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Irritable Bowel Syndrome

Editor: Karen B. Shackelford Updated: 10/30/2022 8:12:03 PM

Introduction

Irritable bowel syndrome (IBS) is one of the most commonly diagnosed gastrointestinal diseases. IBS, in the absence of any other causative disease, is defined as the presence of abdominal pain or discomfort with altered bowel habits. Diagnosis of IBS has evolved since its first discovery, and today the Rome IV diagnostic criteria are used to diagnose IBS. Depending on the subclass of IBS, symptoms can be managed by a variety of medications and nonpharmaceutical agents. Nonetheless, IBS treatment should be individualized, and a significant factor in management remains a strong patient-physician relationship.[1]

Etiology

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Etiology

The etiology of IBS is broad and not clearly understood. However, as below in the pathophysiology section, motility, visceral sensation, brain-gut interaction, and psychosocial distress can all play a role in the development of IBS.

Epidemiology

Nearly 12 percent of patients seek medical care in primary care practices for IBS related complaints.[1][2] Studies have demonstrated that the prevalence of IBS ranges between ten and fifteen percent; however, the majority of these patients do not seek medical care.[1] IBS is most prevalent in South America at approximately 21 percent and least prevalent in Southeast Asia at 7 percent.[3][4] In the United States, Canada, and Isreal, IBS symptoms are 1.5 to 2 times more prevalent among women than men.[5] Moreover, women are more likely to report abdominal pain and constipation, whereas men are more likely to report diarrhea.[5] The prevalence of IBS also decreases with age.[3] IBS can also be broken down into more specific diagnoses, which include IBS with diarrhea (IBS-D), IBS with constipation (IBS-C), and IBS with mixed bowel patterns (IBS-M). The prevalence of these three diagnoses differs in the United States versus Europe. In the United States, there is an equal distribution of these diagnoses, whereas, in Europe, IBS-C or IBS-M can be more prevalent.[6]

Pathophysiology

The pathophysiology of IBS is broad and includes abnormalities involving motility, visceral sensation, brain-gut interaction, and psychosocial distress.[3] One of these can usually be demonstrated in the majority of IBS patients; however, not all symptoms can be attributed to them.[3] Recent studies have also shown altered gut immune activation and intestinal and colonic microbiome are associated with IBS[3][7][8]. Environmental contributors to IBS include early life stressors, food intolerance, antibiotics, and enteric infections.[3] Patients often complain that IBS symptoms are related to food intake. However, a true food allergen has a limited contribution to IBS.[3][9]

Histopathology

Histopathology examination of the intestinal mucosa in those with IBS can show chronic inflammatory cells, mast cells, enteroendocrine cells, and enteric nerves.[10]. IBS-D is typically associated with a greater increase in mucosal T-lymphocytes than IBS-C.[10][11] Moreover, there can be an increased number of nerve fibers that stain positive for neuron-specific enolase, substance P, and 5-HT.[10][12] There also appears to be a significantly increased density of nerve fibers around mast cells.[10][12]

History and Physical

IBS typically consists of abdominal pain or discomfort, altered bowel habits along with constipation, diarrhea, or both. Other complaints in patients with IBS include bloating, distention, symptoms brought on by food intake, and a change in pain location and stool pattern with time.[3]. Concerning features would include onset after the age of 50 years old, severe or progressive symptoms, unexplained weight loss, nocturnal diarrhea, rectal bleeding, iron deficiency anemia, or a family history of organic gastrointestinal diseases such as colon cancer, celiac disease, or inflammatory bowel disease.[3] Additional history that would be important would include travel and social history.

The Rome IV criteria are used to diagnose IBD, which requires at least 3 days a month in the last 3 months associated with 2 or more of the following: improvement in abdominal pain or discomfort with defecation, onset associated with a change in frequency of stool, and/or an onset accompanied by a change in form or appearance of stool[3].

Evaluation

If no alarm findings exist (weight loss, hematochezia, iron deficiency), routine diagnostic testing is not recommended.[1] If symptoms are not typical of IBS or alarm symptoms are present, then a complete blood cell count, comprehensive metabolic panel, inflammatory markers such as erythrocyte sedimentation rate or C-reactive protein, and thyroid stimulating hormone level should be checked.[1] If diarrhea is predominant, fecal leukocytes and stool tests for Clostridium difficile, Giardia, and Cryptosporidium, when appropriate, should be ordered.[1] Testing for celiac disease may be needed as well, and a tissue transglutaminase or TTG-IgA can be obtained.[1] A colonoscopy may be beneficial when there is a family history of inflammatory bowel disease, colon cancer, or alarm symptoms.[1] If the patient has diarrhea, random biopsies should be done on colonoscopy.[1]

