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What is malabsorption?

A wide range of conditions can cause impaired digestion and the malabsorption of nutrients in infants and children1. The management and nutritional support required varies by aetiology, condition and severity2. Learn more about the causes, effects and treatments for malabsorption with this summary of recent evidence.

Understanding malabsorption

Malabsorption is a broad term covering a wide range of conditions that cause impaired digestion and absorption of nutrients1. It may affect the absorption of one or more nutrients by the small intestine, and result in malnutrition if untreated3. Symptoms may include chronic diarrhoea, abdominal distension and pain, flatulence and weight loss1.

 

 

Nutritional support is often required to manage malabsorption2

When and where does malabsorption occur?

Malabsorption can happen at any of the three stages of digestion2.

Table 1: The three stages of digestion2.

1. Luminal 2. Mucosal 3. Postabsorptive
Stomach acids, pancreatic enzymes and bile from the liver break down proteins, fats, and carbohydrates. At this stage micronutrients are released from the food. At the brush border within the small intestinal epithelial cells, the nutrients are absorbed from the intestinal lumen. Once absorbed, the nutrients are transported throughout the body via the circulatory and lymphatic systems to be utilised or stored.

(Taken from Network Health Digest (NHD), Malabsorption: An Overview by Emma Coates, Volume 7. 13 – 3rd August 2017)

Malabsorption of different nutrients1

Malabsorption affects both macro and micronutrient absorption2.

Carbohydrate malabsorption may result from mucosal damage, short bowel syndrome or congenital intestinal enzyme or transport deficiencies4. Damage caused to the intestinal mucosa can lead to brush border enzyme deficiencies such as sucrase-isomaltase, lactase and glucoamylase – present on the villous tips in the jejunum and most of the ileum.

Protein malabsorption alone is rare. Protein digestion survives in most conditions except in cystic fibrosis and intestinal damage can cause protein-losing enteropathy in the gut1,4.

Fat malabsorption alone is uncommon. It is usually associated with protein and carbohydrate malabsorption. Steatorrhoea may occur: the excessive passage of fat in the faeces. Fat-soluble vitamin A, D, E and K deficiency often co-exists1-4.

Table 2: Effects of micronutrient malabsorption2. 

Anaemias

 

Iron deficiency anaemia – often a manifestation of coeliac disease.

Microcytic (iron deficiency) or macrocytic (vitamin B12 deficiency).

Crohn’s disease or ileal resection – can cause megaloblastic anaemia due to vitamin B12 deficiency.

Clotting disorders

 

Vitamin K malabsorption and subsequent hypoprothrombinemia – can lead to complications in blood clotting.

Bone complications

 

Vitamin D deficiency – may lead to osteopenia or osteomalacia. Easy fracture of bones and bone pain.

Secondary hyperparathyroidism – can be caused by the malabsorption of calcium.

Neurological presentations

 

Malabsorption of vitamins B5 (pantothenic acid) and D – can cause generalised motor weakness.

Peripheral neuropathy due to B1 (thiamine), B6 (pyridoxine) and B12 (cobalamin) malabsorption.

Other complications can include night blindness (vitamin A) and seizures (biotin). Loss of sensations such as vibration and position may be due to B12 (cobalamin) deficiency. B12 deficiency also causes breathlessness and fatigue.

Hypocalcemia and hypomagnesemia, due to electrolyte malabsorption – can lead to tetany.

(Taken from Network Health Digest (NHD), Malabsorption: An Overview by Emma Coates, Volume 7. 13 – 3rd August 2017)

Diseases, conditions and treatments

Malabsorption may be the consequence of five main problems3: small intestinal mucosal damage (enteropathy) or short bowel syndrome (congenital or acquired); defects of specific hydrolysis; defects of transport; exocrine pancreatic insufficiency; or reduced biliary secretion.

Table 3: Underlying diseases and treatment in malabsorption2.

Cause Treatment
Coeliac disease

Gluten-free diet +/- vitamin and mineral supplementation, e.g. calcium, iron.

Secondary lactose intolerance may occur and can be addressed with a temporary exclusion diet.

Lactose intolerance

 

Lactose exclusion diet with appropriate dairy replacements, e.g. lactose-free baby formulas in infants, suitable dairy alternatives and weaning advice for young babies.

Appropriate calorie and calcium intake should be monitored across the life span.

Pancreatic insufficiency, 
e.g. in cystic fibrosis (CF)
or pancreatic cancer

Protease and/or lipase replacement therapy. Advice and guidance regarding their use and dietary considerations should be provided. High calorie supplements may be required.

In CF patients, fat-soluble vitamins are routinely prescribed.

Enteral nutritional support is sometimes required.

