Etiology

IBS is believed to be a disorder of altered gastrointestinal motility. There are no specific endoscopic, biochemical, anatomic, microbiologic, or histologic findings in IBS that make the etiology clear, although most feel that it is an illness with often multiple contributing causes.

Inflammatory or immune system involvement

The fact that IBS can accompany inflammatory bowel disease, or follow a bout of bacterial or parasitic dysentery, has led to the hypothesis that there may be an inflammatory or immune component to IBS. Subtle changes have been reported in some patients with IBS, including alterations of gut-homing T lymphocytes, and an unexplained increase in mast cells in colonic mucosa.[25][26] However, in patients with IBS alone, mucosal biopsies are generally felt to be normal.

Intestinal microbiota

Intestinal microbiota may play a role in IBS by their actions on certain foods, especially carbohydrates, and also by their effects on epithelial barrier integrity and enteroendocrine signaling. Although an exact microbial signature is uncertain, IBS appears to be associated with dysbiosis and less diversity of the microbiota.[27][28]

Bacterial overgrowth

Bacterial overgrowth has been demonstrated in some patients with IBS, particularly those with diarrhea predominance.[29]

Bile acid malabsorption

There appears to be a subgroup of patients with IBS and diarrhea who have bile acid malabsorption, despite no history of ileal disease, surgery, or previous cholecystectomy.[30]

Psychological stress or abuse

Stress and emotional tension frequently trigger bouts of IBS, although there are no specific personality profiles or psychiatric diagnoses associated with the condition. A history of physical or sexual abuse has been reported in 32% to 44% of patients.[20][21][22] One meta-analysis found that post-traumatic stress disorder (PTSD) is associated with an increased likelihood of IBS (pooled odds ratio 2.80, 95% CI 2.06 to 3.54, P <0.001).[31]

Pathophysiology

Most evidence suggests that there is dysfunction of the motor and sensory aspects of the digestive tract in people with IBS.[32] There is altered gut reactivity (motility and secretion) in response to various stimuli, which may be environmental (personal life stresses or abuse) or luminal (certain foods, bacterial overgrowth or toxins, or gut distension or inflammation). This altered reactivity can lead to pain as well as constipation or diarrhea.

There is evidence that there is gut hypersensitivity with enhanced perception of visceral type pain and sensations.[1] For instance, when a balloon is distended within the lumen of the lower colon or rectum, patients with IBS experience pain at lower pressures compared with people without IBS.[33] People with IBS also have dysregulation of the brain-gut axis. This may be associated with greater stress reactivity and with modulation or perception of afferent signals from the enteric nervous system.[32]

While the histology of the large and small intestinal mucosa is generally felt to be normal, subtle changes, including alterations of gut-homing T lymphocytes and an unexplained increase in mast cells in colonic mucosa, have been reported in patients with IBS.[25][26] These findings suggest possible immune system involvement.

Classification

Rome IV: subtyping IBS by predominant stool pattern[2]​​​[3]

1. IBS with constipation (IBS-C): hard or lumpy stools for ≥25% of bowel movements and loose (mushy) or watery stools for ≤25% of bowel movements.

2. IBS with diarrhea (IBS-D): loose (mushy) or watery stools for ≥25% of bowel movements and hard or lumpy stool for ≤25% of bowel movements.

3. Mixed IBS (IBS-M): hard or lumpy stools for ≤25% of bowel movements and loose (mushy) or watery stools for ≤25% of bowel movements.

4. Unspecified IBS: insufficient abnormality of stool consistency to meet criteria for IBS-C, IBS-D, or IBS-M.

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