Ulcerative colitis (UC) and Crohn’s disease (CD) are chronic inflammatory conditions of the GI tract. UC was described 150 years ago in 1859 by Wilks and CD was first described by Crohn in 1932. Both are painful, debilitating conditions that follow a relapsing–remitting pattern. Despite decades of research, we cannot yet define the exact cause of either form of IBD. Current opinion favours a complex aetiology that predominantly involves genes and the gut microbiology, though other environmental risk factors, including the presence or absence of smoking in CD and UC respectively and a stressful lifestyle, are still of consideration in IBD. ¹ It has been postulated that several genetic polymorphisms may contribute to risk of IBD and that these may influence the immune response of the gut to normal microflora. Thus in genetically susceptible individuals, microflora that is normally harmless may induce an abnormal immune response with the production of inflammatory cytokines, including tumour necrosis factor-alfa (TNF-α). ² TNF-α is known to have a major role in the pathogenesis of CD and may have an influence on the permeability of the mucosa to antigens. ¹

While UC only affects the colon, CD may occur at any site in the GI tract and though infrequent, can also affect proximal parts of the GI tract including the mouth. Investigation to establish a diagnosis includes endoscopy and haematological tests of inflammation such as C-reactive protein (CRP). In the colon, it can be difficult to distinguish between CD and UC. In the case of UC, endoscopy of the colon reveals a continuous area of lesion that affects the superficial layers of mucosa with no fistulas and very few or no fissures. ³ In UC the rectum is always affected, unlike CD. ⁴ In CD, inflammation is patchy, often described as having a cobblestone appearance. The inflammation is deep, with fissures and fistulas present. Abscesses and strictures occur in advanced disease. Granulomas, a collection of monocyte/macrophage cells within the lamina propria, are a reliable feature of CD. ⁵ Active involvement of the ileum occurs in 40% of patients with CD and this is often the feature that differentiates between UC and CD in distal disease. In 25% of patients with CD, the disease is confined to the colon and in 30% the disease is confined to the small intestine. ³ Both conditions may occur at any age in either sex and their incidence is high in early adulthood. The prevalence of IBD in Europe is approximately 50 per 100,000 with little evidence of a recent increase in incidence. There are wide geographic and racial variations in the incidence of IBD, with a particularly high incidence of CD in American and European Jewish populations while the incidence in Asia and Africa is low. ⁶

Diarrhoea, abdominal pain and weight loss are the most frequent presenting symptoms of CD. Loss of blood in stools is a feature of UC and may be severe. Blood loss occurs less frequently in CD unless there is active involvement of the colon. Poor oral intake is often regarded as the most likely cause of weight loss and malnutrition in IBD, occurring in up to 80% of patients with CD. ³ The cause of malnutrition in active CD includes inflammation leading to malabsorption and diarrhoea. Inflammation reduces the available surface area for absorption of fluid and nutrients and there is decreased hydrolysis of disaccharides, including lactose which may lead to lactose intolerance.

Active inflammation of the terminal ileum decreases the availability of bile salts for recycling via the liver leading to steatorrhoea and reduced absorption of triglycerides and fat soluble vitamins. Inflammation of the terminal ileum also reduces the absorption of vitamin B ₁₂ leading to macrocytic anaemia. Abdominal cramps and diarrhoea reduce appetite and there may be associated nausea and vomiting. In both CD and UC patients may associate abdominal pain and diarrhoea with consumption of specific food and so food avoidance may contribute to weight loss and malnutrition. This is of particular concern when food avoidance occurs without dietetic support. Hypoproteinaemia, subclinical serum levels of vitamin A, D, K, C and B group, may occur and low serum levels of minerals such as iron, zinc, magnesium and selenium all contribute to poor wound healing and reduced immune-competence, thus increasing the risk of infection. ^7,8

Both microcytic and macrocytic anaemia are common in CD, related to a combination of poor oral intake, bleeding from the inflamed mucosa and malabsorption of iron, vitamin B ₁₂ and folate. A recent Canadian study found subclinical iron deficiency anaemia in 40% of subjects while only 13% had a poor oral intake. ⁹ The side effects of drug treatment of IBD with sulfasalazine and methotrexate can compound macrocytic anaemia caused by poor absorption of folate (see Chapter 6, Drug–Nutrient Interactions).

