Gastroenterology training and education

It involves suspecting its presence, confirming its existence and finally demonstrating the cause.

Step 1

Suspecting Malabsorption

• The classical manifestation of malabsorption is steatorrhoea (pale, greasy, voluminous, foul smelling stools) and weight loss despite adequate food intake.
• There may be selective abnormality in the absorption of carbohydrates. This will lead to watery diarrhoea, cramping, bloating, flatulence and milk intolerance.
• May present with isolated nutrient deficiency like IDA, def of vitamins, calcium leading to anaemia, tetany, bruising, bone pain etc.
• The clinical features depend upon the cause and severity of the underlying disease.

Remember-

• All patients with suspected malabsorption of unknown cause should have the following tests-
• Haematology- FBC, B12, folate, ferritin, INR
• Biochemistry- Urea & electrolytes, LFT, albumin, TFT, Mg, PO4, Ca, glucose
• Inflammatory markers- CRP, ESR
• Immunology- coeliac antibody, autoantibody (systemic diseases), Immunoglobulins
• Check Zn, Cu, Selenium- if malabsorption for a long time

Step 2

Confirming Malabsorption

• Faecal fat excretion-
  • 14 C- triolein breadth test- measures 14CO2 in breadth after ingestion of a triglyceride that has been labeled with 14C. fat malabsorption results in decreased pulmonary excretion of 14CO2. It has been reported to have 100% sensitivity and 96% specificity however limitations such as the confounding effects of comorbidities altering fat metabolism or respiratory function have also been documented. Despite its limitations, it is usually the test of choice to detect fat malabsorption.
  • A qualitative assessment on a spot stool using Sudan III stain.  However, its use is not recommended due to its lack of sensitivity and poor reproducibility.
  • The acid steatocrit (a gravimetric assay performed on a spot stool sample) may provide an alternative accurate and simplified method for detecting steatorrhea on a spot stool specimen.
  • Quantitative assessment of a 72 hour stool collection on a 100 gram fat/day diet- if the qualitative tests above are negative. Normal fat excretion is < 6gm/day. Steatorrhea- if fat excretion >14 g/day. More than 6gm/day fat is pathologic; however fecal fat excretion can be increased upto 14g/day in diarrheal diseases even without fat malabsorption.
  • Faecal elastase- faecal elastase is more sensitive and specific than chymotrypsin determination. Among pancreatic function tests, faecal elastase measurement is the most sensitive and specific in the early phases of pancreatic insufficiency. In addition, its values are independent on pancreatic enzyme replacement therapy, thereby extending its utility. Faecal elastase decreases in pancreatitic insufficiency. Faecal elastase helps in differentiating between pancreatic and intestinal causes.
  • Low levels of serum beta-carotene, cholesterol, TG and calcium and a prolonged PT suggest malabsorption of fat and fat soluble vitamins. Beta carotene values less than 100 mcg/dl is suggestive and less than 47mcg/dl is strongly indicative of steatorrhea.
• Low levels of B12, folate, iron and albumin suggest malabsorption of water soluble substances and therefore indicate intestine disease rather than pancreatic or biliary disease.
  • Carbohydrate malabsorption
  • D-xylose test- Limited clinical value today
  • Hydrogen breadth (lactose tolerance) tests- H2 is produced by bacterial action on unabsorbed CH in the colon. Thus in CH malabsorption, a breadth H2 peak will occur 90 minutes after its ingestion when it first arrives in the colon and is broken down by the bacteria.  False positive results are possible particularly with small bowel bacterial overgrowth.  It can be used to diagnose specific forms of carbohydrate malabsorption (eg, lactose, fructose, sucrose isomaltase and others).
  • Concurrent antibiotic administration will alter the results of H2 breadth test as it relies on bacterial fermentation of carbohydrate.
  • Stool pH less than 5.5 is a qualitative indicator of CHO malabsorption. (SCFA and lactic acids are the products of CHO metabolism)
• Protein malabsorption- Not generally tested. The tests are technically difficult and intestinal protein loss is generally due to either bacterial overgrowth or protein losing gastroenteropathy. Enteral protein loss is demonstrable by measurement of the alpha-1 antitrypsin clearance. In massive enteral protein loss, the exact site of protein leakage may be localized by the infusion of 99mTc-albumin and gamma camera scintigraphy.
• d. Specific tests- SeHCAT, Schilling

