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Irritable Bowel Syndrome

  • Author: Jenifer K Lehrer, MD; Chief Editor: BS Anand, MD  more...
Updated: Jun 16, 2015

Practice Essentials

Irritable bowel syndrome (IBS) is a functional GI disorder characterized by abdominal pain and altered bowel habits in the absence of a specific and unique organic pathology, although microscopic inflammation has been documented in some patients.[2] Population-based studies estimate the prevalence of irritable bowel syndrome at 10-20% and the incidence of irritable bowel syndrome at 1-2% per year.

Signs and symptoms

Manifestations of IBS are as follows:

  • Altered bowel habits
  • Abdominal pain
  • Abdominal distention

Altered bowel habits in IBS may have the following characteristics:

  • Constipation variably results in complaints of hard stools of narrow caliber, painful or infrequent defecation, and intractability to laxatives
  • Diarrhea usually is described as small volumes of loose stool, with evacuation preceded by urgency or frequent defecation
  • Postprandial urgency is common, as is alternation between constipation and diarrhea
  • Characteristically, one feature predominates in a single patient, but significant variability exists among patients

Abdominal pain in IBS is protean, but may have the following characteristics:

  • Pain frequently is diffuse without radiation
  • Common sites of pain include the lower abdomen, specifically the left lower quadrant
  • Acute episodes of sharp pain are often superimposed on a more constant dull ache
  • Meals may precipitate pain
  • Defecation commonly improves pain but may not fully relieve it
  • Pain from presumed gas pockets in the splenic flexure may masquerade as anterior chest pain or left upper quadrant abdominal pain

Additional symptoms consistent with irritable bowel syndrome are as follows:

  • Clear or white mucorrhea of a noninflammatory etiology
  • Dyspepsia, heartburn
  • Nausea, vomiting
  • Sexual dysfunction (including dyspareunia and poor libido)
  • Urinary frequency and urgency have been noted
  • Worsening of symptoms in the perimenstrual period
  • Comorbid fibromyalgia
  • Stressor-related symptoms

Symptoms not consistent with irritable bowel syndrome should alert the clinician to the possibility of an organic pathology. Inconsistent symptoms include the following:

  • Onset in middle age or older
  • Acute symptoms (irritable bowel syndrome is defined by chronicity)
  • Progressive symptoms
  • Nocturnal symptoms
  • Anorexia or weight loss
  • Fever
  • Rectal bleeding
  • Painless diarrhea
  • Steatorrhea
  • Gluten intolerance

See Clinical Presentation for more detail.


The Rome III criteria for the diagnosis of irritable bowel syndrome[3] require that patients have had recurrent abdominal pain or discomfort at least 3 days per month during the previous 3 months that is associated with 2 or more of the following:

  • Relieved by defecation
  • Onset associated with a change in stool frequency
  • Onset associated with a change in stool form or appearance
  • Supporting symptoms include the following:
  • Altered stool frequency
  • Altered stool form
  • Altered stool passage (straining and/or urgency)
  • Mucorrhea
  • Abdominal bloating or subjective distention

Four bowel patterns may be seen with irritable bowel syndrome. These patterns include the following:

  • IBS-D (diarrhea predominant)
  • IBS-C (constipation predominant)
  • IBS-M (mixed diarrhea and constipation)
  • IBS-A (alternating diarrhea and constipation)

The usefulness of these subtypes is debatable. Notably, within 1 year, 75% of patients change subtypes, and 29% switch between constipation-predominant IBS and diarrhea-predominant IBS.

A comprehensive history, a physical examination, and tailored laboratory and radiographic studies can establish a diagnosis of irritable bowel syndrome in most patients. The American College of Gastroenterologists does not recommend laboratory testing or diagnostic imaging in patients younger than 50 years with typical IBS symptoms and without the following “alarm features”[4] :

  • Weight loss
  • Iron deficiency anemia
  • Family history of certain organic GI illnesses (eg, inflammatory bowel disease, celiac sprue, colorectal cancer)

Screening studies to rule out disorders other than IBS include the following:

  • Complete blood count with differential to screen for anemia, inflammation, and infection
  • A comprehensive metabolic panel to evaluate for metabolic disorders and to rule out dehydration/electrolyte abnormalities in patients with diarrhea
  • Stool examinations for ova and parasites, enteric pathogens, leukocytes, Clostridium difficile toxin, and possibly Giardia antigen

History-specific studies include the following:

  • Hydrogen breath testing to exclude bacterial overgrowth in patients with diarrhea to screen for lactose and/or fructose intolerance
  • Tissue transglutaminase antibody testing and small bowel biopsy in IBS-D to diagnose celiac disease.
  • Thyroid function tests
  • Serum calcium testing to screen for hyperparathyroidism
  • Erythrocyte sedimentation rate and C-reactive protein measurement are nonspecific screening tests for inflammation

See Workup for more detail.