There is no standard system to define the severity of disease in IBD and a variety of activity indices are in use. The European Crohn’s and Colitis Organisation (ECCO) defines the severity of Crohn’s disease in terms of the Crohn’s disease activity index (CDAI). ⁵

In mild disease, with a CDAI of 150–200, there is < 10% weight loss, with no obstruction, fever, dehydration, abdominal mass or tenderness. The acute phase protein CRP activity may be increased above normal. In moderate disease with a CDAI of 220–450, weight loss may be > 10%, with vomiting. There is no obstruction but CRP is raised above normal.

In severe disease with a CDAI > 450, there may be either advanced cachexia with a BMI < 18 or evidence of obstruction or abscess. Symptoms are persistent and CRP is raised. In contrast, during a period of remission the activity index is usually taken to be < 150. ⁵

The extent of weight loss is related to disease activity. The degree of inflammation influences the acute phase stress response, provoking an elevated resting metabolic rate and increased energy requirement. Simultaneously, abdominal pain, diarrhoea and poor appetite conspire to reduce oral intake, increasing risk of weight loss.

The acute phase response may also inhibit the production of nutrient transport proteins in the mucosa and this may indirectly reduce the absorption of nutrients from the gut and influence the immune competence of the gut mucosa. For example, a reduced circulating level of retinol binding protein is related to the acute phase response in CD. ⁷ In a recent nutritional assessment of patients with IBD, low serum carotene levels were reported in 23% of subjects and there was an inadequate intake of vitamin A in 26% of subjects. ⁹ Deficiency of vitamin A is known to impair mucosal function in the GI tract through loss of microvilli and through loss of mucin and goblet cells. ⁸ This leads to an impaired immune response to pathogens and antigens.

When IBD affects the colon, more so than the small intestine, the immune response may not only be confined to the GI tract. Systemic features of inflammation thought to be related to the activity of proinflammatory cytokines may present. These include arthritis, skin ulceration, inflammation of the eye and hepatitis. The influence of proinflammatory cytokines on bone metabolism may increase risk of osteoporosis. ⁷ Malabsorption of calcium and 25-hydroxycholecalciferol (vitamin D) from the small intestine may also contribute to an increased risk of osteoporosis, compounded by poor dietary intake of calcium and treatment with corticosteroids. ^9,10

The management of Crohn’s disease requires a coordinated multidisciplinary team (MDT) approach including medical, dietetic, nursing and pharmacology practitioners in tandem with the patient. The disease activity, site and extraintestinal symptoms influence the choice of clinical treatment. The aim of treatment in CD is to reduce inflammation, induce remission and maintain optimal nutritional status. The role of the dietitian as part of the MDT is to assess and monitor nutritional status, to promote nutritional support as an important adjunct to pharmacological treatment, to improve or maintain nutritional status and where indicated, to facilitate nutritional support as a primary therapy in CD.

In mild CD the corticosteroid budesonide is the preferred pharmacological treatment, achieving remission in 51–60% over 8–10 weeks. Antibiotics are not recommended in mild disease due to side effects that include nausea, metallic taste and polyneuropathy. ¹⁰ Prednisolone is very effective and the preferred corticosteroid for moderately active ileocaecal CD, but is associated with more side effects than budesonide. ¹⁰

