Malabsorption

Malabsorption
Classification and external resources
Whipple's disease: Alcian blue with apparently eosin counterstain enlarged villus with many macrophages
ICD-10	(K90)
ICD-9	579
DiseasesDB	7698
MedlinePlus	000299
eMedicine	med/1384
MeSH	D008286

Malabsorption is a state arising from abnormality in absorption of food nutrients across the gastrointestinal (GI) tract.

Impairment can be of single or multiple nutrients depending on the abnormality. This may lead to malnutrition and a variety of anaemias.

Classification

Some prefer to classify malabsorption clinically into three basic categories:

(1) selective, as seen in lactose malabsorption.

(2) partial, as observed in a-Beta-lipoproteinaemia.

(3) total as in coeliac disease.

Pathophysiology

The main purpose of the gastrointestinal tract is to digest and absorb nutrients (fat, carbohydrate, protein, and fiber), micronutrients (vitamins and trace minerals), water, and electrolytes. Digestion involves both mechanical and enzymatic breakdown of food. Mechanical processes include chewing, gastric churning, and the to-and-fro mixing in the small intestine. Enzymatic hydrolysis is initiated by intraluminal processes requiring gastric, pancreatic, and biliary secretions. The final products of digestion are absorbed through the intestinal epithelial cells.

Malabsorption constitutes the pathological interference with the normal physiological sequence of digestion (intraluminal process), absorption (mucosal process) and transport (postmucosal events) of nutrients.

Intestinal malabsorption can be due to:

• Mucosal damage (enteropathy)
• Congenital or acquired reduction in absorptive surface
• Defects of specific hydrolysis
• Defects of ion transport
• Pancreatic insufficiency
• Impaired enterohepatic circulation

Causes

Due to infective agents HIV related malabsorption Traveller's diarrhoea Parasites e.g. Giardia lamblia, fish tape worm (B12 malabsorption); roundworm, hookworm (Ancylostoma duodenale and Necator americanus) Tropical sprue Whipple's disease Intestinal tuberculosis

Due to structural defects Blind loops Inflammatory bowel diseases, as in Crohn's Disease Fistulae, diverticulae and strictures Infiltrative conditions such as amyloidosis, lymphoma, eosinophilic gastroenteritis Radiation enteritis Systemic sclerosis and collagen vascular diseases Short bowel syndrome

Due to surgical structural changes Gastrectomy; Vagotomy Bariatric surgery (Weight loss surgery)

Due to mucosal abnormality Coeliac disease Cows' milk intolerance Soya milk intolerance Fructose malabsorption

Due to enzyme deficiencies Lactase deficiency inducing lactose intolerance (constitutional, secondary or rarely congenital) Sucrose intolerance Intestinal disaccharidase deficiency Intestinal enteropeptidase deficiency

Due to digestive failure Pancreatic insufficiencies: Cystic fibrosis Chronic pancreatitis Carcinoma of pancreas Zollinger-Ellison syndrome Bile acid/Bile salt malabsorption Terminal ileal disease such as Crohn's disease Obstructive jaundice Bacterial overgrowth Primary bile acid diarrhea

Due to other systemic diseases affecting GI tract Coeliac disease Hypothyroidism and hyperthyroidism Addison's disease Diabetes mellitus Hyperparathyroidism and Hypoparathyroidism Carcinoid syndrome Malnutrition Fiber Deficiency Abeta-lipoproteinaemia

Clinical features

Small intestine : major site of absorption

They can occur in a variety of ways and features might give a clue to the underlying condition. Symptoms can be intestinal or extra-intestinal - the former predominates in severe malabsorption.

• Diarrhoea, often steatorrhoea, is the most common feature. Watery, diurnal and nocturnal, bulky, frequent stools are the clinical hallmark of overt malabsorption. It is due to impaired water, carbohydrate and electrolyte absorption or irritation from unabsorbed fatty acid. Latter also results in bloating, flatulence and abdominal discomfort. Cramping pain usually suggests obstructive intestinal segment e.g. in Crohn's disease, especially if it persists after defecation.
• Weight loss can be significant despite increased oral intake of nutrients.
• Growth retardation, failure to thrive, delayed puberty in children
• Swelling or oedema from loss of protein
• Anaemias, commonly from vitamin B₁₂, folic acid and iron deficiency presenting as fatigue and weakness.
• Muscle cramp from decreased vitamin D, calcium absorption. Also lead to osteomalacia and osteoporosis
• Bleeding tendencies from vitamin K and other coagulation factor deficiencies.

