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.