Gastro-Intestinal Malabsorption

Malabsorption
Dr. Haseeb Ahmed Bhatti
RMO - Medical Unit III
JPMC Karachi
PREPARED BY DR. HASEEB A. BHATTI

Malabsorption – impaired absorption of
nutrients
• Inadequate assimilation of dietary substances due to defects
in
• Digestion (intra luminal)
• Absorption (mucosal)
• Transport (post mucosal)
• Can affect micronutrients
(vits and minerals) or
macronutrients
(protein/carb/fat)

Sites of absorption of nutrients
within the gastrointestinal tract.
Adapted from: Mahan and Escott-
Stump: Krause's Food, Nutrition and
Diet Therapy, 9/e, p l3, ©1996, with
permission from Elsevier

The Luminal Phase
Impaired nutrient hydrolysis
• The most common cause for impaired
nutrient hydrolysis is pancreatic insufficiency.
• The resultant deficiencies in lipase and
proteases lead to lipid and protein
malabsorption, respectively.
• Inactivation of pancreatic enzymes by gastric
hypersecretion
• Inadequate mixing of nutrients, bile, and
pancreatic enzymes, also causes impaired
hydrolysis.
• Failure to convert a proenzyme to active
form, cause protein maldigestion and
malabsorption. PREPARED BY DR. HASEEB A. BHATTI

Impaired micelle formation
Impaired micelle formation causes a
problem in fat solubilization and
subsequent fat malabsorption.
(1) Decreased bile salt synthesis
(2) Impaired bile secretion from biliary
obstruction or cholestatic jaundice
(3) Impaired enterohepatic bile
circulation
(4) Bile salt deconjugation

 Stasis of intestinal content caused
by a motor abnormality (eg,
scleroderma, diabetic neuropathy,
intestinal obstruction)
 an anatomic abnormality (eg, small
bowel syndrome, stricture, ischemia,
blind loops),
 or small bowel contamination from
enterocolonic fistulas can cause
bacterial overgrowth.

Mucosal phase
• Disaccharidase deficiency can lead to disaccharide malabsorption.
• Lactase deficiency, either primary or secondary, is the most
common form of disaccharidase deficiency.
• Secondary lactase deficiency can be due to acute gastroenteritis
(rotavirus and giardia infection), chronic alcoholism, celiac sprue,
radiation enteritis, regional enteritis, or AIDS enteropathy.
• Immunoglobulin A (IgA) deficiency (most common
immunodeficiency) is due to decreased or absent serum and
intestinal IgA, which clinically appears similar to celiac disease
and is unresponsive to a gluten-free diet.
• Acrodermatitis enteropathica is an autosomal recessive disease
with selective inability to absorb zinc, leading to villous atrophy
and acral dermatitis.
• Nutrient malabsorption is due to inherited or acquired defects.
• Inherited defects include glucose-galactose malabsorption,
abetalipoproteinemia, cystinuria, and Hartnup disease.

Acquired disorders are far more common and are
caused by the following:
(1) Decreased absorptive surface area
(2) Damaged absorbing surface
(3) Infiltrating disease of the intestinal wall
(4) Infections
-Whipple's disease
-Intestinal tuberculosis
-Tropical sprue
-Parasites e.g. Giardia lamblia.

Post - absorptive Phase
• Obstruction of the lymphatic system, both congenital
(eg, intestinal lymphangiectasia, Milroy disease) and
acquired (eg, Whipple disease, neoplasm [including
lymphoma], tuberculosis), impairs the absorption of
chylomicrons and lipoproteins

Risk Factors
•Factors that may increase chance of having
malabsorption include:
oMedical conditions affecting the intestine
oUse of laxatives
oExcessive use of antibiotics
oIntestinal surgery
oExcessive use of alcohol
oTravel to countries with high incidence of intestinal
parasites.

