Irritable bowel syndrome medical therapy: Difference between revisions

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The fact that patients benefit from probiotics shows that the composition of gut microflora determines IBS.  Administration of probiotics alters metabolism and composition of the microflora and decreases flatulence in patients.There is no treatment for [disease name]; the mainstay of therapy is supportive care.
The fact that patients benefit from probiotics shows that the composition of gut microflora determines IBS.  Administration of probiotics alters metabolism and composition of the microflora and decreases flatulence in patients.There is no treatment for [disease name]; the mainstay of therapy is supportive care.
The important role of psychological therapies that act on cerebral cortical sites and [[antidepressants]] as mainstays of therapy in IBS patients, further throws light on the involvement of the CNS in its pathophysiology. In addition to this, the role of [[Probiotic|probiotics]] in modifying signal processing in the brain also proves that IBS is a brain gut disorder.<ref name="pmid23474283">{{cite journal |vauthors=Tillisch K, Labus J, Kilpatrick L, Jiang Z, Stains J, Ebrat B, Guyonnet D, Legrain-Raspaud S, Trotin B, Naliboff B, Mayer EA |title=Consumption of fermented milk product with probiotic modulates brain activity |journal=Gastroenterology |volume=144 |issue=7 |pages=1394–401, 1401.e1–4 |year=2013 |pmid=23474283 |pmc=3839572 |doi=10.1053/j.gastro.2013.02.043 |url=}}</ref>


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Revision as of 15:06, 30 October 2017

Irritable bowel syndrome Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

[1]

The fact that patients benefit from probiotics shows that the composition of gut microflora determines IBS.  Administration of probiotics alters metabolism and composition of the microflora and decreases flatulence in patients.There is no treatment for [disease name]; the mainstay of therapy is supportive care.

The important role of psychological therapies that act on cerebral cortical sites and antidepressants as mainstays of therapy in IBS patients, further throws light on the involvement of the CNS in its pathophysiology. In addition to this, the role of probiotics in modifying signal processing in the brain also proves that IBS is a brain gut disorder.[2]

OR

Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].

OR

The majority of cases of [disease name] are self-limited and require only supportive care.

OR

[Disease name] is a medical emergency and requires prompt treatment.

OR

The mainstay of treatment for [disease name] is [therapy].

OR   The optimal therapy for [malignancy name] depends on the stage at diagnosis.

OR

[Therapy] is recommended among all patients who develop [disease name].

OR

Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].

OR

Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].

OR

Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].

OR

Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].

Diet therapy

Low FODMAP diet

Low FODMAP diet may help acording to a systematic review of randomized controlled trials[3] and a more recent trial[4]. Included in the systematic review was a trial that combined low FODMAPs and high dietary fiber.[5]

High dietary fiber

High dietary fiber, especially soluble fiber (psyllium or ispaghula husks) can help according to a systematic review of randomized controlled trials.[6] This result is driven by a large randomized controlled trial that directly compared soluble and insoluble fiber.[7]

Medical therapy

Clinical practice guidelines by the American College of Gastroenterology address the treatment of irritable bowel syndrome.[8]

Initial treatments

Medications may consist of stool softeners and laxatives in constipation-predominant IBS, and antidiarrheals (e.g., opioidor opioid analogs such as loperamide, diphenoxylate or codeine in diarrhea-predominant IBS for mild symptoms.[9][10][11]

Laxatives
Main article: laxative

For patients who do not adequately respond to dietary fiber, osmotic agents such as polyethylene glycol, sorbitol, and lactulose can help avoid 'cathartic colon' which has been associated with stimulant laxatives.[12] Among the osmotic laxatives, 17 to 26 grams/day of polyethylene glycol (PEG) has been well studied.

Antispasmodics
Main article: antispasmodic

The use of antispasmodic drugs (e.g. anticholinergics such as hyoscyamine or dicyclomine) may help patients, especially those with cramps or diarrhea. A meta-analysis by the Cochrane Collaboration concludes that if 6 patients are treated with antispasmodics, 1 patient will benefit (number needed to treat = 6).[9] Antispasmodics can be divided in two groups: neurotropics and musculotropics. Neurotropics, such as atropine, act at the nerve fibre of the parasympathicus but also affect other nerves and have side effects. Musculotropics such as mebeverine act directly at the smooth muscle of the gastrointestinal tract, relieving spasm without affecting normal gut motility. Since this action is not mediated by the autonomic nervous system, the usual anticholinergic side effects are absent. Antispasmodic drugs are also available in combination with tranquilizers or barbiturates, such as chlordiazepoxide and Donnatal. The value of the combination therapies has not been established.

