IBS affects 10–20% of the adult US population, is the most common diagnosis made by gastroenterologists, and is one of the top 10 reasons for visits to primary care physicians. IBS is the most common functional bowel disorder and affects predominantly women (70% of patients). This may be due to the fact that women more easily report their symptoms of abdominal pain, gas, bloating, and altered bowel movements. It may also be due to hormonal differences between men and women that may affect gut function and alter perception of pain related to abdominal distention. IBS can cause great discomfort, sometimes intermittent or continuous, for many decades in a patient’s life and can have a significantly negative impact on quality of life.

The prevalence of IBS in a typical primary care practice is 12% and in a typical gastroenterology practice is 28%. The estimated total yearly cost of IBS in the United States is $21 billion. One billion dollars is spent in direct costs such as diagnostic tests, physician and emergency department visits, hospitalizations, surgeries, and medications; $20 billion is spent on intangible costs such as reduced work productivity, absenteeism, and travel to consultations. The intangible costs of IBS are human suffering and impaired quality of life. IBS sufferers incur 74% more health care costs than non-IBS sufferers.

IBS primarily affects people in the prime of their lives, mostly between the ages of 20 and 40. Patient surveys from both the United States and the United Kingdom report an average disease duration of 11 years, with one-third of patients having symptoms for much longer. For many patients, symptoms occur frequently and significantly impair emotional, physical, and social well-being. Almost three-fourths of patients report symptoms more than once a week and about half report daily symptoms. In a telephone survey of female IBS sufferers in the United States, almost 40% reported pain and discomfort as intolerable without relief. Women with IBS reported 71% more abdominal surgeries than women without IBS (58% vs 34%). The rates of gallbladder operations, hysterectomies, and appendectomies were twice as high or higher among women with IBS. Twenty-five percent had been hospitalized overnight due to symptoms. Seventy-eight percent of women had limits on what they ate, 43% had limits on sports and recreational activity, 43% on social activity, 40% on vacation or travel, and 28% on sexual activity. Two-thirds of women were concerned about restroom availability wherever they went, one-third avoided group meetings, and 25% got up earlier for work. Even more frustrating was that only 39% of women were diagnosed with IBS by the first physician they saw; 3% saw eight or more physicians before receiving a diagnosis. Time from onset to diagnosis took an average of 3 years, and patients saw an average of three physicians before getting a diagnosis.

Patients with IBS were absent from work or school an average of 13 days per year compared with 5 days per year (P < .001) in patients without IBS. In another study, the quality of life of patients with IBS was significantly worse than that of patients with migraines, asthma, or gastroesophageal reflux disease (GERD). For this study, quality of life was measured in multiple domains, including physical functioning, pain, general health, vitality, social functioning, emotional functioning, and mental health.

Only about 25% of IBS patients actually consult a physician for their symptoms. Of these, only a small percentage visits a gastroenterologist. Patients who consult a primary care physician for their symptoms usually have mild symptoms and effective coping skills and social support. Of IBS patients who consult subspecialists, 60% or more may have psychological disturbances, including anxiety, somatoform or personality disorders, or chronic pain syndromes. Up to 35% of women who consult subspecialists for IBS have a history of sexual abuse.

A. Motility

Although disturbances in small bowel motility have been reported in IBS, none appear specific for the condition. Small bowel motility shows marked diurnal variability, and hence, consistent results can only be obtained with prolonged (at least 24 hour) recordings and large numbers of subjects. Small bowel motor disturbances reported include increased frequency and duration of discrete cluster contractions (DCC), increased frequency of the migrating motor complex (MMC), more retrograde duodenal and jejunal contractions, and an exaggerated motor response to meal ingestion, ileal distention, and cholecystokinin (CCK). Corticotrophin-releasing hormone (CRH) has been reported to increase the number of DCCs. Small bowel transit is faster in IBS patients with diarrhea (IBS-D) compared with constipation (IBS-C), and unlike in healthy controls, colonic distention does not appear to reduce duodenal motility in IBS patients, suggesting an impaired intestine-intestinal inhibitory reflex. The most consistent abnormality in the colon is an exaggerated motility response to meal ingestion. Rectal compliance or increased tension, or both, has also been reported in some studies in patients with IBS. This has been proposed as a possible mechanism for enhanced visceral sensation to balloon distention in IBS.

