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This page is about the functional disorder. For bowel inflammation, see inflammatory bowel disease. For other uses, see IBS (disambiguation).

Irritable bowel syndrome
Other namesIBS
Depiction of a person suffering from Irritable Bowel Syndrome (IBS). The typical symptoms of IBS as well as abnormal colon contractions have been shown.
Pronunciation
SpecialtyGastroenterology

Irritable bowel syndrome (IBS)



Signs and symptoms

[edit]

There may also be urgency for bowel movements, a feeling of incomplete evacuation (tenesmus) or bloating.[1] In some cases, the symptoms are relieved by bowel movements.[2]

People with IBS, more commonly than others, have gastroesophageal reflux, symptoms relating to the genitourinary system, fibromyalgia, headache, backache, and psychiatric symptoms such as depression, sleep disorders,[3]

Cause

[edit]

Recent findings suggest that an allergy triggered peripheral immune mechanism may underlie the symptoms associated with abdominal pain in patients with irritable bowel syndrome.[4] IBS is more prevalent in obese patients.[5]

Risk factors

[edit]

People who are younger than 50, women, and those with a family history of the condition are more likely to develop IBS.[6] Further risk factors are anxiety, depression, and stress.[7] The risk of developing IBS increases six-fold after having a gastrointestinal infection (gastroenteritis).[6] This is also called post-infectious IBD Genetic defects in innate immunity and epithelial homeostasis increase the risk of developing both post-infectious as well as other forms of IBS.[8]

Stress

[edit]

The role of the brain–gut axis in IBD has been suggested since the 1990s[9] and childhood physical and psychological abuse is often associated with the development of IBS.[10] It is believed that psychological stress may trigger IBS in predisposed individuals.[11]

Individuals with IBS also report high rates of sleep disturbances such as trouble falling asleep and frequent arousal throughout the night.[12]

Gastroenteritis

[edit]

Approximately 10 percent of IBS cases are triggered by an acute gastroenteritis infection.[13] The CdtB toxin is produced by bacteria causing gastroenteritis and the host may develop an autoimmunity when host antibodies to CdtB cross-react with vinculin.[14] A link between small intestinal bacterial overgrowth and tropical sprue has been proposed to be involved as a cause of post-infectious IBS.[15]

Bacteria

[edit]

Small intestinal bacterial overgrowth (SIBO) occurs with greater frequency in people who have been diagnosed with IBS compared to healthy controls.[16]

Certain bacteria are found in lower or higher abundance when compared with healthy individuals. Generally Bacteroidota, Bacillota, and Pseudomonadota are increased and Actinomycetota, Bifidobacteria, and Lactobacillus are decreased. Within the human gut, there are common phyla found. The most common is Bacillota. This includes Lactobacillus, which is found to have a decrease in people with IBS, and Streptococcus, which is shown to have an increase in abundance. Within this phylum, species in the class Clostridia are shown to have an increase, specifically Ruminococcus and Dorea. The family Lachnospiraceae presents an increase in IBS-D patients. The second most common phylum is Bacteroidota. In people with IBS, the Bacteroidota phylum has been shown to have an overall decrease, but an increase in the genus Bacteroides. IBS-D shows a decrease for the phylum Actinomycetota and an increase in Pseudomonadota, specifically in the family Enterobacteriaceae.[17]

Gut microbiota

[edit]

Alterations of gut microbiota (dysbiosis) are associated with the intestinal manifestations of IBS, but also with the psychiatric morbidity that coexists in up to 80% of people with IBS.[18]

Protozoa

[edit]

Blastocystis and Dientamoeba fragilis colonisation occurs more commonly in IBS affected individuals but their role in the condition is unclear.[19]

Vitamin D

[edit]

Vitamin D deficiency is more common in individuals affected by IBS.[20][21] Vitamin D is involved in regulating triggers for IBS including the gut microbiome, inflammatory processes and immune responses, as well as psychosocial factors.[22]

Genetics

[edit]

SCN5A mutations are found in a small number of people who have IBS, particularly the constipation-predominant variant (IBS-C).[23][24]

Mechanism

[edit]

Dysregulated brain-gut axis, abnormal serotonin/5-hydroxytryptamine (5-HT) metabolism, and high density of mucosal nerve fibers in the intestines have been implicated in the mechanisms of IBS. A number of 5-HT receptor subtypes were involved in the IBS symptoms, including 5-HT3, 5-HT4, and 5-HT7 receptors. High levels of 5-HT7 receptor-expressing mucosal nerve fibers were observed in the colon of IBS patients. A role of 5-HT7 receptor in intestinal hyperalgesia was demonstrated in mouse models with visceral hypersensitivity, of which a novel 5-HT7 receptor antagonist administered by mouth reduced intestinal pain levels.[25]

