551 results match your criteria Bailliere's clinical gastroenterology[Journal]


Home enteral and parenteral nutrition in children.

Baillieres Clin Gastroenterol 1998 Dec;12(4):877-94

Hôpital Necker-Enfants Malades, Fédération de Pédiatrie, Unité de Gastroentérologie et Nutrition, Paris, France.

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. Read More

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December 1998
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Nutritional support in malnourished paediatric patients.

Authors:
O Goulet

Baillieres Clin Gastroenterol 1998 Dec;12(4):843-76

Service de Gastroentérologie et Nutrition Pédiatrique, Hôpital Necker-Enfants Malades, Paris, France.

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. Read More

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December 1998

Cholestasis and end-stage liver disease.

Baillieres Clin Gastroenterol 1998 Dec;12(4):823-41

Liver Unit, Birmingham Children's Hospital NHS Trust, UK.

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. Read More

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December 1998
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Cystic fibrosis: nutritional consequences and management.

Authors:
D Turck L Michaud

Baillieres Clin Gastroenterol 1998 Dec;12(4):805-22

University of Lille, France.

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. Read More

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December 1998
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Pancreatic diseases (excluding cystic fibrosis).

Authors:
J Sarles

Baillieres Clin Gastroenterol 1998 Dec;12(4):799-803

Hôpital d'Enfants de la Timone, Marseille, France.

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. Read More

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December 1998

Motility disorders in childhood.

Authors:
P J Milla

Baillieres Clin Gastroenterol 1998 Dec;12(4):775-97

Institute of Child Health, University of London, UK.

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. Read More

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December 1998

Short bowel syndrome.

Baillieres Clin Gastroenterol 1998 Dec;12(4):739-73

Institute of Child Health, University of Birmingham, UK.

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. Read More

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December 1998

Nutrition in inflammatory bowel disease.

Baillieres Clin Gastroenterol 1998 Dec;12(4):719-38

University Department of Paediatric Gastroenterology, Royal Free Hospital, London, UK.

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. Read More

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December 1998

Nutritional management in diarrhoeal disease.

Baillieres Clin Gastroenterol 1998 Dec;12(4):697-717

University of Chicago, Department of Pediatrics, Illinois, USA.

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. Read More

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December 1998

Nutritional support of infants and children: supply and metabolism of lipids.

Baillieres Clin Gastroenterol 1998 Dec;12(4):671-96

Division of Metabolic Diseases and Nutrition, Kinderklinik and Kinderpoliklinik, Ludwig-Maximilians-University of Munich, Germany.

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. Read More

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December 1998

Assessment of nutritional status in clinical practice.

Authors:
O Goulet

Baillieres Clin Gastroenterol 1998 Dec;12(4):647-69

Service de Gastroentérologie et Nutrition Pédiatrique, Hôpital des Enfants Malades, Paris, France.

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. Read More

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December 1998
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Protein and energy requirements in healthy and ill paediatric patients.

Authors:
J L Bresson

Baillieres Clin Gastroenterol 1998 Dec;12(4):631-45

Hôpital des Enfants Malades, Paris, France.

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. Read More

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December 1998

Prevalence, incidence and natural history of dyspepsia and functional dyspepsia.

Authors:
G R Locke

Baillieres Clin Gastroenterol 1998 Sep;12(3):435-42

Division in Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, USA.

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. Read More

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September 1998

Dyspepsia in infants and children.

Baillieres Clin Gastroenterol 1998 Sep;12(3):601-24

University Department of Paediatric Gastroenterology, Royal Free Hospital, London, UK.

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 feed-associated irritability in the infant, peri-umbilical pain in the younger child, and heart-burn, 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. Read More

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September 1998

How should new-onset dyspepsia be managed in general and specialist practice?

Authors:
P Bytzer

Baillieres Clin Gastroenterol 1998 Sep;12(3):587-99

Department of Medical Gastroenterology F, Glostrup University Hospital, Ndr. Ringvej, Denmark.

