Maldigestion and
Malabsorption
DR.RAHIMI
 The only clinical situations in which absorption is
increased are hemochromatosis and Wilson's
disease, in which absorption of iron and copper,
respectively, are increased.
 Disorders of absorption must be included in the
differential diagnosis of diarrhea
 The demonstration of the effect of prolonged (>24 h)
fasting on stool output can be very effective in
suggesting that a dietary nutrient is responsible for
the individual's diarrhea.
 The presence of a significant osmotic gap suggests
the presence in stool water of a substance (or
substances) other than Na/K anions that is
presumably responsible for the patient's diarrhe.
MALABSORPTION SYNDROME
PATHOPHYSIOLOGICAL (MECHANISM):
- Is divided into:
A) Intraluminal stage
Impaired hydrolysis and solubilization of nutrients
B) Intestinal stage
C) Lymphatic transport
A) Intraluminal stage
1) Impaired fat absorption:
i) Pancreatic lipase is necessary for triglyceride
hydrolysis in duodenum.
Pancreatic enzyme deficiency leads to fat malabsorption.
ii) Inactivation of pancreatic lipase by low gastric luminal
pH – fat malabsorption.
iii) Interruption of enterohepatic circulation of bile salt –
impaired micelle formation – fat malabsorption.
Absorption of fat soluble vitamins may be impaired as well.
2) Impaired carbohydrate absorption:
Most diseases that causes carbohydrate
malabsorption do so by affecting intestinal stage.
But amylase catalyse hydrolysis of starch to
oligosaccharides.
3) Impaired protein absorption:
Hydrolysis of polypeptides occurs mainly in small
intestine by action of pancreatic enzyme
trypsin,
chymotrypsin.
Deficiency of pancreatic proteases – impaired
protein absorption.
Diseases like:
Chronic pancreatitis
Cystic fibrosis
Ca. pancreatic resection
-
Protein malnutrition
B) Intestinal stage
1) Abnormalities of small intestinal mucosa.
Lactase deficiency
e.g. Congenital or acquired
Result – malabsorption of lactose.
Acquired:- i) Celiac disease
ii) Crohn’s disease
iii) Infective enteritis
2) Impaired epithelial cell transport:
Many diseases cause loss of intestinal surface
area
- malabsorption of many nutrients.
e.g.
i)
Celiac disease
ii) Tropical spure
iii) Extensive surgical resection
iv) Drugs
C) Lymphatic transport:
Lymphatic obstruction – fat malabsorption
e.g. i) Intestinal lymphangiectasia
iii) Tuberculous enteritis
iv) Intestinal lymphoma
D) Decreased availability of ingested nutrients and
cofactors for absorption.
i) Vitamin B12 malabsorption if intrinsic factor is
deficient. e.g. gastrectomy, antiparietal cell Ab.
ii) Bacterial overgrowth –can bind B12.
iii) Patient infected with fist tapeworm – B12
deficiency.
Tests for steatorrhea
 Quantitative test
 72hr stool fat collection – gold standard
>7gm/day – pathologic
 up to 14 g per day (secondary fat malabsorption) could be used
as the upper limit of normal in patients with diarrhea

 Qualitative tests
 Sudan lll stain
Detect clinically significant steatorrhea in
>90% of cases
 Although it cannot be used to exclude steatorrhea; its sole
advantage is its ease of performance.

Acid steatocrit – a gravimetric assay
 NIRA (near infra reflectance analysis)


Equally accurate with 72hr stool fat test
Investigations:
Specific:
Tests of fat absorption:
Quantitative fecal fat
Patient should be on daily diet containing 80-100
grams of fat.
Fecal fat estimated on 72 H collection.
6 grams or more of fat/day is abnormal.
May be due to: - Pancreatic
- Small intestinal
- Hepatobiliary disease
14C-Triolein
Test:
Is triglyceride which is hydrolysed by pancreatic
lipase.
 absorption of metabolism ↑ 14CO2
lung
Tests for pancreatic function:
1) Bentiromide test:
Chymotrypsin
PABA + pepside
PABA  absorbed and conjugated in liver
 urine excretion
2) Schilling test
3) Pancreatic stimulation test
Secretin stimulation –
4) Radiographic techniques:
- Plain abdominal X-ray
- U/S abdomen
- ERCP
- CT abdomen
Schilling test
 The Schilling test can be used clinically to distinguish
between gastric and ileal causes of vitamin B12 deficiency.
 Alternative approaches to diagnosing pernicious
anemia are to document atrophic gastritis by endoscopy
and biopsy, to confirm achlorhydria by acid secretion
analysis and increased serum gastrin levels, and to look for
antibodies in the serum directed against parietal cells or
intrinsic factor.
 Schilling test results are normal in patients with dietary
vitamin B12 deficiency, in protein-bound (foodbound) vitamin B12 malabsorption,[24] and
sometimes in congenital transcobalamin II
deficiency.[124]
 False-positive results on the Schilling test can result from
renal dysfunction or inadequate urine collection
Schilling test
To determine the cause of cobalamine(B12)
malabsorbtio
 Helps to asses the integrity of gastric, pancreatic and
ileal functions.