Abnormalities occur in the gut flora of individuals who have IBS, such as reduced diversity, a decrease in bacteria belonging to the phylum Bacteroidota, and an increase in those belonging to the phylum Bacillota.[18] The changes in gut flora are most profound in individuals who have diarrhoea-predominant IBS. Antibodies against common components (namely flagellin) of the commensal gut flora are a common occurrence in IBS affected individuals.[26]

Chronic low-grade inflammation commonly occurs in IBS affected individuals with abnormalities found including increased enterochromaffin cells, intraepithelial lymphocytes, and mast cells resulting in chronic immune-mediated inflammation of the gut mucosa.[27][28] It is believed that psychological stress can induce increased inflammation and thereby cause IBS to develop in predisposed individuals.[11]

Diagnosis

[edit]

The recommendations for physicians are to minimize the use of medical investigations.[29] The Rome criteria are typically used for diagnosis. They allow the diagnosis to be based only on symptoms, but no criteria based solely on symptoms is sufficiently accurate to diagnose IBS.[30] Worrisome features include onset at greater than 50 years of age, weight loss, blood in the stool, iron-deficiency anemia, or a family history of colon cancer, celiac disease, or inflammatory bowel disease.[31] The criteria for selecting tests and investigations also depends on the level of available medical resources.[32]

The Rome IV criteria for diagnosing IBS include recurrent abdominal pain, on average, at least one day/week in the last three months, associated with additional stool- or defecation-related criteria.[33]

Differential diagnosis

[edit]

Conditions that may present similarly include celiac disease, bile acid malabsorption, colon cancer, and dyssynergic defecation.[31]

Ruling out parasitic infections, lactose intolerance, small intestinal bacterial overgrowth, and celiac disease is recommended before a diagnosis of IBS is made.[34] An ileocolonoscopy with biopsies is useful to exclude Crohn's disease and ulcerative colitis (Inflammatory bowel disease).[35]

Gastrointestinal symptoms of IBS are clinically indistinguishable from those of NCGS, but the presence of any of the following non-intestinal manifestations suggest a possible NCGS: headache or migraine, "foggy mind", chronic fatigue,[36] fibromyalgia,[37][38][39] joint and muscle pain,[36][37][40] leg or arm numbness,[36][37][40] tingling of the extremities,[36][40] dermatitis (eczema or skin rash),[36][40] atopic disorders,[36] allergy to one or more inhalants, foods or metals[36][37] (such as mites, graminaceae, parietaria, cat or dog hair/dander, shellfish, or nickel[37]), depression,[36][37][40] anxiety,[37] anemia,[36][40] iron-deficiency anemia, folate deficiency, asthma, rhinitis, eating disorders,[37] neuropsychiatric disorders (such as schizophrenia,[40][41] autism,[37][40][41] peripheral neuropathy,[40][41] ataxia,[41] attention deficit hyperactivity disorder[36]) or autoimmune diseases.[36] An improvement with a gluten-free diet of immune-mediated symptoms, including autoimmune diseases, once having reasonably ruled out celiac disease and wheat allergy, is another way to realize a differential diagnosis.[36]

Comorbidities

[edit]

IBS occurs in 51% of people with chronic fatigue syndrome and 49% of people with fibromyalgia, and psychiatric disorders occur in 94% of people with IBS.[42][note 1]

  • Channelopathy and muscular dystrophy: IBS and functional GI diseases are comorbidities of genetic channelopathies that cause cardiac conduction defects and neuromuscular dysfunction, and result also in alterations in GI motility, secretion, and sensation.[43]

Classification

[edit]

Management

[edit]

A number of treatments have been found to be effective, including fiber, talk therapy, antispasmodic and antidepressant medication, and peppermint oil.[44][45]

Diet

[edit]

FODMAP

[edit]

FODMAPs are short-chain carbohydrates that are poorly absorbed in the small intestine. A 2018 systematic review found that although there is evidence of improved IBS symptoms with a low-FODMAP diet, the evidence is of very low quality.[46] Symptoms most likely to improve on this type of diet include urgency, flatulence, bloating,[47] abdominal pain, and altered stool output. One national guideline advises a low FODMAP diet for managing IBS when other dietary and lifestyle measures have been unsuccessful.[48] The diet restricts various carbohydrates which are poorly absorbed in the small intestine, as well as fructose and lactose, which are similarly poorly absorbed in those with intolerances to them. Reduction of fructose and fructan has been shown to reduce IBS symptoms in a dose-dependent manner in people with fructose malabsorption and IBS.[49]

