Gastrointestinal Malabsorption

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Food Allergy and Intolerance written for patients

Gastrointestinal malabsorption is a failure to fully absorb nutrients from the gastrointestinal tract. The digestion and absorption of nutrients within the gastrointestinal tract requires a complex interaction between motor, secretory, digestive and absorptive processes that are vulnerable to various potential disturbances which may lead to global or specific malabsorption syndromes[1].

The outcome is malnutrition. Malnutrition may also be caused by inadequate diet with or without malabsorption. See also the separate Malnutrition article.

Malabsorption, from whatever cause, may be accompanied by:

  • Changes in weight and growth:
  • Gastrointestinal symptoms:
    • Chronic diarrhoea is common. Chronic diarrhoea may be defined as the abnormal passage of three or more loose or liquid stools per day for more than four weeks and/or a daily stool weight greater than 200 g/day.
    • Steatorrhoea is often present. There is excessive fat in the stools and they become pale, bulky and offensive in smell. Stools float and are difficult to flush away. They often leave a greasy rim around the pan.
  • Family history:
    • Some diseases associated with malabsorption are found more frequently in families - eg, coeliac disease, Crohn's disease, cystic fibrosis and disaccharidase deficiencies (lactase). It is therefore important to explore the family history carefully.
  • Signs of deficiencies may be apparent. There may be:
    • Non-anaemic iron deficiency.
    • Iron-deficiency anaemia.
    • Folate deficiency or vitamin B12 deficiency.
    • Bleeding, resulting from low vitamin K.
    • Oedema, which occurs in protein/calorie malnutrition.

There may also be clinical features associated with the particular cause of malabsorption. The most common causes in the UK are coeliac disease, Crohn's disease and chronic pancreatitis.

However the malabsorption of simple carbohydrates is the most common type of non-immune-mediated food intolerance, affecting 20-30% of the European population[2].

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Mucosal causes

  • Coeliac disease usually presents in childhood but can present later. It is due to allergy to gluten in the diet that results in subtotal villous atrophy. This considerably reduces the surface area available for absorption. A diet strictly free of gluten will reverse the process. Nowadays, about one child in four with coeliac disease is diagnosed by targeted screening rather than presenting with malabsorption[3].
  • Lactose intolerance.
  • Cow's milk protein allergy.
  • Soya milk intolerance.
  • Fructose intolerance and malabsorption: simultaneous consumption of glucose reduces fructose malabsorption[4].
  • Infection:
  • In patients with an inflammatory bowel disorder and malabsorption, an immune deficiency, including HIV enteropathy, should be considered[5, 6].
  • Intestinal lymphangiectasia and other causes of lymphatic obstruction include lymphoma, tuberculosis and cardiac disease.

Intraluminal causes

Structural causes

Causes outside the gut

In the elderly, causes of malabsorption are as in the young but pancreatic insufficiency can occur without obvious cause and intestinal overgrowth can occur without anatomical abnormality of the bowel[8].

The World Gastroenterology Organisation has produced guidelines for the investigation of malabsorption[9].

Blood tests

  • FBC.
  • Plasma viscosity, ESR, CRP.
  • Vitamin B12 level.
  • Red cell folate.
  • Iron status (usually ferritin but can be iron and iron-binding capacity).
  • Clotting screen for vitamin K deficiency.
  • Serum albumin.
  • Calcium (corrected for albumin level).
  • Anti-endomysial, anti-reticulin and alpha-gliadin antibodies (coeliac screen).
  • LFTs.
  • Serum magnesium.

Iron deficiency causes a microcytic blood picture. Folate or vitamin B12 deficiency causes megaloblastic anaemia but the picture may be mixed.

Patients with unexplained iron deficiency merit screening for coeliac disease[10].


  • Faecal microbiological assessments may be indicated.
  • Sudan stain for fat globules.
  • Tests for secretory function - eg, elastase or chymotrypsin in stool.