Management of irritable bowel syndrome consists primarily of providing psychological support and recommending dietary measures. Pharmacologic treatment is adjunctive and should be directed at symptoms.

Dietary measures may include the following:

  • Fiber supplementation may improve symptoms of constipation and diarrhea
  • Polycarbophil compounds (eg, Citrucel, FiberCon) may produce less flatulence than psyllium compounds (eg, Metamucil)
  • Judicious water intake is recommended in patients who predominantly experience constipation
  • Caffeine avoidance may limit anxiety and symptom exacerbation
  • Legume avoidance may decrease abdominal bloating
  • Lactose, fructose, and/or FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) should be limited or avoided in patients with these contributing disorders
  • Probiotics are being studied for their use in decreasing IBS symptoms

Although the evidence is mixed regarding long-term improvement in GI symptoms with successful treatment of psychiatric comorbidities, the American College of Gastroenterology has concluded the following:

  • Psychological interventions, cognitive-behavioral therapy, dynamic psychotherapy, and hypnotherapy are more effective than placebo
  • Relaxation therapy is no more effective than usual care

Pharmacologic agents used for management of symptoms in IBS include the following:

  • Anticholinergics (eg, dicyclomine, hyoscyamine)
  • Antidiarrheals (eg, diphenoxylate, loperamide)
  • Tricyclic antidepressants (eg, imipramine, amitriptyline)
  • Prokinetics
  • Bulk-forming laxatives
  • Serotonin receptor antagonists (eg, alosetron)
  • Chloride channel activators (eg, lubiprostone)
  • Guanylate cyclase C (GC-C) agonists (eg, linaclotide)
  • Antispasmodics (eg, peppermint oil, pinaverium, trimebutine, cimetropium/dicyclomine) [5]
  • Potentially, rifaxamin (this is still investigational and not FDA approved)

See Treatment and Medication for more detail.



Irritable bowel syndrome (IBS) is a functional GI disorder characterized by abdominal pain and altered bowel habits in the absence of a specific and unique organic pathology. Osler coined the term mucous colitis in 1892 when he wrote of a disorder of mucorrhea and abdominal colic with a high incidence in patients with coincident psychopathology. Since that time, the syndrome has been referred to by sundry terms, including spastic colon, irritable colon, and nervous colon.

In the past, irritable bowel syndrome has been considered a diagnosis of exclusion; however, it is no longer considered a diagnosis of exclusion, but it does have a broad differential diagnosis.[1] No specific motility or structural correlates have been consistently demonstrated; however, experts suggest the use of available guidelines can minimize testing and aid in diagnosis.



Traditional theories regarding pathophysiology may be visualized as a 3-part complex of altered GI motility, visceral hyperalgesia, and psychopathology. A unifying mechanism is still unproven.

Altered GI motility

Altered GI motility includes distinct aberrations in small and large bowel motility.

The myoelectric activity of the colon is composed of background slow waves with superimposed spike potentials. Colonic dysmotility in irritable bowel syndrome manifests as variations in slow-wave frequency and a blunted, late-peaking, postprandial response of spike potentials. Patients who are prone to diarrhea demonstrate this disparity to a greater degree than patients who are prone to constipation.

Small bowel dysmotility manifests in delayed meal transit in patients prone to constipation and in accelerated meal transit in patients prone to diarrhea. In addition, patients exhibit shorter intervals between migratory motor complexes (the predominant interdigestive small bowel motor patterns).

Current theories integrate these widespread motility aberrations and hypothesize a generalized smooth muscle hyperresponsiveness. They describe increased urinary symptoms, including frequency, urgency, nocturia, and hyperresponsiveness to methacholine challenge.

Visceral hyperalgesia

Visceral hyperalgesia is the second part of the traditional 3-part complex that characterizes irritable bowel syndrome.

Enhanced perception of normal motility and visceral pain characterizes irritable bowel syndrome. Rectosigmoid and small bowel balloon inflation produces pain at lower volumes in patients than in controls. Notably, hypersensitivity appears with rapid but not with gradual distention.

Patients who are affected describe widened dermatomal distributions of referred pain. Sensitization of the intestinal afferent nociceptive pathways that synapse in the dorsal horn of the spinal cord provides a unifying mechanism.


Psychopathology is the third aspect. Associations between psychiatric disturbances and irritable bowel syndrome pathogenesis are not clearly defined.