Drugs affecting serotonin (5-HT)

Drugs affecting serotonin (5-HT) in the intestines can help reduce symptoms.[13] Serotonin stimulates the gut motility and so agonists can help constipation predominate irritable bowel while antagonists can help diarrhea predominant irritable bowel:

Agonists
  • Tegaserod, a selective 5-HT4 agonist for IBS-C, is available for relieving IBS constipation in women and chronic idiopathic constipation in men and women. On March 30, 2007, the Food and Drug Administration (FDA) requested that Novartis Pharmaceuticals voluntarily discontinue marketing of Zelnorm (tegaserod) based on the recently identified finding of an increased risk of serious cardiovascular adverse events (heart problems) associated with use of the drug. Novartis agreed to voluntarily suspend marketing of the drug in the United States and in many other countries. On July 27, 2007 the Food and Drug Administration (FDA) approved a limited treatment IND program for Zelnorm in the USA to allow restricted access to the medication for patients in need if no comparable alternative drug or therapy is available to treat the disease. The USA FDA had issued two previous warnings about the serious consequences of Tegaserod. In 2005, Tegaserod was rejected as an IBS medication by the European Union. Tegaserod, marketed as Zelnorm in the United States, was the only agent approved to treat the multiple symptoms of IBS (in women only), including constipation, abdominal pain and bloating. A meta-analysis by the Cochrane Collaboration concludes that if 17 patients are treated with typical doses of tegaserod, 1 patient will benefit (number needed to treat = 17).[14]
  • Selective serotonin reuptake inhibitor anti-depressants (SSRIs), because of their serotonergic effect, would seem to help IBS, especially patients who are constipation predominant. Initial crossover studies[15] and randomized controlled trials[16][17][18] support this role.
Antagonists
  • Alosetron, a selective 5-HT3 antagonist for IBS-D, which is only available for women in the United States under a restricted access program, due to severe risks of side-effects if taken mistakenly by IBS-A or IBS-C sufferers.
  • Cilansetron, also a selective 5-HT3 antagonist, is undergoing further clinical studies in Europe for IBS-D sufferers. In 2005, Solvay Pharmaceuticals withdrew Cilansetron from the United States regulatory approval process after receiving a "not approvable" action letter from the FDA requesting additional clinical trials.

Secretagogues (for constipation)

Linaclotide, a guanylate cyclase C agonist, can reduce symptoms according to a systematic review of trials. [19]

Other agents

Anti-depressants include both tricyclic antidepressants (TCAs) and the newer selective serotonin reuptake inhibitors (SSRIs). In addition to improving symptoms via treating any co-existing depression, TCAs have anti-cholinergic actions while SSRIs are serotonergic. Thus in theory, TCAs would best treat diarrhea-predominant IBS while SSRIs would best treat constipation-predominant IBS. A meta-analysis of randomized controlled trials of mainly TCAs found 3 patients have to be treated with TCAs for one patient to improve (number needed to treat = 3).[20] A separate randomized controlled trial found that TCAs are best for patients with diarrhea-predominant IBS.[21]

Recent studies have suggested that rifaximin can be used as an effective treatment for abdominal bloating and flatulence,[22][23] giving more credibility to the potential role of bacterial overgrowth in some patients with IBS.[24]

The multi-herbal extract Iberogast was found to be significantly superior to placebo via both an abdominal pain scale and an IBS symptom score after four weeks of treatment.[25]

Enteric coated peppermint oil capsules has been advocated for IBS symptoms in adults and children;[26] however, results from trials have been inconsistent.[27][28]

For severe diarrhea-predominant IBS, more potent opioids may be used, such as codeine or propoxyphene; refractory cases may even be treated with paregoric, or, more rarely, deodorized tincture of opium or morphine sulfate. The use of opioids remains controversial due to the lack of evidence supporting their benefit and the potential risk of tolerance,physical dependence and addiction.[29]

Cannabis has theoretical support for its role,[30][31] but has not been subject of clinical studies. Although illegal in many counties, it has been prescribed to patients in nations such as Canada. Some of the argued benefits of cannabis are the reduction of pain and nausea, appetite stimulation, and assisting in falling asleep.