Abnormal cobalamine absorbtion in:
pernicious anemia, ch. Pancreatitis, Achlorohydria,
Bacterial overgrowth, ileal dysfunction
The test :

Administering 58Co-labeled cobalamine p.o.

Cobalamine 1mg i.m. 1hr after ingestion to saturate hepatic
binding sites
Collecting urine for 24 hr
(dependant on normal renal & bladder function)
 Abnormal - <10% excretion in 24 hrs

Schilling Test
1. Ingestion of labeled
Vit B12 and Non- labeled
IM Vit B12
2. Urine labeled
Vit B12 <8%/24 hr=
malabsorption
Intrinsic factor
(Corrects)
Pancreatic enzymes
Antibiotic therapy
Ileal disease or resection
IF def (PA)
Panc exoc def
Bact overgrowth
Carbohydrate absorption test
1) Hydrogen breath test
Hydrogen excretion ↑ in
bacterial overgrowth
small intestinal malabsorption
Carbohydrate absorption test
2) D-xylose test
5-carbon sugar  excreted unchanged in urine
25 grams given
Urine collected for 5 hours
Normally 25% is excreted
In patients with fat malabsorption, this test
differentiates pancreatic from small intestinal
malabsorpton.
D-xylose is normal in pancreatic disease
Serum level of D-xylose at 1-2 hours after ingestion
can be measured.
Test for bacterial overgrowth:
Intestinal aspiration and culture
2) Breath test
3) C-D xylose breath test
1)
Glucose Hydrogen
 most widely used breath test in clinical practice
 With bacterial overgrowth, : the glucose is cleaved by bacteria into carbon dioxide
and hydrogen. rise of 20 parts per million (ppm) above the baseline is
regarded as diagnostic of SIBO.
 Fasting breath hydrogen levels of more than 20 ppm also are considered
positive. High baseline hydrogen levels also are common in untreated celiac
disease and normalize after gluten withdrawal for as-yet-unknown reasons.[
 Patients must avoid smoking and ingestion of nonfermentable carbohydrates, such
as pasta and bread, the night before the test, because these factors can raise baseline
breath hydrogen values. Exercise can induce hyperventilation, thereby reducing
baseline breath hydrogen values, and should be avoided for two hours before the
test.
 sensitivity of 62% and specificity of 83%. Very rapid intestinal transit can lead to a
false-positive test result, because glucose can reach the colon before it can be
absorbed.
Lactulose Hydrogen
 Lactulose is a disaccharide that is not absorbed in the small
intestine but is metabolized by bacteria in the proximal
colon, producing a late peak in exhaled hydrogen.
 In the presence of bacterial overgrowth, an early hydrogen
peak is observed.
 Results of this test may be difficult to interpret with either slow or
fast intestinal transit, and sensitivity and specificity have been
disappointing
 sensitivity and specificity rates of 68% and 44%, respectively.[133]
Sensitivity of the test may be increased by the addition of
scintigraphy to correct for abnormalities of intestinal transit,[150] but
the lactulose hydrogen breath test cannot be
recommended for routine clinical use.
Xylose
 The 14C-xylose and 13C-xylose breath tests measure labeled carbon dioxide
that is produced by breakdown of labeled substrates by bacteria. The
isotope may be radioactive (14C) or stable (13C); the stable isotope has
been used in children.[151] d-Xylose is the most widely used substrate and is
a good substrate for breath testing for SIBO because it is absorbed
completely in the small intestine, is metabolized minimally, and is
catabolized by Gram-negative bacteria. The 14C-d-xylose breath test
appears to perform better than the glucose or lactulose
hydrogen breath test
 The 14C-d-xylose breath test result is considered positive when the
“cumulated dose at four hours exceeds 4.5% of the administered
radioactivity.”[49] Disturbances in intestinal transit particularly affect the
performance of this test, and accuracy may be improved by the addition of
a transit marker (such as barium or diatrizoate meglumine–diatrizoate
sodium [Gastrografin]) and radiologic imaging
Radiography of small intestine:
barium contrast (small-bowel series or study)–
to see
- Blind loop
- Strictures and fistulas (as in Crohn's disease)
- J. diverticular
A normal barium contrast study does not exclude
the possibility of small-intestinal disease.
2) CT enteroclysis and magnetic resonance (MR)
enteroclysis
1)
2)
Intestinal mucosal biopsy: indications ;

A small-intestinal mucosal biopsy is essential
in the evaluation of a patient with documented
steatorrhea or chronic diarrhea (lasting >3
weeks)
Diffuse or focal abnormalities of the small
intestine defined on a small-intestinal series