B. Visceral Hypersensitivity

Abdominal pain and discomfort cause considerable morbidity in IBS patients and are essential components of the Rome III criteria for diagnosis of IBS. Approximately two-thirds of IBS patients demonstrate heightened pain sensitivity to experimental gut stimulation, a phenomenon known as visceral hypersensitivity. Visceral hypersensitivity is thought to play an important role in the development of chronic pain and discomfort in IBS patients. It results from a combination of factors that involve both the peripheral and central nervous systems. During tissue injury, peripheral nociceptor terminals are exposed to a mixture of immune and inflammatory mediators, such as prostaglandins, leukotrienes, serotonin, histamine, cytokines, neurotrophic factors, and reactive metabolites. These inflammatory mediators act on nociceptor terminals, leading to the activation of intracellular signaling pathways, which in turn upregulate their sensitivity and excitability. This phenomenon has been termed peripheral sensitization. Peripheral sensitization is believed to cause pain hypersensitivity at the site of injury or inflammation, also known as primary hyperalgesia (increased sensitivity to painful stimuli) and allodynia (nonpainful stimuli are perceived as painful).

A secondary consequence of peripheral sensitization is the development of an area of hypersensitivity in the surrounding uninjured tissue (secondary hyperalgesia or allodynia). This phenomenon occurs due to an increase in the excitability and receptive fields of spinal neurons and results in recruitment and amplification of both non-nociceptive and nociceptive inputs from the adjacent healthy tissue.

Depending on the setting, about 6–17% of patients with IBS report their symptoms began with an episode of gut inflammation due to gastroenteritis. In addition, an increase in mucosal T lymphocytes has been reported in patients with IBS. Therefore, the environment of nociceptor terminals in the gut of IBS patients is likely to be altered, suggesting a role for peripheral sensitization. Evidence for central sensitization as an important mechanism for the development of visceral hypersensitivity in IBS patients comes from three main observations. First, in response to colon stimulation, patients with IBS have greater radiation of pain to somatic structures in comparison with healthy subjects. Second, a proportion of IBS patients also suffer from fibromyalgia, a condition characterized by somatic hyperalgesia. Finally, patients with IBS also often demonstrate hypersensitivity of proximal areas of the gut. The innervation of the different gut organs overlaps and converges with that of the somatic structures at the level of the spinal cord, and these phenomena can be explained by central sensitization of the spinal segments that demonstrate viscerovisceral and viscerosomatic convergence.

Alterations in brain processing in IBS patients can also contribute to visceral hypersensitivity. Brain imaging studies have begun to address the possible neural mechanisms of hypersensitivity in IBS patients, and a common finding has been compared with healthy controls; patients with IBS exhibit altered or enhanced activation of regions involved in pain processing, such as the anterior cingulated cortex, thalamus, insula, and prefrontal cortices, in response to experimental rectal pain.

C. Postinfective IBS

The prevalence of postinfective IBS varies from 17% in primary care in the United Kingdom to as little as 6% in tertiary care in the United States. Population surveys indicate a relative risk of 11.1–11.9% of developing IBS in the year following a bout of gastroenteritis. Known risk factors include the severity of the initial illness; bacterial toxigenicity; female sex; a range of adverse psychological factors, including neuroticism, hypochondriasis, anxiety, and depression; and adverse life events. Postinfective IBS has been reported after Shigella, Salmonella, and Campylobacter infections and does not appear specific to any organism.

The Walkerton Health Study followed the long-term effects of a large outbreak of acute gastroenteritis related to municipal water contamination involving a population of 5000 people in May 2000. In the initial study, all participants were divided into three strata: (1) those who reported no illness during the outbreak (controls); (2) those who reported an acute illness not substantiated by health records; and (3) those with an acute illness documented by health records (gastrointestinal symptoms, diarrhea lasting ≥3 days, or positive stool culture). Of 4561 participants who enrolled in the study in 2002–2003, 3200 returned in 2004, 2572 returned in 2006, and 2451 returned for their 8-year assessment. At years 2–3, the prevalence of diarrhea-predominant IBS was 28.3%, at year 4, 21.4%, at year 6, 14.3%, and at year 8, 15.4%. The risk factors for developing IBS were female sex, younger age, and fever or weight loss during the acute illness. This remarkable study shows that a substantial number of people will develop IBS, with symptoms that can persist for as long as 8 years, after an acute episode of gastroenteritis. Specific host characteristics and the acute enteritis illness can predict the long-term risk of postinfective IBS.

Histologic studies indicate that postinfective IBS is characterized by increased lymphocyte numbers in mucosal biopsies, an effect that is seen throughout the colon. Where the terminal ileum has been biopsied, increased mast cells have also been noted. Another change following inflammation is enterochromaffin cell hyperplasia. Whereas in most subjects, these changes resolve within 3 months, in IBS patients, the levels of both lymphocytes and enteroendocrine cells remain elevated. Increased enterochromaffin cell numbers are associated with an increase in postprandial 5-HT release, an abnormality shown in both postinfective IBS and in diarrhea-predominant IBS without an obvious postinfective origin. Immediately after gastroenteritis affecting the small bowel, there may be transient lactose intolerance, which is particularly obvious in young children. However, in adults with postinfective IBS, who by definition have had symptoms for over 6 months, the incidence of lactose malabsorption is no different from uninfected controls.