Managing patients with new-onset dyspeptic symptoms represents a real challenge in clinical decision-making. The major controversy has been over the optimal management strategy of patients with new-onset dyspeptic symptoms who do not present with alarm symptoms. Since unaided clinical diagnosis is unreliable, proposed management strategies have included empirical treatment algorithms, computer-assisted predictive score models and Helicobacter pylori-based strategies such as test-and-scope or test-and-treat algorithms. Read More

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September 1998

Treatment of functional dyspepsia.

Baillieres Clin Gastroenterol 1998 Sep;12(3):573-86

Department of Medicine, Dalhousie University, QEII, Victoria General Hospital Site, Dr. R. C. Dickson Centre, Halifax, N.S., Canada.

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. Read More

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September 1998

Are psychosocial factors of aetiological importance in functional dyspepsia?

Authors:
K W Olden

Baillieres Clin Gastroenterol 1998 Sep;12(3):557-71

Division of Gastroenterology, Mayo Clinic, Arizona, USA.

The causes of functional dyspepsia remain unclear. Research has linked other functional gastrointestinal disorders, particularly irritable bowel syndrome, to a history of physical or sexual abuse, psychosocial distress and certain psychiatric disorders. In functional dyspepsia, there is a possibility of certain psychiatric disorders, particularly alcohol abuse and eating disorders, indirectly influencing the development of functional dyspepsia-like symptoms. Read More

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September 1998
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Gastrointestinal sensory abnormalities in functional dyspepsia.

Baillieres Clin Gastroenterol 1998 Sep;12(3):545-56

Department of Gastroenterology, Instituto Nacional de la Nutricion Salvador Zubiran, Mexico DF, Mexico.

Symptoms of functional dyspepsia, such as epigastric pain, bloating or early satiety and nausea, are non-specific and are likely to arise from different mechanisms. Current evidence suggests the presence of at least two subgroups: patients who respond to a prolonged course of acid suppression and patients who show a significant overlap of symptoms with other functional gastrointestinal disorders such as irritable bowel syndrome. An enhanced sensitivity of visceral afferent pathways with or without associated autonomic dysregulation appears to play an important role in the aetiology of symptoms in the second group. Read More

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September 1998

Relevance of gastrointestinal motor disturbances in functional dyspepsia.

Baillieres Clin Gastroenterol 1998 Sep;12(3):533-44

Department of Internal Medicine and Gastroenterology, University of Bologna, Italy.

Gastrointestinal motor abnormalities are frequent findings in patients with functional dyspepsia. However, these abnormalities are rather non-specific and seem to be restricted to a proportion of patients. Furthermore, they are not necessarily time-linked to symptom perception. Read More

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September 1998

Helicobacter pylori and functional dyspepsia: a real causal link?

Baillieres Clin Gastroenterol 1998 Sep;12(3):503-32

Department of Medicine, University Hospital, CHUV, Lausanne, Switzerland.

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. Read More

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September 1998

Role of gastric acid in the aetiology of dyspeptic disease and dyspepsia.

Authors:
K E McColl

Baillieres Clin Gastroenterol 1998 Sep;12(3):489-502

Department of Medicine and Therapeutics, Gardiner Institute, Glasgow, UK.

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. Read More

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September 1998

Organic causes of dyspepsia, and discriminating functional from organic dyspepsia.

Authors:
J E Kellow

Baillieres Clin Gastroenterol 1998 Sep;12(3):477-87

Department of Gastroenterology, Royal North Shore Hospital, University of Sydney, Australia.

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. Read More

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September 1998

Is functional dyspepsia largely explained by gastro-oesophageal reflux disease?

Baillieres Clin Gastroenterol 1998 Sep;12(3):463-76

Northern Oesophago-Gastric Cancer Unit, University of Newcastle upon Tyne, UK.

