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Irritable bowel syndrome

For patient information click here Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Synonyms and keywords: Spastic colon, functional bowel disorder, IBS

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Overview

Irritable bowel syndrome (IBS) is a functional bowel disorder characterized by abdominal pain and alteration of bowel habits. IBS is caused by the complex interaction of various factors such as intrinsic gastrointestinal factors, CNS dysregulation, psychosocial factors, genetic and environmental factors. Intrinsic gastrointestinal factors include motor abnormalities, visceral hypersensitivity, immune activation, and mucosal inflammation, altered gut microbiota and abnormal serotonin pathways. A definite cause of irritable bowel syndrome (IBS) has not yet been established. However, an interplay of several factors contribute to the development of IBS such as emotional disturbances, stress, adverse early life events, history of inflammatory bowel disease, and acute gastrointestinal infections. Irritable bowel syndrome (IBS) may be classified according to Rome IV criteria into four sub types/groups: IBS with predominant constipation, IBS with predominant diarrhea, IBS with mixed bowel habits, and unclassified IBS. In addition, IBS occurring secondary to GI infections is known as post infectious-IBS or PI-IBS. Irritable bowel syndrome must be differentiated from other diseases that cause diarrhea, constipation, and abdominal pain, such as celiac disease, inflammatory bowel disease (Crohn’s disease and ulcerative colitis), thyroid disease (hyper or hypothyroidism), strictures due to ischemia, diverticulitis or ischemia, among others. The diagnosis of IBS depends on the recognition of gastrointestinal symptoms that wax and wane and are exacerbated by psycho-social stress. Therefore, the diagnosis of IBS is based primarily on clinical symptoms and elimination of other organic gastrointestinal diseases. This is due to lack of definitive radiologic or laboratory diagnostic tests in IBS. There are no strict guidelines for the treatment of IBS and the therapy is mostly symptom-based. All IBS patients are required to adapt a diet low in fermentable oligo-, di-, and monosaccharides and polyols (FODMAPs). A psychiatric referral and regular exercise are very helpful for all IBS patients. Pharmacological therapy is adjunctive and only preferred in patients where symptoms of IBS are moderate-severe in intensity and markedly impair the quality of life. Pharmacological therapy administered to patients is based on the predominant symptom, with diarrhea-predominant, constipation-predominant, and pain-predominant subtypes having their own different regimens. New therapies such as herbal medications, tight-junction modulators, mast cell stabilizers, acupuncture, and mind body therapy currently have an uncertain role in the treatment of IBS.

Historical Perspective

Irritable Bowel syndrome(IBS) was first mentioned in the Rocky Mountain Medical Journal in 1950. IBS was described as a psychosomatic disorder, not explained by any biochemical or structural abnormalities. Apley and Nash conducted a famous study on 1000 children in Bristol, United Kingdom and were the first to describe Recurrent Abdominal Pain (RAP) as the predominant feature of IBS. In 1978, the first diagnostic criteria i.e. the Manning criteria was described. It did not specify any required duration for the symptoms of IBS. The subsequent criteria saw a reduction in the required duration of symptoms to facilitate early diagnosis and treatment. In Rome in 1995, an international group of gastroenterologists defined the diagnostic criteria for IBS and this was published in 1999 under the title of the Rome II criteria. This criteria underwent modification and was described as the Rome III criteria. Since June 2016, the criteria being followed is the Rome IV criteria.

Classification

Irritable bowel syndrome (IBS) may be classified according to Rome IV criteria into four sub types/groups: IBS with predominant constipation , IBS with predominant diarrhea, IBS with mixed bowel habits,and IBS unclassified. In addition, IBS occurring subsequent to GI infections is known as Post infectious-IBS or PI-IBS. The rationale behind these different sub types is to maintain consistency of patient selection. This increases understanding of pathophysiological mechanisms, aids in effective diagnosis, treatment and patient recruitment for clinical trials.

Pathophysiology

IBS is caused by the complex interaction of various factors such as intrinsic gastrointestinal factors, CNS dysregulation and psychosocial factors, genetic and environmental factors. Intrinsic gastrointestinal factors include motor abnormalities, visceral hypersensitivity, immune activation and mucosal inflammation, altered gut microbiota and abnormal serotonin pathways. Visceral hypersensitivity is a decreased threshold for the perception of visceral stimuli that affects spinal excitability brain stem and cortical modulation, activation of specific gastrointestinal mediators and recruitment of peripheral silent nociceptors. Immune activation and mucosal inflammation involves an interaction of lymphocytes, mast cells and proinflammatory cytokines. Environmental factors encompass dietary changes and infections. Psychosocial factors such as stress, anxiety and depression directly shape adult connectivity in the executive control network consisting of structures such as the insula, anterior cingulate cortex and the thalamus. Semipermanent/permanent changes in complex neural circuits lead to central pain amplification and contribute to abdominal pain in IBS patients. The dorsolateral prefrontal cortex activity (responsible for vigilance and alertness of the human brain) and the mid-cingulate cortex (engaged in attention pathways and responses) is reduced in IBS patients, which may lead to alterations in the subjective sensations of pain. Genetic factors also play a role in IBS. It has high twin concordance and familial aggregation. It is associated with Single nucleotide polymorphisms (SNPs) in genes involved in immune activation, neuropeptide hormone function, oxidative stress, nociception, permeability of the GI tract, host-microbiota interaction, inflammation, and TNF activity.

Causes

There is no definite cause that has been established for irritable bowel syndrome (IBS). However, an interplay of several factors contribute to the development of IBS such as emotional disturbances, stress, adverse early life events, history of inflammatory bowel disease, and acute gastrointestinal infections. Less common causes of IBS include genetics and hormonal changes.

Differentiating IBS from Other Diseases

Irritable bowel syndrome must be differentiated from other diseases that cause diarrhea, constipation, and abdominal pain, such as Celiac disease, Inflammatory bowel disease(Crohn’s disease and Ulcerative colitis) Thyroid disease (Hyper or Hypothyroidism), strictures due to ischemia, diverticulitis or ischemia, among others.

The differential diagnosis for Irritable bowel syndrome can be listed based on predominant symptoms, such as constipation predominant, diarrhea predominant and pain predominant diseases.

Epidemiology and Demographics

IBS is an extremely common disorder in the population. The incidence of IBS is approximately 200 per 100,000 individuals worldwide. The prevalence of IBS is approximately 11,200 per 100,000 individuals worldwide. The prevalence of IBS varies with geographical and demographic distribution. Females are more commonly affected by IBS than males. The female to male ratio is approximately 1.5-3. The prevalence of IBS in USA and Europe is 10,000-20,000 per 100,000 individuals. In USA and Australia, 1 in every 10 people fulfill the Rome criteria for IBS. In Asia, Africa and South America, IBS is becoming increasingly prevalent as a disease of urbanization and industrialization. This is due to increased access to health care, higher stress levels and differing dietary choices.

Risk Factors

Common risk factors in the development of IBS include stress, anxiety, depression, history of IBD and acute gastrointestinal infections.

Screening

There is insufficient evidence to recommend routine screening for Irritable Bowel Syndrome.

Natural History, Complications, and Prognosis

The symptoms of IBS usually develop in the second decade of life, and start with symptoms such as abdominal pain, diarrhea and constipation. IBS may develop after exposure to early life adverse events, sexual abuse, anxiety, depression and stressors. Psychological conditions may also develop as complications of the disease. If left untreated, patients with IBS may progress to develop malnutrition (resulting from food intolerance), impacted bowel, and poor quality of life. Common complications of IBS include dehydration, hemorrhoids and fatigue. Prognosis is good, as IBS does not lead to life threatening complications or shorten lifespan of an individual. IBS patients tend to have long symptom free intervals interspersed with periods of severe symptoms. Although Irritable bowel syndrome may be a life-long condition, symptoms can often be improved or relieved through treatment.

Diagnosis

As per the Rome IV criteria, the diagnosis of IBS is made when at least two of the following diagnostic criteria are met in association with abdominal pain for ≥1 day per week, in the previous 3 months with an onset of ≥6 months : Change in stool consistency, pain related to defecation and absence of warning signs such as unintentional loss of weight, age ≥50 years, recent change in bowel habit, hematochezia or melena i.e. evidence of overt gastrointestinal bleeding.

The definition of IBS according to Rome IV, is recurrent abdominal pain associated with a change in frequency and/or form of the stool. It considers IBS as a disorder of gut–brain interaction as opposed to being a functional disorder of the GI tract. The term “abdominal discomfort” mentioned in Rome Ⅲ, has been removed in Rome IV to counter ambiguity. In addition to this, the frequency of abdominal pain has been changed from at least 3 days a month in the preceding 3 months (Rome III) to at least one day per week in the preceding 3 months (Rome IV).  The phrase ‘improvement of abdominal pain with defecation’ in Rome III has been changed to“abdominal pain related to defecation” in Rome IV, as some IBS patients may report worsening of pain following defecation. Experts state that physicians should limit evaluation to Rome criteria fulfillment, if no alarm symptoms are present.

History and Symptoms

The diagnosis of IBS relies on recognition of gastrointestinal symptoms that wax and wane for and are exacerbated by psycho social stress. Diagnosis of IBS is based on on clinical symptoms and elimination of other organic gastrointestinal diseases. This is due to lack of definitive radio logic or laboratory diagnostic tests in IBS.The hallmark of IBS is abdominal pain. A positive history of stress, anxiety, depression, panic disorders, gastrointestinal disorders such as IBD and acute GI infection predispose individuals to IBS. The most common symptoms of IBS include presence of abdominal pain and alteration of bowel habits. Less common symptoms of IBS include flatulence and upper GI symptoms such as heartburn, nausea, dyspepsia and vomiting. 

Physical Examination

Patients with IBS usually appear normal on physical exam. Physical examination of patients with IBS may elicit abdominal tenderness in some patients. A digital rectal examination must be performed in all patients to rule out rectal growths, blood in stool and evaluate for dyssynergic defecation (where paradoxical contraction of the rectal sphincter occurs on straining, leading to constipation). Physical findings such as fever, abdominal mass, hepatosplenomegaly, lymph node enlargement, weight loss, peritoneal signs and ascites are absent in IBS and help rule out organic causes.  

Laboratory Findings

The diagnosis of IBS is based on clinical symptoms and elimination of other organic gastrointestinal diseases. This is due to lack of definitive radiologic or laboratory diagnostic tests in IBS. If the history and physical exam are suggestive of IBS in the absence of alarm features, complete blood count, occult blood test, complete metabolic panel and ESR are usually normal. Additional tests may be costly and harmful in young patients with typical IBS symptoms, in the absence of alarm features. To determine the aggressiveness of the diagnostic evaluation, the American Gastroenterological Association has defined certain factors that must be considered such as degree of psychosocial impairment, age and sex of the patient, family history of colorectal cancer etc. In patients that require aggressive diagnostic evaluation, additional diseases such as Celiac disease, IBD, Clostridium difficile infection, Giardiasis, lactase deficiency, bile salt malabsorption and colon cancer should be ruled out.

Electrocardiogram

There are no ECG findings associated with IBS.

X-ray

There are no x-ray findings associated with IBS. However, an x-ray may be helpful in the ruling out obstruction, stool retention and aerophagia during a pain episode. In IBS patients presenting with dyspepsia, upper GI radiographs help rule out other causes. Small bowel barium radiography helps in the diagnosis of ileal and jejunal Crohn’s disease and diverticulae.

CT scan

There are no CT scan findings associated with IBS.

MRI

There are no MRI findings associated with IBS.

USG

There are no ultrasound findings associated with IBS.  IBS patients presenting with with postprandial right upper quadrant pain, must undergo an ultra sonogram of the gallbladder to rule out pain due to cholecystitis. Postmenopausal women presenting with constipation, abdominal distension and pain localized to the lower abdomen should undergo trans vaginal and trans abdominal ultrasonography to rule out ovarian cancer.

Other Imaging Findings

75SeHCAT testing may be helpful in the diagnosis of IBS patients with bile acid diarrhea. The 75SeHCAT test measures the whole-body retention of 75Se-homocholyltaurine, a bile acid radiolabeled with the gamma-emitting isotope selenium-75. Retention of the isotope is measured by gamma-camera scanning performed a week after administration.