Medical Therapy

  • Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].
  • Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].
  • Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].
  • Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].

Disease Name

  • 1 Stage 1 - Name of stage
    • 1.1 Specific Organ system involved 1
      • 1.1.1 Adult
        • Preferred regimen (1): drug name 100 mg PO q12h for 10-21 days (Contraindications/specific instructions)
        • Preferred regimen (2): drug name 500 mg PO q8h for 14-21 days
        • Preferred regimen (3): drug name 500 mg q12h for 14-21 days
        • Alternative regimen (1): drug name 500 mg PO q6h for 7–10 days
        • Alternative regimen (2): drug name 500 mg PO q12h for 14–21 days
        • Alternative regimen (3): drug name 500 mg PO q6h for 14–21 days
      • 1.1.2 Pediatric
        • 1.1.2.1 (Specific population e.g. children < 8 years of age)
          • Preferred regimen (1): drug name 50 mg/kg PO per day q8h (maximum, 500 mg per dose)
          • Preferred regimen (2): drug name 30 mg/kg PO per day in 2 divided doses (maximum, 500 mg per dose)
          • Alternative regimen (1): drug name10 mg/kg PO q6h (maximum, 500 mg per day)
          • Alternative regimen (2): drug name 7.5 mg/kg PO q12h (maximum, 500 mg per dose)
          • Alternative regimen (3): drug name 12.5 mg/kg PO q6h (maximum, 500 mg per dose)
        • 1.1.2.2 (Specific population e.g. 'children < 8 years of age')
          • Preferred regimen (1): drug name 4 mg/kg/day PO q12h（maximum, 100 mg per dose）
          • Alternative regimen (1): drug name 10 mg/kg PO q6h (maximum, 500 mg per day)
          • Alternative regimen (2): drug name 7.5 mg/kg PO q12h (maximum, 500 mg per dose)
          • Alternative regimen (3): drug name 12.5 mg/kg PO q6h (maximum, 500 mg per dose)
    • 1.2 Specific Organ system involved 2
      • 1.2.1 Adult
        • Preferred regimen (1): drug name 500 mg PO q8h
      • 1.2.2 Pediatric
        • Preferred regimen (1): drug name 50 mg/kg/day PO q8h (maximum, 500 mg per dose)
  • 2 Stage 2 - Name of stage
    • 2.1 Specific Organ system involved 1
      Note (1):
      Note (2):
      Note (3):
      • 2.1.1 Adult
        • Parenteral regimen
          • Preferred regimen (1): drug name 2 g IV q24h for 14 (14–21) days
          • Alternative regimen (1): drug name 2 g IV q8h for 14 (14–21) days
          • Alternative regimen (2): drug name 18–24 MU/day IV q4h for 14 (14–21) days
        • Oral regimen
          • Preferred regimen (1): drug name 500 mg PO q8h for 14 (14–21) days
          • Preferred regimen (2): drug name 100 mg PO q12h for 14 (14–21) days
          • Preferred regimen (3): drug name 500 mg PO q12h for 14 (14–21) days
          • Alternative regimen (1): drug name 500 mg PO q6h for 7–10 days
          • Alternative regimen (2): drug name 500 mg PO q12h for 14–21 days
          • Alternative regimen (3):drug name 500 mg PO q6h for 14–21 days
      • 2.1.2 Pediatric
        • Parenteral regimen