Disease that Can Be Diagnosed by Small-Intestinal Mucosal Biopsies
Lesions
Diffuse, Specific
Whipple's disease
Agammaglobulinemia
Abetalipoproteinemia
Patchy, Specific
Intestinal lymphoma
Intestinal lymphangiectasia
Eosinophilic gastroenteritis
Amyloidosis
Crohn's disease
Infection by one or more
microorganisms (see text)
Mastocytosis
Pathologic Findings
Lamina propria contains macrophages containing
PAS+ material
No plasma cells; either normal or absent villi
("flat mucosa")
Normal villi; epithelial cells vacuolated with fat
postprandially
Malignant cells in lamina propria and submucosa
Dilated lymphatics; clubbed villi
Eosinophil infiltration of lamina propria and
mucosa
Amyloid deposits
Noncaseating granulomas
Specific organisms
Mast cell infiltration of lamina propria
Lesions
Diffuse, Nonspecific
Celiac disease
Tropical sprue
Bacterial overgrowth
Pathologic Findings
Short or absent villi; mononuclear
infiltrate; epithelial cell damage;
hypertrophy of crypts
Similar to celiac disease
Patchy damage to villi; lymphocyte
infiltration
Folate deficiency
Short villi; decreased mitosis in
crypts; megalocytosis
Vitamin B12 deficiency
Similar to folate deficiency
Radiation enteritis
Similar to folate deficiency
Zollinger-Ellison syndrome Mucosal ulceration and erosion from
acid
Protein-calorie malnutrition Villous atrophy; secondary bacterial
overgrowth
Drug-induced enteritis
Variable histology
Results of Diagnostic Studies in Different Causes of Steatorrhea
D-Xylose Test
Schilling Test
Duodenal Mucosal
Biopsy
Normal
Chronic pancreatitis Normal
50% abnormal; if
abnormal, normal
with pancreatic
enzymes
Bacterial
overgrowth
syndrome
Normal or only
modestly
abnormal
Often abnormal; if
abnormal, normal
after antibiotics
Usually normal
Ileal disease
Celiac disease
Normal
Decreased
Abnormal
Normal
Intestinal
lymphangiectasia
Normal
Normal
Normal
Abnormal:
probably "flat"
Abnormal:
"dilated
lymphatics"
Malabsorption due to bacteral over growth of
small bowel
Normal small intestine is bacterial sterile due to:



Acid
Int. peristalsis (major)
Immunoglobulin
Cause of bacterial growth.
e.g.




Small intestinal diverticuli
Blind loop
Strictures
DM/ Scleroderma
Pathophysiology
1)
Bacterial over growth: Metabolize bile salt resulting in
deconjugation of bile salt
  Bile Salt
 Impaired intraluminal micelle formation

Malabsorption of fat.
Intestinal mucosa is damaged by
 Bacterial invasion
 Toxin
 Metabolic products
 Damage villi  may cause total villous atrophy.
2)
Clinically:
 Steatorrhea
 Anaemia
 B12 def.
Reversed of symptom after antibiotic treatment.
Diagnosis:
 Breath test
 Cxylose test
 Culture of aspiration (definitive)
Treatment: Antibiotic
 Tetracyclin
 Ciproflexacin
 Metronidazole
 Amoxil
Short Bowel Syndrome
 Three different situations in adults demand
intestinal resections:
(1) mesenteric vascular disease, including
atherosclerosis, thrombotic phenomena, and
vasculitides
(2) primary mucosal and submucosal disease, e.g.,
Crohn's disease
(3) operations without preexisting small intestinal
disease, such as trauma.
Sequella of bowel resection
 Adaptation of remaining bowel:last for up to 6–12 months.
 Enteral nutrition with calorie administration must be




maintained, especially in the early postoperative period
The presence of the colon (or a major portion) is associated
with substantially less diarrhea and lower likelihood of
intestinal failure as a result of fermentation of nonabsorbed
carbohydrates to SCFAs.
Increase in oxalate absorption in the colon
Cholestyramine,
an anion-binding resin, and calcium have proved useful in
reducing the hyperoxaluria.
Gastric hypersecretion ( due to reduced hormonal inhibition of
acid secretion or increased gastrin levels due to reduced smallintestinal catabolism of circulating gastrin)
proton pump
inhibitors can help in reducing the diarrhea and steatorrhea but
only for the first six months.
Absence of the ileocecal valve
decrease in intestinal transit
time and bacterial overgrowth from the colon.
Whipple's Disease
 Etiology:gram-positive bacillus, T. whipplei
 Clinical Presentation:diarrhea, steatorrhea, abdominal pain, weight
loss, migratory large-joint arthropathy, and fever as well as
ophthalmologic and CNS symptoms (dementia,..).
 The steatorrhea in these patients is generally believed secondary to
both small-intestinal mucosal injury and lymphatic obstruction
secondary to the increased number of PAS-positive macrophages in
the lamina propria of the small intestine.
 Diagnosis:tissue biopsies from the small intestine and/or other
organs . PAS-positive macrophages containing the characteristic
small (0.25—1–2 mm) bacilli is suggestive of this diagnosis.
 Treatment:trimethoprim/sulfamethoxazole for approximately 1
year.
Protein-Losing Enteropathy
 Normally, about 10% of total protein catabolism
occurs via the gastrointestinal tract.
 Increased protein loss into the gastrointestinal in
more than 65 different diseases with mucosal
ulceration or nonulcerated mucosa or lymphatic
dysfunction
 Peripheral edema and low serum albumin and
globulin levels in the absence of renal and hepatic
disease.
 Treatment: treat the underlying disease process .