This document presents the official recommendations of the American Gastroenterological Association (AGA) on treatment of patients with dysphagia caused by benign disorders of the distal espophagus. It was approved by the Clinical Practice and Practice Economics Committee on September 27, 1998, and by the AGA Governing Board on November 8, 1998.

Adenocarcinomas at the gastroesophageal junction appear to arise from foci of intestinal metaplasia that develop either in the distal esophagus or the proximal stomach (the gastric cardia). Metaplasia is usually a consequence of chronic inflammation, and it is logical to assume that intestinal metaplasia at the gastroesophageal junction develops as a result of chronic inflammation in the epithelia that normally line the junction region. Intestinal metaplasia in the esophagus is known to be a sequela of chronic inflammation in squamous epithelium caused by gastroesophageal reflux disease, whereas intestinal metaplasia in the distal stomach is often a consequence of chronic gastritis caused by Helicobacter pylori infection. For the gastric cardia, the contributions of gastroesophageal reflux disease, H. pylori infection, and other factors to inflammation, metaplasia, and neoplasia are not clear. If physicians are to develop meaningful preventive strategies and specific therapies for tumors of the proximal stomach, a clear understanding of pathogenesis is important. Recent studies on pathogenetic factors for inflammation in cardiac epithelium (gastric carditis) have yielded contradictory results, perhaps because of fundamental differences in the techniques used by different investigators for identifying and sampling the gastric cardia. This report explores the roots of the controversy regarding the role of gastric carditis in the development of metaplasia and neoplasia at the gastroesophageal junction and suggests practical guidelines for biopsy protocols to be used in future studies that will be necessary to resolve these disputes.

This literature review and the recommendations therein were prepared for the American Gastroenterological Association Clinical Practice and Practice Economics Committee. The paper was approved by the committee on September 27, 1998.

This document presents the official recommendations of the American Gastroenterological Association (AGA) on the Evaluation and Management of Chronic Diarrhea. It was approved by the Clinical Practice and Practice Economics Committee on September 27, 1998, and by the AGA Governing Board on November 8, 1998.

The gastric transitional zones are the junctional zones between the different types of mucosa: antral-body, body-cardia, and antrum-duodenum. In this article, the importance of the transitional zone in determining disease outcome, specifically duodenal ulcer, gastric ulcer, and possibly gastric cancer, is reviewed. Both gastric ulcers and duodenal ulcers are located immediately adjacent to the transitional zones. The transitional zones are dynamic rather than static areas. Local acid levels determine the behavior of Helicobacter pylori at the antral-body transitional zone and, as a consequence, the geographic distribution of gastritis in the stomach and the formation of duodenal ulcer and gastric ulcer. This review also explains that diffuse antral gastritis and multifocal atrophic gastritis are part of the same disease and not separate entities.

The prevalence of home enteral and parenteral nutrition programmes is rising rapidly all over the world, in children as in adults. Home artificial nutrition, especially parenteral nutrition, is an expensive technology but is life-saving for many patients. The only possible alternative to home treatment is keeping patients in hospital, and cost-benefit studies have demonstrated that home nutrition is about 70% more cost-effective than hospital-based therapy. Although home nutrition is usually considered by children and families to lead to an improvement in their quality of life, the complications of these techniques, including psychological consequences, have to be carefully assessed and prevented.

An imbalance between a person's energy requirements and his or her dietary protein and caloric supply is the source of protein energy malnutrition (PEM), which compounds the problems of any underlying disease. Malnutrition may occur quite rapidly in critically ill patients, particularly those suffering from sepsis, setting up a vicious cycle with worsening of the PEM. This chapter examines the main consequences of PEM, the means whereby appropriate nutrition may be provided, and risks for severely malnourished paediatric patients in hospital. If the gastrointestinal tract can be used for refeeding, it should be used. When the gastrointestinal tract is unable to meet the protein and energy requirements, parenteral nutrition (PN) is required. PN is efficient but carries a high risk of metabolic complications known as the refeeding syndrome and directly related to the homeostatic changes secondary to severe PEM. Catch-up growth may be achieved by using appropriate nutritional support. Changes in body composition have to be assessed during the course of renutrition.

