The irritable bowel syndrome (IBS) is a chronic and sometimes disabling functional bowel disorder.1,2 Traditionally, this functional diagnostic label has been applied when no obvious structural or biochemical abnormalities are found, but emerging evidence suggests that distinct pathophysiological
disturbances may account for the symptoms and that IBS is unlikely to be one disease or merely a psychiatric (somatosensory) disorder.2 The Rome IV
criteria,1 derived from a consensus process by a multinational group of experts in functional gastrointestinal disorders, constitute the current standard for diagnosing IBS. According to these criteria, IBS is diagnosed on the basis of recurrent abdominal pain related to defecation or in association with a change in stool frequency or form (Table 1). Bloating is a common accompanying symptom. Symptoms must be chronic, occurring at least once per week, on average, in the previous 3 months, with a duration of at least 6 months.IBS negatively affects quality of life and work productivity. It has been estimated that patients would give up 10 to 15 years of life expectancy for an instant cure of the disease.3 The prevalence of IBS in the United States is between 7% and 16%, and the condition is most common in women and young people.4 Direct costs associated with IBS in the United States have been estimated, conservatively, at more than $1 billion.5 Thus, diagnosing IBS accurately, minimizing invasive investigations,and recommending effective treatment have an important role in efforts to reduce the societal and economic effects of the disease.
Classification
On the basis of the Rome IV criteria, IBS is classified into four subtypes (IBS with diarrhea, IBS with constipation, IBS with mixed symptoms of constipation and diarrhea, or unsubtyped IBS) according to patients’ reports of the proportion of time they have hard or lumpy stools versus loose or watery stools.1 The rationale for these subtypes is to improve the homogeneity of patients recruited for clinical trials, guide effective diagnosis and therapy, and increase knowledge of potential pathophysiological mechanisms.
Rome IV Criteria for the Irritable Bowel Syndrome
Diagnostic Algorithm for the Irritable Bowel Syndrome (IBS)
IBS can be accurately diagnosed with the use of a stepwise approach.Patients with suspected IBS have symptoms of abdominal pain1; the absence of abdominal pain precludes the diagnosis. Disordered bowel habits also need to be present. Abdominal bloating is not required but is frequently present and supports the diagnosis. A detailed history should be obtained to rule out warning signs and to consider disorders that can mimic IBS (e.g.,carbohydrate malabsorption, celiac disease, ovarian cancer, and microscopiccolitis). Physical examination in patients with IBS generally reveals no abnormalities
other than abdominal tenderness, which is more common in the lower abdomen than in the upper abdomen; tenderness is not increased by tensing abdominal wall muscles. The presence of ascites, hepatosplenomegaly,enlarged lymph nodes, or a mass should prompt the clinician to seek an alternative diagnosis. A digital rectal examination should be performed,especially in patients with constipation; overlapping pelvic-floor
dyssynergia can be identified with a careful digital examination. In the absence
of warning signs, the Rome IV criteria should be applied to make a positive diagnosis. The clinician may order appropriate limited diagnostic testing to rule out other, less common, causes of similar symptoms. The Bristol Stool Form Scale can be used to accurately classify the patient as having IBS with constipation, IBS with diarrhea, or IBS with mixed symptoms of constipation and diarrhea. Treatment should be initiated as soon as the diagnosis is made and should focus on the predominant symptoms.
Pathogenesis of IBS
IBS has traditionally been thought of as a brain–gut disorder (Panel A). In susceptible persons (e.g., those with a genetic predisposition or exposure to environmental factors), an abnormal stress response, in combination with psychological distress (e.g., anxiety,depression,or somatization), and an infectious or inflammatory response may alter intestinal permeability and initiate a cascade of events (e.g., infiltration of inflammatory cells, localized edema, and release of cytokines or chemokines) that results in the development of IBS symptoms. Recent data show that immunocytes may play an important role in some patients. Coexisting depression, somatization, and catastrophization may also mediate changes in gut permeability, the immune system, and the microbiome, leading to the development of IBS symptoms. The presence of IBS symptoms may exacerbate symptoms of anxiety, depression,or somatization, further intensifying the gastrointestinal symptoms. Emerging data show that in up to half of patients with IBS, gastrointestinal symptoms develop first, with subsequent development of mood disorders(Panel B). Changes in the gut microbiome and the release of inflammatory mediators may be responsible for the central nervous system (CNS) disorders that arise after the development of IBS symptoms. The ensuing psychological distress may further exacerbate IBS symptoms.
Theoretical Model of the Pathophysiology of IBS
In healthy persons, tight junctions prevent luminal gastrointestinal tract material (e.g., chemicals, bacteria, medications, and food antigens) from entering the subepithelial space, and intestinal flora play a critical role in maintaining pH and nourishing epithelial cells, as well as completing the process of digestion, which results in the production of intestinal gas (e.g., hydrogen, carbon dioxide, and methane). In susceptible persons, however, it is postulated that infection or consumption of certain foods (e.g., foods containing fructans or gluten)increases intestinal permeability by altering tight junctions. Localized inflammation then develops, with a subsequent influx of inflammatory cells. Inflammatory mediators are released, altering neuromuscular function within the luminal gastrointestinal tract. This may lead to symptoms of abdominal pain and accelerated or delayed transit through the gastrointestinal tract with consequent diarrhea or constipation, respectively. Symptoms of bloating and distention may develop, in part because of changes in the normal gut flora and excess gas production, with abnormal intestinosomatic reflex responses. Disaccharidase deficiency (e.g., congenital sucrose–isomaltase deficiency) and alterations in normal ion-channel function may lead to IBS symptoms in some patients. Not all the pathophysiological
processes shown occur in all patients with IBS or in all IBS subtypes. Rather, the wide range of pathophysiological abnormalities identified to date in patients with IBS are shown. TNF-α denotes tumor necrosis factor α.
Interventions for Patients with the Irritable Bowel Syndrome, According to Efficacy, Level of Evidence, Side Effects, and Cost
联系客服
