Irritable bowel syndrome




functional bowel disorder characterized by chronic issues without an organic cause


















































Irritable bowel syndrome
Synonyms Spastic colon, nervous colon, mucous colitis, spastic bowel[1]
Specialty Gastroenterology
Symptoms
Diarrhea, constipation, abdominal pain[1]
Usual onset Before 45 years old[1]
Duration Long term[2]
Causes Unknown[2]
Diagnostic method Based on symptoms[3]
Differential diagnosis
Celiac disease, non-celiac gluten sensitivity, microscopic colitis, inflammatory bowel disease, bile acid malabsorption, colon cancer[3][4]
Treatment
Symptomatic (dietary changes, medication, probiotics, counseling)[5]
Prognosis Normal life expectancy[6]
Frequency 12.5% (developed world)[1][7]

Irritable bowel syndrome (IBS) is a group of symptoms—including abdominal pain and changes in the pattern of bowel movements without any evidence of underlying damage.[1] These symptoms occur over a long time, often years.[2] It has been classified into four main types depending on whether diarrhea is common, constipation is common, both are common, or neither occurs very often (IBS-D, IBS-C, IBS-M, or IBS-U respectively).[1] IBS negatively affects quality of life and may result in missed school or work.[8] Disorders such as anxiety, major depression, and chronic fatigue syndrome are common among people with IBS.[1][9]


The causes of IBS are not clear.[2] Theories include combinations of gut–brain axis problems, gut motility disorders, pain sensitivity, infections including small intestinal bacterial overgrowth, neurotransmitters, genetic factors, and food sensitivity.[2] Onset may be triggered by an intestinal infection,[10] or stressful life event.[11] IBS is a functional gastrointestinal disorder.[1] Diagnosis is based on signs and symptoms in the absence of worrisome features.[3] Worrisome features include onset at greater than 50 years of age, weight loss, blood in the stool, or a family history of inflammatory bowel disease.[3] Other conditions that may present similarly include celiac disease, microscopic colitis, inflammatory bowel disease, bile acid malabsorption, and colon cancer.[3]


There is no known cure for IBS.[5] Treatment is carried out to improve symptoms.[5] This may include dietary changes, medication, probiotics, and counseling.[5] Dietary measures include increasing soluble fiber intake, a gluten-free diet, or a short-term diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs).[3][12][13] The medication loperamide may be used to help with diarrhea while laxatives may be used to help with constipation.[3]Antidepressants may improve overall symptoms and pain.[3]Patient education and a good doctor–patient relationship are an important part of care.[3][14]


About 10 to 15% of people in the developed world are believed to be affected by IBS.[1][7] It is more common in South America and less common in Southeast Asia.[3] It is twice as common in women as men and typically occurs before age 45.[1] The condition appears to become less common with age.[3] IBS does not affect life expectancy or lead to other serious diseases.[6] The first description of the condition was in 1820 while the current term "irritable bowel syndrome" came into use in 1944.[15]





Contents






  • 1 Classification


  • 2 Signs and symptoms


  • 3 Cause


    • 3.1 Post-infectious


    • 3.2 Stress


    • 3.3 Bacteria


    • 3.4 Fungus


    • 3.5 Protozoa


    • 3.6 Vitamin D




  • 4 Mechanism


  • 5 Diagnosis


    • 5.1 Differential diagnosis


    • 5.2 Investigations


    • 5.3 Misdiagnosis


    • 5.4 Comorbidities




  • 6 Management


    • 6.1 Diet


      • 6.1.1 Low-FODMAP diet


      • 6.1.2 Fiber




    • 6.2 Medication


      • 6.2.1 Laxatives


      • 6.2.2 Antispasmodics


      • 6.2.3 Discontinuation of proton pump inhibitors


      • 6.2.4 Tricyclic antidepressants


      • 6.2.5 Serotonin agonists


      • 6.2.6 Serotonin antagonists


      • 6.2.7 Other agents


      • 6.2.8 SIBO therapy




    • 6.3 Psychological therapies


    • 6.4 Stress relief


      • 6.4.1 Probiotics


      • 6.4.2 Herbal remedies


      • 6.4.3 Yoga


      • 6.4.4 Acupuncture






  • 7 Epidemiology


    • 7.1 Gender




  • 8 History


  • 9 Society and culture


    • 9.1 Names


    • 9.2 Economics


      • 9.2.1 United States






  • 10 Research


  • 11 References


  • 12 External links





Classification


IBS can be classified as either diarrhea-predominant (IBS-D), constipation-predominant (IBS-C), or with alternating stool pattern (IBS-A) or pain-predominant.[16] In some individuals, IBS may have an acute onset and develop after an infectious illness characterized by two or more of: fever, vomiting, diarrhea, or positive stool culture. This postinfective syndrome has consequently been termed "postinfectious IBS" (IBS-PI).



Signs and symptoms


The primary symptoms of IBS are abdominal pain or discomfort in association with frequent diarrhea or constipation and a change in bowel habits.[17] Symptoms usually are experienced as acute attacks that subside within one day, but recurrent attacks are likely.[18] There may also be urgency for bowel movements, a feeling of incomplete evacuation (tenesmus), bloating, or abdominal distension.[19] In some cases, the symptoms are relieved by bowel movements.[14] People with IBS, more commonly than others, have gastroesophageal reflux, symptoms relating to the genitourinary system, chronic fatigue syndrome, fibromyalgia, headache, backache, and psychiatric symptoms such as depression and anxiety.[9][19] About a third of men and women who have IBS also report sexual dysfunction typically in the form of a reduction in libido.[20]



Cause


While the causes of IBS are still unknown, it is believed that the entire gut–brain axis is affected.[21][22]


The risk of developing IBS increases six-fold after acute gastrointestinal infection. Postinfection, further risk factors are young age, prolonged fever, anxiety, and depression.[23] Psychological factors, such as depression or anxiety, have not been shown to cause or influence the onset of IBS, but may play a role in the persistence and perceived severity of symptoms.[24] Nevertheless, they may worsen IBS symptoms and quality of life.[24] Antibiotic use also appears to increase the risk of developing IBS.[25] Research has found that genetic defects in innate immunity and epithelial homeostasis increase the risk of developing both post-infectious as well as other forms of IBS.[26]



Post-infectious


Approximately 10 percent of IBS cases are triggered by an acute gastroenteritis infection. Genetic defects relating to the innate immune system and epithelial barrier as well as high stress and anxiety levels appear to increase the risk of developing post-infectious IBS. Post-infectious IBS usually manifests itself as the diarrhea-predominant subtype. Evidence has demonstrated that the release of high levels of proinflammatory cytokines during acute enteric infection causes increased gut permeability leading to translocation of the commensal bacteria across the epithelial barrier; this in turn can result in significant damage to local tissues, which can develop into chronic gut abnormalities in sensitive individuals. However, increased gut permeability is strongly associated with IBS regardless of whether IBS was initiated by an infection or not.[26] A link between small intestinal bacterial overgrowth and tropical sprue has been proposed to be involved in the cause of post-infectious IBS.[27]



Stress


Publications suggesting the role of brain-gut "axis" appeared in the 1990s[28] and childhood physical and psychological abuse is often associated with the development of IBS.[29]


Given the high levels of anxiety experienced by people with IBS and the overlap with conditions such as fibromyalgia and chronic fatigue syndrome, a potential model of IBS involves a disruption of the stress system. The stress response in the body involves the HPA axis and the sympathetic nervous system, both of which have been shown to operate abnormally in people with IBS. Psychiatric illness or anxiety precedes IBS symptoms in two-thirds of people with IBS, and psychological traits predispose previously healthy people to developing IBS after gastroenteritis.[30][31]



Bacteria


Small intestinal bacterial overgrowth occurs with greater frequency in people who have been diagnosed with IBS compared to healthy controls. SIBO is most common in diarrhea-predominate IBS but also occurs in constipation-predominant IBS more frequently than healthy controls. Symptoms of SIBO include bloating, abdominal pain, diarrhea or constipation among others. IBS may be the result of the immune system interacting abnormally with gut microbiota resulting in an abnormal cytokine signalling profile.[32]



Fungus


There is growing evidence that 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.[33] The role of the gut mycobiota, and especially of the abnormal proliferation of the yeast Candida albicans in some people with IBS, was under investigation as of 2005.[34]



Protozoa




Prevalence of protozoal infections in industrialized countries (United States and Canada) in the 21st century[35][36]


Protozoal infections can cause symptoms that mirror specific IBS subtypes,[37] e.g., infection by certain substypes of blastocystis hominis (blastocystosis).[38][39]


As of 2017, evidence indicates that blastocystis colonisation occurs more commonly in IBS affected individuals and is a possible risk factor for developing IBS.[40]Dientamoeba fragilis has also been considered a possible organism to study, though it is also found in people without IBS.[41]



Vitamin D


Vitamin D deficiency is more common in individuals affected by irritable bowel syndrome.[42][43]



Mechanism


There is evidence that abnormalities occur in the gut flora of individuals who have IBS, such as reduced diversity, a decrease in bacteria belonging to the phylum Bacteroidetes, and an increase in those belonging to the phylum Firmicutes.[44] 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.[45] 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.[21][46]


Genetic, environmental, and psychological factors seem to be important in the development of IBS. Studies have shown that IBS has a genetic component even though there is a predominant influence of environmental factors.[47] IBS has been reported in greater quantities in multigenerational families with IBS than in the regular population.[48]



Diagnosis


No specific laboratory or imaging test can be performed to diagnose irritable bowel syndrome. Diagnosis involves excluding conditions that produce IBS-like symptoms, and then following a procedure to categorize the person's symptoms. Ruling out parasitic infections, lactose intolerance, small intestinal bacterial overgrowth, and celiac disease is recommended before a diagnosis of irritable bowel syndrome is made. Colonoscopy is recommended for people over 50 years old.[49] IBS sufferers are at increased risk of being given inappropriate surgeries such as appendectomy, cholecystectomy, and hysterectomy due to their IBS symptoms being misdiagnosed as other medical conditions.[50]



Differential diagnosis


Colon cancer, inflammatory bowel disease, thyroid disorders, and giardiasis can all feature abnormal defecation and abdominal pain. Less common causes of this symptom profile are carcinoid syndrome, microscopic colitis, bacterial overgrowth, and eosinophilic gastroenteritis; IBS is, however, a common presentation, and testing for these conditions would yield low numbers of positive results, so it is considered difficult to justify the expense.[51]


Some people, managed for years for IBS, may have non-celiac gluten sensitivity (NCGS).[4] 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,[52]fibromyalgia,[53][54][55] joint and muscle pain,[52][53][56] leg or arm numbness,[52][53][56]tingling of the extremities,[52][56] dermatitis (eczema or skin rash),[52][56]atopic disorders,[52]allergy to one or more inhalants, foods or metals[52][53] (such as mites, graminaceae, parietaria, cat or dog hair, shellfish, or nickel[53]), depression,[52][53][56]anxiety,[53]anemia,[52][56]iron-deficiency anemia, folate deficiency, asthma, rhinitis, eating disorders,[53]neuropsychiatric disorders (such as schizophrenia,[56][57]autism,[53][56][57]peripheral neuropathy,[56][57]ataxia,[57]attention deficit hyperactivity disorder[52]) or autoimmune diseases.[52] An improvement with a gluten-free diet of immune-mediated symptoms, including autoimmune diseases, once having reasonably ruled out coeliac disease and wheat allergy, is another way to realize a differential diagnosis.[52]


Because many causes of diarrhea give IBS-like symptoms, the American Gastroenterological Association published a set of guidelines for tests to be performed to rule out other causes of these symptoms. These include gastrointestinal infections, lactose intolerance, and coeliac disease.


Research has suggested these guidelines are not always followed.[49] Once other causes have been excluded, the diagnosis of IBS is performed using a diagnostic algorithm. Algorithms include the Manning criteria, the obsolete Rome I and II criteria, and the Kruis criteria, and studies have compared their reliability.[58] The Rome III process was published in 2006 and the Rome IV criteria were published in 2016.


The Rome IV criteria includes recurrent abdominal pain, on average, at least 1 day/week in the last 3 months, associated with two or more of the following criteria:



  • Related to defecation

  • Associated with a change in frequency of stool

  • Associated with a change in form (appearance) of stool.


