Malabsorption

Objectives

• Define malabsorption
• outline main causes of malabs.
• Describe the investigations of the
malabsorption
• describe clinical features, and
management of celiac disease
• Outline the complications of celiac
disease.

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 Malabsorption
Clinical syndrome caused by
diminished intestinal absorption of
one or more dietary nutrients

Pathophysiology
• Premucosal (luminal) factors
• Mucosal factors
• Postmucosal (lymphatic obstruction)

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 Malabsorption
causes
Intraluminal maldigestion
pancreatic exocrine insufficiency
Chronic pancreatitis
Cancer of pancreas
Cystic fibrosis
bacterial overgrowth
biliary disease
bariatric surgery

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 Malabsorption
Mucosal malabsorption
Enteropathy
Coeliac disease
Tropical sprue
Lymphoma
infection (giardiasis)
radiation
hypogammaglobulinaemia
eosinophilic gastroenteritis
chronic ischemia

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 Malabsorption
Post-mucosal obstruction (1° or 2°
lymphatic obstruction)
congenital intestinal lymphangiectasia
acquired lymphatic obstruction
trauma
Tumor
infection

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 Malabsorption
Clinical features
• Diarrhoea watery and voluminous. Bulky
pale and offensive stools (steatorrhoea)
• Abdominal distension
• Borborygmi, cramps
• Weight loss
• Undigested food in the stool
• Symptoms related to deficiencies of
specific vitamins, trace elements

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 Malabsorption
Approach to the Patient

• History and examination limit extensive,

ill-focused, and expensive laboratory and
imaging studies

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 Malabsorption
Investigations
Test to confirm malabsorption
Routine tests
Haematology
• Microcytic anaemia (iron deficiency)
• Macrocytic anaemia (folate or B12 deficiency)
• Increased prothrombin time (vitamin K deficiency)
Biochemistry
• Hypoalbuminaemia
• Hypocalcaemia
• Hypomagnesaemia
• Deficiencies of phosphate, zinc

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 Malabsorption
Specific tests
• Fat malabsorption
Stool fat collection (24 hr > 7 g)
sudan black test ( qualitative test)

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 Malabsorption
• Carbohydrate malabsorption
(Urinary D-Xylose Test)
• D-Xylose, is disaccharide absorbed almost
exclusively in the proximal small intestine.
• The D-xylose test is usually performed by
giving 25 g D-xylose and collecting urine
for 5 h.
• An abnormal test (<4.5 g excretion)

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 Malabsorption
• B12 absorption (Schilling Test)
• 58Co-labeled cobalamin orally and collecting urine
for 24 h.
• Urinary excretion of cobalamin assessed.
• 1 mg cobalamin is administered intramuscularly 1
h following ingestion of the radiolabeled
cobalamin.
• The Schilling test may be abnormal (usually
defined as <10% excretion in 24 h) in :
– pernicious anemia
– chronic pancreatitis,
– blind loop syndrome
– ileal disease

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 Malabsorption
• Radiologic Examination
– flocculation
– segmentation
– mucosal abnormality
– dilation of intestine
– anatomical abnormalities
strictures and fistulas (Crohn's disease)
blind loop syndrome (jejun. diverticula)

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 Malabsorption
Determine the cause
• Small bowel biopsy
• Barium follow-through
• Pancreatic exocrine assessment
• Ultrasound, CT and MRCP

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 Malabsorption
Nonspecific
Diffuse:
• Celiac sprue Short or absent villi
mononuclear infiltrate
increase IE lymphocyte
hypertrophy of crypts

• Tropical sprue Similar to celiac sprue

Patchy:
• Bac. overgrowth Patchy damage to villi
lymphocyte infiltration

•
 Malabsorption
Specific:
• Intestinal lymphoma Malignant cells
in lamina
propria and submucosa
• Intestinal lymphangiectasia Dilated
lymphatics
• Eosinophilic gastroenteritis
Eosinophil infiltration
mucosa
• Infection by microorganisms as
giardiasis
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malabsorption

CBC, Ca, Ph
Albumin, immunogl.
Celiac serology

Barium image
Fat collection
D-xylose test

Duodenal BX
Aspirate culture

normal
Pancreatic function
test
CT abdomen
 Malabsorption
Coeliac disease
• is an immunologically mediated
inflammatory disorder of the small bowel
occurring in genetically susceptible
individuals and resulting from intolerance
to wheat gluten and similar proteins found
in, barley, rye and, to a lesser extent, oats

• The prevalence is approximately 1%

 Malabsorption
Pathophysiology
• The precise mechanism of mucosal
damage is unclear but
immunological responses to gluten
play a key role .
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 Malabsorption
Clinical features
In infancy presents
diarrhoea
failure to thrive
In children present
delayed growth
mild abdominal distension present.
short stature
 Malabsorption
In adults
The presentation is highly variable
florid malabsorption
non-specific symptoms
iron deficiency anaemia with or
without folate deficiency
weight loss
atypical presentation
oral ulceration
dyspepsia and bloating
 Malabsorption
Diagnosis
• Haematology
microcytic hypochromic
macrocytic anaemia
dimorphic anaemia
hyposplenism (target cells, spherocytes
and Howell-Jolly bodies).