          • Preferred regimen (1): drug name 50–75 mg/kg IV q24h for 14 (14–21) days (maximum, 2 g)
          • Alternative regimen (1): drug name 150–200 mg/kg/day IV q6–8h for 14 (14–21) days (maximum, 6 g per day)
          • Alternative regimen (2):  drug name 200,000–400,000 U/kg/day IV q4h for 14 (14–21) days (maximum, 18–24 million U per day) '(Contraindications/specific instructions)'
        • Oral regimen
          • Preferred regimen (1): drug name 50 mg/kg/day PO q8h for 14 (14–21) days (maximum, 500 mg per dose)
          • Preferred regimen (2): drug name (for children aged ≥ 8 years) 4 mg/kg/day PO q12h for 14 (14–21) days (maximum, 100 mg per dose)
          • Preferred regimen (3): drug name 30 mg/kg/day PO q12h for 14 (14–21) days (maximum, 500 mg per dose)
          • Alternative regimen (1): drug name 10 mg/kg PO q6h 7–10 days (maximum, 500 mg per day)
          • Alternative regimen (2): drug name 7.5 mg/kg PO q12h for 14–21 days (maximum, 500 mg per dose)
          • Alternative regimen (3): drug name 12.5 mg/kg PO q6h for 14–21 days (maximum,500 mg per dose)
    • 2.2 Other Organ system involved 2
      Note (1):
      Note (2):
      Note (3):
      • 2.2.1 Adult
        • Parenteral regimen
          • Preferred regimen (1): drug name 2 g IV q24h for 14 (14–21) days
          • Alternative regimen (1): drug name 2 g IV q8h for 14 (14–21) days
          • Alternative regimen (2): drug name 18–24 MU/day IV q4h for 14 (14–21) days
        • Oral regimen
          • Preferred regimen (1): drug name 500 mg PO q8h for 14 (14–21) days
          • Preferred regimen (2): drug name 100 mg PO q12h for 14 (14–21) days
          • Preferred regimen (3): drug name 500 mg PO q12h for 14 (14–21) days
          • Alternative regimen (1): drug name 500 mg PO q6h for 7–10 days
          • Alternative regimen (2): drug name 500 mg PO q12h for 14–21 days
          • Alternative regimen (3):drug name 500 mg PO q6h for 14–21 days
      • 2.2.2 Pediatric
        • Parenteral regimen
          • Preferred regimen (1): drug name 50–75 mg/kg IV q24h for 14 (14–21) days (maximum, 2 g)
          • Alternative regimen (1): drug name 150–200 mg/kg/day IV q6–8h for 14 (14–21) days (maximum, 6 g per day)
          • Alternative regimen (2):  drug name 200,000–400,000 U/kg/day IV q4h for 14 (14–21) days (maximum, 18–24 million U per day)
        • Oral regimen
          • Preferred regimen (1): drug name 50 mg/kg/day PO q8h for 14 (14–21) days (maximum, 500 mg per dose)
          • Preferred regimen (2): drug name 4 mg/kg/day PO q12h for 14 (14–21) days (maximum, 100 mg per dose)
          • Preferred regimen (3): drug name 30 mg/kg/day PO q12h for 14 (14–21) days (maximum, 500 mg per dose)
          • Alternative regimen (1): drug name 10 mg/kg PO q6h 7–10 days (maximum, 500 mg per day)
          • Alternative regimen (2): drug name 7.5 mg/kg PO q12h for 14–21 days (maximum, 500 mg per dose)
          • Alternative regimen (3): drug name 12.5 mg/kg PO q6h for 14–21 days (maximum,500 mg per dose)