Imaging and endoscopy

  • Abdominal ultrasound (gallbladder, liver, pancreas, intestinal wall, adenopathy).
  • Barium follow-through may show structural abnormalities.
  • Ileocolonoscopy including biopsies of colon and ileum.
  • CT; MRI of pancreatic duct-systems or endoscopic retrograde cholangiopancreatography (ERCP).

Breath hydrogen tests

Take samples of end-expired air; give glucose; take more samples at half-hourly intervals. If there is bacterial overgrowth there is an increase in exhaled hydrogen one hour after ingestion.

Nutritional support may be required.

Management otherwise depends upon the cause. For example:

  • Coeliac disease requires a strict gluten-free diet.
  • Pancreatic insufficiency requires the oral administration of enzymes with food.
  • Blockage of the flow of bile requires surgery.
  • Crohn's disease usually responds to steroids.
  • Blind loop syndromes may require further surgery.
  • Where bile salts are not reabsorbed, it may be necessary to give resins to bind them[11].
  • If there is folate deficiency and possibly B12 deficiency too, it is imperative to give an injection of vitamin B12 before starting folate supplementation. Otherwise, there is a risk of precipitating subacute combined degeneration of the cord.

Complications are related to the underlying disease.

Before it was superseded by endoscopy, small bowel biopsy was performed with the Crosby capsule: this is swallowed on the end of a tube and is monitored by X-ray screening until it reaches the jejunum. It is fired by suction, and a biopsy is caught in its jaws. It is then pulled back up.

Further reading & references

  1. Keller J, Layer P; The Pathophysiology of Malabsorption. Viszeralmedizin. 2014 Jun;30(3):150-4. doi: 10.1159/000364794.
  2. Raithel M, Weidenhiller M, Hagel AF, et al; The malabsorption of commonly occurring mono and disaccharides: levels of investigation and differential diagnoses. Dtsch Arztebl Int. 2013 Nov 15;110(46):775-82. doi: 10.3238/arztebl.2013.0775.
  3. Ravikumara M, Tuthill DP, Jenkins HR; The changing clinical presentation of coeliac disease. Arch Dis Child. 2006 Dec;91(12):969-71. Epub 2006 Aug 3.
  4. Latulippe ME, Skoog SM; Fructose malabsorption and intolerance: effects of fructose with and without simultaneous glucose ingestion. Crit Rev Food Sci Nutr. 2011 Aug;51(7):583-92. doi: 10.1080/10408398.2011.566646.
  5. Agarwal S, Mayer L; Gastrointestinal manifestations in primary immune disorders. Inflamm Bowel Dis. 2010 Apr;16(4):703-11. doi: 10.1002/ibd.21040.
  6. Murray JA, Rubio-Tapia A; Diarrhoea due to small bowel diseases. Best Pract Res Clin Gastroenterol. 2012 Oct;26(5):581-600. doi: 10.1016/j.bpg.2012.11.013.
  7. Hackert T, Schutte K, Malfertheiner P; The Pancreas: Causes for Malabsorption. Viszeralmedizin. 2014 Jun;30(3):190-7. doi: 10.1159/000363778.
  8. Schiller LR; Diarrhea and malabsorption in the elderly. Gastroenterol Clin North Am. 2009 Sep;38(3):481-502. doi: 10.1016/j.gtc.2009.06.008.
  9. Malabsorption Practice Guideline, World Gastroenterology Organisation (Feb 2012)
  10. Zamani F, Mohamadnejad M, Shakeri R, et al; Gluten sensitive enteropathy in patients with iron deficiency anemia of unknown origin. World J Gastroenterol. 2008 Dec 28;14(48):7381-5.
  11. Johnston I, Nolan J, Pattni SS, et al; New insights into bile acid malabsorption. Curr Gastroenterol Rep. 2011 Oct;13(5):418-25. doi: 10.1007/s11894-011-0219-3.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but makes no warranty as to its accuracy. Consult a doctor or other healthcare professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Richard Draper
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Document ID:
2183 (v24)
Last Checked:
Next Review:

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