Practice Essentials
Irritable bowel syndrome (IBS) is a disorder of gut-brain interactions (DGBI). DGBIs are a group of gastrointestinal (GI) disorders that occur from alteration of the interconnected gut-brain pathways. This can result in many different symptoms, such as pain, bloating, cramping, nausea, feelings of satiety, and others. [1, 2] Population-based studies estimate the prevalence of IBS at 4-11% [3] and the incidence of IBS at 1-2% per year. [4, 5] It is the seventh most common diagnosis by primary care physicians. [3] IBS contributes to large direct and indirect costs on a personal and societal level.
Signs and symptoms
IBS is a chronic disorder. Manifestations of IBS include the following [6] :
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Abdominal pain
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Change in stool frequency and/or form
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Abdominal pain related to defection; this could be relief or worsening of the pain
Symptoms not consistent with IBS should alert the clinician to the possibility of an organic pathology. Inconsistent symptoms include the following:
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Onset after age 45 years
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Acute symptoms (IBS is defined by chronicity)
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Progressive symptoms
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Nocturnal symptoms
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Unexplained weight loss
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Fever
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Rectal bleeding
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Painless diarrhea
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Steatorrhea
See Presentation for more detail.
Diagnosis
The Rome IV criteria for the diagnosis of IBS require that patients have had recurrent abdominal pain on average at least 1 day per week during the previous 3 months that is associated with two or more of the following [7] :
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Defecation
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A change in stool frequency
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A change in stool form or appearance
In 2021, the Rome IV criteria suggested that IBS can be diagnosed if symptoms have lasted at least 8 weeks (therefore are chronic) and interfere with daily activities, cause worry, or interfere with quality of life. [8]
Supporting symptoms include the following:
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Altered stool passage (straining and/or urgency)
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Nonbloody mucorrhea
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Abdominal bloating or subjective distention. This is common in IBS but is not required for diagnosis.
Four bowel patterns may be seen with IBS, and these remain in the Rome IV classification. [7] These patterns are as follows:
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IBS-D (diarrhea predominant)
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IBS-C (constipation predominant)
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IBS-M (mixed diarrhea and constipation)
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IBS-U (unclassified; the symptoms cannot be categorized into one of the above three subtypes)
IBS subtypes are often dynamic. Notably, within 1 year, 75% of patients change subtypes, and 29% switch between constipation-predominant IBS and diarrhea-predominant IBS. The Rome IV criteria differ from the Rome III criteria in basing bowel habit on stool form solely during days with abnormal bowel movements rather than on the total number of bowel movements. [7] Understanding a patient's IBS subtype helps in selection of therapies. [6]
A comprehensive history, physical examination, and tailored diagnostic testing can establish a diagnosis of IBS in most patients. The American College of Gastroenterology (ACG) updated their IBS management guidance which is highlighted by a positive diagnostic strategy, in contrast to the old strategy that IBS is a diagnosis of exclusion [6, 9] : The following "alarm symptoms," however, should prompt diagnostic testing including colonoscopy [6] :
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Unintentional weight loss
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Rectal bleeding
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Older age of onset (> 45 years)
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Iron deficiency anemia
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Family history of certain organic GI illnesses (eg, inflammatory bowel disease, celiac disease, colorectal cancer)
Further testing using a positive diagnostic strategy is detailed under Workup.
Management
Management of irritable bowel syndrome has progressed with better understanding of pathophysiology, the role of food in causing and treating IBS, the role of comorbid psychiatric disorders, and development of new medications.
