Bailliere's clinical gastroenterology最新文献

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.

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 posttransplantation 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.

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. p]Catch-up growth may be achieved by using appropriate nutritional support. Changes in body composition have to be assessed during the course of renutrition.

This chapter reviews the evidence for a link between functional dyspepsia and Helicobacter pylori infection from three angles. In the section on pathophysiology, we evaluate how H. pylori could theoretically produce dyspeptic symptoms: many mechanisms can be proposed. In the discussion on epidemiology, we evaluate possible associations between the occurrence of symptoms and infection. Here, many studies claiming a coincidence or chronological sequence of infection and symptoms are criticized because of their poor design. In the section on the improvement of functional dyspepsia by the treatment of H. pylori infection, the conclusion is reached that if such an effect occurs at all—which is unlikely—it is very weak. The controversy on the link between H. pylori infection and functional dyspepsia is presently ongoing. Some authors are still trying to save an elegant concept that once looked so plausible but now has the facts against it.

Many functional dyspepsia treatment trials have until recently suffered from important weaknesses in study design. A major problem has been the low number of studies that have used validated outcome measures. Fortunately, progress has been made in this area. The evidence for the efficacy of antacids, H₂-receptor antagonists, omeprazole, domperidone, cisapride and anti-Helicobacter therapy is reviewed. Although several of these have shown benefit, it is unclear whether this may be a result of the inclusion of patients with unrecognized gastro-oesophageal reflux disease. The data on anti-Helicobacter therapy are conflicting.

Pathological processes and diseases of the upper gastrointestinal tract have become increasingly recognized over recent years as childhood entities responsible for a variety of upper gastrointestinal symptoms previously labelled as functional or non-organic. The term ‘dyspepsia’ is an adult one whose definition requires clarification before use in the paediatric context, but it encompasses age-dependent symptoms such as feedassociated irritability in the infant, peri-umbilical pain in the younger child, and heartburn, nausea, and indigestion in the older child as in adults. The possible organic conditions giving rise to such symptoms are multiple and multiorgan and include: gastro-oesophageal reflux; peptic ulcer disease; upper gastrointestinal Crohn's disease; antroduodenal motility disorders; pancreatitis; cholecystitis; cholelithiasis; biliary dyskinesia; and abdominal migraine. However, Munchausen syndrome by proxy must not be forgotten. Non-ulcer dyspepsia, it is now clear, has a basis in altered gastroduodenal motility and may be amenable to propulsion agents. In many individuals the dyspeptic symptoms of recurrent abdominal pain may be altered by psychotherapeutic intervention. Indeed there remains a proportion of children who undoubtedly have a behavioural or psychological base to their complaint. Nevertheless, with the recent increase in diagnostic yield from improved technical investigative aids available to paediatrics in the last 5–10 years, it is clear that the responsibility of the paediatrician to the child to find a cause of their symptoms is paramount. The variety of presenting features, possible causes of these symptoms, and appropriate investigation and treatment will be discussed, and management algorithms based on published literature and personal practice will be offered.

A wide variety of disorders affecting the upper gastrointestinal tract, as well as systemic disorders, are associated with symptoms of dyspepsia. The more important of these conditions are considered in this chapter, with particular reference to their symptom patterns on presentation. The differentiation, on clinical grounds, between these organic causes of dyspepsia and functional dyspepsia remains an important area of research. Those aspects of the history and physical examination most relevant to this distinction are also considered.

Estimates of the prevalence of dyspepsia in the community have varied between studies. This is, in large part, because of differences in the definitions used. Roughly speaking, 15–20% of the general population will report recurrent upper abdominal pain over the course of a year. Most of these people do not have endoscopic abnormalities and thus meet the criteria for functional dyspepsia. These symptoms appear to come and go, which makes determination of the incidence of dyspepsia quite difficult. Most studies have not distinguished whether the onset of symptoms represents recurrence or de novo symptoms. Approximately 5–10% of the population will develop symptoms of dyspepsia in a given year, and 50% of people with dyspepsia will lose their symptoms the following year. Regardless of the exact figures, all studies have demonstrated dyspepsia to be exceedingly common in the community.

The main diseases associated with dyspepsia are peptic ulcer disease, gastro-oesophageal reflux disease and non-ulcer dyspepsia. Increased gastric acid secretion is a characteristic of most duodenal ulcer patients and of a small minority of non-ulcer dyspepsia and gastro-oesophageal reflux disease patients. Although acid secretion is normal in most gastro-oesophageal reflux disease patients, the condition is mainly the result of excess exposure of the distal oesophagus to acid refluxing from the stomach. Increased mucosal sensitivity to acid is involved in the aetiology of dyspeptic symptoms in the majority of patients with peptic ulcer disease and gastro-oesophageal reflux disease, and in a minority of non-ulcer dyspepsia subjects. Gastric acid, therefore, plays an important role in both the aetiology of dyspeptic diseases and in the aetiology of dyspeptic symptoms.