Physicians may choose to use one of these guidelines or may simply choose to rely on their own anecdotal experience with past patients. The algorithm may include additional tests to guard against misdiagnosis of other diseases as IBS. Such "red flag" symptoms may include weight loss, gastrointestinal bleeding, anemia, or nocturnal symptoms. However, red flag conditions may not always contribute to accuracy in diagnosis; for instance, as many as 31% of people with IBS have blood in their stool, many possibly from hemorrhoidal bleeding.[58]


The diagnostic algorithm identifies a name that can be applied to the person's condition based on the combination of symptoms of diarrhea, abdominal pain, and constipation. For example, the statement "50% of returning travelers had developed functional diarrhea while 25% had developed IBS" would mean half the travelers had diarrhea while a quarter had diarrhea with abdominal pain. While some researchers believe this categorization system will help physicians understand IBS, others have questioned the value of the system and suggested all people with IBS have the same underlying disease but with different symptoms.[59]



Investigations


Investigations are performed to exclude other conditions:



  • Stool microscopy and culture (to exclude infectious conditions)

  • Blood tests: Full blood examination, liver function tests, erythrocyte sedimentation rate, and serological testing for coeliac disease

  • Abdominal ultrasound (to exclude gallstones and other biliary tract diseases)


  • Endoscopy and biopsies (to exclude peptic ulcer disease, coeliac disease, inflammatory bowel disease, and malignancies)


  • Hydrogen breath testing (to exclude fructose and lactose malabsorption)



Misdiagnosis


Some common examples of misdiagnosis include infectious diseases, coeliac disease,[60]Helicobacter pylori,[61][62]parasites (non-protozoal).[37][63][64]


Coeliac disease in particular is often misdiagnosed as IBS. The American College of Gastroenterology recommends all people with symptoms of IBS be tested for coeliac disease.[65]


Bile acid malabsorption is also sometimes missed in people with diarrhea-predominant IBS. SeHCAT tests suggest around 30% of people with D-IBS have this condition, and most respond to bile acid sequestrants.[66]


Chronic use of certain sedative-hypnotic drugs, especially the benzodiazepines, may cause irritable bowel-like symptoms that can lead to a misdiagnosis of irritable bowel syndrome.[67]



Comorbidities


Several medical conditions, or comorbidities, appear with greater frequency in people with IBS.



  • Neurological/psychiatric: A study of 97,593 individuals with IBS identified comorbidities such as headache, fibromyalgia, and depression.[68] 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.[9]


  • Inflammatory bowel disease: IBS may be a type of low-grade inflammatory bowel disease.[69] Researchers have suggested IBS and IBD are interrelated diseases,[70] noting that people with IBD experience IBS-like symptoms when their IBD is in remission.[71][72] A three-year study found that patients diagnosed with IBS were 16.3 times more likely to be diagnosed with IBD during the study period.[73] Serum markers associated with inflammation have also been found in patients with IBS.

  • Abdominal surgery: People with IBS were at increased risk of having unnecessary gall bladder removal surgery not due to an increased risk of gallstones, but rather to abdominal pain, awareness of having gallstones, and inappropriate surgical indications.[74] These people also are 87% more likely to undergo abdominal and pelvic surgery and three times more likely to undergo gallbladder surgery.[75] Also, people with IBS were twice as likely to undergo hysterectomy.[76]


  • Endometriosis: One study reported a statistically significant link between migraine headaches, IBS, and endometriosis.[77]

  • Other chronic disorders: Interstitial cystitis may be associated with other chronic pain syndromes, such as irritable bowel syndrome and fibromyalgia. The connection between these syndromes is unknown.[78]



Management


A number of treatments have been found to be effective, including fiber, talk therapy, antispasmodic and antidepressant medication, and peppermint oil.[79][80][81]



Diet


Studies have shown that up to 70% of people with IBS benefited from eating a low FODMAP diet. Symptoms most likely to improve from such a diet include urgency, flatulence, bloating, 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.[82] This 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.[83]


Some people with IBS believe they have some form of dietary intolerance; however, tests attempting to predict food sensitivity in IBS have proven disappointing. A small study reported that an IgG antibody test was somewhat effective in determining food sensitivity in people with IBS, with people on the elimination diet experiencing 10% greater symptom-reduction than those on a sham diet.[84] However, more research is necessary before IgG testing can be recommended.[85]



Low-FODMAP diet


FODMAPs are fermentable oligo-, di-, monosaccharides and polyols, which are poorly absorbed in the small intestine and subsequently fermented by the bacteria in the distal small and proximal large intestine. This is a normal phenomenon, common to everyone. The resultant production of gas potentially results in bloating and flatulence.[86] Although FODMAPs can produce certain digestive discomfort in some people, not only do they not cause intestinal inflammation, but they avoid it, because they produce beneficial alterations in the intestinal flora that contribute to maintain the good health of the colon.[87][88][89] 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.[86]


A low-FODMAP diet consists in 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.[86]


A low-FODMAP diet might help to improve short-term digestive symptoms in adults with irritable bowel syndrome,[90][82][91][13] but its long-term follow-up can have negative effects because it causes a detrimental impact on the gut microbiota and metabolome.[92][82][13][93] It should only be used for short periods of time and under the advice of a specialist.[94] A low-FODMAP diet is highly restrictive in various groups of nutrients and can be impractical to follow in the long-term.[95] More studies are needed to assess the true impact of this diet on health.[82][13]


In addition, the use of a low-FODMAP diet without medical advice can lead to serious health risks, including nutritional deficiencies,
cancer risk or even mortality. A low-FODMAP diet can ameliorate and mask the digestive symptoms of serious diseases that usually present digestive symptoms similar to those of irritable bowel syndrome, such as celiac disease, inflammatory bowel disease and colon cancer. It is crucial to conduct a complete medical evaluation before starting a low-FODMAP diet to ensure a correct diagnosis and that the appropriate therapy can be undertaken.[96] This is especially relevant in the case of celiac disease. 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 an unrecognized celiac disease, avoiding its diagnosis and correct treatment, with the consequent risk of several serious health complications, including various types of cancer.[96][97]


A 2018 systematic review concluded that although there is evidence of improved IBS symptoms from a low FODMAP diet, this is of very low quality.[98]



Fiber


Some evidence suggests soluble fiber supplementation (e.g., psyllium/ispagula husk) is effective.[12] It acts as a bulking agent, and for many people with IBS-D, allows for a more consistent stool. For people with IBS-C, it seems to allow for a softer, moister, more easily passable stool.


However, insoluble fiber (e.g., bran) has not been found to be effective for IBS.[99][100] In some people, insoluble fiber supplementation may aggravate symptoms.[101][102]


Fiber might be beneficial in those who have a predominance of constipation. In people who have IBS-C, soluble fiber can reduce overall symptoms, but will not reduce pain. The research supporting dietary fiber contains conflicting small studies complicated by the heterogeneity of types of fiber and doses used.[103]


One meta-analysis found only soluble fiber improved global symptoms of irritable bowel, but neither type of fiber reduced pain.[103]
An updated meta-analysis by the same authors also found soluble fiber reduced symptoms, while insoluble fiber worsened symptoms in some cases.[104] Positive studies have used 10–30 grams per day of ispaghula (psyllium).[105][106] One study specifically examined the effect of dose, and found 20 g of ispaghula (psyllium) were better than 10 g and equivalent to 30 g per day.[107]



Medication


Medications may consist of stool softeners and laxatives in IBS-C and antidiarrheals (e.g., opiate, opioid, or opioid analogs such as loperamide, codeine, diphenoxylate) if diarrhea is predominant.[108]


Drugs affecting serotonin (5-HT) in the intestines can help reduce symptoms.[109] On the other hand, many people with IBS-D report that SSRI type medications exacerbate spasms and diarrhea. This is thought to be due to the large number of serotonin receptors in the gut. 5HT3 antagonists such as ondansetron are effective in postinfectious IBS and diarrhea-dominant IBS due to their blockade of serotonin on 5HT3 receptors in the gut; the reason for their benefit is believed to be that excessive serotonin in the gut is thought to play a role in the pathogenesis of some subtypes of IBS. Certain atypical antipsychotic medications, such as clozapine and olanzapine, may also provide relief due to serotonergic properties these agents possess, acting on the same receptors as other medications in this specific category.[110] Benefits may include reduced diarrhea, reduced abdominal cramps, and improved general well-being. Any nausea present may also respond to 5HT3 antagonists owing to their antiemetic properties.[111] Serotonin stimulates the gut motility and so agonists can help constipation-predominant irritable bowel, while antagonists can help diarrhea-predominant irritable bowel. Selective serotonin reuptake inhibitors, SSRIs, frequently prescribed for panic and/or anxiety disorder and depression, affect serotonin in the gut, as well as the brain. The bowels are highly dependent on serotonin for neural communication. "Selective serotonin reuptake inhibitor antidepressants seem to promote global well-being in some patients with irritable bowel syndrome and, possibly, some improvement in abdominal pain and bowel symptoms, but this effect appears to be independent of improved depression. Further research is required."[112]


Mast cells and the compound that they secrete are central to the pathophysiology and implicated in the treatment of IBS;[21] some of the secreted mast cell mediators (and associated receptors) which have been implicated in symptoms of IBS or specific subtypes include: histamine (HRH1, HRH2, HRH3), tryptase and chymase (PAR2), serotonin (5-HT3), PGD2 (DP1).[21] Histamine also causes epithelial secretion of chloride ions and water (associated with secretory diarrhea) by signaling through a receptor or ligand-gated ion channel that has not been identified as of 2015.[21] A 2015 review noted that both H1-antihistamines and mast cell stabilizers have shown efficacy in reducing pain associated with visceral hypersensitivity in IBS;[21] other lower quality studies have also suggested the benefit of these agents for IBS.[21] In a related review on idiopathic mast cell activation syndromes (including IBS), a combined treatment approach using antileukotrienes, H1/H2-antihistamines, and a mast cell stabilizer are suggested.[113]



Laxatives


For people who do not adequately respond to dietary fiber, osmotic laxatives such as polyethylene glycol, sorbitol, and lactulose can help avoid "cathartic colon" which has been associated with stimulant laxatives.[114] Among the osmotic laxatives, doses of 17–26 g/d of polyethylene glycol have been well studied.[by whom?]Lubiprostone is a gastrointestinal agent used for the treatment of idiopathic chronic constipation and constipation-predominant IBS.



Antispasmodics


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.[108] 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.[115] The antispasmodic otilonium may also be useful.[116]



Discontinuation of proton pump inhibitors


Proton pump inhibitors (PPIs) used to suppress stomach acid production may cause bacterial overgrowth leading to IBS symptoms. Discontinuation of PPIs in selected individuals has been recommended as it may lead to an improvement or resolution of IBS symptoms.[117]



Tricyclic antidepressants


There is good evidence that low doses of tricyclic antidepressants can be effective for IBS. However, the evidence is less robust as to the effectiveness of other antidepressant classes such as SSRIs. Antidepressants are not effective for IBS in people with depression, possible because lower doses of antidepressants than the doses used to treat depression are required for relief of IBS.[118]



Serotonin agonists




  • Tegaserod (Zelnorm), a selective 5-HT4 agonist for IBS-C, is available for relieving IBS constipation in women and chronic idiopathic constipation in men and women. On March 30, 2007, the FDA requested Novartis Pharmaceuticals to voluntarily discontinue marketing of tegaserod based on the recently identified finding of an increased risk of serious cardiovascular adverse events (heart problems) associated with use of the drug. Novartis agreed to voluntarily suspend marketing of the drug in the United States and in many other countries. On July 27, 2007, the FDA approved a limited-treatment IND program for tegaserod in the US to allow restricted access to the medication for people in need if no comparable alternative drug or therapy is available to treat the disease. The FDA had issued two previous warnings about the serious consequences of tegaserod. In 2005, it was rejected as an IBS medication by the European Union. Tegaserod, marketed as Zelnorm in the United States, was the only agent approved to treat the multiple symptoms of IBS (in women only), including constipation, abdominal pain, and bloating.