Treatment / Management

One of the most important goals in the management of IBS patients is to develop a trusting patient-physician relationship by actively listening, showing empathy, and setting realistic expectations for treatment.[3][13] IBS is a symptom-based disorder, and thus treatment goals are aimed at resolving symptoms such as pain, bloating, cramping, and diarrhea or constipation.[3] For constipation, fiber supplements and laxatives can be helpful whereas, in those with diarrhea, medications such as loperamide or probiotics can be helpful.[3] Moreover, increased physical activity can increase colonic transit time and improve symptoms.[3][14] Patients also often associate food intake with IBS symptoms. Foods such as wheat products, onions, fruits, vegetables, sorbitol, and some dairy can include short-chain, poorly absorbed, highly fermentable carbohydrates, which are known as FODMAPs. FODMAPs have been associated with increased gastrointestinal symptoms in IBS patients.[3] Patients with constant and chronic abdominal symptoms oftentimes can have a response to low dose tricyclic antidepressants (TCAs) or serotonin reuptake inhibitors (SSRIs).[1] Alosetron can be used to treat IBS-D in females but can cause ischemic colitis.

Rifaximin is a nonabsorbable broad-spectrum antibiotic sometimes used to treat patients with irritable bowel syndrome. Patients with irritable bowel syndrome who take rifaximin have less abdominal pain and diarrhea. The effectiveness of rifaximin in patients with IBS is used as evidence to support the idea that bacterial overgrowth plays a role in the etiology of IBS.

Differential Diagnosis

The differential diagnosis of IBS is broad and ultimately depends on whether the patient has predominant diarrhea or constipation.  If a patient has IBS with diarrhea, the differentials includes lactose intolerance, caffeine intake, alcohol intake, gastrointestinal infections (Giardia, Amoeba, HIV), inflammatory bowel disease, medication-induced diarrhea (antibiotic use, proton pump inhibitor, nonsteroidal anti-inflammatory drugs, ACE inhibitor, chemotherapy), celiac disease, malignancies, colorectal cancer, hyperthyroidism, VIPoma, and ischemic colitis.[15] If constipation is the predominant symptoms, then the differentials can include inadequate fiber intake, immobility, Parkinson's disease, multiple sclerosis, spinal injury, diabetes, hypothyroidism, hypercalcemia, medication-induced (opiates, calcium-channel blockers, antidepressants, clonidine), malignancies, bowel obstruction, endometriosis, and diverticular disease. If a patient's history indicates one of these diseases, then appropriate lab testing should be pursued.[15]

Prognosis

IBS has a good prognosis, and the diagnosis is unlikely to change on follow-up.[16] The use of ambulatory health services by IBS patients can be reduced if a positive physician-patient interaction is developed.[16]

Consultations

Important consults include a gastroenterologist and a nutritionist. Gastroenterologists often sub-specialize in IBS care and are invaluable members of the treatment team. A gastroenterologist can tailor treatment plans for the patient and are also likely to be more aware of advancements in the field of IBS. Given that patients often believe certain food intake is associated with their symptoms, and the findings of FODMAPs association with IBS, nutritionists are vital to providing dietary recommendations for the patient.

Deterrence and Patient Education

If a patient has concerns about abdominal pain, bloating, cramping, and changes in bowel habits, a visit to a primary care physician is advised. If IBS is diagnosed, a gastroenterology consultation will be needed as they can guide management and treatment.

Pearls and Other Issues

IBS can be sub-classified into IBS-C, IBS-D, or IBS-M. Although some treatments are the same between the groups, each subclassification is unique and has different treatments focused on the different symptomatologies. 

Enhancing Healthcare Team Outcomes

IBS can be a very disabling syndrome for patients, and it has been shown to be a very common reason for seeking medical attention. It is vital that there is an interprofessional approach when it comes to the care of these patients as it can improve the quality of life, reduce medications needed, and manage the symptoms of IBS much better.[17] The team can include primary care providers, gastroenterologists, specialty-trained nurses, and pharmacists. Nurses provide education to patients and their families, monitor response to treatment, and report patient status to the team. Pharmacists review prescribed medications for dose and interactions, as well as review usage and side effects with patients. [Level 5]

References


[1]

Occhipinti K, Smith JW. Irritable bowel syndrome: a review and update. Clinics in colon and rectal surgery. 2012 Mar:25(1):46-52. doi: 10.1055/s-0032-1301759. Epub     [PubMed PMID: 23449495]


[2]

