Malabsorption

Dr. Hisham M Alkinani

MBBS, MSc, Cardiologist
 Inability to absorp one or more nutrients.
 Characterized by diarrhea, steatorrhoea and weight loss.
 Causes may be broadly divided into:
 1. Intestinal
 2. Pancreatic
 3. Biliary
 4. Other causes
 1. Intestinal (e.g. villous atrophy) eg coeliac disease ,Crohn's
disease, tropical sprue , Whipple's disease ,Giardiasis ,brush
border enzyme deficiencies (e.g. lactase insufficiency) ,
resection , TB, infiltration by lymphoma
 2. Pancreatic (deficiency of pancreatic enzyme production or
secretion) as in chronic pancreatitis ,cystic fibrosis, pancreatic
cancer
 3. Biliary (deficiency of bile-salts needed for emulsification of
fats)
A-Obstruction of CBD: stones , tumors
B-Terminal ilium diseases : TB, Crohns and resection
C-Drugs interfer with enterohepatic circulation as cholestyramine
which bind bile salts prevent it from fats binding
D-Increase utilization by bacteria as blind loop $, DM causing
autonomic neuropathy --:>food stagnation, after surgery ,
scleroderma(fibroblast infiltration -->decrease motility )
• 4. Other causes
• A-Arterial: Mesenteric insufficiency
• B-Veins : as PHTN
• C-Lymphangiectasia
malabsorption

 The luminal phase is stage in which dietary

nutrients are hydrolyzed and solubilized by
secreted digestive enzymes and bile .

 The mucosal phase relies on the integrity of the

brush border membrane to transport digestive
products from lumen into the cells.

 The postabsorptive phase reassembled lipids and

other nutrients are transported via lymphatics and
portal circulation from epithelial cells to other parts
of the body.
malabsorption

 The luminal phase :

 1/impaired nutrients hydrolysis . the most common
cause is pancreatic insufficiency due to chronic
pancreatitis , pancreatic resection, pancreatic cancer,
cystic fibrosis which result in lipase and proteases
deficiencies leading to lipid and protein malabsorption

 Inactivation of pancreatic enzymes by gastric

hypersecretion eg Zollinger-Ellison syndrome .

 Inadequate mixing of nutrients, bile and pancreatic

enzymes eg total and partial gastrectomy , intestinal
resection .
malabsorption

 The luminal phase :

 2/ impaired micelle formation causes problem in fat
solubilization and subsequent fat malabsorption .
And this result from :
a/ decrease bile acids synthesis from severe
parenchymal liver disease ( cirrhosis) .
b/ impaired bile secretion from biliary obstruction or
cholestatic jaundice .
c/ impaired enterohepatic bile circulation eg in small
bowel resection or regional enteritis .
d/ bile salt deconjugation due to small bowel
bacterial overgrowth .
malabsorption

 Mucosal phase :
 1/ impaired brush border hydrolase activity : eg a/
disaccharidase deficiency leading to disaccharide
malabsorption ( lactase deficiency ) , b/
immunoglobulin A deficiency .
2/ impaired nutrient absorption : either inherited or
acquired defects most common caused by a/
decreased absorptive surface area eg intestinal
resection . b/ damaged absorptive surface eg celiac
disease . c/ infiltrating intestinal wall eg lymphoma.
d/ infection eg giardiasis , bacterial overgrowth .
malabsorption

 Postabsorptive phase: obstruction of the

lymphatic system both congenital eg intestinal
lymphangiectasia . And acquired eg whipple
disease and neoplasm eg lymphoma .
malabsorption

 Clinical presentation : due to osmotic load resulting

from the inability of the intestine to absorb certain
nutrients causes the presenting symptoms.
1/ diarrhea the most common ,watery reflecting the
osmotic load .
2/ Steatorrhea result of fat malabsorption which is
pale , bulky and malodorous stools and difficult to
flush .
malabsorption

 Clinical presentation :
3/ weight loss and fatigue .
4/ flatulence and abdominal distention : due to
Bacterial fermentation of unabsorbed food
substances
5/ Edema : hypoalbuminemia
malabsorption

 Clinical presentation :
6/ Anemia : depend on the cause either microcytic
(iron deficiency ) or macrocytic ( B12 deficiency ) .
7/ Bleeding disorders : due to vitamin K
malabsorption .
8/ Metabolic defects of the bones : vitamin D
deficiency
malabsorption

 Clinical presentation :
9/ Neurologic manifestation : electrolytes
disturbances such as hypocalcemia and
hypomagnesemia can lead to tetany . Vitamins
malabsoption can cause generalized motor
weakness , peripheral neuropathy , night blindness
and seizures .
malabsorption

 Physical examination : signs of weight loss, muscle

wasting, Anemia ,bleeding disorders ( vit K);
oedema (protein); metabolic bone disease ( vit D);
neurological features, eg neuropathy.
Dematological signs.
malabsorption

