2. LEARNING OUTCOME
• Define tropical sprue
• Understand the causes, clinical features,
investigations and managements for
tropical sprue
• Define coeliac disease
• Understand the causes, clinical features,
investigations and managements for
coeliac disease
3. MALABSORPTION
“Inadequate assimilation of dietary
substances due to defects in digestion,
absorption, or transport”
Major factors causing malabsorption:
• Defective digestion
• Faulty absorption
4. TROPICAL SPRUE
Definition:
“A malabsorption disease commonly
found in the tropical regions, marked
with abnormal flattening of the villi and
inflammation of the small intestine
lining”
5.
6. ETIOLOGY
The etiology and pathogenesis are
uncertain.
Why?
1) Its occurrence is not evenly distributed in
all tropical areas.
• It is found in specific locations, southern
India, the Philippines and several Caribbean
islands.
• Rarely observed in Africa, Jamaica or
Southeast Asia.
7. 2) An occasional individual will not develop
symptoms of tropical sprue until long after
having left an endemic area.
3) Multiple microorganisms have been
identified on jejunal aspirate with relatively
little consistency among studies but other
studies have favoured a role for a toxin
produced by one or more of these
bacteria; Klebsiella pneumoniae,
Enterobacter cloacae, or E. coli.
9. INVESTIGATION
• Small-intestinal biopsy
– Less villous architectural alteration &
more mononuclear cell infiltrate in the lamina
propria
– However, this resembles coeliac disease
– The way to differentiate these two is by having
gluten-free diet and it will not give clinical or
histologic improvement
10. • Endoscopy
– Abnormal flattening of villi and inflammation of
the lining of the small intestine can be
observed
• Blood test
– Low levels of vitamins A, B12, E, D, and K, as
well as serum albumin, calcium, and folate
• Examination of stool
– Steatorrhoea
12. MANAGEMENT
• Prescribe antibiotic
– tetracycline or Sulfamethoxazole-
Trimethoprim (Co-trimoxazole) for 3 to 6
months
• Supplementation
– vitamins B12
– folic acid
BEFORE
TREATMENT
AFTER TREATMENT
with doxycycline and folic
acid therapy
13. Definition:
“An autoimmune disease where the
immune system reacts abnormally to
gluten causing inflamed and flattened
villi”
Coeliac Disease
Healthy villi Damaged villi
14. ETIOLOGY
• It is not known but environmental,
immunologic and genetic factors appear
to contribute to the disease.
1) Environmental
- Coeliac disease is associated with
gliadin (a component of gluten)
15. 2) Immunologic
- Serum antibodies; IgA antigliadin, IgA
antiendomysial and IgA anti-tTG are
present.
- However, it is not known whether these
antibodies are primary or secondary to
the tissue damage.
16. 3) Genetic factor
- Patients with coeliac disease express the
HLA-DQ2 allele (majority) and DQ2 allele
(minority) but 5% patients do not express
any of these alleles.
- Coeliac diseas varies widely in different
population groups (high in Caucasians,
low in blacks and Asians)
17. PATHOPHYSIOLOGY
• Partial villous atrophy in a mild lesion of small
intestinal lining
• Subtotal/total villous atrophy in a severe lesion of
small intestinal lining
– Forming flat mucosa due to more advanced
villous fusion (particularly of the upper jejunum)
18. • Surface epithelial cells are cuboidal or
low columnar type
• Lamina propria shows increased
number of plasma cells and
lymphocytes
20. CLINICAL FEATURES
• Mild abdominal pain
• Bloating
• Steatorrhoea
• Anaemia
• Episodes of mild diarrhea or constipation
• Loss of appetite
• Weight loss
• Tingling and numbness in your hands and feet
• Vomiting (usually only affects children)
• Alopecia (usually only affects adults)
• Malnutrition
21. INVESTIGATION
• Blood test
– Positive tTG serology
– Low levels of vitamins A, B12, E, D, and K
• Small-intestinal biopsy
• Examination of stool
– Steatorrhoea
22. • Endoscopy
– Usually duodenum appear normal but some
patients showing:-
• scalloping of the small bowel folds
• paucity in the folds
• a "cracked-mud" appearance of mucosa
• prominence of the submucosa blood vessels and a
nodular pattern to the mucosa
23. MANAGEMENT
• Diet
– Lifelong gluten-free diet
• Steroids or immunosuppressants
– Such as azathioprine
– This is only for refractory disease where they
do not improve on a gluten-free diet.
24. REFERENCES
• Longo, D. L., Fauci, A. S., Kasper, D. L., Hauser, S. L., Jameson, J.
L., & Loscalzo, J. (2012). Harrison's principles of internal medicine.
(18th ed., Vol. 2, pp. 2151-2160). McGraw-Hill Companies Inc.
• https://www.mja.com.au/journal/2005/182/10/tropical-sprue-far-
north-queensland
• http://www.celiac.com/articles/8/1/What-is-gluten-What-is-
gliadin/Page1.html
• http://www.solunetti.fi/en/patologia/ohutsuolen_villusatropia_40x/
• http://www.nhs.uk/Conditions/Coeliac-
disease/Pages/Symptoms.aspx