Other Diagnostic Studies

In young patients with symptoms of classic IBS, additional invasive investigations such as endoscopy are not required and increase patient dissatisfaction. However, endoscopic evaluation is performed in difficult cases of IBS where history is unclear but the physical examination is suggestive of the diagnosis. All IBS patients with alarm features must undergo endoscopic evaluation. Moreover, colonoscopy must be considered in patients aged more than 50 years as part of routine colon cancer screening. Sigmoid colon biopsies and duodenal biopsies are required for exclusion of microscopic colitis, Crohn’s disease, and celiac disease. Anorectal manometry is a diagnostic technique used to rule out obstructive defecation (pelvic-floor dyssynergia).

Treatment

Medical Therapy

IBS is heterogeneous in its presentation. There are no strict guidelines for the treatment of IBS and therapy is mostly symptom-based. All IBS patients are required to adopt a diet low in fermentable oligo-, di-, and monosaccharides and polyols (FODMAPs). A psychiatric referral and regular exercise are considered necessary in all IBS patients. Pharmacological therapy is adjunctive and only preferred in patients where symptoms of IBS are moderate-severe in intensity and markedly impair the quality of life. Pharmacological therapy administered to patients is based on the predominant symptom with diarrhea-predominant, constipation-predominant and pain-predominant subtypes having their own different regimens. New therapies such as herbal medicines, tight-junction modulators, mast cell stabilizers, acupuncture, and mind body therapy currently have an uncertain role in the treatment of IBS.

Surgery

Surgical intervention is not recommended for the management of IBS.

Primary Prevention

Effective measures for the primary prevention of IBS include early and effective treatment of stress, anxiety, depression and panic disorders. Early counseling for victims of physical or sexual abuse and avoidance of certain foods such as fatty food, wheat, carbonated drinks, sorbitol and alcohol in those with food sensitivities helps in the primary prevention of IBS.

Secondary Prevention

There are no established measures for the secondary prevention of IBS.

References


Template:WikiDoc Sources

Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Overview

Irritable Bowel syndrome (IBS) was first mentioned in the Rocky Mountain Medical Journal in 1950. IBS was described as a psychosomatic disorder, not explained by any biochemical or structural abnormalities. Apley and Nash conducted a famous study on 1000 children in Bristol, United Kingdom and were the first to describe recurrent abdominal pain (RAP) as the predominant feature of IBS. In 1978, the first diagnostic criteria i.e. the Manning criteria was described. It did not specify any required duration for the symptoms of IBS. The subsequent criteria saw a reduction in the required duration of symptoms to facilitate early diagnosis and treatment. In Rome in 1995, an international group of gastroenterologists defined the diagnostic criteria for IBS and this was published in 1999 under the title of the Rome II criteria. This criteria underwent modification and was described as the Rome III criteria. Since June 2016, the criteria being followed is the Rome IV criteria.

Historical Perspective

Discovery

  • In 1950, the concept of irritable bowel syndrome (IBS) was mentioned for the first time without the recognition of any particular etiology, in the Rocky Mountain Medical Journal.
  •  IBS was described as a psychosomatic disorder, not explained by any biochemical or structural abnormalities. [1]
  • In 1958, Apley and Nash conducted a study on 1000 children in Bristol, United Kingdom and were the first to describe Recurrent Abdominal Pain (RAP), as the predominant feature of IBS.
  • Recurrent abdominal pain was defined as pain in the abdomen occurring over a duration of at least 3 months, with the severity enough to cause significant impairment of function.[2][3]

Landmark Events

Famous Cases

  • The following are a few famous cases of IBS:
    • Adolf Hitler
    • John F Kennedy
    • Kurt Cobain

References

  1. ↑ BROWN PW (1950). “The irritable bowel syndrome”. Rocky Mt Med J. 47 (5): 343–6. PMID 15418074.
  2. ↑ APLEY J, NAISH N (1958). “Recurrent abdominal pains: a field survey of 1,000 school children”. Arch. Dis. Child. 33 (168): 165–70. PMC 2012205. PMID 13534750.
  3. ↑ El-Matary W, Spray C, Sandhu B (2004). “Irritable bowel syndrome: the commonest cause of recurrent abdominal pain in children”. Eur. J. Pediatr. 163 (10): 584–8. doi:10.1007/s00431-004-1503-0. PMID 15290263.
  4. ↑ Rasquin A, Di Lorenzo C, Forbes D, Guiraldes E, Hyams JS, Staiano A, Walker LS (2006). “Childhood functional gastrointestinal disorders: child/adolescent”. Gastroenterology. 130 (5): 1527–37. doi:10.1053/j.gastro.2005.08.063. PMID 16678566.
  5. ↑ Lacy BE, Patel NK (2017). “Rome Criteria and a Diagnostic Approach to Irritable Bowel Syndrome”. J Clin Med. 6 (11). doi:10.3390/jcm6110099. PMID 29072609.
  6. ↑ Iwańczak B, Iwańczak F (2017). “[Functional gastrointestinal disorders in children and adolescents. The Rome IV criteria]”. Pol. Merkur. Lekarski (in Polish). 43 (254): 75–82. PMID 28875974.
  7. ↑ Ghoshal UC (2017). “Chronic constipation in Rome IV era: The Indian perspective”. Indian J Gastroenterol. 36 (3): 163–173. doi:10.1007/s12664-017-0757-1. PMID 28643273.
  8. ↑ Ghoshal UC (2017). “Pros and Cons While Looking Through an Asian Window on the Rome IV Criteria for Irritable Bowel Syndrome: Pros”. J Neurogastroenterol Motil. 23 (3): 334–340. doi:10.5056/jnm17020. PMC 5503282. PMID 28672432.
  9. ↑ Saps M, van Tilburg MA, Lavigne JV, Miranda A, Benninga MA, Taminiau JA, Di Lorenzo C (2016). “Recommendations for pharmacological clinical trials in children with irritable bowel syndrome: the Rome foundation pediatric subcommittee on clinical trials”. Neurogastroenterol. Motil. 28 (11): 1619–1631. doi:10.1111/nmo.12896. PMID 27477090.
  10. ↑ Dang J, Ardila-Hani A, Amichai MM, Chua K, Pimentel M (2012). “Systematic review of diagnostic criteria for IBS demonstrates poor validity and utilization of Rome III”. Neurogastroenterol. Motil. 24 (9): 853–e397. doi:10.1111/j.1365-2982.2012.01943.x. PMID 22632582.
  11. ↑ Olden KW (2003). “The challenge of diagnosing irritable bowel syndrome”. Rev Gastroenterol Disord. 3 Suppl 3: S3–11. PMID 14502111.

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Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Overview

Irritable bowel syndrome (IBS) may be classified according to Rome IV criteria into IBS with predominant constipation , IBS with predominant diarrhea, IBS with mixed bowel habits, and unclassified IBS. In addition, IBS occurring subsequent to gastrointestinal infections is known as post infectious-IBS (PI-IBS). The rationale behind these different sub-types is to maintain consistency of patient selection. This increases understanding of pathophysiological mechanisms, aids in effective diagnosis, treatment, and patient recruitment for clinical trials.

Classification

Irritable bowel syndrome (IBS) may be classified according to Rome IV criteria into 4 sub-types based on predominant type of bowel habits:[1][2][3][4][5][6]

  • IBS with predominant constipation
  • IBS with predominant diarrhea
  • IBS with mixed bowel habits:
  • IBS unclassified:
    • Patients who meet the diagnostic criteria for IBS but whose bowel habits do not fit into any of the above subtypes.
SUBTYPE HARD OR LUMPY STOOLS LOOSE (MUSHY) OR WATERY STOOLS
IBS with constipation ≥ 25 percent  ≤ 25 percent
IBS with diarrhea  ≤ 25 percent ≥ 25 percent
Mixed IBS ≥ 25 percent ≥ 25 percent
Unsubtyped IBS Insufficient abnormality of stool consistency to meet criteria for IBS with constipation, diarrhea, or mixed subtypes.

References

  1. ↑ Longstreth GF (2005). “Definition and classification of irritable bowel syndrome: current consensus and controversies”. Gastroenterol. Clin. North Am. 34 (2): 173–87. doi:10.1016/j.gtc.2005.02.011. PMID 15862928.
  2. ↑ Sayuk GS, Gyawali CP (2015). “Irritable bowel syndrome: modern concepts and management options”. Am. J. Med. 128 (8): 817–27. doi:10.1016/j.amjmed.2015.01.036. PMID 25731138.
  3. ↑ Lacy BE (2016). “Diagnosis and treatment of diarrhea-predominant irritable bowel syndrome”. Int J Gen Med. 9: 7–17. doi:10.2147/IJGM.S93698. PMC 4755466. PMID 26929659.
  4. ↑ Wong RK, Palsson OS, Turner MJ, Levy RL, Feld AD, von Korff M, Whitehead WE (2010). “Inability of the Rome III criteria to distinguish functional constipation from constipation-subtype irritable bowel syndrome”. Am. J. Gastroenterol. 105 (10): 2228–34. doi:10.1038/ajg.2010.200. PMC 3786710. PMID 20502449.
  5. ↑ Thompson WG, Longstreth GF, Drossman DA, Heaton KW, Irvine EJ, Müller-Lissner SA (1999). “Functional bowel disorders and functional abdominal pain”. Gut. 45 Suppl 2: II43–7. PMC 1766683. PMID 10457044.
  6. ↑ Talley NJ, Spiller R (2002). “Irritable bowel syndrome: a little understood organic bowel disease?”. Lancet. 360 (9332): 555–64. doi:10.1016/S0140-6736(02)09712-X. PMID 12241674.
  7. ↑ Holten KB, Wetherington A, Bankston L (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.

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Overview

Irritable Bowel Syndrome is caused by a complex interaction of various factors such as intrinsic gastrointestinal factors, CNS dysregulation and psychosocial factors, genetic, and environmental factors. Intrinsic gastrointestinal factors include motor abnormalities, visceral hypersensitivity, immune activation, mucosal inflammation, altered gut microbiota, and abnormal serotonin pathways. Visceral hypersensitivity refers to a decreased threshold for the perception of visceral stimuli that affects spinal excitability, brain stem and cortical modulation, activation of specific gastrointestinal mediators, and recruitment of peripheral silent nociceptors. Immune activation and mucosal inflammation involves an interaction of lymphocytes, mast cells, and proinflammatory cytokines. Environmental factors encompass dietary changes and infections. Psychosocial factors such as stress, anxiety, and depression directly shape adult connectivity in the executive control network consisting of structures such as the insula, anterior cingulate cortex, and the thalamus. Semipermanent or permanent changes in complex neural circuits lead to central pain amplification contributing to abdominal pain in IBS patients. The dorsolateral prefrontal cortex activity (responsible for vigilance and alertness of the human brain) and the mid-cingulate cortex (engaged in attention pathways and responses) is reduced in IBS patients. This reduction may lead to alterations in the subjective sensations of pain. Genetic factors also play a role in IBS. IBS has a high twin concordance and familial aggregation. IBS is associated with single nucleotide polymorphisms (SNPs) in genes involved in immune activation, neuropeptide hormone function, oxidative stress, nociception, permeability of the GI tract, host-microbiota interaction, inflammation, and TNF activity.

Pathophysiology

Pathogenesis

IBS occurs as a result of an interplay between four main factors:


 
 
 
 
 
CNS dysregulation and psychosocial factors
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Intrinsic gastrointestinal factors:
• Motor abnormalities
• Visceral hypersensitivity
• Immune activation and mucosal inflammation
• Altered gut microbiota
• Abnormal serotonin pathways
 
 
IRRITABLE BOWEL SYNDROME
 
 
 
Genetic factors:
• Twin concordance
• Familial aggregation
• Single nucleotide polymorphisms(SNPs)
• TNF polymorphism
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Environmental factors:
•Diet
•Infections
 
 
 

Environmental factors

Intrinsic gastrointestinal factors


 
 
 
 
 
 
 
 
 
 
 
 
Spinal hyperexcitability
 
Activation of
• N-methyl D aspartate (NMDA) receptor
• nitric oxide
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Central (brainstem and cortical) modulation
 
Increased activation of:
• Anterior cingulate cortex
• Thalamus
• insula
 
 
 
 
 
 
 
 
 
 
 
Visceral hypersensitivity
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Activation of specific gastrointestinal mediators
 
Kinins and serotonin activation lead to afferent nerve fiber sensitization
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Recruitment of peripheral silent nociceptors
 
Increased end organ sensitivity due to hormonal or immune activation
 
 
 
 
 
 




Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Overview

There is no definite cause for irritable bowel syndrome (IBS). However, an interplay of several factors contribute to the development of IBS such as emotional disturbances, stress, adverse early life events, history of inflammatory bowel disease, and acute gastrointestinal infections. Less common causes of IBS include genetics and hormonal changes.