Diagnosis

There is no single, specific test for malabsorption. As for most medical conditions, investigation is guided by symptoms and signs. A range of different conditions can produce malabsorption and it is necessary to look for each of these specifically. Many tests have been advocated, and some, such as tests for pancreatic function are complex, vary between centers and have not been widely adopted. However, better tests have become available with greater ease of use, better sensitivity and specificity for the causative conditions. Tests are also needed to detect the systemic effects of deficiency of the malabsorbed nutrients (such as anaemia with vitamin B12 malabsorption).

Blood tests

• Routine blood tests may reveal anaemia, high CRP or low albumin; which shows a high correlation for the presence of an organic disease. In this setting, microcytic anaemia usually implies iron deficiency and macrocytosis can be caused by impaired folic acid or B12 absorption or both. Low cholesterol or triglyceride may give a clue toward fat malabsorption. Low calcium and phosphate may give a clue toward osteomalacia from low vitamin D.
• Specific vitamins like vitamin D or micro nutrient like zinc levels can be checked. Fat soluble vitamins (A, D, E & K) are affected in fat malabsorption. Prolonged prothrombin time can be caused by vitamin K deficiency.
• Serological studies. Specific tests are carried out to determine the underlying cause.

IgA Anti-transglutaminase antibodies or IgA Anti-endomysial antibodies for Coeliac disease (gluten sensitive enteropathy).

Stool studies

• Microscopy is particularly useful in diarrhoea, may show protozoa like Giardia, ova, cyst and other infective agents.
• Fecal fat study to diagnose steatorrhoea is rarely performed nowadays.
• Low fecal pancreatic elastase is indicative of pancreatic insufficiency. Chymotrypsin and pancreolauryl can be assessed as well

Radiological studies

• Barium follow through is useful in delineating small intestinal anatomy. Barium enema may be undertaken to see colonic or ileal lesions.
• CT abdomen is useful in ruling out structural abnormality, done in pancreatic protocol when visualising pancreas.
• Magnetic resonance cholangiopancreatography (MRCP) to complement or as an alternative to ERCP.

Interventional studies

Biopsy of small bowel showing coeliac disease manifested by blunting of villi, crypt hyperplasia, and lymphocyte infiltration of crypts.

• OGD to detect duodenal pathology and obtain D2 biopsy (for coeliac disease, tropical sprue, Whipple's disease, abetalipoproteinaemia etc.)
• Enteroscopy for enteropathy and jejunal aspirate and culture for bacterial overgrowth
• Capsule Endoscopy is able to visualise the whole small intestine and is occasionally useful.
• Colonoscopy is necessary in colonic and ileal disease.
• ERCP will show pancreatic and biliary structural abnormalities.

Other investigations

• ⁷⁵SeHCAT test to diagnose bile acid malabsorption in ileal disease or primary bile acid diarrhea.
• Glucose hydrogen breath test for bacterial overgrowth
• Lactose hydrogen breath test for lactose intolerance
• Sugar probes or ⁵¹Cr-EDTA to determine intestinal permeability.

Obsolete tests no longer used clinically

• D-xylose absorption test for mucosal disease or bacterial overgrowth. Normal in pancreatic insufficiency.
• Bile salt breath test (¹⁴C-glycocholate) to determine bile salt malabsorption.
• Schilling test to establish cause of B₁₂ deficiency.

Management

Treatment is directed largely towards management of underlying cause:

• Replacement of nutrients, electrolytes and fluid may be necessary. In severe deficiency, hospital admission may be required for nutritional support and detailed advice from dietitians. Use of enteral nutrition by naso-gastric or other feeding tubes may be able to provide sufficient nutritional supplementation. Tube placement may also be done by percutaneous endoscopic gastrostomy, or surgical jejunostomy. In patients whose intestinal absorptive surface is severely limited from disease or surgery, long term total parenteral nutrition may be needed.
• 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 to treat Small Bowel Bacterial overgrowth.
• Cholestyramine or other bile acid sequestrants will help reducing diarrhoea in bile acid malabsorption.

See also

• Fructose malabsorption
• Protein losing enteropathy

External links

• Practice guideline from World Gastroenterology Organisation
• Tests for malabsorption; from British Society for Gastroenterology