Category:IBS treatments

An IBS treatment is a medicine used to manage irritable bowel syndrome, the functional gastrointestinal disorder characterised by chronic abdominal pain associated with altered bowel habit in the absence of structural pathology. The contemporary diagnostic framework, Rome IV (2016), subdivides IBS by predominant bowel pattern: IBS-D (diarrhoea-predominant), IBS-C (constipation-predominant), IBS-M (mixed), and IBS-U (unsubtyped). The pharmacological strategy follows the subtype.

The clinical history of irritable bowel syndrome predates its name; the condition was described by Powell in 1820 as "mucous colitis" and by Cumming in 1849 as a condition in which "the bowels are at one time constipated, at another lax". The modern concept of IBS as a brain-gut-axis disorder, integrating visceral hypersensitivity, motility disturbance, low-grade mucosal immune activation, and a substantial psychological-stress contribution, has emerged from a hundred and fifty years of clinical observation and the past three decades of brain-imaging, visceral-physiology, and microbiome research.

The medicines for IBS divide into several categories. The smooth-muscle antispasmodics (dicyclomine, hyoscyamine, mebeverine in Europe, otilonium and pinaverium in Europe and South America) act on intestinal smooth muscle to reduce the post-prandial colonic spasm that drives a substantial fraction of IBS pain. Peppermint oil in enteric-coated capsules acts by similar smooth-muscle relaxation through L-type calcium channel blockade and has substantial controlled-trial evidence for both pain and bloating in IBS.

For IBS with diarrhoea (IBS-D), the symptomatic medicines are the gut-restricted opioid agonist loperamide (cross-listed under antidiarrheals and opioid receptor agonists; reduces stool frequency without systemic opioid effect), the bile-acid sequestrants (cholestyramine, colesevelam) in patients with documented bile-acid diarrhoea (approximately a quarter of IBS-D cases on dedicated testing), and the 5-HT3 antagonist alosetron (Lotronex, GSK 2000, restricted to women with severe IBS-D after withdrawal in 2000 for ischaemic colitis and reintroduction 2002 under a restricted-distribution program). The mu-opioid agonist / delta-antagonist eluxadoline (Viberzi, Allergan 2015) is approved for IBS-D with the caveat of pancreatitis risk in patients without a gallbladder or with prior pancreatitis. The non-absorbable rifaximin (Salix/Bausch, IBS-D approval 2015 after the TARGET-3 trial) is a gut-restricted antibacterial that improves IBS-D symptoms by an incompletely understood mechanism, presumed to involve modification of the small-intestinal microbiome.^[1]

For IBS with constipation (IBS-C), the symptomatic medicines include the standard osmotic laxatives (polyethylene glycol; cross-listed under osmotic laxatives), the chloride channel activator lubiprostone (Amitiza, Sucampo 2008, opens the type-2 chloride channel in the intestinal epithelium and increases intestinal fluid secretion), the guanylate cyclase C agonists linaclotide (Linzess, Ironwood/AbbVie 2012) and plecanatide (Trulance, Salix 2017) that activate the same target as the heat-stable enterotoxin of E. coli (the natural ligand of the receptor on the intestinal epithelium), and the more recent sodium-hydrogen exchanger inhibitor tenapanor (Ibsrela, Ardelyx 2019) which reduces intestinal sodium absorption and so increases luminal water. The serotonin 5-HT4 agonist tegaserod (Zelnorm, Novartis 2002, withdrawn 2007 for cardiovascular signal, reintroduced 2019 for women under age 65) and prucalopride (Resotran/Motegrity, Shire/Takeda 2018 in U.S., earlier in Europe) act on intestinal motility through enteric-nervous-system serotonergic signaling and are alternatives.