Patients with psychological disturbances relate more frequent and debilitating illness than control populations. Patients who seek medical care have a higher incidence of panic disorder, major depression, anxiety disorder, and hypochondriasis than control populations. A study has suggested that patients with irritable bowel syndrome may have suicidal ideation and/or suicide attempts strictly as a result of their bowel symptoms.[6] Clinical alertness to depression and hopelessness is mandatory. This is underscored by another study that revealed that patient complaints that relate to functional bowel disorders may be trivialized.

An Axis I disorder coincides with the onset of GI symptoms in as many as 77% of patients. A higher prevalence of physical and sexual abuse has been demonstrated in patients with irritable bowel syndrome. Whether psychopathology incites the development of irritable bowel syndrome or vice versa remains unclear.

Microscopic inflammation

Microscopic inflammation has been documented in some patients.[2] This concept is groundbreaking in that irritable bowel syndrome had previously been considered to have no demonstrable pathologic alterations.

Both colonic inflammation and small bowel inflammation have been discovered in a subset of patients with irritable bowel syndrome, as well as in patients with the onset of irritable bowel syndrome after infectious enteritis (postinfectious irritable bowel syndrome). Risk factors for developing postinfectious irritable bowel syndrome include longer duration of illness, the type of pathogen involved, smoking, female gender, an absence of vomiting during the infectious illness, and young age.[7]

Laparoscopic full-thickness jejunal biopsy samples revealed infiltration of lymphocytes into the myenteric plexus and intraepithelial lymphocytes in a subset of patients in one study.[8] Neuronal degeneration of the myenteric plexus was also present in some patients.

Patients with postinfectious irritable bowel syndrome may have increased numbers of colonic mucosal lymphocytes and enteroendocrine cells. Enteroendocrine cells in postinfectious irritable bowel syndrome appear to secrete high levels of serotonin, increasing colonic secretion and possibly leading to diarrhea.

Alterations in the intestinal biome

Small bowel bacterial overgrowth has been heralded as a unifying mechanism for the symptoms of bloating and distention, common to patients with irritable bowel syndrome. This has led to proposed treatments with probiotics and antibiotics.

The fecal microflora also differs among patients with irritable bowel syndrome versus controls. A sophisticated molecular analysis suggested an alteration in the patterns and the contents of gut bacteria.[9]



The causes of irritable bowel syndrome remain poorly defined, but they are being avidly researched.

Postulated etiologies of irritable bowel syndrome

Abnormal transit profiles and an enhanced perception of normal motility may exist. Up to one third of patients with irritable bowel syndrome may have altered colonic transit. Delayed colonic motility may be more common in patients with constipation-predominant irritable bowel syndrome than in healthy controls. Similarly, accelerated colonic transit may be more common in patients with diarrhea-predominant disease than in healthy controls.[10] Local histamine sensitization of the afferent neuron causing earlier depolarization may occur.

Causes related to enteric infection

Colonic muscle hyperreactivity and neural and immunologic alterations of the colon and small bowel may persist after gastroenteritis. Psychological comorbidity independently predisposes the patient to the development of postinfectious irritable bowel syndrome. Psychological illness may create a proinflammatory cytokine milieu, leading to irritable bowel syndrome through an undefined mechanism after acute infection.

Infection with Giardia lamblia has been shown to lead to an increased prevalence of irritable bowel syndrome, as well as chronic fatigue syndrome. In a historic cohort study of patients with G lamblia infection as detected by stool cysts, the prevalence of irritable bowel syndrome was 46.1% as long as 3 years after exposure, compared with 14% in controls.[11]

Central neurohormonal mechanisms

Abnormal glutamate activation of N- methyl-D- aspartate (NMDA) receptors, activation of nitric oxide synthetase, activation of neurokinin receptors, and induction of calcitonin gene–related peptide have been observed.

The limbic system mediation of emotion and autonomic response enhances bowel motility and reduces gastric motility to a greater degree in patients who are affected than in controls. Limbic system abnormalities, as demonstrated by positron emission tomography, have been described in patients with irritable bowel syndrome and in those with major depression.

The hypothalamic-pituitary axis may be intimately involved in the origin. Motility disturbances correspond to an increase in hypothalamic corticotropin-releasing factor (CRF) production in response to stress. CRF antagonists eliminate these changes.

Additional etiologic factors

Intestinal permeability

Intestinal permeability appears to be increased, especially in diarrhea-predominant irritable bowel syndrome.[12]

Alterations in the intestinal biome

As discussed in Pathophysiology, Pimentel and colleagues have proposed that small bowel bacterial overgrowth provides a unifying mechanism for the common symptoms of bloating and gaseous distention in patients with irritable bowel syndrome.[13]

There is a relationship between the organisms that live in the intestine and the immune system, and this relationship is not yet fully understood.[12]

Dietary intolerance

Bloating and distention may also occur from intolerance to dietary fats. Reflex-mediated small bowel gas clearance is more impaired by ingestion of lipids in patients with irritable bowel syndrome than in patients without the disorder.