Dietary measures may include [10] :
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Soluble fiber (for instance, oats, psyllium)
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Adequate hydration
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Limiting known triggers (for instance, lactose, high fruit/FODMAP (low fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) intake, bran, spicy food, fatty food)
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Low FODMAP diet (often helpful to involve a dietician)
Behavioral and psychological interventions are helpful in treating IBS. These treatments are called brain-gut behavior therapies (BGBTs) and can often improve GI symptoms by targeting the gut-brain connection. [2] Examples of effective therapies include disease self-management, cognitive behavioral therapy (CBT), gut-directed hypnotherapy, mindfulness, and psychotherapy. [2]
Pharmacologic agents used for the management of symptoms in IBS are chosen based on patient subtype and symptoms. According to the American Gastroenterological Association (AGA) clinical practice guidelines, these include [4, 5] :
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Anticholinergics/antispasmodics (eg, dicyclomine, hyoscyamine, trimebutine, peppermint oil) [11]
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Antidiarrheals (eg, diphenoxylate, loperamide)
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Neuromodulators such as tricyclics (eg, imipramine, amitriptyline)
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Prokinetic agents (prucalopride)
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Bulk-forming laxatives
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PEG laxatives
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Serotonin receptor antagonists (eg, alosetron, tegaserod)
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Chloride channel activators (eg, lubiprostone)
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Guanylate cyclase C (GC-C) agonists (eg, linaclotide, plecanatide)
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Altering bacterial flora and gas formation (eg, rifaximin) [12]
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Sodium-hydrogen exchange 3 (NHE3) inhibitors (eg, tenapanor) [13]
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Peripherally acting mixed opioid receptor agonist/antagonist (eluxadoline) [4]
See Treatment and Medication for more detail.
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Background
Irritable bowel syndrome (IBS) is a disorder of gut-brain interaction (DGBI). DGBIs are a group of gastrointestinal disorders that occur from alteration of the interconnected gut-brain pathways. This can result in many different symptoms such as pain, bloating, cramping, nausea, feelings of satiety, and others. [1, 2]
Population-based studies estimate the prevalence of irritable bowel syndrome at 4-11% [3] and the incidence of irritable bowel syndrome at 1-2% per year. [4, 5] However, there is significant heterogeneity among studies of IBS prevalence. [14, 15] It is the seventh most common diagnosis by primary care physicians. [3]
Substantial direct medical costs arise from IBS, ranging from $1.5 to $10 billion per year in the United States, [6] 8 billion Euros in Europe, and 123 billion Yuan in China. [16] Certain groups are overrepresented, including women and younger patients, [6] patients with hypermobility spectrum disorders, [17] patients who report adverse reactions to food, [6] and adverse life events including childhood abuse, anxiety, depression, posttraumatic stress disorder, and others. [2, 16] A 2023 study concluded that loss of productivity is the greatest socioeconomic cost of IBS. [18] IBS is not associated with increased mortality. [19]
Pathophysiology
Traditional theories regarding the pathophysiology of irritable bowel syndrome (IBS) visualized IBS as a three-part complex of altered gastrointestinal (GI) motility, visceral hyperalgesia, and psychopathology. [20] More recently, it is understood that IBS is a disorder of gut-brain interaction (DGBI) and, as such, theories inch closer to a unifying mechanism, though with multiple underlying etiologies. [21, 22] These may include altered GI motility, intestinal dysbiosis, visceral hypersensitivity, food triggers, mucosal inflammation and postinfectious reactivity, altered influence of gravity, and others. [21, 23, 24, 25, 26] The interconnectedness of the gut and brain are the key to understanding IBS.
Altered GI motility
Altered motility is often seen in IBS. Yet, no single motility change encompasses all patients with IBS.
