Fast Facts: Inflammatory Bowel Disease

F. Shanahan, D.S. Rampton

Description

Inflammatory bowel disease (IBD) comprises two idiopathic chronic relapsing and remitting inflammatory disorders of the gastrointestinal tract: ulcerative colitis and Crohn’s disease. Understanding of the etiopathogenesis of IBD, and how best to treat it, continues to advance rapidly and has led to the need for this new edition. Chapter 1 has been substantially revised, emphasizing recent data that indicate how the gut microbiome and its human host may interact to cause IBD in genetically susceptible people. In later chapters, the latest thinking on how best to use immunomodulatory and biological drugs is discussed, along with new sections on recently introduced and imminent therapies. This book is aimed at non-specialist doctors (particularly primary care providers and hospital doctors in training), nurses, stoma therapists, dieticians, psychologists, counselors, social workers and other professionals involved in the care of patients with IBD. Contents: • Etiopathogenesis • Clinical features and intestinal complications • Extraintestinal manifestations and complications • Diagnosis • Drugs used to treat IBD • Principles of management • Medical management of ulcerative colitis • Medical management of Crohn’s disease • Surgery • IBD in pregnancy, childhood and old age • Prognosis

Informations

• Publié par: S. Karger AG
• Date de parution: 26 janvier 2021
• Nombre de lectures: 1
• EAN13: 9783318066562
• Langue: English
• Poids de l'ouvrage: 5 Mo