Studies of elimination and challenge diets have suggested that poorly absorbed short-chain carbohydrates, in the form of fructose and fructans, may create symptoms among patients with irritable bowel syndrome, as measured by a visual analogue scale.[14]

Research suggests that neuronal degeneration and myenteric plexus lymphocytosis may exist in the proximal jejunum. Additionally, colonic lymphocytosis and enteroendocrine cell hyperplasia have been demonstrated in some patients.



Population-based studies estimate the prevalence of irritable bowel syndrome at 10-20% and the incidence of irritable bowel syndrome at 1-2% per year. Of people with irritable bowel syndrome, approximately 10-20% seek medical care. An estimated 20-50% of gastroenterology referrals relate to this symptom complex. The incidence is markedly different among countries.

American and European cultures demonstrate similar frequencies of irritable bowel syndrome across racial and ethnic lines. However, within the United States, survey questionnaires indicate a lower prevalence of irritable bowel syndrome in Hispanics in Texas and Asians in California. Populations of Asia and Africa may have a lower prevalence of irritable bowel syndrome. The role of different cultural influences and varying health care–seeking behaviors is unclear.

In Western countries, women are 2-3 times more likely to develop irritable bowel syndrome than men, although males represent 70-80% of patients with irritable bowel syndrome in the Indian subcontinent. Women seek health care more often, but the irritable bowel syndrome–specific influence of this occurrence remains unknown. Other factors, such as a probably greater incidence of abuse in women, may confound interpretation of this statistic.

Patients often retrospectively note the onset of abdominal pain and altered bowel habits in childhood. Approximately 50% of people with irritable bowel syndrome report symptoms beginning before they were aged 35 years. The development of symptoms in people older than 40 years does not exclude irritable bowel syndrome but should prompt a closer search for an underlying organic etiology.



Irritable bowel syndrome is a chronic relapsing disorder characterized by recurrent symptoms of variable severity; however, life expectancy remains similar to that of the general population. Clinicians must be forthcoming with patients because knowledge of the condition may help allay undue fears as their disease waxes and wanes. Irritable bowel syndrome does not increase the mortality or the risk of inflammatory bowel disease or cancer.

Patients with IBS may carry an increased risk of ectopic pregnancy and miscarriage, but not stillbirth. The reasons for this are unknown. Whether the risk increases because of the irritable bowel syndrome itself, or because of another factor such as medications used for IBS, is also unknown.[15]

The principal associated physical morbidities of irritable bowel syndrome include abdominal pain and lifestyle modifications secondary to altered bowel habits. Work absenteeism resulting in lost wages is more frequent in patients with irritable bowel syndrome.


Patient Education

Patient education remains the cornerstone of successful treatment of irritable bowel syndrome. Teach the patient to acknowledge stressors and to develop avoidance techniques. Many patients successfully manage their symptoms with attention to dietary triggers.

For patient education resources, see Digestive Disorders Center, as well as Irritable Bowel Syndrome (IBS), Inflammatory Bowel Disease (IBD), and Chronic Pain.

Contributor Information and Disclosures

Jenifer K Lehrer, MD Attending Physician, Department of Gastroenterology and Hepatology, Aria Health System, Philadelphia

Jenifer K Lehrer, MD is a member of the following medical societies: American College of Gastroenterology, American Medical Association, American Gastroenterological Association

Disclosure: Nothing to disclose.


Gary R Lichtenstein, MD Professor of Medicine, Director, Center for Inflammatory Bowel Disease, Department of Medicine, Division of Gastroenterology, University of Pennsylvania School of Medicine

Gary R Lichtenstein, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.


Douglas M Heuman, MD, FACP, FACG, AGAF Chief of GI, Hepatology, and Nutrition at North Shore University Hospital/Long Island Jewish Medical Center; Professor, Department of Medicine, Hofstra North Shore-LIJ School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association

Disclosure: Novartis Grant/research funds Other; Bayer Grant/research funds Other; Otsuka Grant/research funds None; Bristol Myers Squibb Grant/research funds Other; Scynexis None None; Salix Grant/research funds Other; MannKind Other

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Rajeev Vasudeva, MD, FACG Clinical Professor of Medicine, Consultants in Gastroenterology, University of South Carolina School of Medicine

Rajeev Vasudeva, MD, FACG is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, Columbia Medical Society, South Carolina Gastroenterology Association, and South Carolina Medical Association

Disclosure: Pricara Honoraria Speaking and teaching; UCB Consulting fee Consulting

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