There may be frequent motility changes in IBS, but only 25-75% of IBS patients exhibit motility abnormalities. These suggest rapid small bowel transit in diarrhea-predominant IBS (IBS-D) and slow transit in constipation-predominant IBS (IBS-C), increased frequency and amplitude of high-amplitude propagating contractions (HAPCs) in IBS-D with abdominal pain, greater phasic contractions of the colon after meals, stress, neostigmine, and intravenous (IV) cholecystokinin (CCK), exaggerated gastrocolic reflex, and accelerated whole gut and colon transit in IBS-D but not in IBS-C. [22, 27]
More recent articles using a wireless capsule that records pH and pressure determined that colonic transit is significantly slower in IBS-C patients than in IBS-D and mixed diarrhea and constipation IBS (IBS-M) patients. [28] There was no correlation found between small bowel transit times among patients. [28] Yet other studies using colonic scintigraphy identified rapid colon transit in those with IBS-D and 20% of subjects with IBS-C. [29]
Colon transit studies correlate poorly with symptoms of bloating, flatulence, and abdominal pain. Interestingly, 72% of IBS-D and 86% of IBS-C patients had normal colon transit, though there was a greater proportion of IBS-D patients with accelerated transit (27% vs 1% of IBS-C) and IBS-C patients with delayed transit (12% vs 2% for IBS-C). This suggests that, at least currently, colon transit is not a reliable method to diagnose IBS. [30]
Visceral hyperalgesia
Visceral hyperalgesia is common in IBS. [31] Enhanced perception of normal motility and visceral pain characterizes IBS. Rectosigmoid and small bowel balloon inflation produces pain at lower volumes in patients than in control subjects. Notably, hypersensitivity appears with rapid but not 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.
Food has been shown to trigger DGBIs including IBS. In particular, mechano- and chemosensitivity of the gut may lead to abnormal gut peptide release and change afferent and efferent signaling. In addition, mucosal immune activation from both food and microbiota lead to visceral hypersensitivity through mast cell dependent and independent mechanisms. Mast cell activation in the small and large bowel in IBS enhances production of histamine, proteases, and prostaglandins, stimulating local nerves and affecting afferent signaling through the dorsal root ganglion, resulting in visceral hypersensitivity. [22]
Gut-brain dysregulation, mucosal immune activation, and microbiome relationships
The gut-brain axis includes the gut's nervous system (the enteric nervous system [ENS], the central nervous system [CNS], the gut wall, and the hypothalamic-pituitary-adrenal axis [HPA] axis). [24] As translational studies have shown, the ENS and CNS communicate bidirectionally. GI afferents to the CNS, spinal, and vagal afferents influence efferent changes in intestinal secretion, motility, visceral sensation, and the immune system. [24, 32] Neuron sensitization and neuroimmune activation cause multiple up- and downstream effects, including triggering of pain receptors that lead to visceral hypersensitivity. [22] Hyperactivation of CNS areas, such as the anterior cingulate cortex, amygdala, and midbrain, increased mucosal permeability, heightened intestinal response to corticotropin-releasing hormone (CRH) release, and decreased volume of the dorsolateral prefrontal cortex, which correlates with decreased coping mechanisms. [33]
For example, tryptophan metabolism is increased in IBS and associated with microbial changes such as increased Firmicutes/Bacteroides ratio, increased Streptococcus and Ruminococcus concentrations, and decreased Lactobacillus and Bifidobacterium. [34] As 5-hydroxytryptamine (5-HT; serotonin) is synthesized from tryptophan, 5-HT production and receptor magnitude are stimulated by changes in the gut microbiota. [26] Secondary bile acids have also been noted to stimulate 5-HT production. 5-HT1 and 5-HT4 receptor stimulation on gut afferent nerve endings changes intestinal motility and secretion, and 5-HT3 stimulation increases visceral hypersensitivity. [26]
However, there is no single clearly defined microbiome profile in IBS. Using rRNA sequencing, Swedish IBS patients were found to have similar microbiome profiles to control subjects, though with greater heterogeneity. [35] In a study of 56 IBS patients in the UK, many had microbiome profiles indistinct from healthy controls. Others showed lower amounts of Bacteroides and higher Firmicutes. This changed profile may allow greater intestinal fermentation and thus may lead to symptoms. [35] A 2023 study found lower alpha-diversity (microbial diversity within a single sample) in IBS, though whether this was causative of the IBS or a result of food intake changes (specifically a low fermentable oligosaccharides, disaccharides, monosaccharides, and polyols [FODMAP] diet) was unclear. [36]