References

  1. ↑ Nobaek S, Johansson ML, Molin G, Ahrné S, Jeppsson B (2000). "Alteration of intestinal microflora is associated with reduction in abdominal bloating and pain in patients with irritable bowel syndrome". Am. J. Gastroenterol. 95 (5): 1231–8. doi:10.1111/j.1572-0241.2000.02015.x. PMID 10811333.
  2. ↑ Tillisch K, Labus J, Kilpatrick L, Jiang Z, Stains J, Ebrat B, Guyonnet D, Legrain-Raspaud S, Trotin B, Naliboff B, Mayer EA (2013). "Consumption of fermented milk product with probiotic modulates brain activity". Gastroenterology. 144 (7): 1394–401, 1401.e1–4. doi:10.1053/j.gastro.2013.02.043. PMC 3839572. PMID 23474283.
  3. ↑ Marsh A, Eslick EM, Eslick GD (2016). "Does a diet low in FODMAPs reduce symptoms associated with functional gastrointestinal disorders? A comprehensive systematic review and meta-analysis". Eur J Nutr. 55 (3): 897–906. doi:10.1007/s00394-015-0922-1. PMID 25982757.
  4. ↑ Eswaran SL, Chey WD, Han-Markey T, Ball S, Jackson K (2016). "A Randomized Controlled Trial Comparing the Low FODMAP Diet vs. Modified NICE Guidelines in US Adults with IBS-D". Am J Gastroenterol. doi:10.1038/ajg.2016.434. PMID 27725652.
  5. ↑ Halmos EP, Power VA, Shepherd SJ, Gibson PR, Muir JG (2014). "A diet low in FODMAPs reduces symptoms of irritable bowel syndrome". Gastroenterology. 146 (1): 67–75.e5. doi:10.1053/j.gastro.2013.09.046. PMID 24076059.
  6. ↑ Moayyedi P, Quigley EM, Lacy BE, Lembo AJ, Saito YA, Schiller LR; et al. (2014). "The effect of fiber supplementation on irritable bowel syndrome: a systematic review and meta-analysis". Am J Gastroenterol. 109 (9): 1367–74. doi:10.1038/ajg.2014.195. PMID 25070054. Review in: Ann Intern Med. 2014 Nov 18;161(10):JC10
  7. ↑ Bijkerk CJ, de Wit NJ, Muris JW, Whorwell PJ, Knottnerus JA, Hoes AW (2009). "Soluble or insoluble fibre in irritable bowel syndrome in primary care? Randomised placebo controlled trial". BMJ. 339: b3154. doi:10.1136/bmj.b3154. PMC 3272664. PMID 19713235. Review in: Ann Intern Med. 2010 Jan 19;152(2):JC1-11
  8. ↑ Weinberg DS, Smalley W, Heidelbaugh JJ, Sultan S (2014). "American gastroenterological association institute guideline on the pharmacological management of irritable bowel syndrome". Gastroenterology. 147 (5): 1146–8. doi:10.1053/j.gastro.2014.09.001. PMID 25224526.
  9. ↑ 9.0 9.1 Quartero A, Meineche-Schmidt V, Muris J, Rubin G, de Wit N. "Bulking agents, antispasmodic and antidepressant medication for the treatment of irritable bowel syndrome". Cochrane Database Syst Rev: CD003460. PMID 15846668.
  10. ↑ Lesbros-Pantoflickova D, Michetti P, Fried M, Beglinger C, Blum A (2004). "Meta-analysis: The treatment of irritable bowel syndrome". Aliment Pharmacol Ther. 20 (11–12): 1253–69. PMID 15606387.
  11. ↑ Jailwala J, Imperiale T, Kroenke K (2000). "Pharmacologic treatment of the irritable bowel syndrome: a systematic review of randomized, controlled trials". Ann Intern Med. 133 (2): 136–47. PMID 10896640.
  12. ↑ Joo J, Ehrenpreis E, Gonzalez L, Kaye M, Breno S, Wexner S, Zaitman D, Secrest K (1998). "Alterations in colonic anatomy induced by chronic stimulant laxatives: the cathartic colon revisited". J Clin Gastroenterol. 26 (4): 283–6. PMID 9649012.
  13. ↑ Talley N (2001). "Serotoninergic neuroenteric modulators". Lancet. 358 (9298): 2061–8. PMID 11755632.
  14. ↑ Evans B, Clark W, Moore D, Whorwell P. "Tegaserod for the treatment of irritable bowel syndrome". Cochrane Database Syst Rev: CD003960. PMID 14974049.
  15. ↑ Tack J, Broekaert D, Fischler B, Oudenhove L, Gevers A, Janssens J (2006). "A controlled crossover study of the selective serotonin reuptake inhibitor citalopram in irritable bowel syndrome". Gut. 55 (8): 1095–103. PMID 16401691.
