Rome criteria

The Rome criteria are an international effort to create scientific data to help in the diagnosis and treatment of functional gastrointestinal disorders, such as irritable bowel syndrome, functional dyspepsia and rumination syndrome. 

The Rome Foundation process is an international effort to create scientific data to help in the diagnosis and treatment of functional gastrointestinal disorders, also known as disorders of gut-brain interaction.


The Rome diagnostic criteria are set forth by Rome Foundation.



The Rome criteria have been evolving from the first set of criteria issued in 1989.



The Rome IV update covers epidemiology, pathophysiology, psychosocial and clinical features, and diagnostic evaluation and treatment recommendations for 33 adult and 17 pediatric functional gastrointestinal disorders.



Disorders classified by GI symptoms related to any combination of:



Motility disturbance



Visceral hypersensitivity



Altered mucosal and immune function



Altered gut microbiota



Altered central nervous system (CNS) processing



A Multidimensional Clinical Profile (MDCP) system has been created that incorporates the diagnostic criteria with additional clinical, quality of life, psychosocial, and physiological parameters to create an individualized treatment plan.



In Rome IV, the classification moved from a physiologically based classification to a symptom-based classification, 


and organ regions.



Rome criteria are updated every 6–10 years.



The current Rome IV classification, published in 2016:



A. Esophageal Disorders



A1. Functional chest pain


A2. Functional heartburn


A3. Reflux hypersensitivity


A4. Globus


A5. Functional dysphagia


B. Gastroduodenal Disorders



B1. Functional dyspepsia


B1a. Postprandial distress syndrome (PDS)


B1b. Epigastric pain syndrome (EPS)


B2. Belching disorders


B2a. Excessive supragastric belching


B2b. Excessive gastric belching


B3. Nausea and vomiting disorders


B3a. Chronic nausea vomiting syndrome (CNVS)


B3b. Cyclic vomiting syndrome (CVS)


B3c. Cannabinoid hyperemesis syndrome (CHS)


B4. Rumination syndrome


C. Bowel Disorders



C1. Irritable bowel syndrome (IBS)


IBS with predominant constipation (IBS-C)


IBS with predominant diarrhea (IBS-D)


IBS with mixed bowel habits (IBS-M)


IBS unclassified (IBS-U)


C2. Functional constipation


C3. Functional diarrhea


C4. Functional abdominal bloating/distension


C5. Unspecified functional bowel disorder


C6. Opioid-induced constipation


D. Centrally Mediated Disorders of Gastrointestinal Pain



D1. Centrally mediated abdominal pain syndrome (CAPS)


D2. Narcotic bowel syndrome (NBS)/ Opioid-induced GI hyperalgesia


E. Gallbladder and Sphincter of Oddi disorders



E1. Biliary pain


E1a. Functional gallbladder disorder


E1b. Functional biliary sphincter of Oddi disorder


E2. Functional pancreatic sphincter of Oddi disorder


F. Anorectal Disorders



F1. Fecal incontinence


F2. Functional anorectal pain


F2a. Levator ani syndrome


F2b. Unspecified functional anorectal pain


F2c. Proctalgia fugax


F3. Functional defecation disorders


F3a. Inadequate defecatory propulsion


F3b. Dyssynergic defecation


G. Childhood Functional GI Disorders: Neonate/Toddler



G1. Infant regurgitation


G2. Rumination syndrome


G3. Cyclic vomiting syndrome (CVS)


G4. Infant colic


G5. Functional diarrhea


G6. Infant dyschezia


G7. Functional constipation


H. Childhood Functional GI Disorders: Child/Adolescent



H1. Functional nausea and vomiting disorders


H1a. Cyclic vomiting syndrome (CVS)


H1b. Functional nausea and functional vomiting


H1b1. Functional nausea


H1b2. Functional vomiting


H1c. Rumination syndrome


H1d. Aerophagia


H2. Functional abdominal pain disorders


H2a. Functional dyspepsia


H2a1. Postprandial distress syndrome


H2a2. Epigastric pain syndrome


H2b. Irritable bowel syndrome (IBS)


H2c. Abdominal migraine


H2d. Functional abdominal pain ‒ NOS


H3. Functional defecation disorders


H3a. Functional constipation


H3b. Nonretentive fecal incontinence



Functional gastrointestinal disorders share in common any of several physiological features including: increased motor reactivity, enhanced visceral hypersensitivity, altered mucosal immune and inflammatory function, and altered central nervous system and enteric nervous system regulation.



These interactions between these factors occur through the brain-gut axis.



These factors affect how the FGID manifests in terms of symptoms but also affect the clinical outcome. 



These factors are interconnected and are bidirectional and mutually interactive.



Polymorphisms and genes predisposing individuals to develop FGID: alpha-2 adrenergic and 5-HT receptors; serotonin and norepinephrine transporters, inflammatory markers interleukin-(IL)10, tumor necrosis factor-(TNF) alpha, and TNF super family member 15 (TNF-SF15); intracellular cell signaling G proteins; and ion channels.



The expression of a FGID requires the influence of additional environmental exposures such as infection, and psychophysiological factors, that affect the expression of these genes, leading to symptoms production associated with FGID.



Certain sociocultural factors and family interactions shape reporting of symptoms, the development of FGIDs, and health care seeking. 



Cultural expression of pain varies: ranging from  denial of symptoms to dramatic expression.



Certain environmental exposures are related to the development of FGIDs: 


childhood salmonella infection can be a risk factor for IBS in adulthood.



Psychosocial factors influence the functioning of the GI tract through the brain-gut axis.



G.I. motility, sensitivity, barrier functions affect behavior, treatment plans and the clinical outcome in FGIDs.



FGID is characterized by abnormal motility, visceral hypersensitivity as well as dysregulation of the immune system and barrier function of the GI tract as well as inflammatory changes.



Psychological disstress and emotional response to stress exacerbates gastrointestinal symptoms and may contribute to FGID development.



Altered muscle contractility and tone, bowel compliance, and transit time may contribute to many of the gastrointestinal symptoms of FGID



Visceral hypersensitivity may be associated with FGID with lowered pain threshold for balloon distension of the bowel, or increased sensitivity even to normal intestinal function.



Postinfectious IBS have associated that factors such as mucosal membrane permeability, the intestinal flora, and altered mucosal immune function lead to visceral hypersensitivity. 



Visceral hypersensitivity factors include  genetics, psychological stress, and altered receptor sensitivity at the gut mucosa and myenteric plexus, which are enabled by mucosal immune dysfunction.



Microorganisms play a role in the brain-gut axis.



The bacterial composition of the gastrointestinal tract in IBS patient differs from healthy individuals.



The types of food consumed and diet consumed plays a role in the manifestation of FGID and intestinal microbiota.



Specific diets:  low FODMAP—fermentable oligo-, di-, and monosaccharides and polyols, or gluten restriction in some patients may help and reduce the symptom burden in FGID. 



No one diet has been shown to be recommended for all people with FGID.



The brain-gut axis is the mechanism in which the psychosocial factors influence the GI tract and vice versa. 



Emotional responses stimulate colon motor function and result in decreased colonic transit time, increased contractile activity, the induction of defecation, and symptoms of diarrhea.



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