In IBS, changes may occur in the metabolism of other neurotransmitters and local intestinal mediators, such as dopamine, gamma-aminobutyric acid (GABA), and histamine. [26] Increased intestinal permeability may be greater in all individuals with IBS subtypes versus control subjects. [36]
Postinfection (PI) intestinal changes
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. [37] Neuronal degeneration of the myenteric plexus was also present in some patients. Research into Campylobacter jejuni–associated PI-IBS suggests certain bacterial genes confer increased susceptibility to PI-IBS. These genes caused greater virulence, enhancing adhesion, invasion, interleukin (IL)-8 and tumor necrosis factor alpha (TNFα) secretion on colonocytes, and conferred increased susceptibility to PI-IBS than other strains of C jejuni lacking these genes. [38] Microbiota changes seen in PI-IBS include lower Firmicutes counts, higher Bacteroides and Clostridioides counts, and lower Firmicutes/Bacteroides ratios. [38, 39]
Putative pathophysiologic changes seen in PI-IBS include epithelial changes of increased density of lamina propria enterochromaffin cells, leading to an increase in serotonin secretion with resultant changes in chemo- and mechano-sensation, increased CCK-reactive immune cells, dysbiosis, enhanced proinflammatory cytokine production, epithelial mast cell infiltration, disruption of the epithelial barrier leading to increased mucosal permeability, increased bile acid production, loss of enteric neurons, and others. [38, 39]
Small intestinal bacterial overgrowth (SIBO)
Historically, SIBO was defined as more than 105 of bacteria per mL of jejunal fluid aspirate. As this is cumbersome and has other limitations, the readily available lactulose- and glucose-hydrogen breath tests are used in the vast majority of IBS-related studies. [40] More recently, breath testing for methane has been available, particularly for IBS-C patients. Limitations of these breath tests are beyond the scope of this article. A 2024 translational technique, high-throughput 16S ribosomal RNA sequencing of duodenal aspirates in symptomatic patients undergoing esophagogastroduodenoscopy (EGD), suggests that SIBO may be defined by duodenal aspirate growth on MacConkey agar. [41] This study identified that SIBO may be defined by 103 or more colony-forming units (CFU) per mL of jejunal fluid. At this cutoff, microbial metabolic pathways for carbohydrate fermentation and production of hydrogen and hydrogen sulfide correlated with symptoms and were enhanced. [41]
A 2020 American College of Gastroenterology (ACG) guideline defined SIBO clinically as "the presence of excessive numbers of bacteria in the small bowel causing GI symptoms." [42] Typical symptoms in the majority of patients include bloating, gas, abdominal distention, flatulence, abdominal pain, and diarrhea. [42] Myriad other symptoms including nausea, constipation, fatigue, and poor concentration have been described. [42] Moreover, nutritional consequences are seen in cases of more severe SIBO, including low vitamin B12, elevated folate, steatorrhea, fat-soluble vitamin malabsorption, and weight loss. These malabsorptive findings are most typical in situations of intestinal stasis, anatomic abnormalities, immune deficiency (inherited or acquired), and hypochlorhydria. [40]
Intestinal dysbiosis, such as that in SIBO, may cause IBS by multiple mechanisms as detailed above. In addition, using breath testing and translational techniques, distinct microbe profiles have been described relatively recently as identifying IBS subtypes, particularly IBS-C and IBS-D. [43] Elevated methane breath test results correlate with elevated levels of stool methanogens such as Methanobrevibacter and identified IBS-C subjects. These patients had higher stool microbial diversity. Elevated H2 breath test findings correlated with IBS-D and lower microbial diversity. IBS-D subjects also had higher levels of hydrogen sulfide on breath testing, associated with greater Fusobacterium and Desulfovibrio levels. [43]
Bile acid malabsorption (BAM)
BAM is common in the general population and in IBS, particularly IBS-D. [6, 44] Bile acid is reabsorbed in the terminal ileum; BAM is well-defined in conditions where reabsorption is limited (eg, ileal resection) or delivery is increased (eg, cholecystectomy). BAM has been determined to be frequent in IBS and alternative mechanisms have been proposed. [6, 44]
Central neurohormonal mechanisms
Current neuroimaging studies in IBS often reveal brain structural and functional changes, though with varied findings and no single brain signature of IBS.