 Investigation :
1/ CBC ( Anemia ) .
2/ serum iron , vitamin B12 and folate .
3/ bleeding profile ( prothrombin prolonged due to
vitamin K malabsorption .
4/ Electrolytes imbalances such as hypokalemia ,
hypocalcemia , hypmagnesemia and metabolic
acidosis .
5/ liver function test ( hypoproteinemia and
hypoalbuminemia ) .
6/ fat malabsorption can lead to low serum
cholesterol and triglyceride .
malabsorption

 Treatment :

two basic principle in the management

a/ the correction of nutritional deficiencies .

b/ treatment of the causative diseases .
 short bowel syndrome
• Does not develop unless more than two thirds
of the small intestine have been removed.
• Features include: Abdominal pain , Diarrhea
and steatorrhea ,Fluid depletion , Weight loss
and malnutrition , Fatigue
• Complications caused by malabsorption of
vitamins and minerals
 D-xylose test
• D-xylose is a monosaccharide which is
absorbed through the small intestines and
excreted through the kidneys.
• D-xylose test is helpful in differentiating
between structural and functional causes
of malabsorption.
• This test distinguishes between
malabsorption due to small-intestinal
diseases and malabsorption due to
pancreatic exocrine insufficiency.
• A 5-hour urinary excretion of 5 g or
greater is normal following the oral
administration of 25 g of D-xylose to a
well-hydrated subject.
• Decreased xylose absorption and
excretion are found:
• In patients with damage to the proximal
small intestine
• When there is bacterial overgrowth in the
small intestine (the bacteria catabolise the
xylose)
 Schilling test
• Abnormal in:
• A-Chronic pancreatitis: B12 bounded with
protein cleaved by pancreatic enzymes
• B-Blind loop $: Bacteria consume B12 and
bile salts
• C-Terminal ileal disease
 small intestine biopsy
• To detect cause of intestinal malabsorption
• if D xylose positive
 small intestine biopsy
FINDING DIAGNOSIS
villous atrophy coeliac disease
tropical sprue
hypogammaglobulinaemia
gastrointestinal lymphoma
Whipple's disease
cow's milk intolerance
PAS + macrophage whipple
malignant cells lymphoma
dilated lymphatics intestinal lymphangectasia
amyloid amyloidosis
absence of plasma cells Agammaglobulinemia

ulcers zollinger ellison $

non caseating granuloma Crohn disease
 other investigations
• 1-Folate ,B12, iron:
-All are low if intestinal cause.
-Folate high in bacterial overgrowth
 other investigations
• 2-X-ray:
calcification at L1 vertebrae as in chronic
pancreatitis
 other investigations
3-Anti-Saccaromyces cerevisiae (ASCA):
 other investigations
4-Low serum carotene :
-Early and sensetive indicators of
malabsorption
5-INR; lipid profile
6- Breath hydrogen analysis: For bacterial
overgrowth.20 Take samples of end expired
air; give glucose; take more samples at ½h
intervals; early exhaled hydrogen =
overgrowth.
 treatment of malabsorption
• 1-Diet:
- Low fats intake , low cellulose
-Use medium change TG
2-Drugs:
-B12, Folate and iron
-low dose of steroids +++ enzymes
3-Replace deficient pancreatic enzymes, bile salts
4-TTT of cause : eg stop gluten, antibiotics for
whipple
• Infectious malabsorption Giardia,
Cryptosporidium,microsporidia.
• Tropical sprue: Villous atrophy +
malabsorption occur, the cause is
unknown. Tetracycline 250mg/6h PO +
folic acid 5mg/d PO for 3–6mnths may
help
Coeliac disease ( gluten sensitive
enteropathy )

 Coeliac disease is an inflammatory disorder of the

small intestine caused by sensitivity to the protein
gliadin (alcohol-soluble fraction of gluten which is
protein commonly found in wheat, barley, rye to a
lesser extent, oats ) .
 It is strongly associated with HLA-DQ2 (95% of
patients) and HLA-B8 (80%) as well as
HLA_x0002_DR3 and HLA-DR7
 Pathophysiology :
 T cell mediated hypersensitivity reaction
Mechanism: repeated protein gluten exposure
villous atrophy malabsorption.
Coeliac disease ( gluten sensitive
enteropathy )
Coeliac disease ( gluten sensitive
enteropathy )

 Clinical presentation :
 a/ GIT symptoms :

1/ Diarrhoea 45-85% watery or semiformed

characteristic foul odor.
2/ flatulence.
3/ weight loss 45% .
4/ fatigue and weakness 78-80% usually related to
general poor nutrition , severe anemia .
Occasionally severe hypokalemia due to loss of
potasium in the stool cause muscle weakness.
Coeliac disease ( gluten sensitive
enteropathy )

b/ Non GIT symptoms :