Causes

Irritable bowel syndrome (IBS) results from a complex interaction among multiple factors. These may include psychological, epidemiological, genetic, and infectious factors. To review these factors in detail, click here.

Genetic causes

Genetic causes IBS is associated with high twin concordance, familial aggregation, Single nucleotide polymorphisms and TNF polymorphisms in genes.[1][2]

References

  1. ↑ Makker J, Chilimuri S, Bella JN (2015). “Genetic epidemiology of irritable bowel syndrome”. World J. Gastroenterol. 21 (40): 11353–61. doi:10.3748/wjg.v21.i40.11353. PMC 4616211. PMID 26525775.
  2. ↑ Tanaka Y, Kanazawa M, Fukudo S, Drossman DA (2011). “Biopsychosocial model of irritable bowel syndrome”. J Neurogastroenterol Motil. 17 (2): 131–9. doi:10.5056/jnm.2011.17.2.131. PMC 3093004. PMID 21602989.
  3. ↑ 3.0 3.1 Levy RL, Jones KR, Whitehead WE, Feld SI, Talley NJ, Corey LA (2001). “Irritable bowel syndrome in twins: heredity and social learning both contribute to etiology”. Gastroenterology. 121 (4): 799–804. PMID 11606493.
  4. ↑ 4.0 4.1 Morris-Yates A, Talley NJ, Boyce PM, Nandurkar S, Andrews G (1998). “Evidence of a genetic contribution to functional bowel disorder”. Am. J. Gastroenterol. 93 (8): 1311–7. doi:10.1111/j.1572-0241.1998.440_j.x. PMID 9707057.
  5. ↑ 5.0 5.1 Lembo A, Zaman M, Jones M, Talley NJ (2007). “Influence of genetics on irritable bowel syndrome, gastro-oesophageal reflux and dyspepsia: a twin study”. Aliment. Pharmacol. Ther. 25 (11): 1343–50. doi:10.1111/j.1365-2036.2007.03326.x. PMID 17509102.
  6. ↑ Saito YA, Petersen GM, Locke GR, Talley NJ (2005). “The genetics of irritable bowel syndrome”. Clin. Gastroenterol. Hepatol. 3 (11): 1057–65. PMID 16271334.
  7. ↑ Wouters MM, Lambrechts D, Knapp M, Cleynen I, Whorwell P, Agréus L, Dlugosz A, Schmidt PT, Halfvarson J, Simrén M, Ohlsson B, Karling P, Van Wanrooy S, Mondelaers S, Vermeire S, Lindberg G, Spiller R, Dukes G, D’Amato M, Boeckxstaens G (2014). “Genetic variants in CDC42 and NXPH1 as susceptibility factors for constipation and diarrhoea predominant irritable bowel syndrome”. Gut. 63 (7): 1103–11. doi:10.1136/gutjnl-2013-304570. PMID 24041540.
  8. ↑ Saito YA, Petersen GM, Larson JJ, Atkinson EJ, Fridley BL, de Andrade M, Locke GR, Zimmerman JM, Almazar-Elder AE, Talley NJ (2010). “Familial aggregation of irritable bowel syndrome: a family case-control study”. Am. J. Gastroenterol. 105 (4): 833–41. doi:10.1038/ajg.2010.116. PMC 2875200. PMID 20234344.
  9. ↑ Bengtson MB, Rønning T, Vatn MH, Harris JR (2006). “Irritable bowel syndrome in twins: genes and environment”. Gut. 55 (12): 1754–9. doi:10.1136/gut.2006.097287. PMC 1856463. PMID 17008364.
  10. ↑ Locke GR, Zinsmeister AR, Talley NJ, Fett SL, Melton LJ (2000). “Familial association in adults with functional gastrointestinal disorders”. Mayo Clin. Proc. 75 (9): 907–12. doi:10.4065/75.9.907. PMID 10994826.
  11. ↑ Villani AC, Lemire M, Thabane M, Belisle A, Geneau G, Garg AX, Clark WF, Moayyedi P, Collins SM, Franchimont D, Marshall JK (2010). “Genetic risk factors for post-infectious irritable bowel syndrome following a waterborne outbreak of gastroenteritis”. Gastroenterology. 138 (4): 1502–13. doi:10.1053/j.gastro.2009.12.049. PMID 20044998.
  12. ↑ 12.0 12.1 Gonsalkorale WM, Perrey C, Pravica V, Whorwell PJ, Hutchinson IV (2003). “Interleukin 10 genotypes in irritable bowel syndrome: evidence for an inflammatory component?”. Gut. 52 (1): 91–3. PMC 1773523. PMID 12477767.
  13. ↑ Locke GR, Ackerman MJ, Zinsmeister AR, Thapa P, Farrugia G (2006). “Gastrointestinal symptoms in families of patients with an SCN5A-encoded cardiac channelopathy: evidence of an intestinal channelopathy”. Am. J. Gastroenterol. 101 (6): 1299–304. doi:10.1111/j.1572-0241.2006.00507.x. PMID 16771953.
  14. ↑ Saito YA, Strege PR, Tester DJ, Locke GR, Talley NJ, Bernard CE, Rae JL, Makielski JC, Ackerman MJ, Farrugia G (2009). “Sodium channel mutation in irritable bowel syndrome: evidence for an ion channelopathy”. Am. J. Physiol. Gastrointest. Liver Physiol. 296 (2): G211–8. doi:10.1152/ajpgi.90571.2008. PMC 2643921. PMID 19056759.
  15. ↑ Mahurkar S, Polytarchou C, Iliopoulos D, Pothoulakis C, Mayer EA, Chang L (2016). “Genome-wide DNA methylation profiling of peripheral blood mononuclear cells in irritable bowel syndrome”. Neurogastroenterol. Motil. 28 (3): 410–22. doi:10.1111/nmo.12741. PMC 4760882. PMID 26670691.
  16. ↑ Camilleri M, Carlson P, Zinsmeister AR, McKinzie S, Busciglio I, Burton D, Zucchelli M, D’Amato M (2010). “Neuropeptide S receptor induces neuropeptide expression and associates with intermediate phenotypes of functional gastrointestinal disorders”. Gastroenterology. 138 (1): 98–107.e4. doi:10.1053/j.gastro.2009.08.051. PMC 2813358. PMID 19732772.
  17. ↑ Wong BS, Camilleri M, Carlson P, McKinzie S, Busciglio I, Bondar O, Dyer RB, Lamsam J, Zinsmeister AR (2012). “Increased bile acid biosynthesis is associated with irritable bowel syndrome with diarrhea”. Clin. Gastroenterol. Hepatol. 10 (9): 1009–15.e3. doi:10.1016/j.cgh.2012.05.006. PMC 3565429. PMID 22610000.
  18. ↑ Wong BS, Camilleri M, Carlson PJ, Guicciardi ME, Burton D, McKinzie S, Rao AS, Zinsmeister AR, Gores GJ (2011). “A Klothoβ variant mediates protein stability and associates with colon transit in irritable bowel syndrome with diarrhea”. Gastroenterology. 140 (7): 1934–42. doi:10.1053/j.gastro.2011.02.063. PMC 3109206. PMID 21396369.
  19. ↑ 19.0 19.1 Swan C, Duroudier NP, Campbell E, Zaitoun A, Hastings M, Dukes GE, Cox J, Kelly FM, Wilde J, Lennon MG, Neal KR, Whorwell PJ, Hall IP, Spiller RC (2013). “Identifying and testing candidate genetic polymorphisms in the irritable bowel syndrome (IBS): association with TNFSF15 and TNFα”. Gut. 62 (7): 985–94. doi:10.1136/gutjnl-2011-301213. PMID 22684480.
  20. ↑ 20.0 20.1 Zucchelli M, Camilleri M, Andreasson AN, Bresso F, Dlugosz A, Halfvarson J, Törkvist L, Schmidt PT, Karling P, Ohlsson B, Duerr RH, Simren M, Lindberg G, Agreus L, Carlson P, Zinsmeister AR, D’Amato M (2011). “Association of TNFSF15 polymorphism with irritable bowel syndrome”. Gut. 60 (12): 1671–1677. doi:10.1136/gut.2011.241877. PMC 3922294. PMID 21636646.

Template:WH Template:WS

Differentiating Irritable Bowel Syndrome from other Diseases

Differentiating Irritable Bowel Syndrome from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Overview

Irritable bowel syndrome must be differentiated from other diseases that cause diarrhea, constipation, and abdominal pain, such as Celiac disease, Inflammatory bowel disease(Crohn’s disease and Ulcerative colitis) Thyroid disease (Hyper or Hypothyroidism), strictures due to ischemia, diverticulitis or ischemia, among others.

The differential diagnosis for Irritable bowel syndrome can be listed based on predominant symptoms, such as constipation predominant, diarrhea predominant and pain predominant diseases.

Differentiating Irritable Bowel Syndrome from other Diseases

Diseases with similar symptoms

Differential diagnosis based on predominant symptom(s)

Differential diagnosis based on abdominal pain

The differential diagnosis of IBS based on abdominal pain is as follows:

Abbreviations: RUQ= Right upper quadrant of the abdomen, LUQ= Left upper quadrant, LLQ= Left lower quadrant, RLQ= Right lower quadrant, LFT= Liver function test, SIRS= Systemic inflammatory response syndrome, ERCP= Endoscopic retrograde cholangiopancreatography, IV= Intravenous, N= Normal, AMA= Anti mitochondrial antibodies, LDH= Lactate dehydrogenase, GI= Gastrointestinal, CXR= Chest X ray, IgA= Immunoglobulin A, IgG= Immunoglobulin G, IgM= Immunoglobulin M, CT= Computed tomography, PMN= Polymorphonuclear cells, ESR= Erythrocyte sedimentation rate, CRP= C-reactive protein, TS= Transferrin saturation, SF= Serum Ferritin

Classification of pain in the abdomen based on etiology Disease Clinical manifestations Diagnosis Comments
Symptoms Signs
Fever Rigors and chills Abdominal Pain Jaundice Diarrhea Melena/ hematochezia/ hemtemesis Hypo-

tension

Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging
Abdominal causes Inflammatory causes Pancreato-biliary disorders Acute suppurative cholangitis + + RUQ + − − + + + N
  • Abnormal LFT
  • WBC >10,000
 Ultrasound shows biliary dilatation/stents/tumor Septic shock occurs with features of SIRS
Acute cholangitis + − RUQ + − − − − − N Ultrasound shows biliary dilatation/stents/tumor Biliary drainage (ERCP) + IV antibiotics
Acute cholecystitis + − RUQ + − − − − − Hypoactive Ultrasound shows gallstone and evidence of inflammation Murphy’s sign
Acute pancreatitis + − Epigastric ± − − ± − − N Ultrasound shows evidence of inflammation Pain radiation to back
Primary biliary cirrhosis − − RUQ/Epigastric + − − − − − N
  • Increased AMA level, abnormal LFTs
Primary sclerosing cholangitis + − RUQ + − − − − − N ERCP and MRCP shows
  • Multiple segmental strictures
  • Mural irregularities
  • Biliary dilatation and diverticula
  • Distortion of biliary tree
 The risk of cholangiocarcinoma in patients with primary sclerosing cholangitis is 400 times higher than the risk in the general population.
Cholelithiasis ± − RUQ/Epigastric ± − − − + + N to hyperactive for dislodged stone Ultrasound shows gallstone Murphy’s sign
Gastric causes Peptic ulcer disease ± − Diffuse − − + in perforated + + N
  • Ascitic fluid
    • LDH > serum LDH
    • Glucose < 50mg/dl
    • Total protein > 1g/dl
 Air under diaphragm in upright CXR Upper GI endoscopy for diagnosis
Gastritis ± − Epigastric − + in chronic gastritis −
Gastroesophageal reflux disease − − Epigastric − − − − − −
Gastric outlet obstruction − − Epigastric − − − ± Hyperactive
Gastrointestinal perforation + ± Diffuse ± − +, depends on site + + ±
  • WBC> 10,000
 Air under diaphragm in upright CXR
Dumping syndrome − − Lower and then diffuse
Intestinal causes Acute appendicitis + +in pyogenic appendicitis Starts in epigastrium, migrates to RLQ − − − + in perforated appendicitis + + Hypoactive Ultrasound shows evidence of inflammation Nausea & vomiting, decreased appetite
Acute diverticulitis + ± LLQ − − Hematochezia − + − Hypoactive CT scan and ultrasound shows evidence of inflammation
Inflammatory bowel disease ± − Diffuse ± Hematochezia
Irritable bowel syndrome ± − Diffuse − + − − − − N Tests done to exclude other diseases as it diagnosis of exclusion Tests done to exclude other diseases as it diagnosis of exclusion Symptomatic treatment
Whipple’s disease ± − Diffuse ± − − ± − − N *Endoscopy is used to confirm diagnosis.

