|Functional gastrointestinal disorder|
|Other names||Disorders of gut–brain interaction|
Functional gastrointestinal disorders (FGID), also known as disorders of gut–brain interaction, include a number of separate idiopathic disorders which affect different parts of the gastrointestinal tract and involve visceral hypersensitivity and motility disturbances.
Using the Delphi method, the Rome Foundation and its board of directors, chairs and co-chairs of the ROME IV committees developed the current definition for disorders of gut-brain interaction.
A group of disorders classified by GI symptoms related to any combination of:
Terms such as functional colonic disease (or functional bowel disorder) refer in medicine to a group of bowel disorders which are characterized by chronic abdominal complaints without a structural or biochemical cause that could explain symptoms. Other functional disorders relate to other aspects of the process of digestion.
The consensus review process of meetings and publications organised by the Rome Foundation, known as the Rome process, has helped to define the functional gastrointestinal disorders. Successively, the Rome I, Rome II, Rome III and Rome IV proposed consensual classification system and terminology, as recommended by the Rome Coordinating Committee. These now include classifications appropriate for adults, children and neonates/toddlers.
The current ROME IV classification, published in 2016, is as follows:
A. Esophageal disorders
B. Gastroduodenal disorders
C. Bowel disorders
D. Centrally mediated disorders of gastrointestinal pain
E. Gallbladder and sphincter of Oddi disorders
F. Anorectal disorders
G. Childhood functional GI disorders: Neonate/Toddler
H. Childhood functional GI disorders: Child/Adolescent
FGIDs share in common any of several physiological features including increased motor reactivity, enhanced visceral hypersensitivity, altered mucosal immune and inflammatory function (associated with bacterial dysbiosis), and altered central nervous system and enteric nervous system (CNS-ENS) regulation.
The pathophysiology of FGID has been best conceptualized using biopsychosocial model help to explain the relationships between an individual factors in their early life that in turn can influence their psychosocial factor and physiological functioning. This model also shows the complex interactions between these factors through the brain-gut axis. These factors affect how FGID manifest in terms of symptoms but also affect the clinical outcome. These factors are interconnected and the influences on these factors are bidirectional and mutually interactive.
Early life factors include genetic factors, psychophysiological and sociocultural factors, and environmental exposures.
Psychosocial factors influence the functioning of the GI tract through the brain-gut axis (motility, sensitivity, barrier function). They also affect experience and behavior, treatment selection and the clinical outcome. Psychological stress or one's emotional response to stress exacerbates gastrointestinal symptoms and may contribute to FGID development.
The physiology of 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.
The brain-gut axis is the mechanism in which the psychosocial factors influence the GI tract and vice versa. There is communication between emotional and cognitive centers of the brain to the GI tract and vice versa. Emotions have been shown to stimulate colon motor function and result in decreased colonic transit time, increased contractile activity, the induction of defecation, and symptoms of diarrhea.
Functional gastrointestinal disorders are very common. Globally, irritable bowel syndrome and functional dyspepsia alone may affect 16–26% of the population.
There is considerable research into the causes, diagnosis and treatments for FGIDs. Diet, microbiome, genetics, neuromuscular function and immunological response all interact. A role for mast cell activation has been proposed as one of the factors.
It is well established that mast cell activation can generate epithelial and neuro-muscular dysfunction and promote visceral hypersensitivity and altered motility patterns in FGIDs, postoperative ileus, food allergy and inflammatory bowel disease.
Mast cells and CD3+ T cells are increased in colonic biopsies of patients with IBS vs non-inflamed controls