Protein-energy malnutrition is an inevitable consequence of chronic liver disease, particularly in the developing infant. Severe malnutrition with loss of fat stores and muscle wasting affects between 60% and 80% of infants with liver disease (Beath, 1993a; Holt et al, 1997). Reduced energy intake secondary to anorexia, vomiting and fat malabsorption, in association with a disordered metabolism of carbohydrate and protein, increased energy requirements and vitamin and mineral deficiencies, contributes towards growth failure. Reversal of malnutrition is one of the key aims of liver transplantation and is achieved in the majority of long-term survivors. The aetiology of persistent growth failure post-transplantation is multifactorial and is related to pre-operative malnutrition, glucocorticoid administration, feeding problems and post-operative complications. Strategies to prevent pre- and post-transplant growth failure include early referral for liver transplantation and a multidisciplinary approach to nutritional support, which may increase survival and improve the quality of life and outcome of liver transplantation.

Malnutrition is an adverse prognostic factor in cystic fibrosis, influencing the course of pulmonary disease and correlating inversely with survival. A positive energy balance between energy intake and the combination of total energy expenditure, energy losses and growth-related energy cost is essential to maintain normal nutritional status. Before starting nutritional supplementation, it is important to rule out pathological conditions that may have a deleterious effect on nutritional status: persistent exocrine pancreatic insufficiency, chronic bacterial pulmonary colonization, impaired glucose tolerance, specific nutritional deficits and associated disorders leading to a decrease of energy intake. Several methods are available, ranging from boosted oral nutrition to behavioural intervention, oral supplementation, enteral nutrition and, rarely, parenteral nutrition. The use of elemental nutrients for either oral supplementation or enteral nutrition seems of no nutritional benefit and is more expensive than conventional polymeric nutrients. Provided that the goals of the nutritional supplementation are fulfilled, simpler is often better.

Except for cystic fibrosis, which is the most frequent genetic disorder in the Caucasian population, diseases of the exocrine pancreas are relatively uncommon in children. However, they are many and varied in terms of their pathogenesis and clinical manifestation. They can be classified as: (1) congenital anatomical abnormalities, (2) congenital secretory insufficiencies, and (3) pancreatitis. In all of these diseases, when pancreatic insufficiency (whether partial or complete) is present, the nutritional status of the patients must be investigated regularly, and pancreatic enzymes as well as nutritional supplementations must be prescribed as soon as malnutrition is present, or even prophylactically. The preservation of good nutritional status is the guarantee of a better prognosis.

Motility disorders are very common in childhood, causing a number of gastrointestinal symptoms: recurrent vomiting, abdominal pain and distension, constipation and obstipation, and loose stools. The disorders result from disturbances of gut motor control mechanisms caused by either intrinsic disease of nerve and muscle, central nervous system dysfunction or perturbation of the humoral environment in which they operate. Intrinsic gut motor disease and central nervous system disorder are most usually congenital in origin, and alterations of the humoral environment acquired. Irritable bowel syndrome occurs in children as well as adults and is multifactorial in origin, with an interplay of psychogenic and organic disorders.

Short bowel syndrome has significant morbidity and is potentially lethal especially when intestinal loss is extensive. The pathophysiology of short bowel syndrome, its aetiology, prognosis and our understanding of the mechanisms of adaptation are reviewed. Management by a multi-disciplinary nutritional care team is advocated and should be directed to the maintenance of growth and development, the promotion of intestinal adaptation, the prevention of complications and the establishment of enteral nutrition. The choice of enteral feed, the role of drugs and the use of pro-adaptive nutrients and agents are discussed. Complications including cholestasis and catheter related sepsis are outlined with strategies to reduce them. Finally the roles of secondary surgical interventions including transplantation are discussed.