Inflammatory bowel disease, e.g. Crohn’s disease, ulcerative colitis or pouchitis

 

 

Elemental feeds or liquid diets may be used to promote bowel rest and remission, administered orally or via enteral feeds.

Vitamin and mineral supplementation may be necessary, e.g. regular vitamin B12 injections and iron supplementation.

Corticosteroids and/or anti-inflammatory agents, such as mesalamine. Immunosuppressants, e.g. Azathioprine and Infliximab.

Probiotics may be considered, but there is limited evidence for their use; however, they may be useful in the management of pouchitis and ulcerative colitis.

Short bowel syndrome

 

If there has been extensive intestinal disease or resection, parenteral nutrition may be necessary.

High calorie supplements may be useful for some patients along with vitamin and mineral supplements, e.g. fat soluble vitamins, electrolytes, B12, iron.Antibiotics may be prescribed for bacterial overgrowth.

Liver disease, e.g. biliary atresia

 

Medium-chain triglycerides (MCT)-based feeds and oil may be used in patients experiencing poor weight gain as a consequence of fat malabsorption. MCTs are more easily absorbed and don’t require the body’s usual process for fat metabolism, e.g. micelle formation is not required for absorption and they are transported via the portal route rather than via the lymphatic system.

Fat-soluble vitamin supplements are required for patients with fat malabsorption.

Oral and/or enteral nutritional support may be required.

(Taken from Network Health Digest (NHD), Malabsorption: An Overview by Emma Coates, Volume 7. 13 – 3rd August 2017)

Diagnosis and management of malabsorption

Malabsorption is diagnosed through an array of tests – the estimation of full blood count, erythrocyte sedimentation rate, haematinics in the form of folate, B12 and iron status and serum albumin with serum calcium, phosphate and magnesium is routine5. When managing malabsorption there are two approaches to consider2:

  1. Treat the underlying disease.
  2. Provide nutritional support to encourage adequate growth and correct deficiencies.

Aptamil Pepti-Junior

Aptamil Pepti-Junior – formerly Cow & Gate Pepti-Junior* – is designed to be easy to digest and absorb for cases of malabsorption in infants. It supports growth and maturation of the gut and immune system6, with added long-chain polyunsaturated fatty acids and nucleotides for brain, eye and nervous system development7.

Clinical evidence shows that Aptamil Pepti-Junior is well tolerated by infants with complex gastrointestinal tract intolerances with no major complications observed in long-term usage8. Whey hydrolysates present in Aptamil Pepti-Junior help infants with enteropathy to thrive9. It is suitable as a sole source of nutrition for infants and is specially formulated to:

Enhance digestion and absorption:

– Extensively hydrolysed formula10 for infants and children with malabsorption
– 50% medium chain triglyceride (MCT)

Reduce osmotic load:

– Low osmolality (210 mOsmol/kg H2O)
– Carbohydrate as glucose polymers15

Promote palatability:

– Whey based12-14

*There has been no change to the formulation of this product as a result of the Aptamil rebranding.

  1. Ammoury RF, Croffie JM. Malabsorptive disorders of childhood. Pediatr Rev 2010;31:407.
  2. Coates E. Malabsorption: an overview [Online]. Available at: https://issuu.com/nhpublishingltd/docs/nhd_cpd_earticle_vol_7.13?e=14357770/51776981 [Accessed: November 2017]
  3. Walker-Smith et al. J Pediatr Gastroenterol Nutr 2002;35:S98-105.
  4. Pietzak MM, Thomas DW. Childhood malabsorption. Pediatr Rev 2003;24:195.
  5. British Society of Gastroenterology [Online}. Available at: https://www.bsg.org.uk/pdf_word_docs/malabsorpton.pdf [Accessed: November 2017]
  6. Yu V. J Paediatr Child Health 2002;38:543-9.
  7. Koletzko B et al. J Perinat Med 2008;36:5-14.
  8. Taylor CJ, Jenkins P & Manning D. Clin Nutr 1988;7:183‐90.
  9. Walker‐Smith JA, Digeon B & Phillips AD. Pediatr 1989;149:68‐71.
  10. Keohane PP et al. Gut 1985;26(9):907-13.
  11. Bach AC, Babayan VK. Am J Clin Nutr 1982;36(5):950-62.
  12. Mabin DC et al. Arch Dis Child 1995;73(3):208-10.
  13. Pedrosa M et al. J Investig Allergol Clin Immunol 2006;16(6):351-6.
  14. Miraglia Del Giudice M et al. Ital J Pediatr 2015;41:42.
  15. Shaw V, Lawson M (eds). Clinical Paediatric Dietetics. 4th ed. Oxford: Blackwell Publishing, 2015.