Extensive disease, affecting more than 100 cm of the small intestine, has a severe impact on nutritional status and so medical treatment involves both corticosteroids and immunomodulators to reduce inflammation and so limit the debilitating consequences of disease on nutritional status. Prednisolone or intravenous hydrocortisone is the initial treatment of choice for severely active ileocaecal CD. Following this, the thiopurine immunomodulators, azathioprine or mercaptopurine, are effective at maintaining remission. However, the side effects of thiopurines include bone marrow toxicity and hepatitis and so blood count and liver function must be monitored every 2–3 months. ⁴

When severe ileocaecal disease is resistant to medical treatment, surgery may be considered as a management strategy¹⁰ (please see Chapter 9, Short Bowel Syndrome). In severe disease that is managed conservatively with medication, the potent anti-inflammatory drug infliximab may be considered. This is a chimeric anti-TNF-α monoclonal antibody that binds with this proinflammatory cytokine. ¹¹ Despite the risk of side effects of antibiotics causing nausea and altered taste acuity, thus reducing food intake, they may be necessary when a fever or abscess is present. ¹⁰

Nutritional support is recommended by the ECCO, in addition to medical treatment, to minimise deterioration in nutritional status due to disease and also prior to surgical intervention to reduce the nutritional risk associated with short bowel syndrome. ¹⁰

ECCO recommend that we distinguish between:

The use of liquid diets for nutritional support, as a primary therapy in CD to induce remission, is a well-established treatment. It was introduced during the 1970s to help manage active disease and it may be the treatment of choice for some patients as it reduces exposure to the harmful effect of corticosteroid treatment. ¹² Studies have compared the efficacy of elemental, semi-elemental and whole protein liquid preparations to both induce and maintain remission and there is no clear evidence of benefit of one over the other. ¹³ While the exact nature of the action of nutritional therapy is unclear, its efficacy is thought to transcend improvement in nutritional status and gut rest. It has been suggested that nutritional therapy may influence the inflammatory response of the gut and have a direct immunomodulatory effect by influencing the production of cytokines that act on the microflora of the gut. ²

A recent Cochrane systematic review suggests that the corticosteroid prednisolone is a more effective treatment for inducing remission than nutritional therapy. ¹⁴ For this reason ECCO does not recommend nutrition as a primary therapy in CD, other than in mild disease or in patients who decline drug therapy. They recommend that nutritional therapy is not appropriate as a sole therapy for inducing remission in corticosteroid refractory or corticosteroid-dependent disease, but it may be taken as an adjunct to improve nutritional status. ¹⁰

However, in a recent review of the use of liquid diets in CD, it is argued that if clinical trials were to take account of the issue of compliance, liquid diets would be as effective a means of inducing remission as corticosteroids. It was identified that the ECCO guidance excludes patients with active disease who may benefit from it and discourages consideration of nutritional therapy by gastroenterologists, especially as clinics tend to have poor dietetic support. ¹⁵ Many patients do not complete treatment due to a dislike of the taste of products, taste fatigue, boredom on liquid diets or poor support and lack of regular dietetic contact. However, in patients who do comply and complete the treatment, the remission rate in studies has been shown to be as high as 85%. ¹⁵

When it is decided to offer a patient nutritional therapy to induce remission as a primary treatment, practical considerations include:

On the basis of taste, whole protein formulas such as Modulen IBD (Nestlé) or Alicalm (Nutricia) are usually the liquid treatments of choice and preferred if taken orally. Semi-elemental products, such as Elemental 028 (SHS International), may be best tolerated if taken via the nasogastric route. The quantity of feed and total fluid should aim to provide adequate energy, nitrogen and micronutrient requirements to maintain nutritional status and fluid balance.

Oral liquid feeds can be introduced and managed in the outpatient setting; otherwise a short admission period is required to establish nasogastric feeding. Not surprisingly, tiredness, hunger, diarrhoea and weight loss are frequently experienced and may limit compliance. ¹⁶ If nutritional therapy is tolerated with good compliance there are usually signs of improvement in symptoms within 2 weeks and remission is achieved within 4 weeks.