Although FODMAPs can produce certain digestive discomfort in some people, not only do they not cause intestinal inflammation, but they help avoid it, because they produce beneficial alterations in the intestinal flora that contribute to maintaining the good health of the colon.[50] FODMAPs are not the cause of irritable bowel syndrome nor other functional gastrointestinal disorders, but rather a person develops symptoms when the underlying bowel response is exaggerated or abnormal.[51]

A low-FODMAP diet consists of restricting them from the diet. They are globally trimmed, rather than individually, which is more successful than for example restricting only fructose and fructans, which are also FODMAPs, as is recommended for those with fructose malabsorption.[51]

A low-FODMAP diet might help to improve short-term digestive symptoms in adults with irritable bowel syndrome,[52][48][53][54] but its long-term follow-up can have negative effects because it causes a detrimental impact on the gut microbiota and metabolome.[55][48][54][56] It should only be used for short periods of time and under the advice of a specialist.[57] A low-FODMAP diet is highly restrictive in various groups of nutrients and can be impractical to follow in the long-term.[58] More studies are needed to assess the true impact of this diet on health.[48][54]

In addition, the use of a low-FODMAP diet without verifying the diagnosis of IBS may result in misdiagnosis of other conditions such as celiac disease.[59] Since the consumption of gluten is suppressed or reduced with a low-FODMAP diet, the improvement of the digestive symptoms with this diet may not be related to the withdrawal of the FODMAPs, but of gluten, indicating the presence of unrecognized celiac disease, avoiding its diagnosis and correct treatment, with the consequent risk of several serious health complications, including various types of cancer.[59]

Fiber

[edit]

Soluble fiber supplementation (e.g., psyllium/ispagula husk) may be effective in improving symptoms.[60] However soluble fiber does not appear to reduce pain.[61]

Physical activity

[edit]

Physical activity can have beneficial effects on irritable bowel syndrome.[62] In light of this, the latest British Society of Gastroenterology guidelines on the management of IBS have stated that all patients with IBS should be advised to take regular exercise (strong recommendation, weak certainty evidence),[63] whereas the American College of Gastroenterology guidelines have suggested with a lower certainty of evidence.[64] Physical activity could significantly improve people’s adherence and, consequently, lead to a significant clinical benefit for symptoms of irritable bowel syndrome.[62]

Medication

[edit]

Both H1-antihistamines and mast cell stabilizers have shown efficacy in reducing pain associated with visceral hypersensitivity in IBS.[27]

Laxatives

[edit]

Lubiprostone is a gastrointestinal agent used for the treatment of constipation-predominant IBS.[65]

Antispasmodics

[edit]

The use of antispasmodic drugs (e.g., anticholinergics such as hyoscyamine or dicyclomine) may help people who have cramps or diarrhea. A meta-analysis by the Cochrane Collaboration concludes if seven people are treated with antispasmodics, one of them will benefit.[66] Antispasmodics can be divided into two groups: neurotropics and musculotropics. Musculotropics, such as mebeverine, act directly at the smooth muscle of the gastrointestinal tract, relieving spasm without affecting normal gut motility.[citation needed] Since this action is not mediated by the autonomic nervous system, the usual anticholinergic side effects are absent.[67] The antispasmodic otilonium may also be useful.[68]

Discontinuation of proton pump inhibitors

[edit]

Proton-pump inhibitors (PPIs) used to suppress stomach acid production may cause small intestinal bacterial overgrowth (SIBO) leading to IBS symptoms.[69]

Antidepressants

[edit]

There is good evidence that low doses of tricyclic antidepressants (TCAs) can be effective for IBS.[66][70]

However, the evidence is less robust for the effectiveness of other antidepressant classes such as selective serotonin reuptake inhibitor antidepressants (SSRIs). Because of their serotonergic effect, SSRIs have been studied in IBS, especially for people who are constipation predominant. As of 2015, the evidence indicates that SSRIs do not help.[71] Antidepressants are not effective for IBS in people with depression, possibly because lower doses of antidepressants than the doses used to treat depression are required for relief of IBS.[72]

Other agents

[edit]

Magnesium aluminum silicates and alverine citrate drugs can be effective for IBS.[73][74]

Rifaximin may be useful as a treatment for IBS symptoms, including abdominal bloating and flatulence, although relief of abdominal distension is delayed.[11][75] It is especially useful where small intestinal bacterial overgrowth is involved.[11]