Symptoms of malabsorption
Symptoms can be
1.Extraintestinal
2.Intraintestinal
Diarrhea, often steatorrhea is the most common feature. It isdue to
impaired water, carbohydrate and electrolyte absorption.
Other symptoms include:
• - Weight loss
• -Growth retardation
• -Swelling or edema
• -Anemias
• -Muscle cramps and bleeding tendencies.

Angular Cheilosis
Deficiencies:
Vitamin B-12
Iron
Folate
B vitamins

GLOSSITIS
• Deficiencies of:
• Vitamin B-12
• Iron
• Folate
• Niacin
B-12 deficiency
with
hypersegmented
PMNs

Zinc Deficiency
Acrodermatitis

Acrodermatitis
Loss of hair, skin rash and diarrhea due to zinc deficiency

INVESTIGATIONS – Work up

Work-up
•If you suspect specific cause, test for it
• Details to follow, and more details from Brenda’s lab
lectures
•And/or check CBC (anemia), ferritin, lytes
•Confirm malabsorption:
• 72 h fecal fat collection
• Sudan III stool stain for fat
• D-xylose test (assesses mucosal integrity to
differentiate between mucosa and pancreatic etiology)

Tests for steatorrhea
• Quantitative test
72hr stool fat collection – gold standard
6gm/day – pathologic
P’ts with steatorrhea - >20gm/day
Modest elevation in diarrheal disease
(may not necessarily indicate Malabsorption)
• Qualitative tests
 Sudan lll stain
Detect clinically significant steatorrhea in >90% of cases
Acid steatocrit – a gravimetric assay
Sensitivity – 100%, specificity – 95% , PPV – 90%
NIRA (near infra reflectance analysis)
Equally accurate with 72hr stool fat test
Allows simultaneous measurement of fecal fat, nitrogen, CHO

Schilling test
To determine the cause of cobalamine(B12)
malabsorbtion
• 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 58 Co-labeled cobalamine
- 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

D-Xylose Test
•D-Xylose is a monosacchride which is absorbed
through the small intestine and excreted through the
kidneys.
•Used to asses mucosal function
• The test:
After overnight fast, 25gm D-xylose
Urine collected for next 5 hrs
Abnormal test = <5 gm excretion

D-Xylose Test

A. Normal individual. B. Celiac sprue. C.
Jejunal diverticulosis. D. Crohn's disease

Endoscopy
• Gross morphology – gives diagnostic clue
-Reduced duodenal folds and scalloping of duodenal mucosa – celiac
disease
Use of vital dyes to identify villous atrophy
• Biopsy – to establish Dx
-For p’ts with documented steatorrhea or ch. Diarrhea
• Lesions seen – classified in to three
- Diffuse, specific e.g. whippl’s Disease
- Patchy, specific – crohn’s D., lymphomainfectious causes
- Diffuse, non-specific – Celiac sprue, Tropical sprue autoimmune
enteropathy
• Suspected distal pathology
- push enteroscopy
wireless capsule endoscopy PREPARED BY DR. HASEEB A. BHATTI

Chronic Pancreatitis
• Often due to long-standing alcohol use
• Marked destruction of ducts/acini
• Reduced secretion of digestive
enzymes, fluid, bicarbonate
• Lipases most affected
• Anatomic damage assessed by ERCP or
endoscopic ultrasound (EUS) or
pancreatic calcifications on x-rays

Bile duct
Pancreatic duct

ERCP view
of Chronic
Pancreatitis
Endoscopic Retrograde
CholangioPancreatography
Single arrow points to bile
duct compressed by fibrotic
pancreas
Double arrow points to dilated
pancreatic duct with short
stubby side branches

Celiac Disease
•Aka:
• Celiac Sprue
• Non-tropical sprue
• Gluten-sensitive Enteropathy
•Immunologically mediated disease
caused by intolerance of (gliaden
component of )gluten, which causes
mucosal inflammation and
malabsorption, in genetically
predisposed individuals

