Crohns' disease is a chronic inflammation that can involve any part of the gastrointestinal system from the mouth to the anus. In the small intestine, Crohns' disease typically affects the ileum; however, other parts of the small intestine can be affected. It produces a segmental, full-thickness inflammation, with formation of fissures and abscesses, fistulas, and fibrotic stenoses, and it may follow a chronic relapsing course. The cause of Crohns' disease is unknown, although several hypotheses such as infections (mycobacteria, chlamydia, and viruses) have been put forward. The discovery of susceptibility gene variants in NOD2/CARD-15 suggests predisposition to the disease by abnormalities of the intra-cellular sensors of bacterial lipopolysaccharide and their effect on the caspase and nuclear factor-^B signalling pathways and macrophage function.
The inflammation of Crohns' disease can be treated by the use of defined formula artificial feeds or by the use of drugs, including aminosalicylates, antibiotics, steroids, and immunosuppressives such as azathioprine/mercaptopurine, methotrexate, and infliximab. There is evidence that improving nutritional status alone will reduce Crohns' disease activity. If these measures fail to control the disease, then surgical resections of the diseased segment may be necessary.
Crohns' disease presents an important model for the role of nutritional management in small bowel disease. Nutritional treatment of Crohns' disease may use defined formula feeds to reduce inflammation or may seek to correct nutritional deficiency consequent on reduced food intake (loss of appetite, nausea, abdominal pain, or diarrhea), malabsorption, or the changes in protein and energy metabolism that occur secondary to inflammation. It therefore seeks to:
• maintain adequate nutrition and correct any nutritional deficiencies;
• reduce disease activity;
• maintain nutrition against the background of intestinal failure or short bowel syndrome on a long-term basis; and
• treat or prevent growth failure (consequent on nutritional deficiency and inflammation combined) in children.
A wide range of nutritional deficiencies can arise in patients with Crohns' disease of the small bowel that result in defects in wound healing, increased susceptibility to infection, and specific nutrient deficiency syndromes. Patients become anemic from intestinal bleeding; inadequate iron, folate, and B12 intake; failure to absorb iron in the duodenum or B12 in the ileum; or because of impaired folate absorption. Vitamin B12 can be given by injections to avoid the problem of absorption, folic acid by mouth, and iron orally or, if necessary, by injection. Trace elements and vitamins that are deficient during relapses include zinc, ascorbic acid, calcium, and the fat-soluble vitamins. Osteomalacia, rickets, and osteoporosis may occur due to steroid treatment or malabsorption of calcium and vitamin D. Zinc deficiency can cause mouth and skin problems and results from loss of zinc in watery diarrhea.
Chemically defined artificial liquid diets can achieve induction of remission, although the response rate is slightly less than that achieved with steroids. They are particularly beneficial in children with growth failure or in patients with steroid-resistant disease.
Enteral nutrition is preferred to parenteral nutrition, but parenteral (intravenous) nutrition may be life-saving in patients with short bowel syndrome following multiple resections for Crohns' disease or in patients with treatment-resistant Crohns' disease, and it may have a place in supporting malnourished patients at the time of surgery.
Patients with Crohns' disease tend to self-select low-fiber containing foods and often feel bloated after eating foods high in non-starch polysacchar-ides. Exclusion diets have been tried with some success in Crohns' disease, often following initial treatment with liquid feeds, but there seems to be little consistency between which foods' exclusion benefits different patients. Some patients develop malabsorption of milk sugar (lactose) and a small minority are said to be intolerant of milk protein. Other diets such as yeast exclusion have their advocates but there is little evidence for consistent benefit. Dietary fat reduction should not usually be recommended in underweight patients because the body gains nine calories for each gram of fat eaten, whereas nonhydrated protein and starch provide four calories each. Milk and milk products provide important, easily assimilable sources of protein, energy, and calcium and their exclusion should not be undertaken lightly.
Intolerance to lactose, the sugar of milk, increases with age. Patients who are lactase deficient (the enzyme required to split lactose into two smaller sugars that can be absorbed) pass unabsorbed lactose into the large bowel with resultant cramps and abdominal distension. Any patient with extensive inflammation in the small bowel, where lactase is located, may develop lactose malabsorption, which improves once the inflammation resolves. Evidence of lactose intolerance should be documented before withdrawal from the diet and calcium supplementation considered. Occasionally, a lactose breath test is required to detect lactase deficiency. Some patients with lactose intolerance who still wish to take milk can have lactase enzyme added to the milk or use lactase tablets that can be eaten prior to or while eating foods rich in lactose. Patients can eat aged cheese (reduced lactose content) or yoghurt made with live bacterial culture.
Patients with narrowing of the bowel (strictures) should consider a low-fiber diet to reduce the risk of intestinal obstruction. A low-fiber diet may be deficient in folic acid, ascorbic acid, calcium, and some B vitamins, and these can be supplemented.
Patients with small bowel Crohns' disease with resections may have diarrhea resulting from fat malabsorption (steatorrhea) and may have to restrict their fat intake from 100 to 70 g of fat. If steator-rhea still occurs, medium-chain triglycerides (6-10 carbon atoms) should be substituted for the normal fat diet because these are absorbed directly into the portal system. Oil, powders, or emulsions containing medium-chain triglycerides can be added to food or used in cooking and baking.
Patients with ileal resections due to Crohns' disease are susceptible to calcium oxalate kidney stones. These patients should have a low oxalate diet, modest dietary fat restriction, and dietary supplementation of calcium.
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