  • Selective serotonin reuptake inhibitor antidepressants (SSRIs), because of their serotonergic effect, have been studied to see if they help IBS, especially people who are constipation predominant but as of 2015 the evidence is that SSRIs do not help.[119]



Serotonin antagonists


Alosetron, a selective 5-HT3 antagonist for IBS-D and cilansetron (also a selective 5-HT3 antagonist) were trialed for IBS. Due to severe adverse effects, namely ischemic colitis and severe constipation, they are not available or recommended.[102]



Other agents


Magnesium aluminum silicates and alverine citrate drugs can be effective for IBS.[102]


Evidence is conflicting about the benefit of antidepressants in IBS. Some meta-analyses have found a benefit, while others have not.[120] A meta-analysis of randomized controlled trials of mainly TCAs found three patients have to be treated with TCAs for one patient to improve.[121]


Rifaximin may be useful as a treatment for abdominal bloating and flatulence.[122]


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.[42][43]


Domperidone, a dopamine receptor blocker and a parasympathomimetic, has been shown to reduce bloating and abdominal pain as a result of an accelerated colon transit time and reduced fecal load, that is, a relief from 'hidden constipation'; defecation was similarly improved.[123]


The use of opioids is controversial due to the potential risk of tolerance, physical dependence, and addiction, but can be the only relief for some diarrhea-predominant cases when other treatment has been ineffective.[124]



SIBO therapy


Statistically significant reduction in IBS symptoms occurs following antibiotic therapy for small intestinal bacterial overgrowth.[125] However, recent research has shown that the lactulose hydrogen breath test does not actually measure SIBO, and that SIBO is unlikely to be the cause of IBS.[126]



Psychological therapies


There is low quality evidence from studies with poor methodological quality that psychological therapies can be effective in the treatment of IBS; however there are no significant adverse effects from psychological therapies for IBS.[118] The mind-body or brain-gut interactions has been proposed for IBS, and is gaining increasing research attention.[100]Hypnosis can improve mental well-being, and cognitive behavioural therapy can provide psychological coping strategies for dealing with distressing symptoms, as well as help suppress thoughts and behaviours that increase the symptoms of IBS.[100][102] Although the evidence base for effectiveness of psychotherapy and hypnosis is weak[118] and such therapies are in general not recommended,[50] in treatment-resistant cases where pharmacological therapies over a period of at least 12 months have failed to give relief, NICE clinical guidelines recommend that consideration should be given to psychological treatment strategies such as cognitive behavioural therapy [CBT], hypnotherapy and/or psychological therapy.[127]



Stress relief


Reducing stress may reduce the frequency and severity of IBS symptoms. Techniques that may be helpful include:



  • Relaxation techniques such as meditation

  • Physical activities such as yoga or tai chi

  • Regular exercise such as swimming, walking, or running[128]



Probiotics


Probiotics can be beneficial in the treatment of IBS; taking 10 billion to 100 billion beneficial bacteria per day is recommended for beneficial results. However, further research is needed on individual strains of beneficial bacteria for more refined recommendations.[100][129] Probiotics have positive effects such as enhancing the intestinal mucosal barrier, providing a physical barrier, bacteriocin production (resulting in reduced numbers of pathogenic and gas-producing bacteria), reducing intestinal permeability and bacterial translocation, and regulating the immune system both locally and systemically among other beneficial effects.[50] Probiotics may also have positive effects on the gut-brain axis by their positive effects countering the effects of stress on gut immunity and gut function.[130]


A number of probiotics have been found to be effective, including Lactobacillus plantarum,[50] and Bifidobacteria infantis;[131] but one review found only Bifidobacteria infantis showed efficacy.[132]B. infantis may have effects beyond the gut via it causing a reduction of proinflammatory cytokine activity and elevation of blood tryptophan levels, which may cause an improvement in symptoms of depression.[133] Some yogurt is made using probiotics that may help ease symptoms of IBS.[134] A probiotic yeast called Saccharomyces boulardii has some evidence of effectiveness in the treatment of irritable bowel syndrome.[135]


Certain probiotics have different effects on certain symptoms of IBS. For example, Bifidobacterium breve, B. longum, and Lactobacillus acidophilus have been found to alleviate abdominal pain. B. breve, B. infantis, L. casei, or L. plantarum species alleviated distension symptoms. B. breve, B. infantis, L. casei, L. plantarum, B. longum, L. acidophilus, L. bulgaricus, and Streptococcus salivarius ssp. thermophilus have all been found to affect flatulence levels. Most clinical studies show probiotics do not improve straining, sense of incomplete evacuation, stool consistency, fecal urgency, or stool frequency, although a few clinical studies did find some benefit of probiotic therapy. The evidence is conflicting for whether probiotics improve overall quality of life scores.[136]


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.[136]



Herbal remedies


Peppermint oil appears useful.[137] In a meta-analysis it was found to be superior to placebo for improvement of IBS symptoms, at least in the short term.[138] 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.[79] 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.[100]Iberogast, a multi-herbal extract, was found to be superior in efficacy to placebo.[139]


Only limited evidence exists for the effectiveness of other herbal remedies for IBS. As with all herbs, it is wise to be aware of possible drug interactions and adverse effects.[100]



Yoga


Yoga may be effective for some people with IBS, especially poses which exercise the lower abdomen.[102]



Acupuncture


A meta-analysis found no benefits of acupuncture relative to placebo for IBS symptom severity or IBS-related quality of life.[140]



Epidemiology




Percentage of population with IBS reported in various studies in different countries


The prevalence of IBS varies by country and by age range examined. The bar graph at right shows the percentage of the population reporting symptoms of IBS in studies from various geographic regions (see table below for references). The following table contains a list of studies performed in different countries that measured the prevalence of IBS and IBS-like symptoms:






































































Percentage of population reporting symptoms of IBS in various studies from various geographic areas
Country
Prevalence
Author/year
Notes
Canada
6%[141]
Boivin, 2001

Japan
10%[142]
Quigley, 2006
Study measured prevalence of GI abdominal pain/cramping
United Kingdom
8.2%[143]

10.5%[144]


Ehlin, 2003

Wilson, 2004


Prevalence increased substantially 1970–2004
United States
14.1%[145]
Hungin, 2005
Most undiagnosed
United States
15%[141]
Boivin, 2001
Estimate
Pakistan
14%[146]
Jafri, 2007
Much more common in 16–30 age range. 56% male, 44% female
Pakistan
34%[147]
Jafri, 2005
College students
Mexico City
35%[148]
Schmulson, 2006
n=324. Also measured functional diarrhea and functional vomiting. High rates attributed to "stress of living in a populated city."
Brazil
43%[142]
Quigley, 2006
Study measured prevalence of GI abdominal pain/cramping
Mexico
46%[142]
Quigley, 2006
Study measured prevalence of GI abdominal pain/cramping


Gender


Women are around two to three times more likely to be diagnosed with IBS and four to five times more likely to seek specialty care for it than men.[149] These differences likely reflect a combination of both biological (sex) and social (gender) factors. People diagnosed with IBS are usually younger than 45 years old.[1] Studies of females with IBS show symptom severity often fluctuates with the menstrual cycle, suggesting hormonal differences may play a role.[150] Endorsement of gender-related traits has been associated with quality of life and psychological adjustment in IBS.[151] Gender differences in healthcare-seeking may also play a role.[152] Gender differences in trait anxiety may contribute to lower pain thresholds in women, putting them at greater risk for a number of chronic pain disorders.[153] Finally, sexual trauma is a major risk factor for IBS, with as many as 33% of those affected reporting such abuse. Because women are at higher risk of sexual abuse than men, sex-related risk of abuse may contribute to the higher rate of IBS in women.[154]



History


The concept of an "irritable bowel" appeared in the Rocky Mountain Medical Journal in 1950. 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.[155]



Society and culture



Names


Other names for the condition used in the past included irritable colon, spastic colon, nervous colon, colitis, mucous colitis, and spastic bowel.[156][157]


The terminologies that refer to the colon are inaccurate and discouraged, since the disorder is not limited to this section of the digestive tract. Similarly, the term "colitis" is not accurate as inflammation is not present.[157][158][159] Other reasons why these terms were abandoned were to reflect the understanding that the disorder is not a figment of a person’s imagination.[156]



Economics



United States


The aggregate cost of irritable bowel syndrome in the United States has been estimated at $1.7–10 billion in direct medical costs, with an additional $20 billion in indirect costs, for a total of $21.7–30 billion.[8] A study by a managed care company comparing medical costs for people with IBS to non-IBS controls identified a 49% annual increase in medical costs associated with a diagnosis of IBS.[160] People with IBS incurred average annual direct costs of $5,049 and $406 in out-of-pocket expenses in 2007.[161] A study of workers with IBS found that they reported a 34.6% loss in productivity, corresponding to 13.8 hours lost per 40 hour week.[162] A study of employer-related health costs from a Fortune 100 company conducted with data from the 1990s found people with IBS incurred US $4527 in claims costs vs. $3276 for controls.[163] A study on Medicaid costs conducted in 2003 by the University of Georgia's 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.[164]



Research


Individuals with IBS have been found to have decreased diversity and numbers of bacteroidetes 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.[165][166] 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.[167]


There is increasing evidence for the effectiveness of mesalazine (5-aminosalicylic acid) in the treatment of IBS.[168] 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.[169]


An IgG-mediated food intolerance diet led to a 24% greater deterioration in symptoms compared to those on the elimination diet and food elimination based on IgG antibodies may be effective in reducing IBS symptoms and is worthy of further biomedical research.[84] The main problem with this study was that the differences in symptoms were only observed in exclusion diets is limited, treatment based on "abnormally" high IgG antibodies cannot be recommended.[170]


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.[171] IBS/IBD individuals are less often HLA DQ2/8 positive than in upper functional gastrointestinal disease and healthy populations.[172]


A questionnaire in 2006 designed to learn people's perceptions about IBS, their preferences on the type of information they need, and educational media and expectations from health care providers revealed misperceptions about IBS developing into other conditions, including colitis, malnutrition, and cancer. The survey found that people IBS were most interested in learning about foods to avoid (60%), causes of IBS (55%), medications (58%), coping strategies (56%), and psychological factors related to IBS (55%). The respondents indicated they wanted their physicians to be available by phone or e-mail following a visit (80%), have the ability to listen (80%), and provide hope (73%) and support (63%).[173]



References





  1. ^ abcdefghijk "Definition and Facts for Irritable Bowel Syndrome". NIDDKD. February 23, 2015. Archived from the original on April 2, 2016. Retrieved March 29, 2016..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"""""""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/6/65/Lock-green.svg/9px-Lock-green.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/d/d6/Lock-gray-alt-2.svg/9px-Lock-gray-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/a/aa/Lock-red-alt-2.svg/9px-Lock-red-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}


  2. ^ abcde "Symptoms and Causes of Irritable Bowel Syndrome". NIDDK. February 23, 2015. Archived from the original on April 5, 2016. Retrieved March 29, 2016.


  3. ^ abcdefghijk Chey, WD; Kurlander, J; Eswaran, S (3 March 2015). "Irritable bowel syndrome: a clinical review". JAMA. 313 (9): 949–58. doi:10.1001/jama.2015.0954. PMID 25734736.


  4. ^ ab Levy J, Bernstein L, Silber N (Dec 2014). "Celiac disease: an immune dysregulation syndrome". Curr Probl Pediatr Adolesc Health Care. 44 (11): 324–7. doi:10.1016/j.cppeds.2014.10.002. PMID 25499458.


  5. ^ abcd "Treatment for Irritable Bowel Syndrome". NIDDK. February 23, 2015. Archived from the original on April 6, 2016. Retrieved March 29, 2016.


  6. ^ ab Quigley, Eamonn M.M. (2013). "Treatment level 1". Irritable bowel syndrome : diagnosis and clinical management (First ed.). Chichester, West Sussex: Wiley-Blackwell. ISBN 9781118444740. Archived from the original on September 8, 2017.


