D-Xylose Excretion Test in Small Intestine

Small Intestine: CHO

• D-xylose excretion test: ideal for small intestinal integrity
• D-xylose is not normally present in the diet and is actively absorbed by the small bowel
• >25% of the 5g oral dose is excreted in the urine within 5 hours
• This test is unaffected by biliary or pancreatic disease

Small Intestine: Proteins

• Detect leakage of serum proteins into the bowel due to mucosal inflammation or lymphatic obstruction (protein-losing enteropathy)
• Methods:
  • IV administration of 51Cr labelled albumin: faecal radioactivity >30%/day indicates protein-losing enteropathy
  • Measure faecal alpha-1-antitrypsin: directly proportional to plasma loss in the gut

Fat/Lipids

• Faecal fat excretion: normal output is up to 6g/day on a normal diet of 100g fat/day
• Increased excretion is seen in:
  • Generalized small bowel disease
  • Pancreatic insufficiency
  • Biliary obstruction
  • Terminal ileal disease/resection
• 14C-triolein breath test: decreased excretion of 14CO2 indicates fat malabsorption

Assessment for Vitamins

• Serum Vitamin A and E levels are decreased in fat malabsorption
• Vitamin A, E, and D levels can be requested
• Vitamin K deficiency is assessed by measuring the Vitamin K-dependent prothrombin index

Vitamin B12 Malabsorption

• Suspicion of Vitamin B12 malabsorption: clinical features (fatigue/weakness, peripheral neuropathy), megaloblastic anaemia, low Vit B12
• Schilling test: 1ug 58Co labelled vitamin B12 is given orally with a large 1mg intramuscular dose of unlabelled B12

Digestion and Absorption

• Monosaccharides (glucose, fructose, galactose) are absorbed into enterocytes
• Digestion and absorption of proteins:
  • Mouth: pepsin cleaves internal bonds of proteins
  • Stomach: digestion proceeds further through pancreatic proteases
  • Small intestine: mixtures of amino acids, dipeptide, and tripeptides are absorbed into the blood
• Digestion and absorption of fats:
  • Binds to salivary and dietary R-proteins
  • R-proteins are digested by pancreatic proteases, liberating B12
  • Binds to IF and is absorbed in the terminal ileum

Malabsorption

• May occur due to defects in digestion or absorption phase
• Single nutrient or multiple nutrients may be affected
• 3 phases of digestion/absorption:
  • Luminal
  • Mucosal
  • Post-absorptive

Defects in Digestion and Absorption

• Luminal: decreased lipase/protease secretion (e.g., chronic pancreatitis, intestinal resection, bile duct obstruction, cystic fibrosis)
• Mucosal: mucosal dysfunction (e.g., coeliac disease, disaccharides deficiency)
• Post-absorptive: abnormal lymphatics (e.g., intestinal lymphangiectasia, Whipple's disease)

Clinical Features

• Severe generalised malabsorption:
  • Diarrhoea
  • Steatorrhoea
  • Weight loss
  • Flatulence and abdominal distension
  • Anaemia (iron deficiency/megaloblastic)
  • Oedema
  • Metabolic bone disease
  • Features of vitamin deficiencies (e.g., skin lesions, peripheral neuropathies, petechial haemorrhages)
  • Neurological manifestations

Malabsorption Syndromes

• Coeliac disease (small intestine)
• Cystic fibrosis (pancreas)
• Crohn's disease (small intestine, including terminal ileum)
• Whipple's disease (small intestine + lymphatics)
• Intestinal parasites
• Short bowel syndrome

Non-GIT Causes of Malabsorption

• Hyperthyroidism
• Hypothyroidism
• Addison's disease
• Carcinoid syndrome