Images used to find complications

Extra intestinal findings:
Toxic megacolon + − Diffuse − + − + ± − Hypoactive CT scan shows:

Ultrasound shows:

  • Loss of haustra coli of the colon
  • Hypoechoic and thickened bowel walls with irregular internal margins in the sigmoid and descending colon
  • Prominent dilation of the transverse colon (>6 cm)
  • Insignificant dilation of ileal bowel loops (diameter >18 mm) with increased intraluminal gas and fluid
Tropical sprue + − Diffuse + −
Celiac disease − − Diffuse ±, also dermatitis herpetiformis + − − − − Hyperactive (increased sounds)
Infective colitis +
Hepatic causes Viral hepatitis + − RUQ + − − − +
Liver masses + + in Liver abscess RUQ ± − − + in sepsis
Budd-Chiari syndrome ± − RUQ ± − + in liver failure leading to varices − − − N
Findings on CT scan suggestive of Budd-Chiari syndrome include:
Ascitic fluid examination shows:
Hemochromatosis − − RUQ Dull / aching + with infections and GI involvement − + in cirrhotic patients may be in cardicmyopathy − −
  • >60% TS
  • >240 μg/L SF
  • Raised LFT
    Hyperglycemia
 Ultrasound shows evidence of cirrhosis Extra intestinal findings:
  • hyperpigmentation
  • Diabetes mellitus
  • Arthralgia
  • Impotence in males
  • Cardiomyopathy
  • Atherosclerosis
  • Hypopituitarism
  • Hypothyroidism
  • Extrahepatic cancer
  • Prone to specific infections
Cirrhosis + − RUQ + − varices −
Peritoneal causes Spontaneous bacterial peritonitis + − Diffuse + in cirrhotic patients − − ± − − Hypoactive
  • Ascitic fluid PMN>250 cells/mm³
  • Culture: Positive for single organism
 Ultrasound for evaluation of liver cirrhosis
Hollow Viscous Obstruction Small intestine obstruction − − Diffuse − − − − + ± Hyperactive then absent Leukocytosis Abdominal X ray Nausea & vomiting associated with constipation, abdominal distention
Volvulus − − Diffuse − − − − + − Hypoactive Leukocytosis CT scan and abdominal X ray Nausea & vomiting associated with constipation, abdominal distention
Biliary colic − − RUQ + − − − − − N Increased bilirubin and alkaline phosphatase Ultrasound Nausea & vomiting
Renal colic − − Flank pain − − − − − − N Hematuria CT scan and ultrasound Colicky abdominal pain associated with nausea & vomiting
Vascular Disorders Ischemic causes Mesenteric ischemia ± − Periumbilical − + Hematochezia ± − − Hyperactive Leukocytosis and lactic acidosis CT scan Nausea & vomiting, normal physical examination
Acute ischemic colitis ± ± Diffuse − + Massive + + Hyperactive then absent Leukocytosis CT scan Nausea & vomiting
Hemorrhagic causes Ruptured abdominal aortic aneurysm − − Diffuse − − Massive + − − N Normal CT scan Unstable hemodynamics
Intra-abdominal or retroperitoneal hemorrhage − − Diffuse − − Massive + − − N Anemia CT scan History of trauma
Gynaecological Causes Tubal causes Torsion of the cyst − − RLQ / LLQ − − − ± ± N Increased ESR and CRP Ultrasound Sudden onset sever pain with nausea and vomiting
Acute salpingitis + ± RLQ / LLQ − − − − ± ± N Leukocytosis Pelvic ultrasound Vaginal discharge
Cyst rupture − − RLQ / LLQ − − − + ± ± N Increased ESR and CRP Ultrasound Sudden onset sever pain with nausea and vomiting
Pregnancy Ruptured ectopic pregnancy − − RLQ / LLQ − − − + − − N Positive pregnancy test Ultrasound History of missed period and vaginal bleeding
Extra-abdominal causes Pulmonary disorders Pleural empyema + ± RUQ/Epigastric − − − − − − N
Cardiovascular disorders Myocardial Infarction − − Epigastric − − − + in cardiogenic shock − − N

Differential diagnosis based on constipation

The differential diagnosis of irritable bowel syndrome based on constipation as the predominant symptom is as follows:[1][2][3][4][5][6][7][8][9][10]

Differential Diagnosis for Constipation predominant symptoms Clinical features Diagnosis
Strictures due to diverticultis,inflammatory bowel disease, ischemia or cancer
Hypothyroidism
Medication
  • Medication history.
Neurologic disease
Pelvic floor dysfunction
  • Straining, self digitation
Colonic inertia


Differential Diagnosis based on abdominal pain and diarrhea

Below is a table that overviews the differential based on type of diarrhea. A more detailed table follows.

Diarrhea with abdominal pain/cramping may be caused by infectious diseases, celiac disease,[11] parasites,[12] food allergies[13] and lactose intolerance.[14] See the list of causes of diarrhea for other conditions which can cause diarrhea. Celiac disease in particular is most often misdiagnosed as IBS.[15] The differential diagnosis of irritable bowel syndrome based on abdominal pain and diarrhea is as follows:[16][17][18][19][20][21][22][23][24][25]

Overview based on type of diarrhea

Cause Osmotic gap History Physical exam Gold standard Treatment
< 50 mOsm per kg > 50 mOsm per kg*
Watery Secretory Crohns + –
Zollinger-Ellison syndrome + –
  • Gastrin levels
  • Proton pump inhibitors
  • Octreotide
Hyperthyroidism + –
VIPoma + –
  • Elevated VIPlevels
  • Followed by imaging
Osmotic Lactose intolerance – +
Celiac disease – +
Functional Irritable bowel syndrome – – Abdominal pain or discomfort recurring at least 3 days per month in the past 3 months and associated with 2 or more of the following:
  • Onset associated with change in frequency of stool
 Clinical diagnosis
  • ROME IV criteria
  • Exclusion of organic causes based on laboratory investigations and imaging


Details based on pathology

Irritable bowel syndrome must be diifferentiated from other causes of abdominal pain and diarrhea.

Diseases Clinical manifestations Para-clinical findings Gold standard Additional findings
Symptoms Physical examination
Lab Findings Imaging Histopathology
Abdominal pain Diarrhea Flushing Dyspnea Palpitations Other symptoms Wheezing Telangiectasia Hypotension Tachycardia Systolic murmur of tricuspid regurgitation Other physical findings Urinary 5-hydroxyindoleacetic acid (5-HIAA) Serum Chromogranin A (CgA) Other markers Abdominal computed tomography (CT) Abdominal MRI Somatostatin receptor scintigraphy [SRS], or Octreoscan Metaiodobenzylguanidine (MIBG) scintigraphy Other diagnostic studies Transthoracic echocardiography
Carcinoid Syndrome[26][27][28][29][30][31][32][33][34] Neuroendocrine tumor of midgut [35][36][37][38] +

Mild

+ + + +

Dermatitis

Diarrhea

Dementia

Metastatic tumors in the liver: Right upper quadrant pain, hepatomegaly, and early satiety

+ +/- +/- + + – + + + +
  • Valve thickening with retraction and reduction in the mobility of the tricuspid valve

Pathognomonic radiological sign of midgut NET.

Neuroendocrine tumor of lung[39][40][41][42] + + + + +
    		+ +/- +/- + + – + + Sensitive for detection of liver metastases if present + + – Typical low-grade:bland cells containing regular round nuclei with finely dispersed chromatin and inconspicuous small nucleoli.Mitotic figures are scarce and necrosis is absent.

    Intermediate-grade atypical: presence of Neuroendocrine morphology and either necrosis or 2 to 10 mitoses per 10 HPF

    Irritable Bowel Syndrome[43][44][45][46] +

    Perioidic

    		– – – – – – – – – – – – – – – – Rome IV criteria
    • Recurrent abdominal pain, at least 1day/week in the last 3 months, a/s with 2 or more of the following criteria:

    •Related to defecation

    •Associated with a change in stool frequency

    •Associated with a change in stool form (appearance)

    Malignant neoplasms of small intestine[47][48][49] +/- +/- – – +/- – – +/- – * Abdominal mass – + Abdominal CT scan may be diagnostic of small intestine cancer. Findings on CT scan suggestive of small intestine cancer include intrinsic mass with a short segment of bowel wall thickening MRI and MRI enteroscopy are other advance modalities to diagnose and stage small intestinal cancers – – Enteroscopy, capsule endoscopy and double balloon enteroscopy Biopsy and histopathology
    Crohn disease[50][51][52][53] +/- – – – – – – – – – – – – –
    • Focal ulcerations and acute and chronic inflammation
    Benign cutaneous flushing[54] – – + – – – – – – – – – – – – – – – – – – –
    Systemic mastocytosis[55][56][57][58][59] + + + + – +/- +/- + – – – – – –
    Asthma exacerbation[60][61][62][63] – – – + + + – – + –
    • Tachypnea
    • Prolonged expiratory phase of respiration (decreased I:E ratio)
    • Seated position with use of extended arms to support the upper chest (tripod position)
    • +/- Pulsus paradoxus
    		 – – – — – – – Chest X ray –
    • Loss of the normal pseudostratified structure of airway epithelium
    • Increase in the proportion of goblet cells
    • Fibrotic thickening of the sub-epithelial reticular basement membrane
    • Increased numbers of myofibroblasts
    • Increased vascularity
    • Increased airway smooth muscle mass
    • Increased extracellular matrix
    Anaphylaxis[64][65][66][67][68] + -/+ + + + +/- – + + – – – – – – – – – – History of exposure to insect stings,food alllergy,rubber latex,food additives,,allergy to medications,physical factors such s excercise and cold
    Histaminergic Angioedema[69][70][71][72][73] +/- +/- + + + + – + + – – – – – – – – – –
    • Take proper clinical history of previous similar episodes
    • Medication history
    • Any allergy to insects stings , foods or any ingestion within previous 24 hours
    Medullary Thyroid Carcinoma[74][75][76][77] – +/- +/- +/- – – – – – – – – – – – –

    For metastasis

    		–

    Differential diagnosis based on diarrhea

    The following table outlines the major differential diagnoses based on diarrhea as the major presenting symptom

    Differential Diagnosis for Diarrhea predominant symptoms Clinical features Diagnosis
    Crohn’s disease
    Ulcerative colitis
    Microscopic colitis
    Celiac disease
    Neuroendocrine tumor
    Hyperthyroidism
    • Serum TSH levels
    Lactose intolerance
    • Avoidance trial, lactose breath test
    Infectious causes
    • Abdominal discomfort, diarrhea especially in the setting of recent travel
    Small bowel bacterial overgrowth
    Clostridium difficile infection(Psuedomembranous colitis)