  7. ^ ab Maxion-Bergemann S, Thielecke F, Abel F, Bergemann R; Thielecke; Abel; Bergemann (2006). "Costs of irritable bowel syndrome in the UK and US". PharmacoEconomics. 24 (1): 21–37. doi:10.2165/00019053-200624010-00002. PMID 16445300.CS1 maint: Multiple names: authors list (link)


  8. ^ ab Hulisz D (2004). "The burden of illness of irritable bowel syndrome: current challenges and hope for the future". J Manag Care Pharm. 10 (4): 299–309. PMID 15298528.


  9. ^ abc Whitehead WE, Palsson O, Jones KR; Palsson; Jones (2002). "Systematic review of the comorbidity of irritable bowel syndrome with other disorders: what are the causes and implications?". Gastroenterology. 122 (4): 1140–56. doi:10.1053/gast.2002.32392. PMID 11910364.CS1 maint: Multiple names: authors list (link)


  10. ^ Spiller R, Garsed K; Garsed (May 2009). "Postinfectious irritable bowel syndrome". Gastroenterology. 136 (6): 1979–88. doi:10.1053/j.gastro.2009.02.074. PMID 19457422.


  11. ^ Chang L (March 2011). "The role of stress on physiologic responses and clinical symptoms in irritable bowel syndrome". Gastroenterology. 140 (3): 761–5. doi:10.1053/j.gastro.2011.01.032. PMC 3039211. PMID 21256129.


  12. ^ ab Moayyedi, P; Quigley, EM; Lacy, BE; Lembo, AJ; Saito, YA; Schiller, LR; Soffer, EE; Spiegel, BM; Ford, AC (September 2014). "The effect of fiber supplementation on irritable bowel syndrome: a systematic review and meta-analysis". The American Journal of Gastroenterology. 109 (9): 1367–74. doi:10.1038/ajg.2014.195. PMID 25070054.


  13. ^ abcd Rao SS, Yu S, Fedewa A (2015). "Systematic review: dietary fibre and FODMAP-restricted diet in the management of constipation and irritable bowel syndrome". Aliment. Pharmacol. Ther. 41 (12): 1256–70. doi:10.1111/apt.13167. PMID 25903636.


  14. ^ ab Mayer EA (April 2008). "Clinical practice. Irritable bowel syndrome". N. Engl. J. Med. 358 (16): 1692–9. doi:10.1056/NEJMcp0801447. PMC 3816529. PMID 18420501.


  15. ^ Hatch, Maureen C. (2000). Women and health. San Diego, Calif: Academic Press. p. 1098. ISBN 9780122881459. Archived from the original on September 8, 2017.


  16. ^ Holten KB, Wetherington A, Bankston L; Wetherington; Bankston (2003). "Diagnosing the patient with abdominal pain and altered bowel habits: is it irritable bowel syndrome?". Am Fam Physician. 67 (10): 2157–62. PMID 12776965. Archived from the original on May 15, 2008.CS1 maint: Multiple names: authors list (link)


  17. ^ Schmulson MW, Chang L; Chang (1999). "Diagnostic approach to the patient with irritable bowel syndrome". Am. J. Med. 107 (5A): 20S–26S. doi:10.1016/S0002-9343(99)00278-8. PMID 10588169.


  18. ^ Tamparo, Carol (2011). Fifth Edition: Diseases of the Human Body. Philadelphia, PA: F.A. Davis Company. p. 407. ISBN 978-0-8036-2505-1.


  19. ^ ab Talley NJ (2006). "Irritable bowel syndrome". Intern Med J. 36 (11): 724–8. doi:10.1111/j.1445-5994.2006.01217.x. PMC 1761148. PMID 17040359.


  20. ^ Sperber AD, Dekel R; Dekel (Apr 2010). "Irritable Bowel Syndrome and Co-morbid Gastrointestinal and Extra-gastrointestinal Functional Syndromes". J Neurogastroenterol Motil. 16 (2): 113–9. doi:10.5056/jnm.2010.16.2.113. PMC 2879857. PMID 20535341.


  21. ^ abcdefg Wouters MM, Vicario M, Santos J (2015). "The role of mast cells in functional GI disorders". Gut. 65 (1): 155–68. doi:10.1136/gutjnl-2015-309151. PMID 26194403.


  22. ^ Ohman L, Simrén M; Simrén (2010). "Pathogenesis of IBS: Role of inflammation, immunity and neuroimmune interactions". Nature Reviews Gastroenterology & Hepatology. 7 (3): 163–73. doi:10.1038/nrgastro.2010.4. PMID 20101257.


  23. ^ Thabane M, Kottachchi DT, Marshall JK; Kottachchi; Marshall (2007). "Systematic review and meta-analysis: The incidence and prognosis of post-infectious irritable bowel syndrome". Aliment Pharmacol Ther. 26 (4): 535–44. doi:10.1111/j.1365-2036.2007.03399.x. PMID 17661757.CS1 maint: Multiple names: authors list (link)


  24. ^ ab "World Gastroenterology Organisation Global Guidelines. Irritable Bowel Syndrome: a Global Perspective" (PDF). World Gastroenterology Organisation. Sep 2015. Archived (PDF) from the original on May 27, 2016. Retrieved April 24, 2016.


  25. ^ Shanahan F, Quigley EM; Quigley (May 2014). "Manipulation of the microbiota for treatment of IBS and IBD-challenges and controversies". Gastroenterology. 146 (6): 1554–63. doi:10.1053/j.gastro.2014.01.050. PMID 24486051.


  26. ^ ab Beatty JK, Bhargava A, Buret AG (2014). "Post-infectious irritable bowel syndrome: mechanistic insights into chronic disturbances following enteric infection". World J. Gastroenterol. 20 (14): 3976–85. doi:10.3748/wjg.v20.i14.3976. PMC 3983453. PMID 24744587.


  27. ^ Ghoshal UC, Gwee KA (2017). "Post-infectious IBS, tropical sprue and small intestinal bacterial overgrowth: the missing link". Nat Rev Gastroenterol Hepatol. 14 (7): 435–41. doi:10.1038/nrgastro.2017.37. PMID 28513629.CS1 maint: Uses authors parameter (link)


  28. ^ Fukudo S, Nomura T, Muranaka M, Taguchi F; Nomura; Muranaka; Taguchi (1993). "Brain-gut response to stress and cholinergic stimulation in irritable bowel syndrome. A preliminary study". J. Clin. Gastroenterol. 17 (2): 133–41. doi:10.1097/00004836-199309000-00009. PMID 8031340.CS1 maint: Multiple names: authors list (link)


  29. ^ Barreau F, Ferrier L, Fioramonti J, Bueno L; Ferrier; Fioramonti; Bueno (September 2007). "New Insights in the Etiology and Pathophysiology of Irritable Bowel Syndrome: Contribution of Neonatal Stress Models". Pediatric Research. 62 (3): 240–5. doi:10.1203/PDR.0b013e3180db2949. PMID 17622962.CS1 maint: Multiple names: authors list (link)


  30. ^ Spiller, R; Aziz, Q; Creed, F; Emmanuel, A; Houghton, L; Hungin, P; Jones, R; Kumar, D; Rubin, G; Trudgill, N; Whorwell, P (1 December 2007). "Guidelines on the irritable bowel syndrome: mechanisms and practical management". Gut. 56 (12): 1770–98. doi:10.1136/gut.2007.119446. PMC 2095723. PMID 17488783.


  31. ^ Fukudo, Shin (19 January 2007). "Role of corticotropin-releasing hormone in irritable bowel syndrome and intestinal inflammation". Journal of Gastroenterology. 42 (S17): 48–51. doi:10.1007/s00535-006-1942-7. PMID 17238026.


  32. ^ Ghoshal, UC.; Srivastava, D. (Mar 2014). "Irritable bowel syndrome and small intestinal bacterial overgrowth: meaningful association or unnecessary hype". World J Gastroenterol. 20 (10): 2482–91. doi:10.3748/wjg.v20.i10.2482. PMC 3949258. PMID 24627585.


  33. ^ Collins, SM (August 2014). "A role for the gut microbiota in IBS". Nature Reviews. Gastroenterology & Hepatology. 11 (8): 497–505. doi:10.1038/nrgastro.2014.40. PMID 24751910.


  34. ^ Santelmann, H; Howard, JM (January 2005). "Yeast metabolic products, yeast antigens and yeasts as possible triggers for irritable bowel syndrome". European Journal of Gastroenterology & Hepatology. 17 (1): 21–6. CiteSeerX 10.1.1.567.6030. doi:10.1097/00042737-200501000-00005. PMID 15647635.


  35. ^ Lagacé-Wiens PR, VanCaeseele PG, Koschik C; Vancaeseele; Koschik (2006). "Dientamoeba fragilis: an emerging role in intestinal disease". Canadian Medical Association Journal. 175 (5): 468–9. doi:10.1503/cmaj.060265. PMC 1550747. PMID 16940260.CS1 maint: Multiple names: authors list (link)


  36. ^ Amin OM (2002). "Seasonal prevalence of intestinal parasites in the United States during 2000". Am. J. Trop. Med. Hyg. 66 (6): 799–803. PMID 12224595.


  37. ^ ab Stark D, van Hal S, Marriott D, Ellis J, Harkness J; Van Hal; Marriott; Ellis; Harkness (2007). "Irritable bowel syndrome: a review on the role of intestinal protozoa and the importance of their detection and diagnosis". Int. J. Parasitol. 37 (1): 11–20. doi:10.1016/j.ijpara.2006.09.009. PMID 17070814.CS1 maint: Multiple names: authors list (link)


  38. ^ Wawrzyniak I, Poirier P, Viscogliosi E, Dionigia M, Texier C, Delbac F, Alaoui HE (2013). "Blastocystis, an unrecognized parasite: an overview of pathogenesis and diagnosis". Ther Adv Infect Dis. 1 (5): 167–78. doi:10.1177/2049936113504754. PMC 4040727. PMID 25165551. Recent in vitro and in vivo studies have shed new light on the pathogenic power of this parasite, suggesting that Blastocystis sp. infection is associated with a variety of gastrointestinal disorders, may play a significant role in irritable bowel syndrome, and may be linked with cutaneous lesions (urticaria).


  39. ^ Roberts T, Stark D, Harkness J, Ellis J (2014). "Update on the pathogenic potential and treatment options for Blastocystis sp". Gut Pathog. 6: 17. doi:10.1186/1757-4749-6-17. PMC 4039988. PMID 24883113.


  40. ^ Rostami, A.; Riahi, SM.; Haghighi, A.; Saber, V.; Armon, B.; Seyyedtabaei, SJ. (July 2017). "The role of Blastocystis sp. and Dientamoeba fragilis in irritable bowel syndrome: a systematic review and meta-analysis". Parasitol Res. 116 (9): 2361–2371. doi:10.1007/s00436-017-5535-6. PMID 28668983.


  41. ^ Windsor JJ, Macfarlane L; MacFarlane (May 2005). "Irritable bowel syndrome: the need to exclude Dientamoeba fragilis". Am. J. Trop. Med. Hyg. 72 (5): 501, author reply 501–2. PMID 15891119. Archived from the original on July 17, 2010. Retrieved November 4, 2009.


  42. ^ ab Williams CE, Williams EA, Corfe BM (January 2018). "Vitamin D status in irritable bowel syndrome and the impact of supplementation on symptoms: what do we know and what do we need to know?" (PDF). Eur J Clin Nutr. 72 (10): 1358–1363. doi:10.1038/s41430-017-0064-z. PMID 29367731.


  43. ^ ab Ferguson LR, Laing B, Marlow G, Bishop K (January 2016). "The role of vitamin D in reducing gastrointestinal disease risk and assessment of individual dietary intake needs: Focus on genetic and genomic technologies". Mol Nutr Food Res. 60 (1): 119–33. doi:10.1002/mnfr.201500243. PMID 26251177.


  44. ^ Collins S (2014). "A role for the gut microbiota in IBS". Nature Reviews Gastroenterology & Hepatology. 11 (8): 497–505. doi:10.1038/nrgastro.2014.40. PMID 24751910.