Protocols for return to normal eating vary between gastroenterology units and for many years have been based on the possibility that specific foods may have a precipitating role in the aetiology of CD. While there is no evidence that food intolerance per se is a causative agent in CD, an elimination diet has been shown to be effective in prolonging remission, relative to treatment with steroids. ¹² The LOFFLEX diet is a well-established low fat, low fibre diet based on a modified elimination regimen. ¹⁷ This includes foods normally well tolerated in CD, such as rice, potato, chicken and fish for up to 4 weeks. The addition of supplementary nutritional sip feeds ensure nutritional adequacy. Other foods are then introduced at 4-day intervals over a period of 3–4 weeks until a full normal diet is resumed.

While the mode of action of the LOFFLEX regime is not known, it has been found to be as effective as an elimination diet in maintaining remission in CD. In a recent Cochrane review of enteral nutrition for the maintenance of remission in Crohn’s disease, two small studies were evaluated. ¹³ In one Japanese study, 26 subjects received half of their nutritional requirements by normal diet and half by nutritional support, in comparison to the control group of 25 subjects who followed a normal diet. After almost 12 months only 9 subjects receiving nutritional support had relapsed (35%), compared to 16 on full normal diet (64%). The second study undertaken in the UK evaluated 33 adults with CD who received their energy and nutritional requirements as 35–50% normal diet, supplemented with either a semi-elemental sip feed or whole protein sip feed. This study found no difference in relapse rate between the two sip feeds. However, it did not compare them to normal diet alone. The Cochrane review concludes that these studies suggest that supplementary enteral nutrition with either semi-elemental or whole protein formula may be effective for maintaining remission in CD. While the above studies are small and larger trials are needed, this conclusion supports the use of nutritional support for all patients with CD whether experiencing active CD or during remission, to both enhance nutritional status and as an adjunctive primary therapy for CD. It is feasible that the LOFFLEX diet is effective, not because it reduces intake of poorly tolerated food substances during inflammation, such as fibre or because it may eliminate food allergens, but because it encourages the continuation of nutritional support during a further period of 2–4 weeks of remission.

The role of other forms of nutritional therapy has been studied in Crohn’s disease, including the efficacy of omega-3 fatty acids as fish oil capsules (omega-3 therapy) for maintenance of remission, due to their anti-inflammatory properties. The omega-3 fatty acid eicosapentaenoic acid (EPA) may act by reducing the production of the leukotriene B ₄. ¹⁰ A recent Cochrane review of four studies, involving 166 patients, found a non-statistically significant benefit of omega-3 therapy, taken as capsules, for maintenance of remission. The authors conclude that the evidence does not merit recommending the routine use of omega-3 therapy in CD, but taken as enteric coated capsules, is safe and may be an effective adjunct for the maintenance of remission in CD. ¹⁸

The role of probiotics in the management of IBD has been investigated in recent years, in parallel with studies to investigate the role of the gut microflora in IBD. In a recent study of 15 people with CD and 5 with UC, the anti-inflammatory effect of probiotic yoghurt was investigated and the results compared to 20 healthy control subjects. ¹⁹ All subjects consumed probiotic yoghurt for 30 days and a significant increase in protective T cells in the peripheral blood of IBD patients was found and an improved anti-inflammatory profile including a decrease in serum TNF-α. However, it is suggested that further studies are required to confirm the immunosuppressive action of probiotic yoghurt in IBD. Whether prebiotics, in the form of inulin and oligofrucose, have a protective role in inflammatory disease has also been reviewed as they are known to support growth of the colonic bacteria lactobacilli and bifidobacteria, to promote homeostatis of the gut ecosystem. Early clinical trials suggest that these prebiotics may be effective to treat colonic inflammation in CD and UC. ²⁰

The management of UC also requires a coordinated multidisciplinary approach in tandem with the patient, including medical, dietetic, nursing and pharmacology practitioners. The aim of treatment in UC is to reduce inflammation of the colon, induce remission, support the management of bowel function and maintain optimal nutritional status.

