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MALABSORPTION: AN OVERVIEW Emma Coates Registered Dietitian Emma has been a registered dietitian for 10 years, with experience of adult and paediatric dietetics. She specialised in clinical paediatrics for six years, working in the NHS. She has recently moved into industry and currently works as Metabolic Dietitian for Dr Schar UK.

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Malabsorption is the clinical term to describe any defects occurring during the digestion of food and the absorption of nutrients. Depending on the cause, the digestion or absorption of single or multiple nutrients can be affected. In lactose intolerance and the digestion of a single nutrient, lactose, is affected. However, for example, in coeliac disease, the digestion and absorption of several nutrients are affected. There are a wide range of symptoms related to malabsorption, with abdominal discomfort, bloating, flatulence, diarrhoea and weight loss being commonly reported by patients. Nutritional intervention is often required to manage malabsorption, including the use of exclusion diets, nutritional support and use of specialist nutritional products and/or supplements. In some cases, pharmaceutical intervention is also required. The intervention will depend on the definitive cause of the malabsorption. Our bodies require a consistent supply of nutrients to function and maintain themselves. Nutrients are used in many complex pathways in order to produce energy, enzymes, hormones, proteins, cells, tissues and bone and to fight infections. The diet we eat supplies the essential nutrients to complete these vital tasks.

WHERE AND WHEN DOES MALABSORPTION OCCUR?

The food we eat is digested in three stages. Table 1 shows each stage and gives examples of some of the conditions associated with those stages. It is important to understand the mechanism of malabsorption in order to realise the impact it may have on the health of the patient. There are various stages of malabsorption depending on which point it occurs in the normal process of digestion and absorption within the gastrointestinal tract. Disruption of the normal digestive process can lead to malabsorption. The aetiology of the malabsorption will determine the type and severity of the symptoms and deficiencies observed. Also whether the situation is acute or likely to become chronic. FAT DIGESTION

During the luminal stage, long chain triglycerides are split into fatty acids and monoglycerides by lipase and colipase (pancreatic enzymes). They are then

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Table 1: stages of digestion and conditions causing malabsorption Luminal

Examples of conditions

Mucosal

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.

Biliary atresia; Cholestasis; Cystic fibrosis; Lactose intolerance; Cancers including pancreatic cancer, lymphoma or stomach cancer; Pancreatic insufficiency or diseases; Zollinger-Ellison syndrome; Medications that inhibit stomach acid production, such as phenytoin.

Coeliac disease; Inflammatory bowel disease; Radiation enteritis; Decreased intrinsic factor production; Surgery, such as a bowel resection or gastric bypass; Short bowel syndrome; Scleroderma; GI tract infections including viral, bacterial and parasitic infections; Whipple disease; Tropical spruce.

Liver diseases or cancer; Lymphangiectasia; Intrinsic factor deficiency, e.g. pernicious anaemia; Blocked lacteals due to lymphoma or TB.

combined with bile acids and phospholipids, which form micelles. The micelles are transported through the jejunal enterocytes to be reconstituted to make chylomicrons when combined with protein, phospholipids and cholesterol. Chylomicrons are transported via the lymphatic system to ensure fats are utilised or stored. Medium-chain triglycerides (MCTs) are absorbed directly by passively diffusing from the GI tract to the portal system. MCTs do not require any modification for absorption, unlike longer chain fatty acids. There is also no requirement for bile salts in order to digest MCTs. Patients experiencing malabsorption, or particular fatty-acid metabolism disorders, can be treated with MCT as part of their diet or feeds due to the relative ease of MCT digestion by the body. Steatorrhea, defined as excess fat in the stools, is a clear symptom in fat malabsorption. Patients experience pale, bulky and offensive stools, which are difficult to flush away. It is

commonly observed in pancreatic insufficient cystic fibrosis patients when Pancreatic Enzyme Replacement Therapy (PERT) is not effectively managed or taken by the patient. Patients with Crohnâ&#x20AC;&#x2122;s disease, pancreatitis disease, short bowel syndrome and liver disease are highly likely to experience steatorrhea. When fats are unabsorbed, fat-soluble vitamins (A, D, E, K) and possibly some minerals will be trapped within the fatty molecules. This leads to deficiencies, which can be managed by supplementation of the affected nutrients and the use of enzyme replacement therapy, such as lipase replacement in cystic fibrosis and pancreatitis patients. The absorption of fats can be affected by bacterial overgrowth due to the deconjugation and dehydroxylation of bile salts. This has a limiting effect on fat absorption. Diarrhoea occurs due to the unabsorbed bile salts, which stimulate water secretion in the large intestine.

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References 1. Wright C. CN Focus 2012;4(3):17-19. 2. Sharma M et al. Colorectal Disease 2013;15: 885-891. 3. Data on file. 4. Malnutrition Advisory Group (MAG) 2011.Malnutrition Universal Screening Tool. www.bapen.org.uk/pdfs/must/must_full.pdf. Accessed September 2016. *Of those who were at medium or high risk of malnutrition at baseline, 67% were at low risk of malnutrition on study completion.