Tests for Bile Acid Malabsorption
This can cause symptoms of chronic diarrhoea. Three types of bile acid malabsorption are recognised:
Type 1: following ileal disease or resection or bypass surgery.
Type 2: primary idiopathic malabsorption.
Type 3: associated with cholecystectomy, peptic ulcer surgery, chronic pancreatitis, coeliac disease and diabetes mellitus.
Bile acids are cathartic to colonic mucosa, and impair sodium and water absorption. A trial of cholestyramine may be appropriate in some patients with chronic diarrhoea for which other causes have been excluded; however, the Selenium-75 labeled Homotaurocholic Acid Test (75SeHCAT) is necessary in some.  The SeHCAT test involves the administration of a selenium75 labeled synthetic bile acid (selenium-homotaurocholic acid) orally, followed by measurement of retention of the bile acid by whole body scan or gamma camera at seven days (abnormal is less than 5 percent, normal is >12%, equivocal is between 5 and 12%).

Step 3

Finding the cause

History-

• Abdominal pain is unusual in malabsorption except in chronic pancreatitis, Crohns disease and pseudo obstruction (Scleroderma)
• Always ask about an h/o recurrent peptic ulcer disease (ZES)
• Always ask h/o previous surgery
• Take a careful alcohol history- it takes 10-20 years for pancreatic insufficiency to develop in alcoholics
• Some diseases associated with malabsorption are found more frequently in families- like coeliac, Crohns, lactase def- so take a careful family history.
• H/o travel to endemic areas of tropical sprue, giardiasis, or other GI infections
• Is there an increased likelihood of HIV infection?
• Does the patient have clinical features of thyrotoxicosis, Addison’s disease, Whipple’s disease or diabetic neuropathy?

If the case warrants further evaluation- Proceed stepwise as-

• H2-breath tests for carbohydrate malabsorption (lactose, fructose), coeliac antibodies, search for giardia lamblia, enteropathogenic bacteria, parasites and ova.
• Abdominal ultrasound (gallbladder; liver; pancreas; intestinal wall aspects; adenopathy; etc.)
• OGD including biopsies from stomach (autoimmune gastritis? H. pylori?) and duodenum
• Ileocolonoscopy including biopsies of colon and ileum
• If pancreatic disease with secretory insufficiency is suspected- check tests for secretory function like chymotrypsin or elastase in stool, CT/ERCP of pancreas
• If small bowel disease is still within the D/D- do small bowel x-rays (fistulae, diverticula, blind loops, short bowel, etc.), Schilling-test (Vit B12), Glucose-H2-test (bacterial overgrowth), Angiography of celiac and mesenteric arteries (ischemic bowel damage).

Practical approach to Malabsorption

Remember 3 major malabsorptive conditions- small bowel mucosal disease, small bowel bacterial overgrowth, and pancreatic insufficiency

Step A- Possible coeliac disease- D2 biopsies
Step B- If other diagnoses suspected- Do Triolein breadth test (TBT)
Step C- If TBT is abnormal- a. pancreatic insuff b. Small bowel bacterial overgrowth, c. diffuse enteropathy (radiology, endoscopy, biopsy, microbiology)
Step D- If TBT normal- a. CHO malabsorption b. Bile acid malabsorption c. segmental enteropathy (radiology, endoscopy, biopsy)

Discuss the mechanisms of malabsorption?

Mechanisms of fat malabsorption

• Pancreatic insufficiency
• Bile acid deficiency
• Small intestinal bacterial overgrowth
• Loss of absorptive surface area
• Defective enterocyte function
• Lymphatic disorders

Mechanisms of CHO malabsorption

• Selective disaccharidase deficiency
• Disruption of brush border/enterocyte function
• Loss of mucosal surface area
• Pancreatic insufficiency (loss of amylase)

Mechanisms of Protein malabsorption

• Pancreatic insufficiency (loss of pancreatic proteases)
• Disorders with impaired enterocyte function
• Disorders with decreased absorptive surface
• Protein-losing enteropathy