    References

    1. ↑ Rasquin A, Di Lorenzo C, Forbes D, Guiraldes E, Hyams JS, Staiano A, Walker LS (2006). “Childhood functional gastrointestinal disorders: child/adolescent”. Gastroenterology. 130 (5): 1527–37. doi:10.1053/j.gastro.2005.08.063. PMID 16678566.
    2. ↑ Cash BD, Schoenfeld P, Chey WD (2002). “The utility of diagnostic tests in irritable bowel syndrome patients: a systematic review”. Am. J. Gastroenterol. 97 (11): 2812–9. doi:10.1111/j.1572-0241.2002.07027.x. PMID 12425553.
    3. ↑ Hamm LR, Sorrells SC, Harding JP, Northcutt AR, Heath AT, Kapke GF, Hunt CM, Mangel AW (1999). “Additional investigations fail to alter the diagnosis of irritable bowel syndrome in subjects fulfilling the Rome criteria”. Am. J. Gastroenterol. 94 (5): 1279–82. doi:10.1111/j.1572-0241.1999.01077.x. PMID 10235207.
    4. ↑ Prott G, Shim L, Hansen R, Kellow J, Malcolm A (2010). “Relationships between pelvic floor symptoms and function in irritable bowel syndrome”. Neurogastroenterol. Motil. 22 (7): 764–9. doi:10.1111/j.1365-2982.2010.01503.x. PMID 20456760.
    5. ↑ Voderholzer WA, Schatke W, Mühldorfer BE, Klauser AG, Birkner B, Müller-Lissner SA (1997). “Clinical response to dietary fiber treatment of chronic constipation”. Am. J. Gastroenterol. 92 (1): 95–8. PMID 8995945.
    6. ↑ Spiller R, Camilleri M, Longstreth GF (2010). “Do the symptom-based, Rome criteria of irritable bowel syndrome lead to better diagnosis and treatment outcomes?”. Clin. Gastroenterol. Hepatol. 8 (2): 125–9, discussion 129–36. doi:10.1016/j.cgh.2009.12.018. PMID 20152787.
    7. ↑ Rao SS, Valestin J, Brown CK, Zimmerman B, Schulze K (2010). “Long-term efficacy of biofeedback therapy for dyssynergic defecation: randomized controlled trial”. Am. J. Gastroenterol. 105 (4): 890–6. doi:10.1038/ajg.2010.53. PMC 3910270. PMID 20179692.
    8. ↑ Chey WD, Nojkov B, Rubenstein JH, Dobhan RR, Greenson JK, Cash BD (2010). “The yield of colonoscopy in patients with non-constipated irritable bowel syndrome: results from a prospective, controlled US trial”. Am. J. Gastroenterol. 105 (4): 859–65. doi:10.1038/ajg.2010.55. PMC 2887227. PMID 20179696.
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    15. ↑ http://digestive.niddk.nih.gov/ddiseases/pubs/celiac/ – The United States National Institutes of Health Celiac Disease Page
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    37. ↑ Signs and symptoms of carcinoid syndrome. National Cancer Institute. http://www.cancer.gov/types/gi-carcinoid-tumors/patient/gi-carcinoid-treatment-pdq
    38. ↑ Modlin IM, Kidd M, Latich I, Zikusoka MN, Shapiro MD (May 2005). “Current status of gastrointestinal carcinoids”. Gastroenterology. 128 (6): 1717–51. PMID 15887161.
    39. ↑ Gustafsson BI, Kidd M, Chan A, Malfertheiner MV, Modlin IM (July 2008). “Bronchopulmonary neuroendocrine tumors”. Cancer. 113 (1): 5–21. doi:10.1002/cncr.23542. PMID 18473355.
    40. ↑ Jeung, Mi-Young; Gasser, Bernard; Gangi, Afshin; Charneau, Dominique; Ducroq, Xavier; Kessler, Romain; Quoix, Elisabeth; Roy, Catherine (2002). “Bronchial Carcinoid Tumors of the Thorax: Spectrum of Radiologic Findings”. RadioGraphics. 22 (2): 351–365. doi:10.1148/radiographics.22.2.g02mr01351. ISSN 0271-5333.
    41. ↑ Nessi R, Basso Ricci P, Basso Ricci S, Bosco M, Blanc M, Uslenghi C (April 1991). “Bronchial carcinoid tumors: radiologic observations in 49 cases”. J Thorac Imaging. 6 (2): 47–53. PMID 1649924.
    42. ↑ Melmon KL, Sjoerdsma A, Mason DT (October 1965). “Distinctive clinical and therapeutic aspects of the syndrome associated with bronchial carcinoid tumors”. Am. J. Med. 39 (4): 568–81. PMID 5831899.
    43. ↑ Ford AC, Forman D, Bailey AG, Axon AT, Moayyedi P (May 2008). “Irritable bowel syndrome: a 10-yr natural history of symptoms and factors that influence consultation behavior”. Am. J. Gastroenterol. 103 (5): 1229–39, quiz 1240. doi:10.1111/j.1572-0241.2007.01740.x. PMID 18371141.
    44. ↑ Simren M, Palsson OS, Whitehead WE (April 2017). “Update on Rome IV Criteria for Colorectal Disorders: Implications for Clinical Practice”. Curr Gastroenterol Rep. 19 (4): 15. doi:10.1007/s11894-017-0554-0. PMC 5378729. PMID 28374308.
    45. ↑ “American Gastroenterological Association medical position statement: irritable bowel syndrome”. Gastroenterology. 123 (6): 2105–7. December 2002. doi:10.1053/gast.2002.37095b. PMID 12454865.
    46. ↑ Mearin F, Lacy BE, Chang L, Chey WD, Lembo AJ, Simren M, Spiller R (February 2016). “Bowel Disorders”. Gastroenterology. doi:10.1053/j.gastro.2016.02.031. PMID 27144627.
    47. ↑ McLaughlin PD, Maher MM (July 2013). “Primary malignant diseases of the small intestine”. AJR Am J Roentgenol. 201 (1): W9–14. doi:10.2214/AJR.12.8492. PMID 23789703.
    48. ↑ Hatzaras I, Palesty JA, Abir F, Sullivan P, Kozol RA, Dudrick SJ, Longo WE (March 2007). “Small-bowel tumors: epidemiologic and clinical characteristics of 1260 cases from the connecticut tumor registry”. Arch Surg. 142 (3): 229–35. doi:10.1001/archsurg.142.3.229. PMID 17372046.
    49. ↑ Lepage C, Bouvier AM, Manfredi S, Dancourt V, Faivre J (December 2006). “Incidence and management of primary malignant small bowel cancers: a well-defined French population study”. Am. J. Gastroenterol. 101 (12): 2826–32. doi:10.1111/j.1572-0241.2006.00854.x. PMID 17026561.
    50. ↑ Hara AK, Swartz PG (2009). “CT enterography of Crohn’s disease”. Abdom Imaging. 34 (3): 289–95. doi:10.1007/s00261-008-9443-1. PMID 18649092.
    51. ↑ Baumgart, Daniel C; Sandborn, William J (2012). “Crohn’s disease”. The Lancet. 380 (9853): 1590–1605. doi:10.1016/S0140-6736(12)60026-9. ISSN 0140-6736.
    52. ↑ Feuerstein, Joseph D.; Cheifetz, Adam S. (2017). “Crohn Disease: Epidemiology, Diagnosis, and Management”. Mayo Clinic Proceedings. 92 (7): 1088–1103. doi:10.1016/j.mayocp.2017.04.010. ISSN 0025-6196.
    53. ↑ García-Bosch, O.; Ordás, I.; Aceituno, M.; Rodríguez, S.; Ramírez, A. M.; Gallego, M.; Ricart, E.; Rimola, J.; Panes, J. (2016). “Comparison of Diagnostic Accuracy and Impact of Magnetic Resonance Imaging and Colonoscopy for the Management of Crohn’s Disease”. Journal of Crohn’s and Colitis. 10 (6): 663–669. doi:10.1093/ecco-jcc/jjw015. ISSN 1873-9946.
    54. ↑ Izikson, Leonid; English, Joseph C.; Zirwas, Matthew J. (2006). “The flushing patient: Differential diagnosis, workup, and treatment”. Journal of the American Academy of Dermatology. 55 (2): 193–208. doi:10.1016/j.jaad.2005.07.057. ISSN 0190-9622.
    55. ↑ Hartmann, Karin; Escribano, Luis; Grattan, Clive; Brockow, Knut; Carter, Melody C.; Alvarez-Twose, Ivan; Matito, Almudena; Broesby-Olsen, Sigurd; Siebenhaar, Frank; Lange, Magdalena; Niedoszytko, Marek; Castells, Mariana; Oude Elberink, Joanna N.G.; Bonadonna, Patrizia; Zanotti, Roberta; Hornick, Jason L.; Torrelo, Antonio; Grabbe, Jürgen; Rabenhorst, Anja; Nedoszytko, Boguslaw; Butterfield, Joseph H.; Gotlib, Jason; Reiter, Andreas; Radia, Deepti; Hermine, Olivier; Sotlar, Karl; George, Tracy I.; Kristensen, Thomas K.; Kluin-Nelemans, Hanneke C.; Yavuz, Selim; Hägglund, Hans; Sperr, Wolfgang R.; Schwartz, Lawrence B.; Triggiani, Massimo; Maurer, Marcus; Nilsson, Gunnar; Horny, Hans-Peter; Arock, Michel; Orfao, Alberto; Metcalfe, Dean D.; Akin, Cem; Valent, Peter (2016). “Cutaneous manifestations in patients with mastocytosis: Consensus report of the European Competence Network on Mastocytosis; the American Academy of Allergy, Asthma & Immunology; and the European Academy of Allergology and Clinical Immunology”. Journal of Allergy and Clinical Immunology. 137 (1): 35–45. doi:10.1016/j.jaci.2015.08.034. ISSN 0091-6749.
    56. ↑ Lee, Jason K; Whittaker, Scott J; Enns, Robert A; Zetler, Peter (2008). “Gastrointestinal manifestations of systemic mastocytosis”. World Journal of Gastroenterology. 14 (45): 7005. doi:10.3748/wjg.14.7005. ISSN 1007-9327.
    57. ↑ Horan RF, Austen KF (March 1991). “Systemic mastocytosis: retrospective review of a decade’s clinical experience at the Brigham and Women’s Hospital”. J. Invest. Dermatol. 96 (3): 5S–13S, discussion 13S–14S. PMID 2002264.
    58. ↑ Sokol, Harry; Georgin-Lavialle, Sophie; Grandpeix-Guyodo, Catherine; Canioni, Danielle; Barete, Stéphane; Dubreuil, Patrice; Lortholary, Olivier; Beaugerie, Laurent; Hermine, Olivier (2010). “Gastrointestinal involvement and manifestations in systemic mastocytosis”. Inflammatory Bowel Diseases. 16 (7): 1247–1253. doi:10.1002/ibd.21218. ISSN 1078-0998.
    59. ↑ Bedeir A, Jukic DM, Wang L, Mullady DK, Regueiro M, Krasinskas AM (November 2006). “Systemic mastocytosis mimicking inflammatory bowel disease: A case report and discussion of gastrointestinal pathology in systemic mastocytosis”. Am. J. Surg. Pathol. 30 (11): 1478–82. doi:10.1097/01.pas.0000213310.51553.d7. PMID 17063092.
    60. ↑ Fuhlbrigge A, Peden D, Apter AJ, Boushey HA, Camargo CA, Gern J, Heymann PW, Martinez FD, Mauger D, Teague WG, Blaisdell C (March 2012). “Asthma outcomes: exacerbations”. J. Allergy Clin. Immunol. 129 (3 Suppl): S34–48. doi:10.1016/j.jaci.2011.12.983. PMC 3595577. PMID 22386508.
    61. ↑ Limb SL, Brown KC, Wood RA, Wise RA, Eggleston PA, Tonascia J, Adkinson NF (December 2005). “Irreversible lung function deficits in young adults with a history of childhood asthma”. J. Allergy Clin. Immunol. 116 (6): 1213–9. doi:10.1016/j.jaci.2005.09.024. PMID 16337448.
    62. ↑ Aldington S, Beasley R (May 2007). “Asthma exacerbations. 5: assessment and management of severe asthma in adults in hospital”. Thorax. 62 (5): 447–58. doi:10.1136/thx.2005.045203. PMC 2117186. PMID 17468458.
    63. ↑ Dougherty RH, Fahy JV (February 2009). “Acute exacerbations of asthma: epidemiology, biology and the exacerbation-prone phenotype”. Clin. Exp. Allergy. 39 (2): 193–202. doi:10.1111/j.1365-2222.2008.03157.x. PMC 2730743. PMID 19187331.
    64. ↑ Peavy RD, Metcalfe DD (August 2008). “Understanding the mechanisms of anaphylaxis”. Curr Opin Allergy Clin Immunol. 8 (4): 310–5. doi:10.1097/ACI.0b013e3283036a90. PMC 2683407. PMID 18596587.
    65. ↑ Tupper J, Visser S (October 2010). “Anaphylaxis: A review and update”. Can Fam Physician. 56 (10): 1009–11. PMC 2954079. PMID 20944042.
    66. ↑ Kemp SF, Lockey RF (September 2002). “Anaphylaxis: a review of causes and mechanisms”. J. Allergy Clin. Immunol. 110 (3): 341–8. PMID 12209078.
    67. ↑ Bjornsson HM, Graffeo CS (December 2010). “Improving diagnostic accuracy of anaphylaxis in the acute care setting”. West J Emerg Med. 11 (5): 456–61. PMC 3027438. PMID 21293765.
    68. ↑ “Usefulness and Limitations of Sequential Serum Tryptase for the Diagnosis of Anaphylaxis in 102 Patients – FullText – International Archives of Allergy and Immunology 2013, Vol. 160, No. 2 – Karger Publishers”.
    69. ↑ Busse PJ, Smith T (August 2017). “Histaminergic Angioedema”. Immunol Allergy Clin North Am. 37 (3): 467–481. doi:10.1016/j.iac.2017.03.001. PMID 28687103.
    70. ↑ Hahn J, Hoffmann TK, Bock B, Nordmann-Kleiner M, Trainotti S, Greve J (July 2017). “Angioedema”. Dtsch Arztebl Int. 114 (29–30): 489–496. doi:10.3238/arztebl.2017.0489. PMC 5569554. PMID 28818177.
    71. ↑ Bernstein JA, Cremonesi P, Hoffmann TK, Hollingsworth J (December 2017). “Angioedema in the emergency department: a practical guide to differential diagnosis and management”. Int J Emerg Med. 10 (1): 15. doi:10.1186/s12245-017-0141-z. PMC 5389952. PMID 28405953.
    72. ↑ Bernstein JA, Moellman J (November 2012). “Emerging concepts in the diagnosis and treatment of patients with undifferentiated angioedema”. Int J Emerg Med. 5 (1): 39. doi:10.1186/1865-1380-5-39. PMC 3518251. PMID 23131076.
    73. ↑ Kaplan AP (June 2008). “Angioedema”. World Allergy Organ J. 1 (6): 103–13. doi:10.1097/WOX.0b013e31817aecbe. PMC 3651192. PMID 23282406.
    74. ↑ Pacini F, Castagna MG, Cipri C, Schlumberger M (August 2010). “Medullary thyroid carcinoma”. Clin Oncol (R Coll Radiol). 22 (6): 475–85. doi:10.1016/j.clon.2010.05.002. PMID 20627492.
    75. ↑ Roy M, Chen H, Sippel RS (2013). “Current understanding and management of medullary thyroid cancer”. Oncologist. 18 (10): 1093–100. doi:10.1634/theoncologist.2013-0053. PMC 3805151. PMID 24037980.
    76. ↑ Mian C, Perrino M, Colombo C, Cavedon E, Pennelli G, Ferrero S, De Leo S, Sarais C, Cacciatore C, Manfredi GI, Verga U, Iacobone M, De Pasquale L, Pelizzo MR, Vicentini L, Persani L, Fugazzola L (May 2014). “Refining calcium test for the diagnosis of medullary thyroid cancer: cutoffs, procedures, and safety”. J. Clin. Endocrinol. Metab. 99 (5): 1656–64. doi:10.1210/jc.2013-4088. PMID 24552221.
    77. ↑ Bae YJ, Schaab M, Kratzsch J (2015). “Calcitonin as Biomarker for the Medullary Thyroid Carcinoma”. Recent Results Cancer Res. 204: 117–37. doi:10.1007/978-3-319-22542-5_5. PMID 26494386.