  45. ^ Cremon C, Carini G, De Giorgio R, Stanghellini V, Corinaldesi R, Barbara G; Carini; De Giorgio; Stanghellini; Corinaldesi; Barbara (May 2010). "Intestinal dysbiosis in irritable bowel syndrome: etiological factor or epiphenomenon?". Expert Rev. Mol. Diagn. 10 (4): 389–93. doi:10.1586/erm.10.33. PMID 20465494.CS1 maint: Multiple names: authors list (link)


  46. ^ Schmulson M, Bielsa MV, Carmona-Sánchez R, et al. (2014). "[Microbiota, gastrointestinal infections, low-grade inflammation, and antibiotic therapy in irritable bowel syndrome: an evidence-based review]". Rev Gastroenterol Mex (in Spanish). 79 (2): 96–134. doi:10.1016/j.rgmx.2014.01.004. PMID 24857420.


  47. ^ Tally, NJ (Dec 2006). "Genes and environment in irritable bowel syndrome: one step forward". Gut. 55 (12): 1694–6. doi:10.1136/gut.2006.108837. PMC 1856457. PMID 17124153.


  48. ^ Saito, Yuri A. (Mar 2011). "The Role of Genetics in IBS". Gastroenterology Clinics of North America. 40 (1): 45–67. doi:10.1016/j.gtc.2010.12.011. PMC 3056499. PMID 21333900.


  49. ^ ab Yawn BP, Lydick E, Locke GR, Wollan PC, Bertram SL, Kurland MJ; Lydick; Locke; Wollan; Bertram; Kurland (2001). "Do published guidelines for evaluation of Irritable Bowel Syndrome reflect practice?". BMC Gastroenterology. 1: 11. doi:10.1186/1471-230X-1-11. PMC 59674. PMID 11701092.CS1 maint: Multiple names: authors list (link)


  50. ^ abcd Bixquert Jiménez M (Aug 2009). "Treatment of irritable bowel syndrome with probiotics. An etiopathogenic approach at last?". Rev Esp Enferm Dig. 101 (8): 553–64. doi:10.4321/s1130-01082009000800006. PMID 19785495. Archived from the original on October 6, 2014.


  51. ^ C. Hauser (2005). Mayo Clinic Gastroenterology and Hepatology Board Review. CRC Press. p. 225–. ISBN 978-0-203-50274-7. Archived from the original on May 10, 2013. Retrieved October 24, 2010.


  52. ^ abcdefghijkl Fasano A, Sapone A, Zevallos V, Schuppan D (May 2015). "Nonceliac gluten sensitivity". Gastroenterology (Review). 148 (6): 1195–204. doi:10.1053/j.gastro.2014.12.049. PMID 25583468.


  53. ^ abcdefghi Volta U, Caio G, De Giorgio R, Henriksen C, Skodje G, Lundin KE (Jun 2015). "Non-celiac gluten sensitivity: a work-in-progress entity in the spectrum of wheat-related disorders". Best Pract Res Clin Gastroenterol. 29 (3): 477–91. doi:10.1016/j.bpg.2015.04.006. PMID 26060112.


  54. ^ Rossi A, Di Lollo AC, Guzzo MP, Giacomelli C, Atzeni F, Bazzichi L, Di Franco M (2015). "Fibromyalgia and nutrition: what news?". Clin Exp Rheumatol. 33 (1 Suppl 88): S117–25. PMID 25786053.


  55. ^ San Mauro Martín I, Garicano Vilar E, Collado Yurrutia L, Ciudad Cabañas MJ (Dec 2014). "[Is gluten the great etiopathogenic agent of disease in the XXI century?] [Article in Spanish]" (PDF). Nutr Hosp. 30 (6): 1203–10. doi:10.3305/nh.2014.30.6.7866. PMID 25433099. Archived (PDF) from the original on November 6, 2015.


  56. ^ abcdefghi Catassi C, Bai J, Bonaz B, Bouma G, Calabrò A, Carroccio A, Castillejo G, Ciacci C, Cristofori F, Dolinsek J, Francavilla R, Elli L, Green P, Holtmeier W, Koehler P, Koletzko S, Meinhold C, Sanders D, Schumann M, Schuppan D, Ullrich R, Vécsei A, Volta U, Zevallos V, Sapone A, Fasano A (2013). "Non-celiac gluten sensitivity: the new frontier of gluten related disorders". Nutrients (Review). 5 (10): 3839–53. doi:10.3390/nu5103839. ISSN 2072-6643. PMC 3820047. PMID 24077239.


  57. ^ abcd Lebwohl B, Ludvigsson JF, Green PH (Oct 2015). "Celiac disease and non-celiac gluten sensitivity". BMJ (Review). 351: h4347. doi:10.1136/bmj.h4347. PMC 4596973. PMID 26438584.


  58. ^ ab Fass R, Longstreth GF, Pimentel M, Fullerton S, Russak SM, Chiou CF, Reyes E, Crane P, Eisen G, McCarberg B, Ofman J; Longstreth; Pimentel; Fullerton; Russak; Chiou; Reyes; Crane; Eisen; McCarberg; Ofman (2001). "Evidence- and consensus-based practice guidelines for the diagnosis of irritable bowel syndrome". Arch. Intern. Med. 161 (17): 2081–8. doi:10.1001/archinte.161.17.2081. PMID 11570936.CS1 maint: Multiple names: authors list (link)


  59. ^ Talley NJ (2006). "A unifying hypothesis for the functional gastrointestinal disorders: really multiple diseases or one irritable gut?". Reviews in Gastroenterological Disorders. 6 (2): 72–8. PMID 16699476.


  60. ^ Spiegel BM, DeRosa VP, Gralnek IM, Wang V, Dulai GS; Derosa; Gralnek; Wang; Dulai (2004). "Testing for celiac sprue in irritable bowel syndrome with predominant diarrhea: a cost-effectiveness analysis". Gastroenterology. 126 (7): 1721–32. doi:10.1053/j.gastro.2004.03.012. PMID 15188167.CS1 maint: Multiple names: authors list (link)


  61. ^ Su YC, Wang WM, Wang SY, Lu SN, Chen LT, Wu DC, Chen CY, Jan CM, Horowitz M; Wang; Wang; Lu; Chen; Wu; Chen; Jan; Horowitz (August 2000). "The association between Helicobacter pylori infection and functional dyspepsia in patients with irritable bowel syndrome". Am. J. Gastroenterol. 95 (8): 1900–5. doi:10.1111/j.1572-0241.2000.02252.x. PMID 10950033.CS1 maint: Multiple names: authors list (link)


  62. ^ Gerards C, Leodolter A, Glasbrenner B, Malfertheiner P; Leodolter; Glasbrenner; Malfertheiner (2001). "H. pylori infection and visceral hypersensitivity in patients with irritable bowel syndrome". Dig Dis. 19 (2): 170–3. doi:10.1159/000050673. PMID 11549828.CS1 maint: Multiple names: authors list (link)


  63. ^ Grazioli B, Matera G, Laratta C, Schipani G, Guarnieri G, Spiniello E, Imeneo M, Amorosi A, Focà A, Luzza F; Matera; Laratta; Schipani; Guarnieri; Spiniello; Imeneo; Amorosi; Focà; Luzza (March 2006). "Giardia lamblia infection in patients with irritable bowel syndrome and dyspepsia: a prospective study". World J. Gastroenterol. 12 (12): 1941–4. PMC 4087522. PMID 16610003. Archived from the original on August 15, 2009.CS1 maint: Multiple names: authors list (link)


  64. ^ Vernia P, Ricciardi MR, Frandina C, Bilotta T, Frieri G; Ricciardi; Frandina; Bilotta; Frieri (1995). "Lactose malabsorption and irritable bowel syndrome. Effect of a long-term lactose-free diet". The Italian Journal of Gastroenterology. 27 (3): 117–21. PMID 7548919.CS1 maint: Multiple names: authors list (link)


  65. ^
    Brandt LJ, Chey WD, Foxx-Orenstein AE, Schiller LR, Schoenfeld PS, Spiegel BM, Talley NJ, Quigley EM; Brandt; Chey; Foxx-Orenstein; Schiller; Schoenfeld; Spiegel; Talley; Quigley (January 2009). "An Evidence-Based Systematic Review on the Management of Irritable Bowel Syndrome" (PDF). Am J Gastroenterol. 104 (Supplement 1): S1–S35. doi:10.1038/ajg.2008.122. PMID 19521341. Archived (PDF) from the original on December 5, 2010.CS1 maint: Multiple names: authors list (link)



  66. ^ Wedlake L, A'Hern R, Russell D, Thomas K, Walters JR, Andreyev HJ; a'Hern; Russell; Thomas; Walters; Andreyev (2009). "Systematic review: the prevalence of idiopathic bile acid malabsorption as diagnosed by SeHCAT scanning in patients with diarrhoea-predominant irritable bowel syndrome". Alimentary Pharmacology & Therapeutics. 30 (7): 707–17. doi:10.1111/j.1365-2036.2009.04081.x. PMID 19570102.CS1 maint: Multiple names: authors list (link)


  67. ^ C Heather Ashton (1987). "Benzodiazepine Withdrawal: Outcome in 50 Patients". British Journal of Addiction. 82: 655–71.


  68. ^ Cole JA, Rothman KJ, Cabral HJ, Zhang Y, Farraye FA; Rothman; Cabral; Zhang; Farraye (2006). "Migraine, fibromyalgia, and depression among people with IBS: a prevalence study". BMC Gastroenterology. 6: 26. doi:10.1186/1471-230X-6-26. PMC 1592499. PMID 17007634.CS1 maint: Multiple names: authors list (link)


  69. ^ Bercik P, Verdu EF, Collins SM; Verdu; Collins (2005). "Is irritable bowel syndrome a low-grade inflammatory bowel disease?". Gastroenterol. Clin. North Am. 34 (2): 235–45, vi–vii. doi:10.1016/j.gtc.2005.02.007. PMID 15862932.CS1 maint: Multiple names: authors list (link)


  70. ^ Quigley EM (2005). "Irritable bowel syndrome and inflammatory bowel disease: interrelated diseases?". Chinese Journal of Digestive Diseases. 6 (3): 122–32. doi:10.1111/j.1443-9573.2005.00202.x. PMID 16045602.


  71. ^ Simrén M, Axelsson J, Gillberg R, Abrahamsson H, Svedlund J, Björnsson ES; Axelsson; Gillberg; Abrahamsson; Svedlund; Björnsson (2002). "Quality of life in inflammatory bowel disease in remission: the impact of IBS-like symptoms and associated psychological factors". Am. J. Gastroenterol. 97 (2): 389–96. doi:10.1111/j.1572-0241.2002.05475.x. PMID 11866278.CS1 maint: Multiple names: authors list (link)


  72. ^ Minderhoud IM, Oldenburg B, Wismeijer JA, van Berge Henegouwen GP, Smout AJ; Oldenburg; Wismeijer; Van Berge Henegouwen; Smout (2004). "IBS-like symptoms in patients with inflammatory bowel disease in remission; relationships with quality of life and coping behavior". Dig. Dis. Sci. 49 (3): 469–74. doi:10.1023/B:DDAS.0000020506.84248.f9. PMID 15139501.CS1 maint: Multiple names: authors list (link)


  73. ^ García Rodríguez LA, Ruigómez A, Wallander MA, Johansson S, Olbe L; Ruigómez; Wallander; Johansson; Olbe (2000). "Detection of colorectal tumor and inflammatory bowel disease during follow-up of patients with initial diagnosis of irritable bowel syndrome". Scand. J. Gastroenterol. 35 (3): 306–11. doi:10.1080/003655200750024191. PMID 10766326.CS1 maint: Multiple names: authors list (link)


  74. ^ Corazziari E, Attili AF, Angeletti C, De Santis A; Attili, AF; Angeletti, C; De Santis, A (2008). "Gallstones, cholecystectomy and irritable bowel syndrome (IBS) MICOL population-based study". Dig Liver Dis. 40 (12): 944–50. doi:10.1016/j.dld.2008.02.013. PMID 18406218.CS1 maint: Multiple names: authors list (link)


  75. ^ Cole JA, Yeaw JM, Cutone JA, Kuo B, Huang Z, Earnest DL, Walker AM; Yeaw; Cutone; Kuo; Huang; Earnest; Walker (2005). "The incidence of abdominal and pelvic surgery among patients with irritable bowel syndrome". Dig. Dis. Sci. 50 (12): 2268–75. doi:10.1007/s10620-005-3047-1. PMID 16416174.CS1 maint: Multiple names: authors list (link)


  76. ^ Longstreth GF, Yao JF; Yao (2004). "Irritable bowel syndrome and surgery: a multivariable analysis". Gastroenterology. 126 (7): 1665–73. doi:10.1053/j.gastro.2004.02.020. PMID 15188159.