•Hereditary insensitivity to gliadin fraction of
gluten
•Gluten-sensitive T cells activated by exposure,
cause inflammatory response - leads to mucosal
villous atrophy and crypt hyperplasia
•N. America 1/5000
•Female 2:1 male
Celiac Disease

Pathophysiology

Presentation
There is no typical
• Infants
• Symptoms appear after cereals introduced
• FTT (failure to thrive), anorexia, pallor, hypotonia, abdominal distention
• Older kids
Anemia, growth and/or pubertal delays, anorexia, diarrhea
• Adults
Anorexia, weakness,
Diarrhea, steatorrhea,
Anemia (predominantly iron def anemia)
Glossitis, angular stomatitis, aphthous ulcers
Decreased fertility (reduction in steroid hormones)
Evidence of - Ca/vit D deficiency
Dermatitis herpetiformis (10%)

Dermatitis herpetiformis
Dermatitis herpetiformis (sometimes known as Duhring’s
disease, the gluten rash or the celiac rash), is a long-term
(chronic) skin condition that causes itchy, blistering, burning
skin rash symmetrically on the elbows, knees, buttocks, back,
or scalp
Treatment:
Gluten free diet
Dapsone

Diagnosis
•Clinical suspicion
• Use clues like unexplained Fe deficient anemia
•FHX
•Labs
–72 hr fecal fat
–D-xylose absorption test
• Tissue transglutaminase (IgA)
• Anti gliaden antibody (IgA)
• Anti reticulin antibody (IgA)
• Total IgA (check to make sure there is no IgA
deficiency)
• Antibody levels decrease with gluten-free diet, so you can
use this to determine if the pt is really following the diet

Normal
Small Bowel Biopsies
Celiac Sprue
Villi and mature enterocytes destroyed
Deep crypts (hyperplasia) (arrows)
Villous atrophy-Lack of or shortening of villi
Increased epithelial cells

Celiac Treatment
•Gluten free diet
• No wheat, rye, barley or anything that has gluten in it
• No breads, bagels, pastries, pasta and pizza
• Gluten used as thickener frequently, so need education
to facilitate avoidance
• Must do dietitian referral, advise support group
•Sx will resolve in 1-2 weeks (usually)

Prognosis & Complications
•Prog 10-30% mortality without treatment
•Complications:
• Intestinal lymphomas
• Refractory disease
• Increase in other GI malignancies

Whipple's Disease
• Cause: by the bacteria Tropheryma whipplei.
• Effect:
-Chronic multisystem disease associated with diarrhea,
steatorrhea, weight loss, arthralgia, and central nervous
system (eg. dementia,memory loss, oculomasticatory myorythmia) and
cardiac problems (endocarditis)
• Diagnosis:
- identification of T. whipplei by polymerase chain reaction
(PCR).
- PAS-positive macrophages in the small intestine and other
organs with evidence of disease.

TREATMENT
At present, the favored method of treatment is the daily
parenteral administration of 1.2 million units of
benzylpenicillin (penicillin G) and streptomycin 1 g for a
period of 2 weeks.
-This is followed by treatment with cotrimoxazole
(trimethoprim 160 mg and sulfamethoxazole 800 mg) twice
daily for 1 to 2 years.
The treatment
should begin and
end with a PCR
analysis of
cerebrospinal fluid,
in order to
definitively diagnose
infection of the CNS
with Whipple's
disease and to
document the
disappearance of the PREPARED BY DR. HASEEB A. BHATTI

Bacterial Overgrowth Syndrome
•Usually secondary to anatomic alterations or
motility disorders (congenital or acquired) that
promote stasis of intestinal contents
•Normal small bowel has <105 bact/mL
•Low count maintained by peristalsis, gastric acid,
mucus, intact ileocecal valve function