    Template:WH Template:WS |}

    Epidemiology and Demographics

    Epidemiology and Demographics

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

    Overview

    Irritable bowel disease (IBS) is an extremely common disorder among the general population. The incidence of IBS is approximately 200 per 100,000 individuals worldwide. The prevalence of IBS is approximately 11,200 per 100,000 individuals worldwide. The prevalence of IBS varies with geographical and demographic distribution. Females are more commonly affected by IBS than males. The female to male ratio is approximately 1:2. The prevalence of IBS in USA and Europe is 10,000-20,000 per 100,000 individuals. In USA and Australia, 1 in every 10 people fulfill the Rome IV criteria for IBS. In Asia, Africa and South America, IBS is becoming increasingly prevalent as a disease of urbanization and industrialization. This is due to increased access to health care, higher stress levels and differing dietary choices.

    Epidemiology and Demographics

    Incidence

    Prevalence

    Age

    • IBS commonly affects individuals younger than 35 years of age.[18]
    • The incidence of IBS decreases with age.
    • The prevalence of IBS is 25% lower in individuals over 50 years of age.[15] [19]

    Race

    • There is no racial predilection to IBS.[20]

    Gender

    • Females are more commonly affected by IBS than males. The female to male ratio is approximately 1:2. This is due to social and biological factors.[21]

    Social factors:

    • Females are predominantly affected by IBS as the likelihood of diagnosis of IBS is 2-3 times more in women as compared to men. This is because health care seeking behavior for symptoms is 4-5 times higher in women as compared to men.[16][22][23][24] [25][26][27]

    Biological factors:

    Children

    • In the Western pediatric population, IBS is the commonest cause of functional recurrent abdominal pain (RAP) as it accounts for more than 50% of all cases.[35][36]

    Developed and developing countries

    • In USA and Australia, 1 in every 10 people fulfill the Rome IV criteria  for IBS.[37]
    • In Asia, Africa and South America, IBS is becoming increasingly prevalent as a disease of urbanization and industrialization. This is due to increased access to health care, higher stress levels and differing dietary choices. [6][38][6][39][7][40]

    References

    1. ↑ 1.0 1.1 Choung RS, Locke GR (2011). “Epidemiology of IBS”. Gastroenterol. Clin. North Am. 40 (1): 1–10. doi:10.1016/j.gtc.2010.12.006. PMID 21333897.
    2. ↑ Thompson WG, Longstreth GF, Drossman DA, Heaton KW, Irvine EJ, Müller-Lissner SA (1999). “Functional bowel disorders and functional abdominal pain”. Gut. 45 Suppl 2: II43–7. PMC 1766683. PMID 10457044.
    3. ↑ Talley NJ, Spiller R (2002). “Irritable bowel syndrome: a little understood organic bowel disease?”. Lancet. 360 (9332): 555–64. doi:10.1016/S0140-6736(02)09712-X. PMID 12241674.
    4. ↑ Boyce PM, Talley NJ, Burke C, Koloski NA (2006). “Epidemiology of the functional gastrointestinal disorders diagnosed according to Rome II criteria: an Australian population-based study”. Intern Med J. 36 (1): 28–36. doi:10.1111/j.1445-5994.2006.01006.x. PMID 16409310.
    5. ↑ Corazziari E (2004). “Definition and epidemiology of functional gastrointestinal disorders”. Best Pract Res Clin Gastroenterol. 18 (4): 613–31. doi:10.1016/j.bpg.2004.04.012. PMID 15324703.
    6. ↑ 6.0 6.1 6.2 Gwee KA (2005). “Irritable bowel syndrome in developing countries–a disorder of civilization or colonization?”. Neurogastroenterol. Motil. 17 (3): 317–24. doi:10.1111/j.1365-2982.2005.00627.x. PMID 15916618.
    7. ↑ 7.0 7.1 Gwee KA, Ghoshal UC, Chen M (2017). “Irritable bowel syndrome in Asia: pathogenesis, natural history, epidemiology and management”. J. Gastroenterol. Hepatol. doi:10.1111/jgh.13987. PMID 28901578.
    8. ↑ Quigley EM, Fried M, Gwee KA, Khalif I, Hungin AP, Lindberg G, Abbas Z, Fernandez LB, Bhatia SJ, Schmulson M, Olano C, LeMair A (2016). “World Gastroenterology Organisation Global Guidelines Irritable Bowel Syndrome: A Global Perspective Update September 2015”. J. Clin. Gastroenterol. 50 (9): 704–13. doi:10.1097/MCG.0000000000000653. PMID 27623513.
    9. ↑ Agréus L, Svärdsudd K, Nyrén O, Tibblin G (1995). “Irritable bowel syndrome and dyspepsia in the general population: overlap and lack of stability over time”. Gastroenterology. 109 (3): 671–80. PMID 7657095.
    10. ↑ Husain N, Chaudhry IB, Jafri F, Niaz SK, Tomenson B, Creed F (2008). “A population-based study of irritable bowel syndrome in a non-Western population”. Neurogastroenterol. Motil. 20 (9): 1022–9. doi:10.1111/j.1365-2982.2008.01143.x. PMID 18492027.
    11. ↑ Thompson WG, Irvine EJ, Pare P, Ferrazzi S, Rance L (2002). “Functional gastrointestinal disorders in Canada: first population-based survey using Rome II criteria with suggestions for improving the questionnaire”. Dig. Dis. Sci. 47 (1): 225–35. PMID 11837727.
    12. ↑ Heaton KW, O’Donnell LJ, Braddon FE, Mountford RA, Hughes AO, Cripps PJ (1992). “Symptoms of irritable bowel syndrome in a British urban community: consulters and nonconsulters”. Gastroenterology. 102 (6): 1962–7. PMID 1587415.
    13. ↑ Jones R, Lydeard S (1992). “Irritable bowel syndrome in the general population”. BMJ. 304 (6819): 87–90. PMC 1880997. PMID 1737146.
    14. ↑ Wilson S, Roberts L, Roalfe A, Bridge P, Singh S (2004). “Prevalence of irritable bowel syndrome: a community survey”. Br J Gen Pract. 54 (504): 495–502. PMC 1324800. PMID 15239910.
    15. ↑ 15.0 15.1 Lovell RM, Ford AC (2012). “Global prevalence of and risk factors for irritable bowel syndrome: a meta-analysis”. Clin. Gastroenterol. Hepatol. 10 (7): 712–721.e4. doi:10.1016/j.cgh.2012.02.029. PMID 22426087.
    16. ↑ 16.0 16.1 Drossman DA, Li Z, Andruzzi E, Temple RD, Talley NJ, Thompson WG, Whitehead WE, Janssens J, Funch-Jensen P, Corazziari E (1993). “U.S. householder survey of functional gastrointestinal disorders. Prevalence, sociodemography, and health impact”. Dig. Dis. Sci. 38 (9): 1569–80. PMID 8359066.
    17. ↑ Grundmann O, Yoon SL (2010). “Irritable bowel syndrome: epidemiology, diagnosis and treatment: an update for health-care practitioners”. J. Gastroenterol. Hepatol. 25 (4): 691–9. doi:10.1111/j.1440-1746.2009.06120.x. PMID 20074154.
    18. ↑ Maxwell PR, Mendall MA, Kumar D (1997). “Irritable bowel syndrome”. Lancet. 350 (9092): 1691–5. PMID 9400529.
    19. ↑ Tang YR, Yang WW, Liang ML, Xu XY, Wang MF, Lin L (2012). “Age-related symptom and life quality changes in women with irritable bowel syndrome”. World J. Gastroenterol. 18 (48): 7175–83. doi:10.3748/wjg.v18.i48.7175. PMC 3544019. PMID 23326122.
    20. ↑ Haas JS, Phillips KA, Sonneborn D, McCulloch CE, Baker LC, Kaplan CP, Pérez-Stable EJ, Liang SY (2004). “Variation in access to health care for different racial/ethnic groups by the racial/ethnic composition of an individual’s county of residence”. Med Care. 42 (7): 707–14. PMID 15213496.
    21. ↑ Thompson WG (1997). “Gender differences in irritable bowel symptoms”. Eur J Gastroenterol Hepatol. 9 (3): 299–302. PMID 9096434.
    22. ↑ Payne S (2004). “Sex, gender, and irritable bowel syndrome: making the connections”. Gend Med. 1 (1): 18–28. PMID 16115580.
    23. ↑ Lovell RM, Ford AC (2012). “Effect of gender on prevalence of irritable bowel syndrome in the community: systematic review and meta-analysis”. Am. J. Gastroenterol. 107 (7): 991–1000. doi:10.1038/ajg.2012.131. PMID 22613905.
    24. ↑ Kennedy TM, Jones RH, Hungin AP, O’flanagan H, Kelly P (1998). “Irritable bowel syndrome, gastro-oesophageal reflux, and bronchial hyper-responsiveness in the general population”. Gut. 43 (6): 770–4. PMC 1727355. PMID 9824603.
    25. ↑ Voci SC, Cramer KM (2009). “Gender-related traits, quality of life, and psychological adjustment among women with irritable bowel syndrome”. Qual Life Res. 18 (9): 1169–76. doi:10.1007/s11136-009-9532-9. PMID 19728159.
    26. ↑ Quigley EM, Bytzer P, Jones R, Mearin F (2006). “Irritable bowel syndrome: the burden and unmet needs in Europe”. Dig Liver Dis. 38 (10): 717–23. doi:10.1016/j.dld.2006.05.009. PMID 16807154.
    27. ↑ Manning AP, Thompson WG, Heaton KW, Morris AF (1978). “Towards positive diagnosis of the irritable bowel”. Br Med J. 2 (6138): 653–4. PMC 1607467. PMID 698649.
    28. ↑ Jackson NA, Houghton LA, Whorwell PJ, Currer B (1994). “Does the menstrual cycle affect anorectal physiology?”. Dig. Dis. Sci. 39 (12): 2607–11. PMID 7995186.
    29. ↑ Walker EA, Katon WJ, Roy-Byrne PP, Jemelka RP, Russo J (1993). “Histories of sexual victimization in patients with irritable bowel syndrome or inflammatory bowel disease”. Am J Psychiatry. 150 (10): 1502–6. doi:10.1176/ajp.150.10.1502. PMID 8379554.
    30. ↑ Heitkemper MM, Chang L (2009). “Do fluctuations in ovarian hormones affect gastrointestinal symptoms in women with irritable bowel syndrome?”. Gend Med. 6 Suppl 2: 152–67. doi:10.1016/j.genm.2009.03.004. PMC 3322543. PMID 19406367.
    31. ↑ Goffaux P, Michaud K, Gaudreau J, Chalaye P, Rainville P, Marchand S (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.
    32. ↑ Rajindrajith S, Devanarayana NM (2012). “Subtypes and Symptomatology of Irritable Bowel Syndrome in Children and Adolescents: A School-based Survey Using Rome III Criteria”. J Neurogastroenterol Motil. 18 (3): 298–304. doi:10.5056/jnm.2012.18.3.298. PMC 3400818. PMID 22837878.
    33. ↑ Dong L, Dingguo L, Xiaoxing X, Hanming L (2005). “An epidemiologic study of irritable bowel syndrome in adolescents and children in China: a school-based study”. Pediatrics. 116 (3): e393–6. doi:10.1542/peds.2004-2764. PMID 16140684.
    34. ↑ Rasquin A, Di Lorenzo C, Forbes D, Guiraldes E, Hyams JS, Staiano A, Walker LS (2006). “Childhood functional gastrointestinal disorders: child/adolescent”. Gastroenterology. 130 (5): 1527–37. doi:10.1053/j.gastro.2005.08.063. PMID 16678566.
    35. ↑ Hyams JS, Treem WR, Justinich CJ, Davis P, Shoup M, Burke G (1995). “Characterization of symptoms in children with recurrent abdominal pain: resemblance to irritable bowel syndrome”. J. Pediatr. Gastroenterol. Nutr. 20 (2): 209–14. PMID 7714688.
    36. ↑ El-Matary W, Spray C, Sandhu B (2004). “Irritable bowel syndrome: the commonest cause of recurrent abdominal pain in children”. Eur. J. Pediatr. 163 (10): 584–8. doi:10.1007/s00431-004-1503-0. PMID 15290263.
    37. ↑ Cremonini F, Talley NJ (2005). “Irritable bowel syndrome: epidemiology, natural history, health care seeking and emerging risk factors”. Gastroenterol. Clin. North Am. 34 (2): 189–204. doi:10.1016/j.gtc.2005.02.008. PMID 15862929.
    38. ↑ Grodzinsky E, Hallert C, Faresjö T, Bergfors E, Faresjö AO (2012). “Could gastrointestinal disorders differ in two close but divergent social environments?”. Int J Health Geogr. 11: 5. doi:10.1186/1476-072X-11-5. PMC 3330019. PMID 22309613.
    39. ↑ Hulshof KF, Brussaard JH, Kruizinga AG, Telman J, Löwik MR (2003). “Socio-economic status, dietary intake and 10 y trends: the Dutch National Food Consumption Survey”. Eur J Clin Nutr. 57 (1): 128–37. doi:10.1038/sj.ejcn.1601503. PMID 12548307.
    40. ↑ Talley NJ, Phillips SF, Bruce B, Twomey CK, Zinsmeister AR, Melton LJ (1990). “Relation among personality and symptoms in nonulcer dyspepsia and the irritable bowel syndrome”. Gastroenterology. 99 (2): 327–33. PMID 2365186.