Functional dyspepsia is a chronic disorder of unknown aetiology. The lack of endoscopic abnormalities in patients with this disorder has led many physicians to believe that gastro-oesophageal reflux disease may be responsible for most symptoms. Our group has addressed this issue, by pathophysiological studies in a large cohort of Dundee patients with persistent dyspeptic symptoms. Read More

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September 1998

Is functional dyspepsia just a subset of the irritable bowel syndrome?

Baillieres Clin Gastroenterol 1998 Sep;12(3):443-61

Department of Medicine, University of North Carolina, Chapel Hill 27599-7080, USA.

To determine whether functional dyspepsia and irritable bowel syndrome are different entities, epidemiological data, factor analysis studies, physiological data and associated psychological symptoms were reviewed. Between 30% and 60% of patients with either diagnosis also meet the criteria for the other diagnosis, a level greater than expected to occur by chance but not sufficient to infer an identity. Most factor analysis studies identify independent clusters of symptoms corresponding to functional dyspepsia and irritable bowel syndrome. Read More

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September 1998

Nomenclature of dyspepsia, dyspepsia subgroups and functional dyspepsia: clarifying the concepts.

Baillieres Clin Gastroenterol 1998 Sep;12(3):417-33

Department of Gastroenterology, University of Essen, Germany.

There is international agreement that dyspepsia refers to pain or discomfort centered in the upper abdomen. However, the term 'discomfort' has been variably defined. While other symptoms may often be simultaneously present, gastro-oesophageal reflux disease can usually be clearly distinguished by the presence of predominant heartburn. Read More

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September 1998

Other hereditary diseases and the liver.

Baillieres Clin Gastroenterol 1998 Jun;12(2):369-407

Department of Paediatrics, Children's Hospital of The King's Daughters, Norfolk, Virginia, USA.

In this chapter, an abbreviated account is presented on the subject of hereditary diseases and the liver. However, it is incomplete because Alagille syndrome, storage disorders, alpha-1-antitrypsin deficiency and Wilson disease are not included as they appear in other chapters of this volume. Biliary atresia is omitted because all available evidence does not support any significant genetic association. Read More

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The hereditary hyperbilirubinaemias.

Baillieres Clin Gastroenterol 1998 Jun;12(2):355-67

Eastern Virginia Medical School, Norfolk, USA.

The presence of jaundice in the neonate, infant or young child presents a broad differential diagnosis. The 'disease' may be benign, as in breast-milk jaundice, or potentially fatal, as in hereditary fructose intolerance. The cause of the jaundice may be a primary hepatic disorder, such as extrahepatic biliary atresia, or secondary to a non-hepatic cause, such as haemolysis or sepsis. Read More

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Glycogen storage diseases and the liver.

Authors:
A Burchell

Baillieres Clin Gastroenterol 1998 Jun;12(2):337-54

Department of Obstetrics & Gynaecology, Ninewells Hospital & Medical School, University of Dundee, Scotland, UK.

Carbohydrate metabolism in the liver is responsible for plasma glucose homeostasis. Liver glycogen storage diseases are metabolic disorders which result in abnormal storage amounts and/or forms of glycogen, and often (but not always) have hepatomegaly and hypoglycaemia as presenting features. To understand the clinical complexity of the glycogen storage diseases, it is necessary to understand the properties and regulation of the proteins involved in glycogen metabolism. Read More

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The inheritance of alcoholic liver disease.

Baillieres Clin Gastroenterol 1998 Jun;12(2):317-35

Centre for Liver Research, Medical School, Newcastle upon Tyne, UK.

Available evidence supports the concept that alcoholic liver disease (ALD) is a multifactorial disease with a heritable component. A number of polymorphic genes with small and additive effects will thus encode susceptibilty to this 'polygenic' disease. Molecular genetic studies of ALD are in their infancy, and methods available for the genetic dissection of complex traits are discussed. Read More

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Autoimmune polyglandular syndromes.

Baillieres Clin Gastroenterol 1998 Jun;12(2):293-315

Department of Gastroenterology and Hepatology, Hannover Medical School, Germany.