In UC the most frequent pharmacological treatment is the anti-inflammatory drug aminosalicylate (5-ASA), indicated for UC of mild to moderate severity and during periods of remission. This drug is available in several forms, as enemas, suppositories or oral form and choice will depend on the site and severity of disease. Though usually well tolerated, a range of side effects from mild, such as headache, to severe, such as renal involvement, necessitates close medical monitoring. ⁴

As with CD, corticosteroids such as prednisolone may be prescribed for more severe disease. Total colitis requires hospital admission and treatment with IV hydrocortisone and oral 5-ASA. Enteral nutrition support and IV fluids are usually required in preference to parenteral nutrition (see Chapters 10 and 11, Enteral Nutrition and Parenteral Nutrition, respectively).

The role of the dietitian as part of the MDT is to assess and monitor nutritional status and to facilitate nutritional support when indicated, to improve or maintain nutritional status. Unlike CD, there is no indication for use of nutritional support as a primary therapy in UC. Weight loss may occur due to chronic abdominal cramp, diarrhoea and poor appetite during periods of relapse and anaemia is common due to poor oral intake and blood loss in stools. Patients should undergo nutritional screening with an appropriate nutritional screening tool, such as MUST, in an outpatient clinic or on admission to hospital and referred for nutritional support, as indicated. ²¹

The rationale for nutritional support in patients at risk of malnutrition is outlined in the 2006 NICE Clinical Guideline 32, Nutrition Support in Adults. ²² This include a review of the physical and psycho-social side effects of malnutrition and the following are of particular relevance in IBD: impaired immune response, impaired wound healing, reduced muscle strength and fatigue, water and electrolyte disturbance, vitamin and mineral deficiencies and impaired psycho-social function. In patients requiring oral nutrition support who are not at risk of re-feeding syndrome, aim to provide:

Unfortunately there is a lack of clinical evidence to underpin the efficacy of nutritional support for management of malnutrition in IBD. A recent Cochrane review, entitled ‘Dietary Advice for Illness-Related Malnutrition in Adults’, included only one study of patients with CD and none with UC. ²³ This report examines dietary advice as food products, oral nutritional supplements or both, in 36 studies involving 2714 people with disease-related malnutrition, often cancer. Pooled results from four studies suggest that dietary supplements are more effective than food advice to improve weight and energy intake. From examination of five studies they report a significantly greater weight gain in groups receiving dietary advice plus supplements than either dietary advice or supplements alone. These were small short-term studies and did not include patients with UC; however, the authors conclude that there is insufficient information to suggest that nutritional intervention should vary according to the underlying condition. ²³

Many patients follow self-imposed dietary restrictions because they associate their symptoms with certain foods. Fruit and vegetables with a high content of dietary fibre may be poorly tolerated and so patients tend to choose a low fibre diet. They often also avoid fried foods and spicy foods. Although lactose intolerance is rare in UC, dairy foods are often perceived to exacerbate symptoms. While maintaining respect for the patient’s view, acceptable alternative sources of calcium and vitamin D should be discussed and encouraged and small quantities of dairy foods included as tolerated. Adequacy of intake of energy, protein, micronutrient and fluid must be considered, as outlined above. ²²

A recent Cochrane report has reviewed studies comparing the use of probiotics in combination with placebo or standard medical treatment (5-ASAs, sulfasalazine or corticosteroids) for induction of remission in ulcerative colitis. ²⁴ A meta-analysis was not performed due to the differences in methodology between the trials considered. The authors conclude that there is limited evidence that probiotics may reduce disease activity in mild to moderate UC when taken with standard treatment, but they do not improve overall remission rates. Their effect in severe UC is unknown. ²³ Larger randomised control trials are required.

Surgery may be indicated in UC if the patient does not respond to treatment as indicated by a raised temperature, falling Hb, potassium and albumen, raised white cell count and bloody diarrhoea, or if toxic dilation of the colon occurs in advanced disease. ¹¹

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