For instance, a 2022 systematic review of 22 functional magnetic resonance imaging (fMRI) studies in IBS patients versus control subjects found increased or decreased brain activity in areas associated with the processing of pain (caudate, insula, hypothalamus, cingulate cortex, prefrontal cortex, and others). [45] This suggests sensitization of visceral pain pathways, and it persists in IBS in remission. Functional connectivity studies often find hippocampal dysfunction in IBS; however, enhanced, unchanged, and suppressed connectivity to higher brain regions have been found. [45]
Aberrant activation and functional connectivity involving the amygdala and insula features prominently in fMRI studies in IBS. The amygdala is activated in anticipatory pain. The insula (location of self-awareness and emotional arousal and regulation) is activated in IBS, and its connection with limbic and cortical regions is activated both at rest and during painful stimuli in IBS. [46] Taken together, studies suggest dysfunction in the areas of pain anticipation and processing, self-regulation and self-awareness, emotion, and others in IBS.
The hypothalamic-pituitary axis appears involved in the pathogenesis of IBS. Motility disturbances such as colonic hypermotility and delayed gastric emptying correspond to a production increase in the hypothalamic corticotropin-releasing factor (CRF) in response to stress. CRF antagonists eliminate these changes. [32] IBS-D patients manifest elevated morning (AM) cortisol levels but lower adrenocorticotropic hormone (ACTH) levels, suggesting HPA axis dysfunction. [47]
The majority of the body's serotonin is produced in the gut. It is stored in enterochromaffin cells and undergoes reuptake by the serotonin transporter (SERT) in gut epithelial cells and platelets. [32] Serotonin stimulates gut motility, secretion, vasodilation, activates vagal and spinal afferents that mediate sensation, and may promote local gut inflammation. Circulating postprandial 5-HT is elevated in IBS-D and PI-IBS but reduced in IBS-C. [32] Mucosal SERT expression is decreased in IBS-D and IBS-C, which enhances local mast cell and intraepithelial lymphocyte production, leading to local inflammation. [48]
Other proteins may be altered in IBS, including mucosal chromogranins and secretogranins, glucagon-like peptide 1, melatonin, [32] and neurotransmitters such as glutamate, GABA, norepinephrine, and acetylcholine. [48]
IBS often coexists with depression, anxiety, or other psychiatric disorders. Many of the changes described above are also present in patients with comorbid anxiety, depression, posttraumatic stress disorder, and a history of abuse, among other conditions.
Gravity
A novel hypothesis published in 2022 suggested that "ineffective anatomical, physiological, and neuropsychological gravity management systems" may cause IBS. [25] This hypothesis puts forth that gravity resistance mechanisms evolved to support our intestinal function in the upright posture. Aberrant gravitational force resistance, detection, and vigilance mechanisms within an individual may then contribute to the development of IBS. [25] This hypothesis potentially explains the increase in comorbid IBS in patients with hypermobility spectrum disorders such as hypermobile Ehlers-Danlos syndrome. [17, 25]
Etiology
Multiple possible etiologies of irritable bowel syndrome (IBS) have been proposed. Please refer to the Pathophysiology section for detailed discussions.