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    Risk Factors

    Risk Factors

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

    Overview

    Common risk factors in the development of irritable bowel syndrome (IBS) include stress, anxiety, depression, history of IBD and acute gastrointestinal infections.

    Risk Factors

    Common risk factors in the development of IBS may be categorized as psychological, epidemiological, genetic, and infectious.

    Common risk factors

    Common risk factors in the development of IBS include:

    Psychological risk factors:[1][2][3][4]

    Psychiatric risk factors:[2][3][5][6]

    • History of physical or sexual abuse or adverse early life events

    Past medical history

    Less common risk factors

    References

    1. ↑ Devanarayana NM, Mettananda S, Liyanarachchi C, Nanayakkara N, Mendis N, Perera N, Rajindrajith S (2011). “Abdominal pain-predominant functional gastrointestinal diseases in children and adolescents: prevalence, symptomatology, and association with emotional stress”. J. Pediatr. Gastroenterol. Nutr. 53 (6): 659–65. doi:10.1097/MPG.0b013e3182296033. PMID 21697745.
    2. ↑ 2.0 2.1 Qin HY, Cheng CW, Tang XD, Bian ZX (2014). “Impact of psychological stress on irritable bowel syndrome”. World J. Gastroenterol. 20 (39): 14126–31. doi:10.3748/wjg.v20.i39.14126. PMC 4202343. PMID 25339801.
    3. ↑ 3.0 3.1 Bharucha AE, Chakraborty S, Sletten CD (2016). “Common Functional Gastroenterological Disorders Associated With Abdominal Pain”. Mayo Clin. Proc. 91 (8): 1118–32. doi:10.1016/j.mayocp.2016.06.003. PMC 4985027. PMID 27492916.
    4. ↑ Ibrahim NK (2016). “A systematic review of the prevalence and risk factors of irritable bowel syndrome among medical students”. Turk J Gastroenterol. 27 (1): 10–6. doi:10.5152/tjg.2015.150333. PMID 26674980.
    5. ↑ 5.0 5.1 5.2 Cole JA, Rothman KJ, Cabral HJ, Zhang Y, Farraye FA (2006). “Migraine, fibromyalgia, and depression among people with IBS: a prevalence study”. BMC Gastroenterol. 6: 26. doi:10.1186/1471-230X-6-26. PMC 1592499. PMID 17007634.
    6. ↑ Hausteiner-Wiehle C, Henningsen P (2014). “Irritable bowel syndrome: relations with functional, mental, and somatoform disorders”. World J. Gastroenterol. 20 (20): 6024–30. doi:10.3748/wjg.v20.i20.6024. PMC 4033442. PMID 24876725.
    7. ↑ 7.0 7.1 Major G, Spiller R (2014). “Irritable bowel syndrome, inflammatory bowel disease and the microbiome”. Curr Opin Endocrinol Diabetes Obes. 21 (1): 15–21. doi:10.1097/MED.0000000000000032. PMC 3871405. PMID 24296462.
    8. ↑ Ceuleers H, Van Spaendonk H, Hanning N, Heirbaut J, Lambeir AM, Joossens J, Augustyns K, De Man JG, De Meester I, De Winter BY (2016). “Visceral hypersensitivity in inflammatory bowel diseases and irritable bowel syndrome: The role of proteases”. World J. Gastroenterol. 22 (47): 10275–10286. doi:10.3748/wjg.v22.i47.10275. PMC 5175241. PMID 28058009.
    9. ↑ Halliez MC, Buret AG (2013). “Extra-intestinal and long term consequences of Giardia duodenalis infections”. World J. Gastroenterol. 19 (47): 8974–85. doi:10.3748/wjg.v19.i47.8974. PMC 3870550. PMID 24379622.
    10. ↑ Simrén M, Barbara G, Flint HJ, Spiegel BM, Spiller RC, Vanner S, Verdu EF, Whorwell PJ, Zoetendal EG (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.
    11. ↑ Jeffery IB, Quigley EM, Öhman L, Simrén M, O’Toole PW (2012). “The microbiota link to irritable bowel syndrome: an emerging story”. Gut Microbes. 3 (6): 572–6. doi:10.4161/gmic.21772. PMC 3495796. PMID 22895081.
    12. ↑ Ibarra C, Herrera V, Pérez de Arce E, Gil LC, Madrid AM, Valenzuela L, Beltrán CJ (2016). “[Parasitosis and irritable bowel syndrome]”. Rev Chilena Infectol (in Spanish; Castilian). 33 (3): 268–74. doi:10.4067/S0716-10182016000300003. PMID 27598274.
    13. ↑ Giddings SL, Stevens AM, Leung DT (2016). “Traveler’s Diarrhea”. Med. Clin. North Am. 100 (2): 317–30. doi:10.1016/j.mcna.2015.08.017. PMC 4764790. PMID 26900116.
    14. ↑ Keithlin J, Sargeant J, Thomas MK, Fazil A (2014). “Systematic review and meta-analysis of the proportion of Campylobacter cases that develop chronic sequelae”. BMC Public Health. 14: 1203. doi:10.1186/1471-2458-14-1203. PMC 4391665. PMID 25416162.
    15. ↑ Grover M (2014). “Role of gut pathogens in development of irritable bowel syndrome”. Indian J. Med. Res. 139 (1): 11–8. PMC 3994726. PMID 24604037.
    16. ↑ Keithlin J, Sargeant J, Thomas MK, Fazil A (2014). “Chronic sequelae of E. coli O157: systematic review and meta-analysis of the proportion of E. coli O157 cases that develop chronic sequelae”. Foodborne Pathog. Dis. 11 (2): 79–95. doi:10.1089/fpd.2013.1572. PMC 3925333. PMID 24404780.
    17. ↑ Connor BA, Riddle MS (2013). “Post-infectious sequelae of travelers’ diarrhea”. J Travel Med. 20 (5): 303–12. doi:10.1111/jtm.12049. PMID 23992573.
    18. ↑ Ghoshal UC, Shukla R, Ghoshal U (2017). “Small Intestinal Bacterial Overgrowth and Irritable Bowel Syndrome: A Bridge between Functional Organic Dichotomy”. Gut Liver. 11 (2): 196–208. doi:10.5009/gnl16126. PMC 5347643. PMID 28274108.
    19. ↑ Gallo A, Passaro G, Gasbarrini A, Landolfi R, Montalto M (2016). “Modulation of microbiota as treatment for intestinal inflammatory disorders: An uptodate”. World J. Gastroenterol. 22 (32): 7186–202. doi:10.3748/wjg.v22.i32.7186. PMC 4997632. PMID 27621567.
    20. ↑ Distrutti E, Monaldi L, Ricci P, Fiorucci S (2016). “Gut microbiota role in irritable bowel syndrome: New therapeutic strategies”. World J. Gastroenterol. 22 (7): 2219–41. doi:10.3748/wjg.v22.i7.2219. PMC 4734998. PMID 26900286.
    21. ↑ Shreiner AB, Kao JY, Young VB (2015). “The gut microbiome in health and in disease”. Curr. Opin. Gastroenterol. 31 (1): 69–75. doi:10.1097/MOG.0000000000000139. PMC 4290017. PMID 25394236.
    22. ↑ Goodwin L, White PD, Hotopf M, Stansfeld SA, Clark C (2013). “Life course study of the etiology of self-reported irritable bowel syndrome in the 1958 British birth cohort”. Psychosom Med. 75 (2): 202–10. doi:10.1097/PSY.0b013e31827c351b. PMID 23324872.
    23. ↑ Makker J, Chilimuri S, Bella JN (2015). “Genetic epidemiology of irritable bowel syndrome”. World J. Gastroenterol. 21 (40): 11353–61. doi:10.3748/wjg.v21.i40.11353. PMC 4616211. PMID 26525775.
    24. ↑ Mulak A, Taché Y, Larauche M (2014). “Sex hormones in the modulation of irritable bowel syndrome”. World J. Gastroenterol. 20 (10): 2433–48. doi:10.3748/wjg.v20.i10.2433. PMC 3949254. PMID 24627581.
    25. ↑ Mawe GM, Coates MD, Moses PL (2006). “Review article: intestinal serotonin signalling in irritable bowel syndrome”. Aliment. Pharmacol. Ther. 23 (8): 1067–76. doi:10.1111/j.1365-2036.2006.02858.x. PMID 16611266.
    26. ↑ Mulak A, Paradowski L (2005). “[Migraine and irritable bowel syndrome]”. Neurol. Neurochir. Pol. (in Polish). 39 (4 Suppl 1): S55–60. PMID 16419571.
    27. ↑ Cámara-Lemarroy CR, Rodriguez-Gutierrez R, Monreal-Robles R, Marfil-Rivera A (2016). “Gastrointestinal disorders associated with migraine: A comprehensive review”. World J. Gastroenterol. 22 (36): 8149–60. doi:10.3748/wjg.v22.i36.8149. PMC 5037083. PMID 27688656.
    28. ↑ Cady RK, Farmer K, Dexter JK, Hall J (2012). “The bowel and migraine: update on celiac disease and irritable bowel syndrome”. Curr Pain Headache Rep. 16 (3): 278–86. doi:10.1007/s11916-012-0258-y. PMID 22447132.
    29. ↑ Vehof J, Zavos HM, Lachance G, Hammond CJ, Williams FM (2014). “Shared genetic factors underlie chronic pain syndromes”. Pain. 155 (8): 1562–8. doi:10.1016/j.pain.2014.05.002. PMID 24879916.
    30. ↑ Chirila I, Petrariu FD, Ciortescu I, Mihai C, Drug VL (2012). “Diet and irritable bowel syndrome”. J Gastrointestin Liver Dis. 21 (4): 357–62. PMID 23256117.
    31. ↑ Akhondi, Negin; Memar Montazerin, Sahar; Soltani, Sanaz; Saneei, Parvane; Hassanzadeh Keshteli, Ammar; Esmaillzadeh, Ahmad; Adibi, Peyman (2019). “General and abdominal obesity in relation to the prevalence of irritable bowel syndrome”. Neurogastroenterology & Motility. 31 (4): e13549. doi:10.1111/nmo.13549. ISSN 1350-1925.