All information correct at the time of print. December 2016

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Table 2: Micronutrients and malabsorption Iron deficiency anaemia - often a manifestation of coeliac disease. Anaemias

Clotting disorders Bone complications

Microcytic (iron deficiency) or macrocytic (vitamin B12 deficiency). Crohn’s disease or ileal resection - can cause megaloblastic anaemia due to vitamin B12 deficiency. Vitamin K malabsorption and subsequent hypoprothrombinemia - can lead to complications in blood clotting. 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. Malabsorption of vitamins B5 (pantothenic acid) and D - can cause generalised motor weakness

Neurological presentations

Peripheral neuropathy due to B1 (thiamine), B6 (pyridoxine) and B12 (cobalamin) malabsorption. Other complications can include night blindness (vitamin A), 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.

Table 3: Examples of underlying diseases and treatment in malabsorption Disease/condition Coeliac disease

Lactose intolerance

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

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

Short gut syndrome

Liver disease, e.g. biliary atresia

Treatment 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 exclusion diet with appropriate dairy replacements, e.g. lactosefree 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. 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. 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. 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. 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.

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There are various stages of malabsorption depending on which point it occurs in the normal process of digestion and absorption within the gastrointestinal tract.

CARBOHYDRATE DIGESTION

Carbohydrate and disaccharides digestion begins with the pancreatic enzyme, amylase and later the brush border enzymes, maltase, isomaltase, sucrase and lactase which continue to work on breaking down the complex sugars to create monosaccharides. The majority of the newly created monosaccharides are absorbed in the upper small intestine. Unabsorbed carbohydrates are fermented by colonic bacteria to create a variety of waste products, such as carbon dioxide, methane, hydrogen and short chain fatty acids including butyrate, propionate, acetate and lactate. The gases can be absorbed or excreted via breathing or flatulence. However, when malabsorption of carbohydrates occurs, excessive production of gas can cause abdominal distention, discomfort and bloating. Diarrhoea presents when there is an excess of the short chain fatty acids. Lactose intolerance (the appearance of clinical gastrointestinal symptoms after ingestion of lactose) is a common cause of the symptoms described above, with varying degrees of severity and longevity within the condition itself. The various types of lactase deficiency include congenital, primary and secondary lactase deficiency. Primary lactose deficiency occurs as lactase production decreases when the diet becomes less reliant on milk and dairy products. Usually, it presents after the age

of two, but symptoms can take years to present, even into adulthood. Secondary lactase deficiency occurs as a result of a condition or surgery affecting the small intestine. For example, secondary lactose intolerance can occur in the short term after a gastrointestinal infection. A temporary exclusion of lactose from the diet will be required with gradual reintroduction once symptoms are settled and the underlying condition is resolved or stabilised. Congenital lactose intolerance is a rare genetic disorder where little or no lactase is produced. A complete lifelong exclusion of lactose-containing foods and drinks is required in this instance. In primary and secondary lactase deficiency, there may be varying tolerance to lactose, therefore, individual assessment will reveal the level of restriction required. PROTEIN DIGESTION

Protein digestion is initiated by gastric pepsin within the stomach. It also stimulates release of cholecystokinin, which is vital for the secretion of pancreatic enzymes. A brush border enzyme, enterokinase, triggers trypsinogen, the precursor to trypsin. This pathway converts many pancreatic proteases into their active forms. Activated pancreatic enzymes act to hydrolyse proteins into oligopeptides. These are then absorbed directly, or hydrolysed into amino acids.

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When protein is malabsorbed, symptoms such as diarrhoea, abdominal discomfort and bloating may occur. Oedema and ascites are symptoms of severe protein malabsorption. Peripheral oedema is caused by hypoalbuminemia when there has been chronic protein malabsorption, or from loss of protein into the intestinal lumen. Ascites can develop when there are severe protein losses. Protein losses can be caused by extensive obstruction of the lymphatic system, seen in intestinal lymphangiectasia. As faecal nitrogen is difficult to measure, tests to confirm protein malabsorption are rarely performed. MICRONUTRIENT DEFICIENCIES

Malabsorption affects both macro- and micronutrients. Deficiencies of micronutrients can present as a collection or more selectively. Table 2 shows some of the effects caused by micronutrient deficiencies associated with malabsorption.

DIAGNOSIS

There is a vast array of tests performed to diagnose malabsorption and its underlying causes. A good general overview can be found at: British Society of Gastroenterology. Tests for malabsorption which is available at: www.bsg. org.uk/pdf_word_docs/malabsorbtion.pdf MANAGEMENT AND TREATMENT

When treating a patient who is experiencing malabsorption there are two approaches to consider: 1. Treat the underlying disease, e.g. coeliac disease. 2. Provide nutritional support to correct deficiencies, encourage adequate growth in children and prevent weight loss in adults. Table 3 shows just some examples of the under-lying diseases and treatment in malabsorption.

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Questions relating to: Malabsorption: an overview. Type your answers below, download and save or print for your records, or print and complete by hand. Q.1

Explain the aetiology and symptoms of malabsorption.

Q.2

Describe the three stages of digestion.

Q.3

What nutritional interventions are required to manage malabsorption?

Q.4

Explain why Medium-chain triglycerides can be used as treatment for malabsorption in fatty acid metabolism disorders.

Q.5

What are the symptoms of fat malabsorption?

Q.6

Give details of two conditions relating to malabsorption of carbohydrates.

Q.7

Explain the symptoms and conditions of chronic protein malabsorption.

Q.8

What are the two approaches to the management and treatment of malabsorption?

Q.9

Explain the treatment for malabsorption in Inflammatory bowel disease.

Please type additional notes here . . .