Drossman DA, Camilleri M, Mayer EA, Whitehead WE. AGA technical review on irritable bowel syndrome. Gastroenterology. 2002 Dec:123(6):2108-31     [PubMed PMID: 12454866]


[3]

Chey WD, Kurlander J, Eswaran S. Irritable bowel syndrome: a clinical review. JAMA. 2015 Mar 3:313(9):949-58. doi: 10.1001/jama.2015.0954. Epub     [PubMed PMID: 25734736]


[4]

Lovell RM, Ford AC. Global prevalence of and risk factors for irritable bowel syndrome: a meta-analysis. Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. 2012 Jul:10(7):712-721.e4. doi: 10.1016/j.cgh.2012.02.029. Epub 2012 Mar 15     [PubMed PMID: 22426087]

Level 2 (mid-level) evidence

[5]

Lovell RM, Ford AC. Effect of gender on prevalence of irritable bowel syndrome in the community: systematic review and meta-analysis. The American journal of gastroenterology. 2012 Jul:107(7):991-1000. doi: 10.1038/ajg.2012.131. Epub 2012 May 22     [PubMed PMID: 22613905]

Level 1 (high-level) evidence

[6]

Guilera M, Balboa A, Mearin F. Bowel habit subtypes and temporal patterns in irritable bowel syndrome: systematic review. The American journal of gastroenterology. 2005 May:100(5):1174-84     [PubMed PMID: 15842596]

Level 1 (high-level) evidence

[7]

Simrén M, Barbara G, Flint HJ, Spiegel BM, Spiller RC, Vanner S, Verdu EF, Whorwell PJ, Zoetendal EG, Rome Foundation Committee. Intestinal microbiota in functional bowel disorders: a Rome foundation report. Gut. 2013 Jan:62(1):159-76. doi: 10.1136/gutjnl-2012-302167. Epub 2012 Jun 22     [PubMed PMID: 22730468]


[8]

Dupont HL. Review article: evidence for the role of gut microbiota in irritable bowel syndrome and its potential influence on therapeutic targets. Alimentary pharmacology & therapeutics. 2014 May:39(10):1033-42. doi: 10.1111/apt.12728. Epub 2014 Mar 25     [PubMed PMID: 24665829]

Level 3 (low-level) evidence

[9]

Park MI, Camilleri M. Is there a role of food allergy in irritable bowel syndrome and functional dyspepsia? A systematic review. Neurogastroenterology and motility. 2006 Aug:18(8):595-607     [PubMed PMID: 16918724]

Level 3 (low-level) evidence

[10]

Kirsch R, Riddell RH. Histopathological alterations in irritable bowel syndrome. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc. 2006 Dec:19(12):1638-45     [PubMed PMID: 17013373]


[11]

Chadwick VS, Chen W, Shu D, Paulus B, Bethwaite P, Tie A, Wilson I. Activation of the mucosal immune system in irritable bowel syndrome. Gastroenterology. 2002 Jun:122(7):1778-83     [PubMed PMID: 12055584]


[12]

Wang LH, Fang XC, Pan GZ. Bacillary dysentery as a causative factor of irritable bowel syndrome and its pathogenesis. Gut. 2004 Aug:53(8):1096-101     [PubMed PMID: 15247174]


[13]

Drossman DA. 2012 David Sun lecture: helping your patient by helping yourself--how to improve the patient-physician relationship by optimizing communication skills. The American journal of gastroenterology. 2013 Apr:108(4):521-8. doi: 10.1038/ajg.2013.56. Epub 2013 Mar 19     [PubMed PMID: 23511457]


[14]

Song BK, Cho KO, Jo Y, Oh JW, Kim YS. Colon transit time according to physical activity level in adults. Journal of neurogastroenterology and motility. 2012 Jan:18(1):64-9. doi: 10.5056/jnm.2012.18.1.64. Epub 2012 Jan 16     [PubMed PMID: 22323989]


[15]

Lucak S. Diagnosing irritable bowel syndrome: what's too much, what's enough? MedGenMed : Medscape general medicine. 2004 Mar 12:6(1):17     [PubMed PMID: 15208529]


[16]

Owens DM, Nelson DK, Talley NJ. The irritable bowel syndrome: long-term prognosis and the physician-patient interaction. Annals of internal medicine. 1995 Jan 15:122(2):107-12     [PubMed PMID: 7992984]


[17]

Shani-Zur D, Wolkomir K. [Irritable Bowel Syndrome treatment: a multidisciplinary approach]. Harefuah. 2015 Jan:154(1):52-5, 66     [PubMed PMID: 25796677]

Level 3 (low-level) evidence