1/ anemia .
2/ bleeding diathesis due to impaired absorption of fat
soluble vitamin k .
3/ bone pain and fracture due to defective Ca
transport by the diseased small intestine and also
due to vitamin D deficiency .
Coeliac disease ( gluten sensitive
enteropathy )

4/neurologic symptoms:
result from hypocalcemia include motor weakness ,
sensory loss and ataxia. seizure might develop because
of cerebral calcification.
5/ skin disorder include dermatitis herpetiformis (
pruritic papulovesicular skin lesion involving the
extensor surfaces of the extremities , trunk ,buttock,
scalp and neck .
6/ Hormonal disorder such as amenorrhea, delayed
menarche and infertility and impotence in men .
Coeliac disease ( gluten sensitive
enteropathy )

Failure to thrive or faltering growth (in children)

Sudden or unexpected weight loss
Unexplained iron-deficiency anaemia, or other
unspecified anaemia
Coeliac disease ( gluten sensitive
enteropathy )

 Clinical presentation : physical examination reveal the

following :
1/ abdominal examination shows distended due to
intestinal loops fill with fluid and gas. Ascitis can be
detected in severe hypoproteinemia .
2/ weight loss .
3/ orthostatic hypotension .
4/ peripheral edema .
5/ ecchymosis , dermatitis herpetiformis .
6/ cheilosis and glossitis .
• Autoimmune thyroid disease
• Dermatitis herpetiformis
• Irritable bowel syndrome
• Type 1 diabetes
• First-degree relatives (parents, siblings or
children) with coeliac disease
Investigations :

 1/ Haematology and biochemistry : A full blood

count may show microcytic or macrocytic anemia from
iron or folate or B12 deficiency .

 Biochemical tests may reveal reduced concentrations

of calcium, magnesium, total protein, albumin or
vitamin D.
 tissue transglutaminase (TTG) antibodies (IgA) are the first-choice
 Selective IgA deficiency is more common in patients with
coeliac disease. For this reason IgA levels should be checked
when serological tests are ordered.
If the patient has selective IgA deficiency tissue transglutaminase
IgG can be measured.
 Patients normally need to be following a gluten-free diet for at least
6 months before the serology becomes negatives.
 If patients are already taking a gluten-free diet they should be asked,
if possible, to reintroduce gluten for at least 6 weeks prior to testing.
 endomyseal antibody (IgA) 90% sensitive and almost 100% specific.
 Anti-endomysial antibodies are sensitive and specific, but miss the disease in
about 5% of the population who are IgA deficient.
 anti-casein antibodies are also found in some patients
Coeliac disease ( gluten sensitive
enteropathy )
 Investigations :
 Duodenal biopsy :
 gold standard for diagnosis:
villous atrophy
crypt hyperplasia
increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes
 abdominal radiograph with barium
contrast Decreased jejunal folds,
increased ileal folds( jejunization" of the
ileum to enhance nutrient absorption).
Coeliac disease ( gluten sensitive
enteropathy )

 Treatment :
 Lifelong gluten-free diet , patients become experts.
Rice, maize, soya, potatoes.
 Patients should be followed up after initiation of a
gluten-free diet, with assessment of symptoms, weight
and nutritional status, and blood taken for
measurement of tTG or anti-endomysial antibodies.
 correct existing deficiencies of iron, folate, calcium
and/or vitamin D
Coeliac disease ( gluten sensitive
enteropathy )

 Treatment :
 follow-up
 Tissue transglutaminase antibodies may be
checked to check compliance with a gluten free diet.
Coeliac disease ( gluten sensitive
enteropathy )

• Complications :
1/ Anaemia .
2/ 2° lactose-intolerance .
3/ GI T-cell lymphoma (rare; suspect if refractory
symptoms or decrease weight) .
Enteropathy associated T Cell lymphoma (EATL) is a
form of Non-Hodgkins
4/ increase risk of malignancy (eg oesophageal) .
5. Hyposplenism (Splenic atrophy): seen in 50% of cases
and responds poorly to gluten withdrawal.
Tropical sprue

• It is thought that an initial GI infection results in small bowel stasis,

opportunistic colonisation by organisms such as coliforms such as
Klebsiella, E choli and Enterobacter species , and then a degree of
villous atrophy leading to malabsorption and B12, folate deficiency.
• symptoms may not appear untill as long as 10 years after the pt has left
the tropic area.
• Features :
• Patients classically have a history of recent travel to a tropical area
present with indigestion, cramps within 2 or 3 weeks after an acute
enteric infection.
• Megaloblastic anemia due to folate or B12 deficiency is a common
finding.
• Diagnosis: Jejunal biopsy reveals: Mild villous atrophy , ↑↑ villous
crypts ,Mononuclear cellular infiltrates ,Enlarged epithelial cells
• barium swallow may show thickening of mucosal folds
 Treatment:
 The main treatment for tropical sprue is broad-
spectrum antibiotics (i.e.,tetracycline) and
vitamin supplementation (i.e., folic acid, vitamin
B12).
 Tetracyclines up to 6 months
 Ampicillin may be used as an alternative in
patients who are intolerant of tetracyclines.
 Folate and B12 deficiencies should also be
corrected
Whipple’s disease