Nutrition is clearly disturbed by active intestinal inflammation. Appetite is reduced, yet energy substrates are diverted into the inflammatory process, and thus weight loss is characteristic. The nutritional disturbance represents part of a profound defect of somatic function. Linear growth and pubertal development in children are notably retarded, body composition is altered, and there may be significant psychosocial disturbance. Macrophage products such as tumour necrosis factor-alpha and interleukins-1 and 6 may be the central molecules that link the inflammatory process to this derangement of homeostasis. Intriguingly, there is also increasing evidence that an aggressive nutritional programme may in itself be sufficient to reduce the mucosal inflammatory response. Recent evidence suggests that enteral nutrition alone may reduce many pro-inflammatory cytokines to normal and allow mucosal healing. In addition, specific nutritional components, such as n-3 polyunsaturated fatty acids, may have an anti-inflammatory effect as they may alter the pattern of leukotrienes generated during the immune response. The recent discovery of the specific molecular mediators of appetite and body composition, such as leptin and myostatin, may allow increased therapeutic specificity and further improvement in the nutritional treatment of the inflammatory bowel diseases.

Adequate nutritional intervention in diarrhoeal disease in children is crucial in obtaining optimal control of a disorder that may become life-threatening. During recent years, important advances have been made in our understanding of the pathophysiology of diarrhoeal states, in the formulation of oral rehydration solutions and in the role of micro- and macronutrients in diarrhoeal disorders. This chapter outlines some of the relevant concepts in the pathophysiology of diarrhoeal disease and provides a rationale for nutritional intervention. Guidelines for nutritional management in the settings of acute-onset diarrhoea, post-enteritis protracted diarrhoea and chronic non-specific diarrhoea are provided, mostly based on controlled clinical trials and meta-analyses of evidence-based medicine.

The quantity and quality of dietary lipids and their metabolism are of major importance for the growth, body composition, development and long-term health of children, both in health and disease. Lipids are the major source of energy in early childhood and supply essential lipid-soluble vitamins and polyunsaturated fatty acids that are required in relatively high amounts during early growth. Lipids affect the composition of membrane structures, and modulate membrane functions as well as the functional development of the central nervous system. Some long-chain polyunsaturated fatty acids serve as precursors for bioactive lipid mediators, including prostaglandins, thromboxanes and leukotrienes, which are powerful regulators of numerous cell functions such as thrombocyte aggregation, inflammatory reactions and immune functions. Here we review some aspects of the biochemistry and physiology of lipids and their implications for lipoprotein metabolism, energy balance and the lipid supply during early childhood through the placenta, human milk, enteral diets and parenteral lipid emulsions.

As most diseases can have nutritional consequences, the assessment of nutritional status may help to detect an underlying disease, to identify nutritional disorders related to a given disease, and to quantify the impact of nutritional therapy. The aims and methods used for nutritional assessment depend on the circumstances in which nutritional assessment is performed. Whatever the context or aim, nutritional status is assessed through a simple, mainly clinical approach, based on the past history, dietary intake, auxological analysis, anthropometric measurements, body compartment and biological parameters. Accurate techniques for measuring body compartments are available in children such as dual-energy X-ray absorptiometry to assess fat body mass or bioelectrical impedance analysis for body water and lean body mass. Measuring energy expenditure allows for a more accurate monitoring of the patient's energy needs and decreases the risks associated with underfeeding or overfeeding. In clinical practice, the analysis should be longitudinal and take into account situations carrying a risk of malnutrition. Preventive use of nutritional assessment allows nutritional support to be introduced in a timely fashion, thereby avoiding morbidity/mortality and limiting the long-term impact of malnutrition on growth and development.

A reappraisal of available data, together with new studies, suggests that normal infants' energy and protein requirements might be substantially lower than previously estimated. For example, the safe level of protein intake would amount to only 10 g per day during the first 2 years of life and to about 12 g per day during the third. This has direct consequences for the management of malnourished children, particularly for defining an optimal protein:energy ratio. A reduced food intake has long been accepted as the main cause of malnutrition. However, evidence has accumulated suggesting that metabolic dysregulation may also play a part. This is particularly true for proteins. Net protein deposition in the growing child results from protein synthesis rates being higher than protein breakdown. However, this setting can be disrupted by a significant increase in protein breakdown in response to cytokines. This mechanism, which is found in acute as well as in chronic inflammatory processes, may lead to severe protein malnutrition and is not always amenable to nutritional support.