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    Screening

    Screening

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

    Overview

    There is insufficient evidence to recommend routine screening for irritable bowel syndrome.

    Screening

    There is insufficient evidence to recommend routine screening for irritable bowel syndrome.


    References

    Natural History, Complications and Prognosis

    Natural History, Complications and Prognosis

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

    Overview

    The symptoms of irritable bowel syndrome (IBS) usually develop in the second decade of life, and start with symptoms such as abdominal pain, diarrhea and constipation. IBS may develop after exposure to early life adverse events, sexual abuse, anxiety, depression and stressors. Psychological conditions may also develop as complications of the disease. If left untreated, patients with IBS may progress to develop malnutrition (resulting from food intolerance), impacted bowel, and poor quality of life. Common complications of IBS include dehydration, hemorrhoids and fatigue. Prognosis is good, as IBS does not lead to life threatening complications or shorten lifespan of an affected individual. IBS patients tend to have long symptom free intervals interspersed with periods of severe symptoms. Although Irritable bowel syndrome may be a life-long condition, symptoms can often be improved or relieved through treatment.

    Natural History, Complications, and Prognosis

    Natural History

    Complications

    Complications of irritable bowel syndrome may include:

    Prognosis

    • Prognosis is good, as IBS does not lead to life threatening complications or shorten lifespan of an individual.
    • IBS patients tend to have long symptom free intervals interspersed with periods of severe symptoms.
    • Irritable bowel syndrome may be a life-long condition, but symptoms can often be improved or relieved through treatment.
    • Less than 5 percent of IBS patients develop another gastrointestinal disease.

    References

    1. ↑ 1.0 1.1 Klem F, Wadhwa A, Prokop LJ, Sundt WJ, Farrugia G, Camilleri M, Singh S, Grover M (2017). “Prevalence, Risk Factors, and Outcomes of Irritable Bowel Syndrome After Infectious Enteritis: A Systematic Review and Meta-analysis”. Gastroenterology. 152 (5): 1042–1054.e1. doi:10.1053/j.gastro.2016.12.039. PMID 28069350.
    2. ↑ 2.0 2.1 Hausteiner-Wiehle C, Henningsen P (2014). “Irritable bowel syndrome: relations with functional, mental, and somatoform disorders”. World J. Gastroenterol. 20 (20): 6024–30. doi:10.3748/wjg.v20.i20.6024. PMC 4033442. PMID 24876725.
    3. ↑ 3.0 3.1 Fond G, Loundou A, Hamdani N, Boukouaci W, Dargel A, Oliveira J, Roger M, Tamouza R, Leboyer M, Boyer L (2014). “Anxiety and depression comorbidities in irritable bowel syndrome (IBS): a systematic review and meta-analysis”. Eur Arch Psychiatry Clin Neurosci. 264 (8): 651–60. doi:10.1007/s00406-014-0502-z. PMID 24705634.
    4. ↑ 4.0 4.1 Csef H, Bornhauser N (2003). “[Psychosomatic aspects of chronic diarrhea]”. MMW Fortschr Med (in German). 145 (50): 35–7. PMID 14963969.
    5. ↑ 5.0 5.1 Chakiath RJ, Siddall PJ, Kellow JE, Hush JM, Jones MP, Marcuzzi A, Wrigley PJ (2015). “Descending pain modulation in irritable bowel syndrome (IBS): a systematic review and meta-analysis”. Syst Rev. 4: 175. doi:10.1186/s13643-015-0162-8. PMC 4674951. PMID 26652749.
    6. ↑ 6.0 6.1 Farndale R, Roberts L (2011). “Long-term impact of irritable bowel syndrome: a qualitative study”. Prim Health Care Res Dev. 12 (1): 52–67. doi:10.1017/S1463423610000095. PMID 21426615.
    7. ↑ 7.0 7.1 Lea R, Whorwell PJ (2004). “Psychological influences on the irritable bowel syndrome”. Minerva Med. 95 (5): 443–50. PMID 15467519.
    8. ↑ El-Serag HB, Pilgrim P, Schoenfeld P (2004). “Systemic review: Natural history of irritable bowel syndrome”. Aliment. Pharmacol. Ther. 19 (8): 861–70. doi:10.1111/j.1365-2036.2004.01929.x. PMID 15080847.
    9. ↑ Olafsdottir LB, Gudjonsson H, Jonsdottir HH, Björnsson E, Thjodleifsson B (2012). “Natural history of irritable bowel syndrome in women and dysmenorrhea: a 10-year follow-up study”. Gastroenterol Res Pract. 2012: 534204. doi:10.1155/2012/534204. PMC 3312222. PMID 22474441.
    10. ↑ Halder SL, Locke GR, Schleck CD, Zinsmeister AR, Melton LJ, Talley NJ (2007). “Natural history of functional gastrointestinal disorders: a 12-year longitudinal population-based study”. Gastroenterology. 133 (3): 799–807. doi:10.1053/j.gastro.2007.06.010. PMID 17678917.
    11. ↑ Morley JE, Steinberg KE (2009). “Diarrhea in long-term care: a messy problem”. J Am Med Dir Assoc. 10 (4): 213–7. doi:10.1016/j.jamda.2009.01.007. PMID 19426933.
    12. ↑ Mearin F, Ciriza C, Mínguez M, Rey E, Mascort JJ, Peña E, Cañones P, Júdez J (2016). “Clinical Practice Guideline: Irritable bowel syndrome with constipation and functional constipation in the adult”. Rev Esp Enferm Dig. 108 (6): 332–63. doi:10.17235/reed.2016.4389/2016. PMID 27230827.
    13. ↑ “Definition & Facts of Hemorrhoids | NIDDK”.
    14. ↑ Arora G, Mannalithara A, Mithal A, Triadafilopoulos G, Singh G (2012). “Concurrent conditions in patients with chronic constipation: a population-based study”. PLoS ONE. 7 (10): e42910. doi:10.1371/journal.pone.0042910. PMC 3470567. PMID 23071488.
    15. ↑ Tan KY, Seow-Choen F (2007). “Fiber and colorectal diseases: separating fact from fiction”. World J. Gastroenterol. 13 (31): 4161–7. PMC 4250613. PMID 17696243.
    16. ↑ Helvaci MR, Algin MC, Kaya H (2009). “Irritable bowel syndrome and chronic gastritis, hemorrhoid, urolithiasis”. Eurasian J Med. 41 (3): 158–61. PMC 4261279. PMID 25610094.
    17. ↑ Peery AF, Sandler RS, Galanko JA, Bresalier RS, Figueiredo JC, Ahnen DJ, Barry EL, Baron JA (2015). “Risk Factors for Hemorrhoids on Screening Colonoscopy”. PLoS ONE. 10 (9): e0139100. doi:10.1371/journal.pone.0139100. PMC 4583402. PMID 26406337.
    18. ↑ Han CJ, Yang GS (2016). “Fatigue in Irritable Bowel Syndrome: A Systematic Review and Meta-analysis of Pooled Frequency and Severity of Fatigue”. Asian Nurs Res (Korean Soc Nurs Sci). 10 (1): 1–10. doi:10.1016/j.anr.2016.01.003. PMID 27021828.
    19. ↑ Spiegel BM, Gralnek IM, Bolus R, Chang L, Dulai GS, Mayer EA, Naliboff B (2004). “Clinical determinants of health-related quality of life in patients with irritable bowel syndrome”. Arch. Intern. Med. 164 (16): 1773–80. doi:10.1001/archinte.164.16.1773. PMID 15364671.
    20. ↑ Levy RL, Von Korff M, Whitehead WE, Stang P, Saunders K, Jhingran P, Barghout V, Feld AD (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.
    21. ↑ Olgart LM, Edwall B, Gazelius B (1989). “Neurogenic mediators in control of pulpal blood flow”. J Endod. 15 (9): 409–12. doi:10.1016/S0099-2399(89)80173-6. PMID 2700202.
    22. ↑ Canavan C, West J, Card T (2014). “The epidemiology of irritable bowel syndrome”. Clin Epidemiol. 6: 71–80. doi:10.2147/CLEP.S40245. PMC 3921083. PMID 24523597.
    23. ↑ Briggs A, Yazdany S (1974). “Resistance of Bacillus spores to combined sporicidal treatments”. J. Appl. Bacteriol. 37 (4): 623–31. PMID 4436161.
    24. ↑ Chey WD, Nojkov B, Rubenstein JH, Dobhan RR, Greenson JK, Cash BD (2010). “The yield of colonoscopy in patients with non-constipated irritable bowel syndrome: results from a prospective, controlled US trial”. Am. J. Gastroenterol. 105 (4): 859–65. doi:10.1038/ajg.2010.55. PMC 2887227. PMID 20179696.

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    Diagnosis

    Diagnosis

    History and Symptoms | Physical Examination | Laboratory Findings | X Ray | CT | MRI | Ultrasound | Other Imaging Findings | Other Diagnostic Studies

    Treatment

    Treatment

    Medical Therapy | Monitoring | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy

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