  16. ↑ Vahedi H, Merat S, Rashidioon A, Ghoddoosi A, Malekzadeh R (2005). "The effect of fluoxetine in patients with pain and constipation-predominant irritable bowel syndrome: a double-blind randomized-controlled study". Aliment Pharmacol Ther. 22 (5): 381–5. PMID 16128675.
  17. ↑ Creed F, Fernandes L, Guthrie E, Palmer S, Ratcliffe J, Read N, Rigby C, Thompson D, Tomenson B (2003). "The cost-effectiveness of psychotherapy and paroxetine for severe irritable bowel syndrome". Gastroenterology. 124 (2): 303–17. PMID 12557136.
  18. ↑ Tabas G, Beaves M, Wang J, Friday P, Mardini H, Arnold G (2004). "Paroxetine to treat irritable bowel syndrome not responding to high-fiber diet: a double-blind, placebo-controlled trial". Am J Gastroenterol. 99 (5): 914–20. PMID 15128360.
  19. ↑ Videlock EJ, Cheng V, Cremonini F (2013). "Effects of linaclotide in patients with irritable bowel syndrome with constipation or chronic constipation: a meta-analysis". Clin Gastroenterol Hepatol. 11 (9): 1084–1092.e3, quiz e68. doi:10.1016/j.cgh.2013.04.032. PMID 23644388.
  20. ↑ Jackson J, O'Malley P, Tomkins G, Balden E, Santoro J, Kroenke K (2000). "Treatment of functional gastrointestinal disorders with antidepressant medications: a meta-analysis". Am J Med. 108 (1): 65–72. PMID.
  21. ↑ Drossman D, Toner B, Whitehead W, Diamant N, Dalton C, Duncan S, Emmott S, Proffitt V, Akman D, Frusciante K, Le T, Meyer K, Bradshaw B, Mikula K, Morris C, Blackman C, Hu Y, Jia H, Li J, Koch G, Bangdiwala S (2003). "Cognitive-behavioral therapy versus education and desipramine versus placebo for moderate to severe functional bowel disorders". Gastroenterology. 125 (1): 19–31. PMID.
  22. ↑ Sharara AI, Aoun E, Abdul-Baki H, Mounzer R, Sidani S, Elhajj I (2006). "A randomized double-blind placebo-controlled trial of rifaximin in patients with abdominal bloating and flatulence". Am J Gastroenterol. 101 (2): 326–33. PMID.
  23. ↑ Pimentel M, Park S, Mirocha J, Kane S, Kong Y (2006). "The effect of a nonabsorbed oral antibiotic (rifaximin) on the symptoms of the irritable bowel syndrome: a randomized trial". Ann Intern Med. 145 (8): 557–63. PMID.
  24. ↑ Quigley EM (2006). "Germs, gas and the gut; the evolving role of the enteric flora in IBS". Am J Gastroenterol. 101 (2): 334–5. PMID.
  25. ↑ Madisch A, Holtmann G, Plein K, Holz J (2004). "Treatment of irritable bowel syndrome with herbal preparations: results of a double-blind, randomized, placebo-controlled, multi-centre trial". Aliment Pharmacol Ther. 19: 271&ndash, 9.
  26. ↑ Hadley SK, Gaarder SM (2005). "Treatment of irritable bowel syndrome". Am Fam Physician. 72 (12): 2501–6. PMID.
  27. ↑ Nash P, Gould S, Bernardo D (1986). "Peppermint oil does not relieve the pain of irritable bowel syndrome". Br J Clin Pract. 40 (7): 292–3. PMID.
  28. ↑ Liu J, Chen G, Yeh H, Huang C, Poon S (1997). "Enteric-coated peppermint-oil capsules in the treatment of irritable bowel syndrome: a prospective, randomized trial". J Gastroenterol. 32 (6): 765–8. PMID.
  29. ↑ Warfield, Carol A. (2003). Principles and Practice of Pain Medicine. McGraw-Hill Professional. ISBN 0071443495. Unknown parameter |coauthors= ignored (help)
  30. ↑ Massa F, Storr M, Lutz B (2005). "The endocannabinoid system in the physiology and pathophysiology of the gastrointestinal tract". J Mol Med. 83 (12): 944–54. PMID.
  31. ↑ Russo E. "Clinical endocannabinoid deficiency (CECD): can this concept explain therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions?". Neuro Endocrinol Lett. 25 (1–2): 31–9. PMID.

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