Autoimmune polyglandular syndrome type 1 (APS1) is characterized by a variable combination of disease components: (1) mucocutaneous candidiasis; (2) autoimmune tissue destruction; (3) ectodermal dystrophy. The disease is caused by mutations in a single gene called APECED (autoimmune polyendocrinopathy-candidiasis-ectodermal-dystrophy) or AIRE (autoimmune regulator) coding for a putative transcription factor featuring two zinc-finger (PHD-finger) motifs. APS1 shows a penetrance of 100%, lack of female preponderance and lack of association with HLA-DR. Read More

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June 1998
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Arteriohepatic dysplasia (Alagille syndrome; Watson-Alagille syndrome).

Baillieres Clin Gastroenterol 1998 Jun;12(2):275-91

Department of Medicine, University of Queensland, Australia.

Alagille syndrome (AS) (arteriohepatic dysplasia, Alagille-Watson syndrome) is a multi-system disorder with hepatic, skeletal, eye, cardiac and renal manifestations. It results from mutation of the JAG1 gene, located on chromosome 20, which encodes a ligand for Notch receptor(s). The interactions of Notch receptors and their ligands are crucial in controlling cell fate decisions in a variety of developmental processes. Read More

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Alpha 1-antitrypsin deficiency.

Baillieres Clin Gastroenterol 1998 Jun;12(2):257-73

Department of Medicine, Malmö University Hospital, Sweden.

Alpha 1-Antitrypsin deficiency (PiZ) is frequent in Caucasian populations. The predominant clinical correlates of this inborn error, i.e. Read More

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June 1998
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Wilson disease.

Authors:
E A Roberts D W Cox

Baillieres Clin Gastroenterol 1998 Jun;12(2):237-56

Division of Gastroenterology and Nutrition, Hospital for Sick Children, Toronto, Ontario, Canada.

Wilson disease is a recessively inherited disorder of copper transport. Clinical features are highly variable, with any combination of neurological, hepatic or psychiatric illness. The age of onset varies from 3 to 50 years of age. Read More

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Juvenile haemochromatosis.

Authors:
C Camaschella

Baillieres Clin Gastroenterol 1998 Jun;12(2):227-35

Dipartimento di Scienze Cliniche e Biologiche Università di Torino, Italy.

Juvenile haemochromatosis (JH) is an autosomal recessive disorder which leads to early-onset, severe iron overload. The disease affects both sexes equally. Iron parameters and tissue iron distribution are similar to those in middle-life haemochromatosis (which is linked to the HFE gene). Read More

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Haemochromatosis.

Baillieres Clin Gastroenterol 1998 Jun;12(2):209-25

Department of Gastroenterology, Princess Alexandra Hospital, Brisbane, Queensland, Australia.

Primary, hereditary or genetic haemochromatosis is one of the most common inherited disorders in a Caucasian populations with a disease frequency of 1:300-400 and a carrier frequency of approximately 10%. The basic genetic defect remains unknown, although the haemochromatosis gene has now been cloned and is known to be a member of the MHC non-classical class I family. Many factors--environmental, genetic and non-genetic in nature--influence the degree of iron loading in affected individuals. Read More

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Adjuvant post-operative therapy.

Baillieres Clin Gastroenterol 1998 Mar;12(1):179-99

Department of Medicine, University of Liverpool, UK.

About 90% of patients with Crohn's disease require surgery at some time in their lives but the clinical recurrence rate after surgery is about 50% within 5 years, with 50% requiring further surgery within 10 years. Endoscopic evidence of relapse can be found in 75% within 12 weeks of resection. There is therefore a major problem to be solved. Read More

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Prognostic parameters of Crohn's disease recurrence.

Authors:
S A Strong

Baillieres Clin Gastroenterol 1998 Mar;12(1):167-77

Department of Colorectal Surgery, Cleveland Clinic Foundation, OH 44195, USA.

