The intestinal mucosa is a rapidly proliferative tissue, with a highly dynamic cell population. Its total cellular mass is well controlled and can adapt, with hypo- or hyperplasia, to a wide variety of stimuli. Luminal nutrients, hormonal factors, and pancreatic and biliary secretions have all been implicated in the regulation of intestinal mucosal adaptation. Similarly, the same factors appear essential for the maintenance of exocrine pancreatic structure and function. The polyamines (putrescine, spermidine, and spermine) and the key enzyme controlling their synthesis (ornithine decarboxylase, ODC) are important for many cell growth processes, and may play important roles in intestinal and pancreatic adaptation. During intestinal adaptation in response to jejunectomy, lactation and pancreatico-biliary diversion (PBD), intestinal contents of ODC and polyamines are increased, paralleling increases in mucosal proliferative indices and DNA synthesis. With administration of the specific inhibitor of ODC (difluoromethylornithine, DFMO) the increases in ODC and polyamines are suppressed, and intestinal adaptation is abrogated. In pancreatic hyperplasia induced by caerulein, pancreatic polyamines are increased. With DFMO administration, caerulein-induced increases in pancreatic DNA synthesis were inhibited and pancreatic hypertrophy was partially suppressed. PBD-induced pancreatic hypertrophy, however, was not affected by DFMO. Thus, the role of polyamines in the adaptation of the pancreas, with a relatively quiescent proliferative status, is as yet undefined. It seems clear, however, that the induction of ODC and the resultant increase in polyamine biosynthesis are critical for the normal growth and especially for adaptive hyperplasia of the intestinal mucosa.

Major loss of body protein mass in inflammatory bowel disease is much less common than weight loss, which is often attributable to losses of other body, particularly water and fat. It does occur, however, in a few patients, especially in those with compromised food intake. It is due principally to the combined effects of diminished intake and excessive intestinal losses of amino nitrogen. Nitrogen metabolism is influenced not only by protein nutritional state and net nitrogen intake but also by disease activity. There is some evidence for abnormally low secretion of growth hormone in adolescents with inflammatory bowel disease and growth failure. Low serum albumin concentrations are not necessarily related to protein undernutrition and are the combined result of relatively reduced albumin synthesis, increased intestinal losses, and maldistribution between intravascular and extravascular spaces. Concentrations in the plasma of IgG and acute phase reactants may be raised despite increased losses into the bowel lumen. The prevention of total body protein depletion is achieved principally by maintaining adequate and often not supranormal intakes of a balanced source of amino nitrogen in a balanced diet given orally, enterally, or parenterally, combined with a medical or surgical approach to reduce disease activity: supranormal energy intakes are not beneficial.

Nutrient depletion is a common complication of inflammatory bowel disease, and some of the consequences can be severe. Although it is often easy to recognise the most severely undernourished subjects, those with lesser degrees of malnutrition may prove more difficult to detect. Measurements of many nutritional variables will be abnormal in patients with inflammatory bowel disease, especially in those with Crohn's disease, but are not always relevant to the clinical management of patients. Anthropometric means of assessment, in particular, measurement of mid arm circumference, can act as a simple, reproducible method of detecting those most at risk of appreciable undernutrition.

The measurement of selected anthropometric, biochemical and immunological variables, and clinical judgment can be used to assess nutritional state. Nutritional assessment has three main aims: to define the type and severity of malnutrition; to identify high risk patients; to monitor the efficacy of nutritional support. The problems associated with the various methods to assess the nutritional state and the applications of nutritional assessment in clinical practice are presented and discussed.

The efficacy of branched chain amino acids in two consecutive clinical studies in patients with severe hepatic encephalopathy was tested. In the preliminary uncontrolled study 19 patients with grade 3-4 hepatic encephalopathy were given an intravenous solution containing leucine 11 g/l, isoleucine 9 g/l, and valine 8.4 g/l in 20% dextrose. A complete recovery of mental state was obtained in all patients in a mean time of 20.5 hours. In a subsequent controlled study 40 patients with grade 3-4 hepatic encephalopathy were randomly assigned to receive intravenous branched chain amino acid in 20% dextrose (group A) or oral lactulose (group B). Twelve patients (70.6%) in group A and eight (47%) in group B regained consciousness in a mean time of 27.6 and 31.5 hours, respectively. The difference in the recovery rate between the two groups, although evident, was not significant. Intravenous branched chain amino acids are thus at least as effective as lactulose in reversing hepatic coma. These data argue strongly in favour of a therapeutic effect of branched chain amino acids in the treatment of hepatic encephalopathy in patients with chronic liver failure.

Malnutrition results in a wide variety of metabolic responses, depending on circumstances, from reactions to pure deprivation of nutrients to include the added stress of injury and sepsis. Important differences of response exist between adults and children. Weight loss with changes in carbohydrate, fat, and protein metabolism are well documented. Disturbances of fluid and electrolyte balance are newer areas of interest as are changes in requirements for micronutrients such as trace metals. Many of these metabolic changes are under hormonal control. The intestinal tract shares in the response to malnutrition, and the consequent changes in mucosal function determine the ability of the intestine to handle enteral feeds. Such a route for nutritional support is important in protecting intestinal function not only in absorption but also in hormone production. Enteral feeding is increasingly having an important role in the interactions between acute diarrhoeal disease and malnutrition.

Although malnutrition is associated with poor clinical outcome, it cannot be inferred that better nutrition will improve clinical outcome. Efficacy of a proposed regimen is best established by prospective, randomised, controlled trials. Cost effectiveness is only an issue if efficacy exists. Patients with long term temporary, or permanent, inadequate bowel syndrome are candidates for parenteral nutrition. Most of the prospective, randomised, controlled trials testing the value of nutritional support in other diseases, however, have failed to show that this treatment has a beneficial clinical effect. Areas where these trials have shown a possible clinical benefit include the perioperative care of patients with upper gastrointestinal cancer, elemental diet treatment of Crohn's disease, and branched chain amino acid infusions in hepatic encephalopathy. Even in these instances, it is not clear that such treatment will prove to be cost effective (compared with other currently available treatments).

Nutritional support, administered via the enteral or parenteral routes, has been widely introduced in the treatment of inflammatory bowel disease over the past decade. The precise place of total parenteral nutrition, however, as a sole or adjunct treatment of inflammatory bowel disease, has yet to be defined.

Although many patients with inflammatory bowel disease are malnourished, the role of nutritional support is still controversial. It is universally accepted that with adequate nutritional support patients will put on weight and that their biochemical functions may improve; the question nevertheless remains: does this help the patient get over his or her disease more quickly and, more importantly, does this affect morbidity and mortality? There are several ways of providing nutritional support and all need careful evaluation.

Enteral feeding solutions can be contaminated by bacterial micro-organisms already present in the ingredients, or introduced during preparation or transport, or in the hospital ward. During jejunostomy feeding without pump or filter, ascending bacterial invasion of the feeding bag is possible. In patients with lowered immune response contaminated feedings can cause serious septic clinical problems. The progressive loss of the nutritional value of the enteral feeding solution by bacterial contamination has to be considered for all patients.

Complications may arise during enteral feeding that are usually related to the diameter and rigidity of the tube or the delivery, composition, and sterility of the feed uses. By using a soft, fine bore tube to deliver a sterile feed of known composition, by continuous infusion rather than as a bolus, most of these complications can be avoided.

In this review different types of patients who usually require nutritional support are considered and recommendations made as to when nutritional support should be started, how long it should be continued, and which substrates should be preferentially used by which route.