  77. ^ Tietjen GE, Bushnell CD, Herial NA, Utley C, White L, Hafeez F; Bushnell; Herial; Utley; White; Hafeez (2007). "Endometriosis is associated with prevalence of comorbid conditions in migraine". Headache. 47 (7): 1069–78. doi:10.1111/j.1526-4610.2007.00784.x. PMID 17635599.CS1 maint: Multiple names: authors list (link)


  78. ^ "Interstitial cystitis: Risk factors". Mayo Clinic. January 20, 2009. Archived from the original on May 16, 2008.


  79. ^ ab Ford AC, Talley NJ, Spiegel BM, Foxx-Orenstein AE, Schiller L, Quigley EM, Moayyedi P; Talley; Spiegel; Foxx-Orenstein; Schiller; Quigley; Moayyedi (2008). "Effect of fibre, antispasmodics, and peppermint oil in the treatment of irritable bowel syndrome: systematic review and meta-analysis". BMJ. 337: a2313. doi:10.1136/bmj.a2313. PMC 2583392. PMID 19008265.CS1 maint: Multiple names: authors list (link)


  80. ^ Ford, AC; Quigley, EM; Lacy, BE; Lembo, AJ; Saito, YA; Schiller, LR; Soffer, EE; Spiegel, BM; Moayyedi, P (September 2014). "Effect of antidepressants and psychological therapies, including hypnotherapy, in irritable bowel syndrome: systematic review and meta-analysis". The American Journal of Gastroenterology. 109 (9): 1350–65, quiz 1366. doi:10.1038/ajg.2014.148. PMID 24935275.


  81. ^ Khanna, Reena; MacDonald, John K.; Levesque, Barrett G. (2014-07-01). "Peppermint oil for the treatment of irritable bowel syndrome: a systematic review and meta-analysis". Journal of Clinical Gastroenterology. 48 (6): 505–12. doi:10.1097/MCG.0b013e3182a88357. ISSN 1539-2031. PMID 24100754.


  82. ^ abcd Staudacher HM, Irving PM, Lomer MC, Whelan K (April 2014). "Mechanisms and efficacy of dietary FODMAP restriction in IBS". Nat Rev Gastroenterol Hepatol (Review). 11 (4): 256–66. doi:10.1038/nrgastro.2013.259. PMID 24445613. An emerging body of research now demonstrates the efficacy of fermentable carbohydrate restriction in IBS. [...] However, further work is urgently needed both to confirm clinical efficacy of fermentable carbohydrate restriction in a variety of clinical subgroups and to fully characterize the effect on the gut microbiota and the colonic environ¬ment. Whether the effect on luminal bifidobacteria is clinically relevant, preventable, or long lasting, needs to be investigated. The influence on nutrient intake, dietary diversity, which might also affect the gut microbiota,137 and quality of life also requires further exploration as does the possible economic effects due to reduced physician contact and need for medication. Although further work is required to confirm its place in IBS and functional bowel disorder clinical pathways, fermentable carbohydrate restriction is an important consideration for future national and international IBS guidelines.


  83. ^ Fedewa A, Rao SS (2014). "Dietary fructose intolerance, fructan intolerance and FODMAPs". Curr Gastroenterol Rep. 16 (1): 370. doi:10.1007/s11894-013-0370-0. PMC 3934501. PMID 24357350.


  84. ^ ab Atkinson W, Sheldon TA, Shaath N, Whorwell PJ; Sheldon; Shaath; Whorwell (2004). "Food elimination based on IgG antibodies in irritable bowel syndrome: a randomised controlled trial". Gut. 53 (10): 1459–64. doi:10.1136/gut.2003.037697. PMC 1774223. PMID 15361495.CS1 maint: Multiple names: authors list (link)


  85. ^ Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC (2006). "Functional bowel disorders". Gastroenterology. 131 (2): 688. doi:10.1053/j.gastro.2006.06.027.


  86. ^ abc Peter R Gibson & Susan J Shepherd (2010). "Evidence-based dietary management of functional gastrointestinal symptoms: The FODMAP approach". Journal of Gastroenterology and Hepatology. 25 (2): 252–8. doi:10.1111/j.1440-1746.2009.06149.x. PMID 20136989.


  87. ^ Makharia A, Catassi C, Makharia GK (2015). "The Overlap between Irritable Bowel Syndrome and Non-Celiac Gluten Sensitivity: A Clinical Dilemma". Nutrients (Review). 7 (12): 10417–26. doi:10.3390/nu7125541. PMC 4690093. PMID 26690475.


  88. ^ Greer JB, O'Keefe SJ (2011). "Microbial induction of immunity, inflammation, and cancer". Front Physiol (Review). 1: 168. doi:10.3389/fphys.2010.00168. PMC 3059938. PMID 21423403.


  89. ^ Andoh A, Tsujikawa T, Fujiyama Y (2003). "Role of dietary fiber and short-chain fatty acids in the colon". Curr Pharm des (Review). 9 (4): 347–58. PMID 12570825.CS1 maint: Multiple names: authors list (link)


  90. ^ Turco R, Salvatore S, Miele E, Romano C, Marseglia GL, Staiano A (2018). "Does a low FODMAPs diet reduce symptoms of functional abdominal pain disorders? A systematic review in adult and paediatric population, on behalf of Italian Society of Pediatrics". Ital J Pediatr (Systematic Review). 44 (1): 53. doi:10.1186/s13052-018-0495-8. PMC 5952847. PMID 29764491.


  91. ^ Marsh A, Eslick EM, Eslick GD (2015). "Does a diet low in FODMAPs reduce symptoms associated with functional gastrointestinal disorders? A comprehensive systematic review and meta-analysis". Eur J Nutr. 55 (3): 897–906. doi:10.1007/s00394-015-0922-1. PMID 25982757.


  92. ^ Tuck, CJ; Muir, JG; Barrett, JS; Gibson, PR (2014). "Fermentable oligosaccharides, disaccharides, monosaccharides and polyols: role in irritable bowel syndrome". Expert Rev Gastroenterol Hepatol. 8 (7): 819–34. doi:10.1586/17474124.2014.917956. PMID 24830318.


  93. ^ Heiman ML, Greenway FL (2016). "A healthy gastrointestinal microbiome is dependent on dietary diversity". Mol Metab (Review). 5 (5): 317–20. doi:10.1016/j.molmet.2016.02.005. PMC 4837298. PMID 27110483.


  94. ^ Staudacher HM, Whelan K (2017). "The low FODMAP diet: recent advances in understanding its mechanisms and efficacy in IBS". Gut (Review). 66 (8): 1517–27. doi:10.1136/gutjnl-2017-313750. PMID 28592442.


  95. ^ Hou JK, Lee D, Lewis J (October 2014). "Diet and inflammatory bowel disease: review of patient-targeted recommendations". Clin. Gastroenterol. Hepatol. (Review). 12 (10): 1592–600. doi:10.1016/j.cgh.2013.09.063. PMC 4021001. PMID 24107394. Even less evidence exists for the efficacy of the SCD, FODMAP, or Paleo diet. Furthermore, the practicality of maintaining these interventions over long periods of time is doubtful. At a practical level, adherence to defined diets may result in an unnecessary financial burden or reduction in overall caloric intake in people who are already at risk for protein-calorie malnutrition.


  96. ^ ab Barrett JS (2017). "How to institute the low-FODMAP diet". J Gastroenterol Hepatol (Review). 32 Suppl 1: 8–10. doi:10.1111/jgh.13686. PMID 28244669. Common symptoms of IBS are bloating, abdominal pain, excessive flatus, constipation, diarrhea, or alternating bowel habit. These symptoms, however, are also common in the presentation of coeliac disease, inflammatory bowel disease, defecatory disorders, and colon cancer. Confirming the diagnosis is crucial so that appropriate therapy can be undertaken. Unfortunately, even in these alternate diagnoses, a change in diet restricting FODMAPs may improve symptoms and mask the fact that the correct diagnosis has not been made. This is the case with coeliac disease where a low-FODMAP diet can concurrently reduce dietary gluten, improving symptoms, and also affecting coeliac diagnostic indices.3,4 Misdiagnosis of intestinal diseases can lead to secondary problems such as nutritional deficiencies, cancer risk, or even mortality in the case of colon cancer.


  97. ^ "Celiac disease". World Gastroenterology Organisation Global Guidelines. July 2016. Archived from the original on 17 March 2017. Retrieved 4 June 2018.


  98. ^ Dionne J, Ford AC, Yuan Y, Chey WD, Lacy BE, Saito YA, et al. (2018). "A Systematic Review and Meta-Analysis Evaluating the Efficacy of a Gluten-Free Diet and a Low FODMAPs Diet in Treating Symptoms of Irritable Bowel Syndrome". Am J Gastroenterol. 113 (9): 1290–1300. doi:10.1038/s41395-018-0195-4. PMID 30046155.


  99. ^ Francis CY, Whorwell PJ; Whorwell (Jul 2, 1994). "[Bran and irritable bowel syndrome: time for reappraisal]". Lancet. 344 (8914): 39–40. doi:10.1016/S0140-6736(94)91055-3. PMID 7912305.


  100. ^ abcdef Shen YH, Nahas R; Nahas (Feb 2009). "Complementary and alternative medicine for treatment of irritable bowel syndrome". Can Fam Physician. 55 (2): 143–8. PMC 2642499. PMID 19221071.


  101. ^ Bijkerk CJ, de Wit NJ, Muris JW, Whorwell PJ, Knottnerus JA, Hoes AW; De Wit; Muris; Whorwell; Knottnerus; Hoes (Aug 27, 2009). "Soluble or insoluble fibre in irritable bowel syndrome in primary care? Randomised placebo controlled trial". BMJ. 339 (b3154): b3154. doi:10.1136/bmj.b3154. PMC 3272664. PMID 19713235.CS1 maint: Multiple names: authors list (link)


  102. ^ abcde Ducrotté P (Nov 2007). "[Irritable bowel syndrome: current treatment options]". Presse Med. 36 (11 Pt 2): 1619–26. doi:10.1016/j.lpm.2007.03.008. PMID 17490849.


  103. ^ ab Bijkerk CJ, Muris JW, Knottnerus JA, Hoes AW, de Wit NJ; Muris; Knottnerus; Hoes; De Wit (2004). "Systematic review: the role of different types of fiber in the treatment of irritable bowel syndrome". Aliment Pharmacol Ther. 19 (3): 245–51. doi:10.1111/j.0269-2813.2004.01862.x. PMID 14984370.CS1 maint: Multiple names: authors list (link)


  104. ^ Bijkerk CJ, de Wit NJ, Muris JW, Whorwell PJ, Knottnerus JA, Hoes AW; De Wit; Muris; Whorwell; Knottnerus; Hoes (2009). "Systematic Soluble or insoluble fiber in irritable bowel syndrome in primary care? Randomised placebo controlled trial". BMJ. 339 (b): 3154–. doi:10.1136/bmj.b3154. PMC 3272664. PMID 19713235.CS1 maint: Multiple names: authors list (link)


  105. ^ Prior A, Whorwell PJ; Whorwell (1987). "Double blind study of ispaghula in irritable bowel syndrome". Gut. 28 (11): 1510–3. doi:10.1136/gut.28.11.1510. PMC 1433676. PMID 3322956.


  106. ^ Jalihal A, Kurian G; Kurian (1990). "Ispaghula therapy in irritable bowel syndrome: improvement in overall well-being is related to reduction in bowel dissatisfaction". J Gastroenterol Hepatol. 5 (5): 507–13. doi:10.1111/j.1440-1746.1990.tb01432.x. PMID 2129822.