Patients with Crohn's disease are haunted by the likelihood of recurrence following resection of their disease. In an effort to better counsel patients about their relative risk, many centres have evaluated a myriad of factors thought to be harbingers of recurrence. Insightful review of the numerous studies requires consideration of the definition of recurrence, length and manner of follow-up, and statistical tools used for analysis of the data. Read More

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Place of laparoscopic surgery in Crohn's disease.

Baillieres Clin Gastroenterol 1998 Mar;12(1):157-65

Department of Surgery, Royal London Hospital, Whitechapel, London, UK.

Laparoscopic surgery for patients with Crohn's disease is feasible and safe. It may be conducted in appropriately selected patients including those with localized abscess, phlegmon, simple intra-abdominal fistulas, and perianastomotic recurrent disease. However, as the technique is just evolving and has yet to be shown to be of advantage over conventional open surgery, it should not be considered as a standard care. Read More

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Controversies in Crohn's disease.

Authors:
J J Murray

Baillieres Clin Gastroenterol 1998 Mar;12(1):133-55

Department of Colon and Rectal Surgery, Lahey Hitchcock Medical Center, Burlington, MA 01805, USA.

Despite recent advances in the medical therapy of Crohn's disease, surgery continues to play a central role in the treatment of the disease. The strategy for surgical management of Crohn's disease continues to evolve. This chapter reviews many of the controversies surrounding surgical palliation of complications of Crohn's disease. Read More

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March 1998
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Crohn's disease in adolescents.

Authors:
A M Griffiths

Baillieres Clin Gastroenterol 1998 Mar;12(1):115-32

Division of Gastroenterology/Nutrition, Hospital for Sick Children, Toronto, Ontario, Canada.

The clinical features of Crohn's disease manifest during adolescence are varied as in adults. The potential complication of growth impairment and concomitant delay in pubertal development is unique to this population. Cytokines released from the inflamed bowel and chronic nutritional insufficiency are the major factors in the pathophysiology of growth inhibition. Read More

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March 1998
2 Reads

Crohn's disease: nutrition and nutritional therapy.

Baillieres Clin Gastroenterol 1998 Mar;12(1):93-114

Department of Medicine, University of Edinburgh, Western General Hospital, Scotland.

Disordered nutrition is common in Crohn's disease and is multifactorial. Regular and systematic monitoring of at least a minimum set of nutrition data is an essential component of care of children and adults with Crohn's disease. However, even in children, monitoring of growth and development may be deficient. Read More

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Medical therapy of active Crohn's disease.

Baillieres Clin Gastroenterol 1998 Mar;12(1):73-92

Department of Medicine, Orebro Medical Centre Hospital, Sweden.

Active Crohn's disease constitutes a major problem in gastroenterology. Symptoms vary with site, extent and local complications of the disease as well as with the absence or presence of extraintestinal manifestations. Due to the troublesome consequences of the disease new treatments have continuously been tried. Read More

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Crohn's disease: new imaging techniques.

Authors:
K Carroll

Baillieres Clin Gastroenterol 1998 Mar;12(1):35-72

Queen Elizabeth Hospital, University Hospital Birmingham NHS Trust, Edgbaston, UK.

This chapter reviews the current state of imaging in Crohn's disease. Imaging plays an important role in the diagnosis and management of Crohn's disease. Imaging is complementary to the clinical assessment of the patient and other investigations including endoscopy. Read More

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The differential diagnosis of Crohn's disease and ulcerative colitis.

Authors:
D S Sanders

Baillieres Clin Gastroenterol 1998 Mar;12(1):19-33

Department of Pathology, Medical School, University of Birmingham and UHB Trust, Edgbaston, UK.

Most cases of inflammatory bowel disease (IBD) can be correctly labelled as Crohn's disease (CD) or ulcerative colitis (UC) with careful initial gross and microscopic examination of biopsy and resection specimens together with close clinical and radiological correlation. Until we understand more of the aetiology and immunology of IBD we should admit that there are limitations imposed by current diagnostic criteria, consider the use of reporting proforma to improve diagnostic accuracy, and accept that in a small number of patients clinicopathological features will overlap, and CD may masquerade as UC. Read More

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Pathogenesis of Crohn's disease.