Postinfection IBS (PI-IBS)
The multiple putative mechanisms by which infectious gastroenterocolitis may result in PI-IBS is described under Pathophysiology. While viral infections are more common, bacterial and protozoal infections are more likely to result in long-term PI-IBS. [39] Infectious gastroenterocolitis is a strong predictor of IBS development. Its risk increases 4.2 times within 1 year after an acute infectious episode versus individuals without an acute infectious episode. Of those with acute infectious gastroenterocolitis, about 10% will develop PI-IBS. The pattern is typically mixed- or diarrhea-predominant. [38]
Risk factors include severe symptoms, being women, being younger patients, absence of vomiting during illness, higher premorbid or coexistent anxiety or depression, [38] and smoking. [23] When assessed within 1 year of acute bacterial, viral, and protozoal infection, 13%, 19%, and 7% of patients, respectively, developed IBS. Prevalence rates change with time, however. When assessed more than 1 year after acute infection, rates were 13%, 4%, and 53%, respectively, after bacterial, viral, and protozoal infection. [38]
Infections that have been associated with PI-IBS include but are not limited to Clostridioides difficile, Vibrio cholerae, Campylobacter, Shigella, Salmonella, Escherichia coli, Giardia, coronavirus disease 2019 (COVID-19), norovirus, and rotavirus. [38, 49]
For instance, infection with Giardia lamblia leads to an increased prevalence of IBS, 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 IBS was 46.1% for as long as 3 years after exposure, compared with 14% in control subjects. [50] Approximately 25% of patients with Clostridioides difficile infection develop PI-IBS. [49]
Small intestine bacterial overgrowth (SIBO)
Up to 78% of patients with IBS have SIBO. The vast majority of SIBO studies in IBS have used the glucose- or lactulose-hydrogen breath test to identify SIBO [42] and, more recently, added the methane breath test for subjects with IBS-C. [43] Multiple conditions elevate the risk of SIBO, including the following [40] :
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Small bowel dysmotility, as seen in diabetic autonomic neuropathy, scleroderma, amyloidosis, hypothyroidism, intestinal pseudo-obstruction, gastroparesis, Parkinson disease, and chronic opioid use
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Anatomic alteration, including postsurgical (Billroth II, bariatric surgery, end-to-side anastomosis, surgically created blind loops), stricture-related narrowing (radiation damage, Crohn disease), small bowel diverticula, gastrocolic or jejunocolic fistula, and resection of the ileocecal valve
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Innate or acquired immunosuppression, such as common variable immunodeficiency and acquired immunodeficiency syndrome (AIDS)
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Hypochlorhydria (disease- or medication-related)
Dietary factors
Up to 50% of IBS patients report that specific foods induce or worsen IBS symptoms. [6] However, immunoglobulin (Ig) E–related food allergies are not more common in IBS. Thus, IBS-related food-induced symptoms likely occur from food intolerance or sensitivity. [6]
Much attention has been paid to FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols). These highly fermentable and poorly absorbable sugars cause symptoms in the majority of IBS patients, and following a low FODMAP diet has been shown to improve symptoms. The mechanisms are protean and more complex than the gas and abdominal distention created by increased fermentation. Food products can induce intestinal dysbiosis, with downstream effects resulting in IBS symptoms. Gut microbiota interactions with food products may change afferent and local neurotransmission, secretion of proteins (eg, 5-HT, histamine, tryptamine, proteases), proinflammatory cytokine release, and enhance gut mechanosensitivity, among other possibilities. Specific biomarkers are being investigated to measure some of these changes. [22]
Nonceliac gluten sensitivity (NCGS) receives a lot of attention. There is overlap with FODMAPs here as sensitivity to fructans may yield gluten sensitivity. Other components of wheat may also induce local gut inflammation independent of gluten. [22]
Disaccharidase deficiency (lactase, fructase, sucrase, isomaltase) is common in the general population and more common in IBS patients. [51] Relatively recent evidence shows an association between functional variants in the sucrase-isomaltase (SI) gene and an increased risk of IBS. In one study, investigators sequenced SI exons in seven familial cases, as well as screened for four congenital sucrase-isomaltase deficiency (CSID) mutations and a common SI coding polymorphism in a multicenter cohort comprising 1887 patients and control subjects. [52] The investigators found that individuals affected by the SI mutations that code for defective or enzymatic activity in disaccharides had a predisposition to IBS. [52] Similarly, another multinational genotype study of 2207 patients indicates that there is an increased prevalence of rare sucrase-isomaltase pathogenic variants in those affected by IBS. [53]
Environmental factors
A systematic review found a potential association between environmental risk factors and the development of IBS, particularly air pollution. [54] In addition, there was a link between microbial exposure, following a natural disaster or a result of poor sanitation, and IBS development and gut dysbiosis. An IBS risk also existed in those who had early pet ownership or other exposures. [54]
Epidemiology
Population-based studies often estimate the prevalence of irritable bowel syndrome (IBS) at 4.1% (Rome IV criteria) to 10.1% (Rome III criteria) [5] or up to 11%, [3] and the incidence of IBS at 1-2% per year. [4, 5] It is the seventh most common diagnosis by primary care physicians. [3] IBS contributes to large direct and indirect costs on a personal and societal level.
