continuously.

28. INHERITANCE PATTERN
 Celiac disease tends to cluster in families.
 If we carry HLA DQ2 and/or DQ8, your risk of
developing celiac disease is 3% instead of
the general population risk of 1%.
 Parents, siblings, or children (first-degree
relatives) of people with celiac disease have
between a 4 and 15 percent chance of
developing the disorder.
 However, the inheritance pattern is unknown.

29. If Celiac Disease goes untreated?
• Lactose intolerance
• Vitamin and mineral
defeciency
• Osteopenia and
osteoporosis
• Iron deficiency anemia
• Lymphoma
• Fertility problems
• Nervous system disorders

30. TREATMENT
 Celiac disease cannot be cured. Your
symptoms will go away and the villi in
the lining of the intestines will heal if you
follow a lifelong gluten-free diet.
 Do not eat foods, drink beverages, or
take medicines that contain wheat,
barley, rye, and possibly oats.
 Your health care provider may need to
prescribe vitamin and mineral
supplements.
 When you are diagnosed, get help from
a registered dietitian who specializes in
celiac disease and the gluten free diet.

31. • Vitamin C and E, which have
antioxidant activity can be
supplemented to CD patients.
• Fruits and vegetables
containing polyphenols and
carotenoids can be helpful
since they have anti-
inflammatory and anti-oxidant
properties.
• Fatty acids are also helpful
since it could influence

32. GLUTEN FREE FLOUR
 Gluten free flour is a term that is applied to
flours that are made of non-gluten containing
products.
 There are many kinds of gluten free flours
available at supermarkets these days, along
with many “all purpose” gluten free flour
blends that are designed to be an easy to use
replacement for wheat flour.
 Commercially available gluten free flours are
all made with different mixtures and these
mixtures vary widely from brand to brand.
 They might contain rice flour, teff flour, tapioca
flour, sorghum flour, potato starch, garbanzo
flour or buckwheat flour.

33.  These flours could also contain
nut flours, made from very
finely ground almonds or other
nuts.
 Xanthan gum is a binder that is
frequently added to gluten free
flour mixes to give the flour
some elasticity and make it
easy to use right out of the
bag.
 Since the base ingredients for
gluten free flour can be very
different, different brands can

36. The Celiac Sprue Association (CSA) is
a member based organization dedicated
to helping individuals with celiac disease
worldwide through research, education and
support.
The Celiac Sprue Association gives a
trusted source of information about the
gluten-free products that consumers rely
on and enjoy every day.
CELIAC SPRUE ASSOCIATION