NHD issue 149 Malabsorption

CONDITIONS & DISORDERS

MALABSORPTION 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.

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.

There is 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.

THE STAGES OF DIGESTION

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.

The food we eat is digested in three stages. Table 1 overleaf 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.

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 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 Crohn’s disease, pancreatitis disease, short bowel syndrome and liver disease are highly likely to experience steatorrhea.

Emma Coates Editor Emma has been a Registered Dietitian for 12 years, with experience of adult and paediatric dietetics.

FURTHER READING Visit: www.

NHDmag.com/ malabsorption

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CONDITIONS & DISORDERS Table 1: Stages of digestion and conditions causing malabsorption

Examples of conditions

Luminal

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, eg, pernicious anaemia; Blocked lacteals due to lymphoma or TB.

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.

CARBOHYDRATE DIGESTION

Digestion of carbohydrates and disaccharides 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. Most 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 shortchain fatty acids including butyrate, propionate, acetate and lactate. The gases can be absorbed or 32

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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 shortchain 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

CONDITIONS & DISORDERS Table 2: Micronutrients and malabsorption 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), 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.

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.

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.

PROTEIN DIGESTION

DIAGNOSIS, MANAGEMENT AND TREATMENT

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.

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

There are numerous tests performed to diagnose malabsorption and its underlying causes including: • a detailed patient history; • blood tests to screen for consequences of malabsorption; • stool fat testing to confirm malabsorption (if unclear); • diagnosis via endoscopy, contrast x-rays, or other tests based on findings.

More specific diagnostic tests (eg, upper endoscopy, colonoscopy, barium x-rays) are indicated to diagnose several causes of malabsorption.

When treating a patient who is experiencing malabsorption there are two approaches to consider: 1 Treat the underlying disease, eg, coeliac disease.

2 Provide nutritional support to correct deficiencies, encourage adequate growth in children and prevent weight loss in adults.

For examples of underlying diseases and treatment in malabsorption and for further reading, visit: www.NHDmag.com/malabsorption. www.NHDmag.com November 2019 - Issue 149

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