 Whipple's disease is a rare multi-system disorder

 Caused by Tropheryma whippelii, a Gram positive bacterium
 most common in white males aged 40-50 years (M:F ratio 9:1).
 The macrophages can easily observed infiltrating the tissue with light
microscopy and when periodic acid –schiff stain is used for histologic
section .
Whipple’s disease

 Clinical features :
1/ Often starts insidiously with arthralgia (chronic,
migratory, seronegative arthropathy affecting mainly
peripheral joints) .

2/ GI symptoms commonly include colicky abdominal

pain, weight loss, steatorrhea/ diarrhoea .

3/ Systemic symptoms such as chronic cough, fever,

sweats, lymphadenopathy and skin
hyperpigmentation.
Whipple’s disease

 Clinical features :
4/ Cardiac involvement may lead to endocarditis, which
is typically blood culture negative .

5/ CNS features include a reversible dementia,

ophthalmoplegia, and facial myoclonus . CNS
involvement may occur without GI involvement .
Whipple’s disease

 Endoscopay and jejunal biopsy shows stunted villi.

There is deposition of macrophages in the lamina
propria-containing granules which stain positive for
Periodic Acid-Schiff (PAS). Similar cells may be found
in affected samples, eg CSF, cardiac valve tissue,
lymph nodes, synovial fluid .
Whipple’s disease

 Management :
 Whipple’s disease is often fatal if untreated .

 Treatment should include antibiotics which cross the

blood–brain barrier.
 oral co-trimoxazole for a year is thought to have the
lowest relapse rate, sometimes preceded by a course
of IV penicillin
 other option: initial two week course of parenteral
penicillin and streptomycin; followed by a prolonged
course (one year) of tetracycline.
___________________________________________
Small bowel bacterial overgrowth
(blind loop syndrome)

 is a disorder characterised by excessive amounts of

bacteria in the small bowel resulting in gastrointestinal
symptoms of bloating, abdominal distension and
diarrhoea .
 Risk factors :
 Scleroderma ,absent gastric acid secretion ,small
bowel diverticulae ,fistulae between the small and
large bowel ,small bowel strictures ,diabetes mellitus
(diabetic neuropathy) ,adhesions.
Features:

 Steatorrhoea and flatulence are classic presenting

features of small bowel bacterial overgrowth.
 chronic diarrhea
 bloating, flatulence
 abdominal pain
 Biochemically there is classically a low vitamin B12 level
and normal or elevated folate level as a result of
bacterial metabolism of B12 to folate.
Investigation

 The gold standard investigation of

bacterial overgrowth is small bowel
aspiration and culture
 Other possible investigations include:

-hydrogen breath test

-14C-xylose breath test
Management

 correction of underlying disorder

 antibiotic therapy: rifaximin is now the
treatment of choice due to relatively low
resistance.
 Co-amoxiclav or metronidazole are also
effective in the majority of patients.
• Ulcerative Colitis
• Treatment can be divided into inducing
and
• maintaining remission
• Inducing remission
• • Treatment depends on the extent and
• severity of disease
• • Rectal aminosalicylates or steroids: for
• distal colitis rectal mesalazine has been
Ulcerative Colitis
Treatment can be divided into inducing and
maintaining remission
Inducing remission
• Treatment depends on the extent and
severity of disease
• Rectal aminosalicylates or steroids: for
distal colitis rectal mesalazine has been
shown to be superior to rectal steroids
• Oral aminosalicylates or steroids
• Severe colitis should be referred to
hospital
Maintaining remission
• Oral aminosalicylates e.g. Mesalazine
Active disease
• Mesalazine: whilst evidence base is limited
widely used in active disease
• Steroids (oral, topical or intravenous)
• Azathioprine is used as a second-line
treatment in active disease
• Mercaptopurine (also called 6-
mercaptopurine, 6-MP)
• Methotrexate is used in patients intolerant
of azathioprine or refractory disease. Usually
given
intramuscularly, but not effective in
maintaining remission. Significant anemia is
a contraindication for methotrexate.
• Infliximab is useful in refractory disease
and fistulating crohn's. Patients typically
continue on
azathioprine or methotrexate
Perianal disease: Metronidazole is first-line
Enteral feeding
• May be used in addition to or instead of
other measures to induce remission
Surgery
• Around 80% of patients with Crohn's
disease will eventually have surgery