Authors:
H J Hodgson

Baillieres Clin Gastroenterol 1998 Mar;12(1):1-17

Imperial College School of Medicine, Division of Medicine, Hammersmith Hospital, London, UK.

In the absence of a single initiating aetiological factor, most workers envisage Crohn's disease as the manifestation of poorly regulated immune and inflammatory processes within the gut wall. Initially these responses may arise as a response to common antigens associated with the gut--bacterial products being amongst the most obvious candidates. In genetically predisposed individuals there is overexpression both of local immune response mechanisms in the gut wall (T-cells, B-cells and macrophages) and of systemic inflammatory cells (predominantly polymorphonuclear leukocytes), which are attracted into the inflamed gut through activation of adhesion molecules on the vascular endothelium. Read More

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Biliary malignancies.

Baillieres Clin Gastroenterol 1997 Dec;11(4):801-36

Department of Surgical Gastroenterology, Sanjay Gandhi Post-graduate Institute of Medical Sciences (SGPGIMS), Lucknow, India.

Biliary malignancies, including cancers of the intrahepatic and extrahepatic bile ducts, gallbladder and ampulla, should be considered in the differential diagnosis of patients with obstructive jaundice. Cancers of the intrahepatic bile ducts and ampulla are managed as liver and peri-ampullary tumours respectively. Extrahepatic bile duct cancers are diagnosed by cholangiography and evaluated for resectability by imaging and angiography. Read More

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December 1997

Sclerosing cholangitis.

Baillieres Clin Gastroenterol 1997 Dec;11(4):781-800

Division of Liver Transplantation, Mayo Clinic, Rochester, MN 55905, USA.

Primary sclerosing cholangitis (PSC) is a chronic, progressive cholestatic liver disease whose aetiopathogenesis is unknown. PSC is frequently associated with inflammatory bowel disease, in particular chronic ulcerative colitis, is most commonly observed in young males and is clinically characterized by fatigue, pruritus and jaundice. The diagnosis is supported by a cholestatic biochemical profile and histological abnormalities, and confirmed by visualization of an abnormal biliary tree. Read More

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December 1997

Benign post-operative bile duct strictures.

Authors:
K D Lillemoe

Baillieres Clin Gastroenterol 1997 Dec;11(4):749-79

Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, MD 21287-4603, USA.

The vast majority of post-operative bile duct strictures occur following cholecystectomy, these injuries having been seen at an increased frequency since the introduction of laparoscopic cholecystectomy. Bile duct injuries usually present early in the post-operative period, obstructive jaundice or evidence of a bile leak being the most common mode of presentation. In patients presenting with a post-operative bile duct stricture months to years after surgery, cholangitis is the most common symptom. Read More

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December 1997
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Biliary fistulae and haemorrhage.

Authors:
S J Savader

Baillieres Clin Gastroenterol 1997 Dec;11(4):741-8

Russell H. Morgan Department of Radiology and Radiological Sciences, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.

Percutaneous biliary drainage is the most common aetiology of haemobilia. Bile duct fistulae can also arise from the hepatic or portal vein, most commonly as a result of trauma. Percutaneous methods for treating haemobilia from all these sources are discussed in detail. Read More

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December 1997

Biliary motility disorders.

Authors:
J Toouli

Baillieres Clin Gastroenterol 1997 Dec;11(4):725-40

Department of Surgery, Flinders Medical Centre, Bedford Park, Adelaide, Australia.

Disordered motility of the biliary tract may be associated with the aetiology of common biliary tract conditions, such as gallstones. In this instance, treatment of the gallstone disease alleviates symptoms in the majority of patients. However, in up to 10% of patients, biliary motility disorders may present in the absence of gallstones or in patients after cholecystectomy. Read More

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December 1997
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