What Extra Bacteria Do
•Consume nutrients, especially B12 and carbs
• B12 (cyanocobalamin) deficiency
• Calorie deprivation/weight loss
•Produce folate, so this is NOT a cause of folate
deficiency (folate def causes macrocytic anemia)
•Deconjugate bile salts
• Fat malabsorption
• Steatorrhea and diarrhea

Bac-t Overgrowth Dx
•Frequently, empiric antibiotic therapy resulting in
improvement is basis for diagnosis…but abx can
worsen many conditions on the ddx
•Better: quantitative culture of intestinal fluid.
Look for bac-t count>105/mL
•Or C-xylose breath test (less invasive)

Bact Overgrowth Tx
•10-14 days oral abx
• Tetracycline
• Amox/clavanulate
• Cephalexin
• TMP/SMX
• Metronidazole
•Correct underlying condition
•Correct nutritional deficiencies

Carbohydrate Intolerance
•Inability to digest certain carbs due to lack of one
or more enzymes
•Sx: watery diarrhea, abdominal distention,
flatulence, nausea, borborygmi, abd cramping
(hooray for lactaid!)
•Etiology:
• Acquired (primary)
• Secondary
• Congenital (rare)

Lactase Deficiency
•Primary adult hypolactasia
•Most common carb intolerance
•Lactase normally in high levels in neonates but
decrease after weaning in most ethnic groups
• 80% blacks and hispanics
• Near 100% Asians
• Only 15-20% Caucasians

Secondary Lactase Deficiency
• Bacterial overgrowth or stasis syndromes
• Increased fermentation of dietary lactose in the small bowel,
leading to symptoms of lactose intolerance.
• Mucosal injury
Villus flattening or damage to the intestinal epithelium
• Celiac disease
• Crohn’s disease
• Radiation enteritis, chemotherapy
• HIV enteropathy
• Whipple’s disease

Lactase-Deficient Patient with low activity enzyme
other individuals may also downregulate genes, etc.
Protein stained Lactase activity stained

Dx/Tx
•Dx by:
• Careful hx
• Dietary challenge
• H2 breath test
•Tx with:
• Lactose avoidance
• Lactase supplements
• Ca+ supplements

Short Bowel Syndrome
•Malabsorption due to extensive small bowel
resection (often because of Crohn’s, mesenteric
infarction, radiation enteritis)
•Symptom severity depends on length and
function of remaining bowel
•Diarrhea and nutritional deficiencies

Jejunum
• Primary digestive and absorptive site for most nutrients
• BUT
• If removed, the ileum will adapt by changing villous
structure
• Gradual clinical improvement as adaptive process
continues

Ileum
• Primary site for B12 and bile acid absorption
• No compensatory mechanism for loss of ileum
• Malabsorption of fats, fat-soluble vitamins, and B12
• Bile acids in large intestine cause secretory diarrhea
SBS Tx
• Small feedings
• Anti-diarrheals
• TPN if needed

MANAGEMENT of MALABSORPTION
SYNDROME
• Replacement of nutrients, electrolytes and fluid may be
necessary.
• In severe deficiency, hospital admission may berequired for
parenteral administration.
• Pancreatic enzymes are supplemented orally in pancreatic
insufficiency.
• Dietary modification is important in some conditions:
• Gluten-free diet in coeliac disease.
• Lactose avoidance in lactose intolerance.
• Antibiotic therapy will treat Small Bowel Bacterial
overgrowth.

References
1. Dr. L. Schiller, MD. AGA DDSEP8 Chapter 9, Diarrhea.
2. Dr. Schiller,MD., Dr. JH Sellin,MD. Chapter 16: Sleisenger &
Fordtran’s Gastrointestinal and Liver Diseases, Pathology,
Diagnosis, Treatment. 10th edition.
3. ASGE guidelines. Journal GIE 2010 vol 71,
No. 6:2010.
4. Dr. Ali Rezaie, Curr. GI Reports, SIBO , (2016)18.8.

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Gastro-Intestinal Malabsorption

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