• Biochemical tests
calcium, phosphate
vitamin D
total s. protein, albumin
 Malabsorption
serology
Antiendomysial Ab (IgA) detectable by
immunofluorescence in most untreated cases.
sensitive (85-95%) and specific
(approximately 99%) for the diagnosis IgG
antibodies, must be analysed in patients with
coexisting IgA deficiency.
Anti tissue transglutaminase Ab
replaced other blood tests in many countries
as it is easier to perform,and more accurate in
patients with IgA deficiency
Antigliadin Ab (IgG, IgA) low sensitivity and
specificity used only < 2 years age
 Malabsorption
Endoscopic finding
• flat doudenal folds or thin
• Serrated doudenal folds

Duodenal biopsy
The histological features are characteristic

• Short or absent villi

• hypertrophy of crypts
• Increase IE lymphocyte
• mononuclear infiltrate
 Malabsorption
Important causes of villous atrophy
• Coeliac disease
• Tropical sprue
• Dermatitis herpetiformis
• Lymphoma
• AIDS enteropathy
• Giardiasis
• Hypogammaglobulinaemia
• Radiation
• Whipple's disease
• Zollinger-Ellison syndrome
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 Malabsorption

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 Malabsorption
Disease associations of coeliacdisease
• Insulin-dependent diabetes mellitus (2-8%)
• Thyroid disease (5%)
• Primary biliary cirrhosis (3%)
• Sjögren's syndrome (3%)
• IgA deficiency (2%)
• Pernicious anaemia
• Inflammatory bowel disease
• Sarcoidosis
• Myasthenia gravis
• Dermatitis herpetiformis
• Down's syndrome
• Squamous carcinoma of oesophagus
• Microscopic colitis
• Splenic atrophy
• pancreatic insufficiency
 Malabsorption
Management
• Exclusion of wheat, barley, rye
• Life-long gluten-free diet
• Correct existing deficiencies
• Frequent dietary counseling
• Mineral and vitamin supplements
• Regular monitoring of symptoms, weight
and nutrition is essential
 Malabsorption
Complications

• Ulcerative jejuno -ileitis 'refractory'

celiac
• Enteropathy -associated T-cell lymphoma
Wt loss
abdominal pain
anorexia
fever
• Small bowel carcinoma
 Malabsorption
Poor response
▪ Dietary compliance should be assessed
▪ Exclusion of the other conditions
pancreatic insufficiency
microscopic colitis
• complications
ulcerative jejunitis
T-cell lymphoma.
 Malabsorption
Tropical sprue
• Chronic malabsorption in a patient from
the tropics, associated with abnormalities
of small intestinal structure and function.

• 5-10% of tropical area popu affected.

 Malabsorption
Etiology
pathogenesis of tropical sprue are
uncertain
Infective agent
• often begins after an acute diarrhoeal
illness.
• Isolation of Escherichia coli, Enterobacter
and Klebsiella
• Response to Abs

• Folic acid deficiency

 Malabsorption
Clinical features

• chronic diarrhoea
• abdominal distension
• anorexia, fatigue and
• weight loss
• features of malabsorption
megaloblastic anaemia (folic acid
malabsorption)
other deficiencies
 Malabsorption
The course of the disease
• Remissions and relapses may occur.

The differential diagnosis

• infective cause of diarrhea.
giardiasis
 Malabsorption
Diagnosis
▪ chronic diarrhea plus malabsorption
▪ patient in tropics
▪ small-intestinal mucosal biopsy partial
villous atrophy
▪ Celiac screen -ve
▪ No response to GFD

Management

• Tetracycline 250 mg 6-hourly with folic

acid (5 mg daily) for 28 days is the
treatment of choice
 Malabsorption
Small bowel bacterial overgrowth
(blind loop syndrome)

• group of disorders with diarrhea,

steatorrhea, and macrocytic anemia due to
the proliferation of colonic-type bacteria
within the small intestine

The normal duodenum and jejunum contain

less than 104/mL organisms
 Malabsorption
Pathophysiology

Disorders which impair the normal

physiological mechanisms controlling
bacterial proliferation in the intestine
causing:
▪ deconjugation of bile acids
▪ bacterial utilisation of vitamin B12.
 Malabsorption
Etiology
• Hypo- or achlorhydria
Pernicious anaemia
Partial gastrectomy
Long-term PPI therapy
• Impaired intestinal motility
Scleroderma
Diabetic autonomic neuropathy
Chronic intestinal pseudo-obstruction
• Structural abnormalities
Gastric surgery (blind loop after Billroth II
operation)
Jejunal diverticulosis
Enterocolic fistulas (e.g. Crohn's disease)
Strictures (e.g. Crohn's disease)
• Impaired immune function
Hypogammaglobulinaemia
 Malabsorption
Clinical features
▪ watery diarrhoea and/or steatorrhoea

▪ anemia due to B12 deficiency

▪ symptoms from the underlying intestinal

cause.
 Malabsorption
Investigations

▪ Barium follow-through may reveal blind

loops or fistulas.

▪ Endoscopic duodenal biopsies exclude

mucosal disease such as coeliac disease.

▪ Jejunal contents for bacteriological

examination can be aspirated at endoscopy
▪ Schilling test abnormal
▪ Serum vitamin B12 concentration is low.
 Malabsorption
Management
▪ Surgical treatment of the underlying cause
▪ B12 supplementation is needed in chronic
cases.
▪ Antibiotics (2-3 weeks)
➢ Tetracycline 250 mg 6-hourly
➢ Metronidazole 400 mg 8-hourly or
➢ ciprofloxacin 250 mg 12-hourly