Extrait

Fast Facts: Inflammatory Bowel Disease
First published 2000; second edition 2006; third edition 2008, reprinted 2009 and 2010; fourth edition 2014; fifth edition 2016
Sixth edition 2020
Text 2020 David S Rampton, Fergus Shanahan
2020 in this edition S. Karger Publishers Limited
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ISBN 978-3-318-06655-5
Rampton DS (David)
Fast Facts: Inflammatory Bowel Disease/
David S Rampton, Fergus Shanahan
Cover image: Endoscopic view of a colon affected by Crohn s disease, showing extensive ulceration (white areas). Camal, ISM/Science Photo Library.
Medical illustrations by Dee McLean, London, UK. Typesetting by Amnet, Chennai, India. Printed in the UK with Xpedient Print.
List of abbreviations
Introduction
Etiopathogenesis
Clinical features and intestinal complications
Extraintestinal manifestations and complications
Diagnosis
Drugs used to treat IBD
Principles of management
Medical management of ulcerative colitis
Medical management of Crohn s disease
Surgery
IBD in pregnancy, childhood and old age
Prognosis
Useful resources
Index
List of abbreviations
5-ASA: 5-aminosalicylate
ADA: anti-drug antibodies
AS: ankylosing spondylitis
ASCA: anti- Saccharomyces cerevisiae antibody
ATG16L1: autophagy-related 16 like 1 (gene)
BMI: body mass index
CBC: complete blood count
CD: Crohn s disease
CMV: cytomegalovirus
COX: cyclo-oxygenase
CRP: C-reactive protein
CT: computed tomography
CUTE: colitis of uncertain type or etiology
ERCP: endoscopic retrograde cholangiopancreatography
HIV: human immunodeficiency virus
HLA: human leukocyte antigen
IBD: inflammatory bowel disease
IBS: irritable bowel syndrome
IFN: interferon
Ig: immunoglobulin
IL: interleukin
IRGM: immunity-related GTPase family, M protein (gene)
JAK: Janus kinase
LRRK2: leucine-rich repeat kinase 2 (gene)
MAP: mitogen-activated protein
MDP: muramyl dipeptide
MMP: methyl mercaptopurine
MMX: multimatrix
MP: mercaptopurine
MRCP: magnetic resonance cholangiopancreatography
MRI: magnetic resonance imaging
NF- B: nuclear (transcription) factor B
NOD2: nucleotide-binding oligomerization domain containing 2 (gene)
NSAID: non-steroidal anti-inflammatory drug
pANCA: perinuclear antineutrophil cytoplasmic antibody
PCR: polymerase chain reaction
PML: progressive multifocal leukoencephalopathy
PPAR: peroxisome proliferator-activated receptor
SeHCAT: 75 selenium homocholic acid taurine
TB: tuberculosis
99 Tc-HMPAO: 99 technetium hexamethylpropyleneamine oxime
TGF: transforming growth factor
TGN: thioguanine nucleotide
Th: T helper cell
TNF: tumor necrosis factor
TPMT: thiopurine methyltransferase
Treg: regulatory T cell
UC: ulcerative colitis
Introduction
Inflammatory bowel disease (IBD) comprises two idiopathic chronic relapsing and remitting inflammatory disorders of the gastrointestinal tract: ulcerative colitis and Crohn s disease. Our understanding of the etiopathogenesis of IBD, and how best to treat it, continues to advance rapidly and has led to the need for this new edition.
We have substantially revised the opening chapter, emphasizing recent data that indicate how the gut microbiome and its human host may interact to cause IBD in genetically susceptible people. We also discuss the latest thinking on how best to use immunomodulatory and biological drugs, whether alone or in combination, along with new sections on recently introduced and imminent therapies.
Converting the concept of personalized therapy from an aim into a reality will continue to be a focus of clinical research. Detailed assessment of the genotype, immune function and other features of the individual will help us to identify who will respond well and who will be at risk of side effects from specific drugs: treatment for individual patients will then be selected more appositely.
We must also continue to embrace the holistic approach to management of these chronic diseases. Doctors often used to overlook problems such as anemia, mood disturbance, fatigue and osteoporosis, yet each of these is a common if not always easily reversible contributor to impaired quality of life for people with IBD. In this time of increasing specialization, high-technology diagnostics, molecular therapeutics and evidence-based everything, the doctor-patient relationship will come under increasing scrutiny and change. Technology helps to clarify the objective aspects of the disease but not the unique subjective experience of the person with the illness.
Health professionals caring for people with IBD need to care about people with IBD. This requires an interest in the condition, a commitment to long-term follow-up and more than a little compassion. This book is aimed at non-specialist doctors (particularly primary care providers and hospital doctors in training), nurses, stoma therapists, dieticians, psychologists, counselors, social workers and other professionals involved in the care of patients with IBD. Medical students should also find it helpful. We hope, too, that people with IBD may benefit from reading this overview of their illness.
1 Etiopathogenesis
Overview
The collective term inflammatory bowel disease (IBD) obscures the distinctive nature of Crohn s disease and ulcerative colitis. These are separate conditions, with some overlapping and several distinct features. Crohn s disease in particular and ulcerative colitis to a lesser degree are heterogeneous, with more than one underlying defect or mechanism leading to a similar clinical outcome. In addition, different mechanisms may account for different subsets of disease.
Like many other chronic inflammatory disorders, tissue damage is immune-mediated and arises from a variable interaction between genetic susceptibility factors and environmental modifiers, the most proximate of which is the indigenous gut microbiota ( Figure 1.1 ). The importance of the role of the gut microbiome in the etiopathogenesis of IBD is being increasingly recognized as researchers unravel its complexity and its multiple interactions with the human host ( Table 1.1 ). 1
Early human lifestyle and risk of IBD
The epidemiological features of Crohn s disease and ulcerative colitis in modern societies are well established ( Table 1.3 ), but hide key insights derived from global studies. 3 The most consistent observation has been the abrupt increase in incidence and prevalence of both forms of IBD within one to two generations in societies undergoing socioeconomic development. This cannot be attributed to genetic changes alone.
Evidence from migration. Studies of migrants from developing to developed countries have shown that the influence of modern lifestyle and the environment begins during birth and infancy, long before the onset of disease. The younger a migrant is when moving from a country with a low risk of IBD to a region with high frequencies of IBD, the greater the risk of developing IBD.

Figure 1.1 Combined events ( perfect storm ) leading to cycles of IBD. Lifestyle influences associated with socioeconomic development operate in early childhood, particularly the first 3-4 years when the gut microbiome is being assembled and the immune and other systems within the host are maturing. External triggers such as infections, drugs and tobacco may act directly on the host and/or on the microbiome. Dietary changes in modern societies include consumption of low-fiber, processed, energy-dense, high-animal-fat foods. The genetics of IBD is outlined in Table 1.2 .

TABLE 1.1
The gut microbiome 1
The gut contains more than 1000 bacterial species, bacteriophages (phageome), viruses (virome) and fungi (mycobiome), the importance of which to human health and disease is only just being realized.
The gut (mainly the colon) contains more bacteria than the human body has cells. The number of genes in the microbiome (metagenome) is threefold higher than in the human genome.
The gut microbiome interacts widely with the human host, influencing not only digestion and absorption, but also the host s mucosal defence mechanisms, immune function and metabolism.
The composition and function of the microb