Of people with IBS, approximately 30% seek medical care. [14] An estimated 10% of gastroenterology referrals relate to this symptom complex. [55] The prevalence is markedly different among countries, with the lowest reported in South Asia (7%) and the highest in South America (21%). [14] A 2018 study by Quigley suggested that in Asia, the lowest prevalence was in China (6%), with a higher prevalence in Japan (15%) and South Korea (16%). [21] However, the Rome Foundation found in 2017 that there was significant heterogeneity among studies of IBS prevalence. In the same year, an expert literature review among community-based studies worldwide suggested that the lowest prevalence is in France (1.1%) and the highest is in Mexico (35.5%); a 7.1% prevalence was found in the US/Europe/Australia/New Zealand. [15]
Adolescent and young adult women are most commonly affected with IBS. [21] In Western countries, women are 2-3 times more likely to develop IBS than men, although in the Indian subcontinent males represent 70-80% of patients with IBS.
Patients often retrospectively note the onset of abdominal pain and altered bowel habit in childhood. Approximately 50% of people with IBS report symptoms beginning before age 35 years. The development of symptoms later in life does not exclude IBS but should prompt a closer search for an underlying organic etiology.
Prognosis
Irritable bowel syndrome (IBS) is a chronic disorder. At 7-year follow-up, 55% of IBS patients remained with IBS, a more stable prevalence than those with other gastrointestinal conditions such as gastroesophageal reflux disease (GERD) and dyspepsia. [56]
Psychologic comorbidity is seen in 70% of IBS patients, with IBS symptom severity correlating with an increased number of comorbid psychologic disorders. When followed for 1 year, increased psychologic comorbidity also correlated with increased healthcare seeking, treatments used, severity and continuity of symptoms, and impact on daily activities. [16]
Patients with IBS also experience greater work absenteeism, presenteeism, and negative impact of disease on work productivity. [18]
Individuals 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 IBS itself, or due to another factor such as medications used for IBS, is unknown. [57]
IBS patients do not have an increased risk of all-cause or cause-specific mortality. [19]
Patient Education
Good communication between patient and provider is key. Patient education remains a cornerstone of irritable bowel syndrome (IBS) care. Understanding that IBS is chronic is imperative to set reasonable expectations. Many patients may not be familiar with the concept of the gut-brain axis, yet understanding the basic interplay of the gut and brain will assist the patient in understanding that IBS is complicated but treatable. It will also help the patient grasp the importance of intervention for comorbid psychologic disorders, such as different therapy and mindfulness approaches.
Clinicians may also wish to refer patients to the following short video, which provides a simplified but clear and concise overview about what IBS is and its epidemiology, risk factors, and management options, as well as a brief explanation of the difference between IBS and inflammatory bowel disease (IBD).
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Irritable Bowel Syndrome (IBS). What is IBS? IBS is a condition that involves recurrent abdominal pain, as well as abnormal bowel motility, which can include diarrhea and/or constipation.