The pain and psychiatric components of IBS are addressed by the low-dose tricyclic antidepressants (amitriptyline, nortriptyline, imipramine, desipramine at 10-50 mg at bedtime, well below antidepressant doses) and the SNRIs (duloxetine, venlafaxine), used for central pain modulation and the visceral-hypersensitivity component. SSRIs are useful in IBS with psychiatric comorbidity but their efficacy on bowel symptoms alone is limited. The newer fixed-combination clidinium-chlordiazepoxide (an antimuscarinic plus benzodiazepine) is sometimes prescribed for refractory pain but its benzodiazepine component has restricted contemporary use.

The non-pharmacological foundation of IBS management, the low-FODMAP diet developed by Sue Shepherd and colleagues at Monash University in the 2000s, is a substantial therapeutic intervention in its own right and is the only intervention with consistent superior outcomes to placebo across multiple trials. Cognitive-behavioural therapy, gut-directed hypnotherapy, and the recent dietary-and-cognitive-mechanism digital therapeutics (Mahana IBS, the prescription-app approved by the FDA in 2020) extend the non-pharmacological toolkit. The contemporary clinical approach combines a subtype-specific pharmacological strategy with low-FODMAP elimination and reintroduction, with cognitive-behavioural therapy or gut-directed hypnotherapy for patients with substantial psychological-stress contribution, and with the underlying recognition that IBS is a chronic disease in which symptom control rather than cure is the realistic goal.

By subtype and target:

• Antispasmodics:
  • Antimuscarinics (cross-indexed under antimuscarinics): dicyclomine, hyoscyamine
  • Calcium channel blockers (smooth-muscle-selective, primarily European): mebeverine, otilonium, pinaverium
  • Peppermint oil (enteric-coated): IBgard, Pepogest
• IBS-D specific:
  • Loperamide (gut-restricted opioid; OTC)
  • Alosetron (5-HT3 antagonist; restricted distribution)
  • Eluxadoline (mu-agonist / delta-antagonist; pancreatitis caution)
  • Rifaximin (gut-restricted antibacterial; cross-indexed under antibacterials)
  • Bile-acid sequestrants: cholestyramine, colesevelam (in bile-acid diarrhoea)
• IBS-C specific:
  • Osmotic laxatives (cross-indexed under osmotic laxatives): polyethylene glycol, lactulose, magnesium-containing
  • Chloride channel activator: lubiprostone (Amitiza)
  • Guanylate cyclase C agonists: linaclotide (Linzess), plecanatide (Trulance)
  • Sodium-hydrogen exchanger 3 inhibitor: tenapanor (Ibsrela)
  • 5-HT4 agonists: tegaserod (Zelnorm; restricted), prucalopride (Motegrity)
• Pain and central modulation:
  • Tricyclic antidepressants (low-dose): amitriptyline, nortriptyline, imipramine, desipramine
  • SNRIs: duloxetine, venlafaxine
  • SSRIs (for IBS with psychiatric comorbidity)
  • Pregabalin (visceral hypersensitivity)
• Adjunctive:
  • Probiotics (selected strains with positive trial data, including Bifidobacterium infantis 35624; evidence variable)
  • Soluble fibre (psyllium for IBS-C; insoluble fibre worsens symptoms)

The boundary of this category is "medicine used in the management of irritable bowel syndrome." The medicines used in inflammatory bowel disease are listed under IBD medications separately, despite the symptomatic overlap. The medicines used in diverticular disease (antibacterials for diverticulitis; fibre for diverticulosis prevention) are not in this category. The medicines used in chronic idiopathic constipation (the same lubiprostone, linaclotide, plecanatide, prucalopride, tenapanor, also approved in non-IBS chronic constipation) are cross-listed but their indication-specific approvals differ. The non-pharmacological interventions (low-FODMAP diet, cognitive-behavioural therapy, gut-directed hypnotherapy, the digital therapeutics) are foundational to IBS management but not medicines and are mentioned only for clinical-decision context.

This category page is an encyclopedia article about its subject. The actual index of medicines belonging to the category is generated automatically by the wiki engine, from category-membership declarations on the individual medicine pages, and appears at the foot of the page below the references.