  107. ^ Kumar A, Kumar N, Vij JC, Sarin SK, Anand BS; Kumar; Vij; Sarin; Anand (1987). "Optimum dosage of ispaghula husk in patients with irritable bowel syndrome: correlation of symptom relief with whole gut transit time and stool weight". Gut. 28 (2): 150–5. doi:10.1136/gut.28.2.150. PMC 1432983. PMID 3030900.CS1 maint: Multiple names: authors list (link)


  108. ^ ab Ruepert L, Quartero AO, de Wit NJ, van der Heijden GJ, Rubin G, Muris JW; Quartero; De Wit; Van Der Heijden; Rubin; Muris (2011). "Bulking agents, antispasmodics and antidepressants for the treatment of irritable bowel syndrome". Cochrane Database Syst Rev (8): CD003460. doi:10.1002/14651858.CD003460.pub3. PMID 21833945.CS1 maint: Multiple names: authors list (link)


  109. ^ Talley NJ (2001). "Serotoninergic neuroenteric modulators". Lancet. 358 (9298): 2061–8. doi:10.1016/S0140-6736(01)07103-3. PMID 11755632.


  110. ^ Pae CU1, Lee SJ, Han C, Patkar AA, Masand PS; Lee; Han; Patkar; Masand (May 2013). "Atypical antipsychotics as a possible treatment option for irritable bowel syndrome". Expert Opin Investig Drugs. 22 (5): 565–72. doi:10.1517/13543784.2013.782392. PMID 23506326.CS1 maint: Multiple names: authors list (link)


  111. ^ Spiller R, Lam C; Lam (July 2012). "An Update on Post-infectious Irritable Bowel Syndrome: Role of Genetics, Immune Activation, Serotonin and Altered Microbiome". J Neurogastroenterol Motil. 18 (3): 258–68. doi:10.5056/jnm.2012.18.3.258. PMC 3400813. PMID 22837873.


  112. ^ Creed F (2005). "How do SSRIs help patients with irritable bowel syndrome?". Gut. 55 (8): 1065–7. doi:10.1136/gut.2005.086348. PMC 1856284. PMID 16849340.


  113. ^ Frieri M (2015). "Mast Cell Activation Syndrome". Clin Rev Allergy Immunol. 54 (3): 353–365. doi:10.1007/s12016-015-8487-6. PMID 25944644.


  114. ^ Joo JS, Ehrenpreis ED, Gonzalez L, Kaye M, Breno S, Wexner SD, Zaitman D, Secrest K; Ehrenpreis; Gonzalez; Kaye; Breno; Wexner; Zaitman; Secrest (1998). "Alterations in colonic anatomy induced by chronic stimulant laxatives: the cathartic colon revisited". J Clin Gastroenterol. 26 (4): 283–6. doi:10.1097/00004836-199806000-00014. PMID 9649012.CS1 maint: Multiple names: authors list (link)


  115. ^ Paul Barber; Joy Parkes; Diane Blundell (June 1, 2012). Further Essentials of Pharmacology for Nurses. McGraw-Hill Education (UK). pp. 34–. ISBN 978-0-335-24398-3. Archived from the original on February 16, 2017.


  116. ^ Annaházi, A; Róka, R; Rosztóczy, A; Wittmann, T (28 May 2014). "Role of antispasmodics in the treatment of irritable bowel syndrome". World Journal of Gastroenterology. 20 (20): 6031–43. doi:10.3748/wjg.v20.i20.6031. PMC 4033443. PMID 24876726.


  117. ^ Simrén M, Barbara G, Flint HJ, Spiegel BM, Spiller RC, Vanner S, Verdu EF, Whorwell PJ, Zoetendal EG; Barbara; Flint; Spiegel; Spiller; Vanner; Verdu; Whorwell; et al. (Jan 2013). "Intestinal microbiota in functional bowel disorders: a Rome foundation report". Gut. 62 (1): 159–76. doi:10.1136/gutjnl-2012-302167. PMC 3551212. PMID 22730468.CS1 maint: Multiple names: authors list (link)


  118. ^ abc Song KH, Jung HK, Kim HJ, Koo HS, Kwon YH, Shin HD, Lim HC, Shin JE, Kim SE, Cho DH, Kim JH, Kim HJ (April 2018). "Clinical Practice Guidelines for Irritable Bowel Syndrome in Korea, 2017 Revised Edition". J Neurogastroenterol Motil. 24 (2): 197–215. doi:10.5056/jnm17145. PMC 5885719. PMID 29605976.


  119. ^ Xie, C; Tang, Y; Wang, Y; Yu, T; Wang, Y; Jiang, L; Lin, L (7 August 2015). "Efficacy and Safety of Antidepressants for the Treatment of Irritable Bowel Syndrome: A Meta-Analysis". PLOS ONE. 10 (8): e0127815. doi:10.1371/journal.pone.0127815. PMC 4529302. PMID 26252008.


  120. ^ "UpToDate Inc". (Subscription required (help)).


  121. ^ Jackson JL, O'Malley PG, Tomkins G, Balden E, Santoro J, Kroenke K; O'Malley; Tomkins; Balden; Santoro; Kroenke (2000). "Treatment of functional gastrointestinal disorders with antidepressant medications: a meta-analysis". Am J Med. 108 (1): 65–72. doi:10.1016/S0002-9343(99)00299-5. PMID 11059442.CS1 maint: Multiple names: authors list (link)


  122. ^ Quigley EM (2006). "Germs, gas and the gut; the evolving role of the enteric flora in IBS". Am J Gastroenterol. 101 (2): 334–5. doi:10.1111/j.1572-0241.2006.00445.x. PMID 16454839.


  123. ^ Raahave D, Christensen E, Loud FB, Knudsen LL. "Correlation of bowel symptoms with colonic transit, length, and faecal load in functional faecal retention" 2009; 56: 83–8


  124. ^ Warfield, Carol A.; Zahid H. Bajwa (2003). Principles and Practice of Pain Medicine. McGraw-Hill Professional. ISBN 978-0-07-144349-4.


  125. ^ Lin HC (Aug 18, 2004). "Small intestinal bacterial overgrowth: a framework for understanding irritable bowel syndrome". JAMA: The Journal of the American Medical Association. 292 (7): 852–8. doi:10.1001/jama.292.7.852. PMID 15316000.


  126. ^ Spiegel, Brennan M.R. (June 2011). "Questioning the Bacterial Overgrowth Hypothesis of Irritable Bowel Syndrome: An Epidemiologic and Evolutionary Perspective". Clinical Gastroenterology and Hepatology. 9 (6): 461–9. doi:10.1016/j.cgh.2011.02.030. PMID 21397724.


  127. ^ Irritable Bowel Syndrome in Adults Archived May 26, 2014, at the Wayback Machine.: Diagnosis and management of irritable bowel syndrome in primary care; NICE clinical guideline 61, Issue Feb 2008


  128. ^ "Irritable Bowel Syndrome (IBS) – Treatment". NHS Choices. National Health Service. Archived from the original on October 18, 2012. Retrieved October 21, 2012.


  129. ^ Nikfar S, Rahimi R, Rahimi F, Derakhshani S, Abdollahi M; Rahimi; Rahimi; Derakhshani; Abdollahi (December 2008). "Efficacy of probiotics in irritable bowel syndrome: a meta-analysis of randomized, controlled trials". Dis. Colon Rectum. 51 (12): 1775–80. doi:10.1007/s10350-008-9335-z. PMID 18465170.CS1 maint: Multiple names: authors list (link)


  130. ^ Konturek PC, Brzozowski T, Konturek SJ; Brzozowski; Konturek (Dec 2011). "Stress and the gut: pathophysiology, clinical consequences, diagnostic approach and treatment options". J Physiol Pharmacol. 62 (6): 591–9. PMID 22314561.CS1 maint: Multiple names: authors list (link)


  131. ^ "New Studies Examine the Evidence on Probiotics in IBS" (PDF) (Press release). American College of Gastroenterology. October 31, 2005. Archived from the original (PDF) on February 10, 2006.


  132. ^ Brenner DM, Moeller MJ, Chey WD, Schoenfeld PS; Moeller; Chey; Schoenfeld (April 2009). "The utility of probiotics in the treatment of irritable bowel syndrome: a systematic review". Am. J. Gastroenterol. 104 (4): 1033–49, quiz 1050. doi:10.1038/ajg.2009.25. PMID 19277023.CS1 maint: Multiple names: authors list (link)


  133. ^ Aragon G, Graham DB, Borum M, Doman DB; Graham; Borum; Doman (Jan 2010). "Probiotic therapy for irritable bowel syndrome". Gastroenterol Hepatol (NY). 6 (1): 39–44. PMC 2886445. PMID 20567539.CS1 maint: Multiple names: authors list (link)


  134. ^ "IBS diet: Can yogurt ease symptoms?". Mayo Clinic. May 21, 2008. Archived from the original on February 9, 2010.


  135. ^ McFarland, LV. (May 2010). "Systematic review and meta-analysis of Saccharomyces boulardii in adult patients". World J Gastroenterol. 16 (18): 2202–22. doi:10.3748/wjg.v16.i18.2202. PMC 2868213. PMID 20458757.


  136. ^ ab Ortiz-Lucas M, Tobías A, Saz P, Sebastián JJ; Tobías; Saz; Sebastián (Jan 2013). "Effect of probiotic species on irritable bowel syndrome symptoms: A bring up to date meta-analysis". Rev Esp Enferm Dig. 105 (1): 19–36. doi:10.4321/s1130-01082013000100005. PMID 23548007.CS1 maint: Multiple names: authors list (link)


  137. ^ Wilkins T, Pepitone C, Alex B, Schade RR; Pepitone; Alex; Schade (Sep 1, 2012). "Diagnosis and management of IBS in adults". American Family Physician. 86 (5): 419–26. PMID 22963061.CS1 maint: Multiple names: authors list (link)


  138. ^ Khanna, Reena; MacDonald, John J.; Levesque, Barrett (2014). "Peppermint oil for the treatment of irritable bowel syndrome: A systematic review and meta-analysis". Journal of Clinical Gastroenterology. 48 (6): 505–12. doi:10.1097/MCG.0b013e3182a88357. PMID 24100754.


  139. ^ Rösch W, Liebregts T, Gundermann KJ, Vinson B, Holtmann G; Liebregts; Gundermann; Vinson; Holtmann (2006). "Phytotherapy for functional dyspepsia: a review of the clinical evidence for the herbal preparation STW 5". Phytomedicine. 13 Suppl 5: 114–21. doi:10.1016/j.phymed.2006.03.022. PMID 16978851.CS1 maint: Multiple names: authors list (link)


  140. ^ Manheimer E, Cheng K, Wieland LS, Min LS, Shen X, Berman BM, Lao L; Cheng; Wieland; Min; Shen; Berman; Lao (2012). "Acupuncture for treatment of irritable bowel syndrome". Cochrane Database Syst Rev. 5 (5): CD005111. doi:10.1002/14651858.CD005111.pub3. PMC 3718572. PMID 22592702.CS1 maint: Multiple names: authors list (link)


  141. ^ ab
    Boivin M (October 2001). "Socioeconomic impact of irritable bowel syndrome in Canada". Can. J. Gastroenterol. 15 (Suppl B): 8B–11B. PMID 11694908.