D. Stress Response

The response of an organism to external stressors is mediated through the integration of the hypothalamic-pituitary-adrenal axis (HPA) and the sympathetic branch of the autonomic nervous system with the host immune system. A recent model for the pathogenesis of IBS proposes altered stress circuits in predisposed individuals, which are triggered by external stressors resulting in the development of gut symptoms. In postinfective IBS, the persistence of chronic inflammatory mucosal changes and enterochromaffin cell hyperplasia that persists after eradication of the infectious organism are consistent with an inadequate physiologic response to gut inflammation, in particular, an inadequate cortisol or altered sympathetic response. The key interplay between the autonomic nervous system and the HPA axis in regulating gut mucosal immunology has been explored through research looking at how the stress response, which activates both of these systems, may be important in IBS. Environmental stressors are important in predisposing toward IBS and in perpetuating the symptoms of IBS. Prior life stressors and a history of childhood abuse predispose toward developing IBS in later life. Psychiatric illness episodes or anxiety-provoking situations preceded the onset of bowel symptoms in two-thirds of IBS patients being treated in tertiary care centers; in addition, IBS patients report significantly more negative life events than matched peptic ulcer patients. In addition, psychological traits such as hypochondriasis, anxiety, and depression predispose previously healthy individuals who develop gastroenteritis to go on to develop symptoms of IBS. In fact, a subgroup of IBS patients have an exaggerated endocrine stress response, as shown by a heightened release of adrenocorticotropic hormone and cortisol in response to exogenous corticotropin-releasing factor administration. This exaggerated stress response seems to be associated with mucosal immune activation.

IBS is a disease that can be caused by many factors. Disturbed bowel motility, visceral hypersensitivity, bacterial overgrowth, and psychological problems can all contribute to causing or exacerbating IBS. There are several important, take-home points in treating IBS. First, clinicians must take a good history and rule out “red flags.” Celiac sprue, bacterial overgrowth, and microscopic colitis, among many other conditions, can masquerade as IBS. Second, clinicians should provide reassurance and close follow-up at first to make sure the diagnosis is correct. Recall that the Rome III criteria have high specificity in making the diagnosis of IBS. Third, despite the lack of evidence-based studies, diet plays a role in exacerbating gastrointestinal symptoms, and a good dietary history should be taken. Fourth, clinicians should not forget the psychological component of IBS. Many patients with IBS have coexisting depression and anxiety, and patients with severe IBS often have a history of physical and sexual abuse. Lastly, there are only a few newer medications with good data from randomized controlled trials. Given the paucity of specific medicines with positive results in the evidence-based medical literature, treatment is often a trial and error process. However, a combination of dietary and lifestyle changes, relaxation training or psychotherapy, and individualized IBS medicines tailored to each patient’s symptoms usually improves quality of life.

A. Symptoms and Signs

As the Rome III criteria indicate (Table 24–1), the key features are abdominal pain or discomfort that is clearly linked to bowel function, either being relieved by defecation or associated with a change in stool form or consistency. These symptoms are not explained by biochemical or structural abnormalities. Symptoms should be present for at least 6 months to clearly distinguish those from other conditions such as infections, which often pass quickly, or progressive diseases such as bowel cancer that are usually diagnosed within 6 months of symptom onset. Symptoms that are common in IBS but are not part of the Rome III criteria include bloating, abnormal stool form (hard, loose, or both), abnormal stool frequency (<3 times/week or >3 times/week), straining at defecation, urgency, feeling of incomplete evacuation, and the passage of mucus per rectum. Most patients experience flares intermittently, with symptoms lasting 2–4 days followed by periods of remission. In women, symptoms can be worse at the time of menstruation and can cycle with the menstrual cycle. One common symptom of IBS not part of the Rome III criteria is repeated defecation in the morning (morning rush) when stool consistency changes from solid to liquid as the colon contents are evacuated.

One important exception to the Rome III criteria is patients who feel abdominal pain continuously. The diagnosis in this case is likely functional abdominal pain, an unusual, particularly severe condition in which patients respond poorly to treatment and often have severe underlying psychological disturbances.

IBS is considered a painful condition, and those with painless bowel dysfunction are labeled as having “functional constipation” or “functional diarrhea.” Some of the distinguishing characteristics of IBS-C and functional constipation are detailed in Table 24–2.

1. IBS subtype classification

The Rome III subclassification is based solely on stool consistency and not frequency, urgency, and straining and is thus easy to use (Table 24–3

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