In individuals with IBS and low levels of vitamin D supplementation is recommended. Some evidence suggests that vitamin D supplementation may improve symptoms of IBS, but further research is needed before it can be recommended as a specific treatment for IBS.[20][21]

Psychological therapies

[edit]

There is inconsistent evidence from studies with poor methodological quality that psychological therapies can be effective in the treatment of IBS.[72] Preliminary research shows that psychotherapeutic interventions are correlated with reductions in both autonomic nervous system dysregulation and gastrointestinal symptoms.[12]

Probiotics

[edit]

Probiotics may exert their beneficial effects on IBS symptoms via preserving the gut microbiota, normalisation of cytokine blood levels, improving the intestinal transit time, decreasing small intestine permeability, and by treating small intestinal bacterial overgrowth of fermenting bacteria.[76] A fecal transplant does not appear useful as of 2019.[77]

Herbal remedies

[edit]

[45] An earlier meta-analysis suggested the results of peppermint oil were tentative as the number of people studied was small and blinding of those receiving treatment was unclear.[78] Safety during pregnancy has not been established, however, and caution is required not to chew or break the enteric coating; otherwise, gastroesophageal reflux may occur as a result of lower esophageal sphincter relaxation. Occasionally, nausea and perianal burning occur as side effects.[79] A comprehensive meta-analysis using twelve random trials resulted that the use of peppermint oil is an effective therapy for adults with irritable bowel syndrome.[80]

Research into cannabinoids as treatment for IBS is limited. GI propulsion, secretion, and inflammation in the gut are all modulated by the ECS (Endocannabinoid system), providing a rationale for cannabinoids as treatment candidates for IBS.[81]


Epidemiology

[edit]

Gender

[edit]

People diagnosed with IBS are usually younger than 45 years old.[82]

History

[edit]

The concept of an "irritable bowel" was introduced by P. W. Brown, first in The Journal of the Kansas Medical Society in 1947[83] and later in the Rocky Mountain Medical Journal in 1950.[84] The term was used to categorize people who developed symptoms of diarrhea, abdominal pain, and constipation, but where no well-recognized infective cause could be found. Early theories suggested the irritable bowel was caused by a psychosomatic or mental disorder.[85]

Society and culture

[edit]

Economics

[edit]

United States

[edit]

A study on Medicaid costs conducted in 2003 by the University of Georgia College of Pharmacy and Novartis found IBS was associated in an increase of $962 in Medicaid costs in California, and $2191 in North Carolina. People with IBS had higher costs for physician visits, outpatients visits, and prescription drugs. The study suggested the costs associated with IBS were comparable to those found for people with asthma.[86]

Research

[edit]

Individuals with IBS have been found to have decreased diversity and numbers of Bacteroidota microbiota. Preliminary research into the effectiveness of fecal microbiota transplant in the treatment of IBS has been very favourable with a 'cure' rate of between 36 percent and 60 percent with remission of core IBS symptoms persisting at 9 and 19 months follow up.[87][88] Treatment with probiotic strains of bacteria has shown to be effective, though not all strains of microorganisms confer the same benefit and adverse side effects have been documented in a minority of cases.[89]

There is increasing evidence for the effectiveness of mesalazine (5-aminosalicylic acid) in the treatment of IBS.[90] Mesalazine is a drug with anti-inflammatory properties that has been reported to significantly reduce immune mediated inflammation in the gut of IBS affected individuals with mesalazine therapy resulting in improved IBS symptoms as well as feelings of general wellness in IBS affected people. It has also been observed that mesalazine therapy helps to normalise the gut flora which is often abnormal in people who have IBS. The therapeutic benefits of mesalazine may be the result of improvements to the epithelial barrier function.[91] Treatment based on "abnormally" high IgG antibodies cannot be recommended.[92]

Differences in visceral sensitivity and intestinal physiology have been noted in IBS. Mucosal barrier reinforcement in response to oral 5-HTP was absent in IBS compared to controls.[93] IBS/IBD individuals are less often HLA DQ2/8 positive than in upper functional gastrointestinal disease and healthy populations.[94]

Efficacy of mast cell directed therapies in irritable bowel syndrome is an area of ongoing research.[95]

In other species

[edit]

A similar syndrome is found in rats (Rattus spp.).[96] In rats a short-chain fatty acid receptor is involved, a free fatty acid receptor 2 subtype – GPR43 – that is expressed in both enteroendocrine cells and mucosal mast cells.[96] These cells then respond in an exaggerated way to the IBS rat's own large quantity of maldigestion products.[96]

Notes

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