  142. ^ abc
    Quigley EM, Locke GR, Mueller-Lissner S, Paulo LG, Tytgat GN, Helfrich I, Schaefer E; Locke; Mueller-Lissner; Paulo; Tytgat; Helfrich; Schaefer (July 2006). "Prevalence and management of abdominal cramping and pain: a multinational survey". Aliment. Pharmacol. Ther. 24 (2): 411–9. doi:10.1111/j.1365-2036.2006.02989.x. PMID 16842469.CS1 maint: Multiple names: authors list (link)



  143. ^ Ehlin AG, Montgomery SM, Ekbom A, Pounder RE, Wakefield AJ; Montgomery; Ekbom; Pounder; Wakefield (August 2003). "Prevalence of gastrointestinal diseases in two British national birth cohorts". Gut. 52 (8): 1117–21. doi:10.1136/gut.52.8.1117. PMC 1773740. PMID 12865268.CS1 maint: Multiple names: authors list (link)


  144. ^ Wilson S, Roberts L, Roalfe A, Bridge P, Singh S; Roberts; Roalfe; Bridge; Singh (July 2004). "Prevalence of irritable bowel syndrome: a community survey". Br J Gen Pract. 54 (504): 495–502. PMC 1324800. PMID 15239910.CS1 maint: Multiple names: authors list (link)


  145. ^
    Hungin AP, Chang L, Locke GR, Dennis EH, Barghout V; Chang; Locke; Dennis; Barghout (June 2005). "Irritable bowel syndrome in the United States: prevalence, symptom patterns and impact". Aliment. Pharmacol. Ther. 21 (11): 1365–75. doi:10.1111/j.1365-2036.2005.02463.x. PMID 15932367.CS1 maint: Multiple names: authors list (link)



  146. ^ Jafri W, Yakoob J, Jafri N, Islam M, Ali QM; Yakoob; Jafri; Islam; Ali (June 2007). "Irritable bowel syndrome and health seeking behaviour in different communities of Pakistan". J Pak Med Assoc. 57 (6): 285–7. PMID 17629228.CS1 maint: Multiple names: authors list (link)


  147. ^ Jafri W, Yakoob J, Jafri N, Islam M, Ali QM; Yakoob; Jafri; Islam; Ali (2005). "Frequency of irritable bowel syndrome in college students". J Ayub Med Coll Abbottabad. 17 (4): 9–11. PMID 16599025.CS1 maint: Multiple names: authors list (link)


  148. ^ Schmulson M, Ortíz O, Santiago-Lomeli M, Gutiérrez-Reyes G, Gutiérrez-Ruiz MC, Robles-Díaz G, Morgan D; Ortíz; Santiago-Lomeli; Gutiérrez-Reyes; Gutiérrez-Ruiz; Robles-Díaz; Morgan (2006). "Frequency of functional bowel disorders among healthy volunteers in Mexico City" (PDF). Dig. Dis. 24 (3–4): 342–7. doi:10.1159/000092887. PMID 16849861. Archived (PDF) from the original on May 16, 2011.CS1 maint: Multiple names: authors list (link)


  149. ^ Payne S (2004). "Sex, gender, and irritable bowel syndrome: Making the connections". Gender Medicine. 1 (1): 18–28. doi:10.1016/S1550-8579(04)80007-X. PMID 16115580.


  150. ^ Jackson NA, Houghton LA, Whorwell PJ, Currer B; Houghton; Whorwell; Currer (1994). "Does the menstrual cycle affect anorectal physiology?". Digestive Diseases and Sciences. 39 (12): 2607–11. doi:10.1007/bf02087697. PMID 7995186.CS1 maint: Multiple names: authors list (link)


  151. ^ Voci SC, Cramer KM; Cramer (2009). "Gender-related traits, quality of life, and psychological adjustment among women with irritable bowel syndrome". Quality of Life Research : An International Journal of Quality of Life Aspects of Treatment, Care and Rehabilitation. 18 (9): 1169–76. doi:10.1007/s11136-009-9532-9. PMID 19728159.


  152. ^ Drossman DA, Li Z, Andruzzi E, Temple RD, Talley NJ, Thompson WG, Whitehead WE, Janssens J, Funch-Jensen P, Corazziari E; Li; Andruzzi; Temple; Talley; Thompson; Whitehead; Janssens; et al. (1993). "U.S. Householder survey of functional gastrointestinal disorders. Prevalence, sociodemography, and health impact". Digestive Diseases and Sciences. 38 (9): 1569–80. doi:10.1007/bf01303162. PMID 8359066.CS1 maint: Multiple names: authors list (link)


  153. ^ Goffaux P, Michaud K, Gaudreau J, Chalaye P, Rainville P, Marchand S; Michaud; Gaudreau; Chalaye; Rainville; Marchand (2011). "Sex differences in perceived pain are affected by an anxious brain". Pain. 152 (9): 2065–73. doi:10.1016/j.pain.2011.05.002. PMID 21665365.CS1 maint: Multiple names: authors list (link)


  154. ^ Walker EA, Katon WJ, Roy-Byrne PP, Jemelka RP, Russo J; Katon; Roy-Byrne; Jemelka; Russo (1993). "Histories of sexual victimization in patients with irritable bowel syndrome or inflammatory bowel disease". The American Journal of Psychiatry. 150 (10): 1502–6. doi:10.1176/ajp.150.10.1502. PMID 8379554.CS1 maint: Multiple names: authors list (link)


  155. ^ Brown PW (1950). "The irritable bowel syndrome". Rocky Mountain Medical Journal. 47 (5): 343–6. PMID 15418074.


  156. ^ ab "Definition & Facts for Irritable Bowel Syndrome. What is IBS? | NIDDK". National Institute of Diabetes and Digestive and Kidney Diseases. February 2015. Archived from the original on 4 October 2017. Retrieved 15 March 2018.


  157. ^ ab Spiller R, Aziz Q, Creed F, Emmanuel A, Houghton L, Hungin P, et al. (2007). "Guidelines on the irritable bowel syndrome: mechanisms and practical management". Gut (Practice Guideline. Review). 56 (12): 1770–98. doi:10.1136/gut.2007.119446. PMC 2095723. PMID 17488783.


  158. ^ Camilleri M (2012). "Irritable bowel syndrome: how useful is the term and the 'diagnosis'?". Therap Adv Gastroenterol. 5 (6): 381–6. doi:10.1177/1756283X12442223. PMC 3491678. PMID 23152731.


  159. ^ García MD, García JI, Pereda A (2002). "Trastornos intestinales funcionales (equivalentes del colon irritable)". Sociedad Española de Gastroenterología, Hepatología y Nutrición Pediátrica (Review) (in Spanish). 57 (3): 253–63. doi:10.1016/S1695-4033(02)77914-9.


  160. ^ Levy RL, Von Korff M, Whitehead WE, Stang P, Saunders K, Jhingran P, Barghout V, Feld AD; von Korff; Whitehead; Stang; Saunders; Jhingran; Barghout; Feld (2001). "Costs of care for irritable bowel syndrome patients in a health maintenance organization". Am J Gastroenterol. 96 (11): 3122–9. doi:10.1111/j.1572-0241.2001.05258.x. PMID 11721759.CS1 maint: Multiple names: authors list (link)


  161. ^ Nyrop KA, Palsson OS, Levy RL, Korff MV, Feld AD, Turner MJ, Whitehead WE; Palsson; Levy; von Korff; Feld; Turner; Whitehead (2007). "Costs of health care for irritable bowel syndrome, chronic constipation, functional diarrhoea and functional abdominal pain". Aliment Pharmacol Ther. 26 (2): 237–48. doi:10.1111/j.1365-2036.2007.03370.x. PMID 17593069.CS1 maint: Multiple names: authors list (link)


  162. ^ Paré P, Gray J, Lam S, Balshaw R, Khorasheh S, Barbeau M, Kelly S, McBurney CR; Gray; Lam; Balshaw; Khorasheh; Barbeau; Kelly; McBurney (2006). "Health-related quality of life, work productivity, and health care resource utilization of subjects with irritable bowel syndrome: baseline results from LOGIC (Longitudinal Outcomes Study of Gastrointestinal Symptoms in Canada), a naturalistic study". Clinical Therapeutics. 28 (10): 1726–35, discussion 1710–1. doi:10.1016/j.clinthera.2006.10.010. PMID 17157129.CS1 maint: Multiple names: authors list (link)


  163. ^ Leong SA, Barghout V, Birnbaum HG, Thibeault CE, Ben-Hamadi R, Frech F, Ofman JJ; Barghout; Birnbaum; Thibeault; Ben-Hamadi; Frech; Ofman (2003). "The economic consequences of irritable bowel syndrome: a US employer perspective". Arch. Intern. Med. 163 (8): 929–35. doi:10.1001/archinte.163.8.929. PMID 12719202.CS1 maint: Multiple names: authors list (link)


  164. ^ Martin BC, Ganguly R, Pannicker S, Frech F, Barghout V; Ganguly; Pannicker; Frech; Barghout (2003). "Utilization Patterns and Net Direct Medical Costs Medicaid of Irritable Bowel Syndrome". Curr Med Res Opin. 19 (8): 771–80. doi:10.1185/030079903125002540. PMID 14687449. Archived from the original on December 20, 2003.CS1 maint: Multiple names: authors list (link)


  165. ^ Aroniadis OC, Brandt LJ; Brandt (January 2013). "Fecal microbiota transplantation: past, present and future". Curr. Opin. Gastroenterol. 29 (1): 79–84. doi:10.1097/MOG.0b013e32835a4b3e. PMID 23041678.


  166. ^ Smits LP, Bouter KE, de Vos WM, Borody TJ, Nieuwdorp M; Bouter; De Vos; Borody; Nieuwdorp (November 2013). "Therapeutic potential of fecal microbiota transplantation". Gastroenterology. 145 (5): 946–53. doi:10.1053/j.gastro.2013.08.058. PMID 24018052.CS1 maint: Multiple names: authors list (link)


  167. ^ Ford, Alexander C; Quigley, Eamonn M M; Lacy, Brian E; Lembo, Anthony J; Saito, Yuri A; Schiller, Lawrence R; Soffer, Edy E; Spiegel, Brennan M R; Moayyedi, Paul (2014). "Efficacy of Prebiotics, Probiotics, and Synbiotics in Irritable Bowel Syndrome and Chronic Idiopathic Constipation: Systematic Review and Meta-analysis". The American Journal of Gastroenterology. 109 (10): 1547–61. doi:10.1038/ajg.2014.202. ISSN 0002-9270. PMID 25070051.


  168. ^ Klotz U (February 2012). "The pharmacological profile and clinical use of mesalazine (5-aminosalicylic acid)". Arzneimittelforschung. 62 (2): 53–8. doi:10.1055/s-0031-1299685. PMID 22344548.


  169. ^ Barbara G, Stanghellini V, Cremon C; et al. (2009). "Aminosalicylates and other anti-inflammatory compounds for irritable bowel syndrome". Dig Dis. 27 Suppl 1: 115–21. doi:10.1159/000268131. PMID 20203507.CS1 maint: Multiple names: authors list (link) CS1 maint: Explicit use of et al. (link)


  170. ^ Philpott H, Nandurkar S, Lubel J, Gibson PR; Nandurkar; Lubel; Gibson (2012). "Alternative investigations for irritable bowel syndrome". Journal of Gastroenterology and Hepatology. 28 (1): 73–7. doi:10.1111/j.1440-1746.2012.07291.x. PMID 23033865.CS1 maint: Multiple names: authors list (link)


  171. ^ Keszthelyi D, Troost FJ, Jonkers DM, van Eijk HM, Lindsey PJ, Dekker J, Buurman WA, Masclee AA (Aug 2014). "Serotonergic reinforcement of intestinal barrier function is impaired in irritable bowel syndrome". Aliment. Pharmacol. Ther. 40 (4): 392–402. doi:10.1111/apt.12842. PMID 24943480.CS1 maint: Multiple names: authors list (link)


  172. ^ DiGiacomo D, Santonicola A, Zingone F, Troncone E, Caria MC, Borgheresi P, Parrilli G, Ciacci C (Apr 28, 2013). "Human leukocyte antigen DQ2/8 prevalence in non-celiac patients with gastrointestinal diseases". World J. Gastroenterol. 19 (16): 2507–13. doi:10.3748/wjg.v19.i16.2507. PMC 3646141. PMID 23674852.CS1 maint: Multiple names: authors list (link)


  173. ^ Halpert AD, Thomas AC, Hu Y, Morris CB, Bangdiwala SI, Drossman DA; Thomas; Hu; Morris; Bangdiwala; Drossman (2006). "A survey on patient educational needs in irritable bowel syndrome and attitudes toward participation in clinical research". J Clin Gastroenterol. 40 (1): 37–43. doi:10.1097/01.mcg.0000190759.95862.08. PMID 16340632.CS1 maint: Multiple names: authors list (link)




External links











Classification
D



  • ICD-10: K58


  • ICD-9-CM: 564.1


  • MeSH: D043183


  • DiseasesDB: 30638


External resources


  • MedlinePlus: 000246


  • eMedicine: med/1190


  • Patient UK:
    Irritable bowel syndrome



  • Irritable bowel syndrome at Curlie










Popular posts from this blog

Y

Mount Tamalpais

Indian Forest Service