Agents that relax and loosen the bowels and stools
"Purgative" redirects here. For other uses, seePurgation.
Glycerin suppositories used as laxatives.
Laxatives,purgatives, oraperients are substances that loosenstools[1] and increasebowel movements. They are used to treat and preventconstipation.
Laxatives vary as to how they work and the side effects they may have. Certainstimulant,lubricant, andsaline laxatives are used to evacuate thecolon forrectal and bowel examinations, and may be supplemented byenemas under certain circumstances. Sufficiently high doses of laxatives may causediarrhea. Some laxatives combine more than one active ingredient, and may be administeredorally orrectally.
Emollient laxatives, also known as stool softeners, areanionic surfactants that enable additional water and fats to be incorporated in the stool, making movement through the bowels easier.
Lubricant laxatives are substances that coat the stool with slippery lipids and decrease colonic absorption of water so the stool slides through the colon more easily. Lubricant laxatives also increase the weight of stool and decrease intestinal transit time.[9]
Mineral oils, such asliquid paraffin, are generally the only nonprescription lubricant laxative available, but due to the risk of lipid pneumonia resulting from accidental aspiration, mineral oil is not recommended, especially in children and infants.[10][11] Mineral oil may decrease the absorption of fat-soluble vitamins and some minerals.[9]
Hyperosmotic laxatives cause the intestines to hold more water, creating anosmotic gradient, which adds more pressure and stimulates bowel movement.[12][10]
Properties
Site of action: colon
Onset of action: 12–72 hours (oral), 0.25–1 hour (rectal)
Lactulose works by theosmotic effect, which retains water in the colon; lowering thepH through bacterial fermentation to lactic, formic, and acetic acids; and increasing colonicperistalsis. Lactulose is also indicated inportal-systemic encephalopathy. Glycerin suppositories work mostly by hyperosmotic action, but thesodium stearate in the preparation also causes local irritation to the colon.[citation needed]
Saline laxatives are nonabsorbable, osmotically active substances that attract and retain water in the intestinal lumen, increasing intraluminal pressure that mechanically stimulates evacuation of the bowel. Magnesium-containing agents also cause the release ofcholecystokinin, which increases intestinal motility and fluid secretion.[3] Saline laxatives may alter a patient's fluid and electrolyte balance.
Properties
Site of action: small and large intestines
Onset of action: 0.5–3 hours (oral), 2–15 minutes (rectal)
Stimulant laxatives are substances that act on the intestinalmucosa ornerve plexus, altering water andelectrolyte secretion.[13] They also stimulate peristaltic action and can be dangerous under certain circumstances.[14]
Prolonged use of stimulant laxatives can create drug dependence by damaging the colon'shaustral folds, making users less able to move feces through their colon on their own. A study of patients with chronic constipation found that 28% of chronic stimulant laxative users lost haustral folds over the course of one year, while none of the control group did.[15]
These are motility stimulants that work through activation of5-HT4 receptors of theenteric nervous system in thegastrointestinal tract. However, some have been discontinued or restricted due to potentially harmful cardiovascular side effects.
Tegaserod (brand nameZelnorm) was removed from the general U.S. and Canadian markets in 2007, due to reports of increased risks of heart attack or stroke. It is still available to physicians for patients in emergency situations that are life-threatening or require hospitalization.[16]
Prucalopride (brand name Resolor) is a current drug approved for use in the EU since October 15, 2009,[17] in Canada (brand name Resotran) since December 7, 2011,[18] and in the United States since December 2018.
Lubiprostone is used in the management of chronic idiopathic constipation and irritable bowel syndrome. It causes the intestines to produce a chloride-rich fluid secretion that softens the stool, increases motility, and promotes spontaneous bowel movements.
For adults, arandomized controlled trial foundPEG (MiraLax or GlycoLax) 17 grams once per day to be superior totegaserod at 6 mg twice per day.[21] A randomized controlled trial found greater improvement from two sachets (26 g) of PEG versus two sachets (20 g) of lactulose.[22] 17 g per day of PEG has been effective and safe in a randomized, controlled trial for six months.[23] Another randomized, controlled trial found no difference between sorbitol and lactulose.[24]
For children, PEG was found to be more effective than lactulose.[25]
Although some patients with eating disorders such asanorexia nervosa andbulimia nervosa abuse laxatives in an attempt to lose weight, laxatives act to speed up the transit of feces through the large intestine, which occurs after the absorption of nutrients in the small intestine is already complete. Thus, studies of laxative abuse have found that effects on body weight reflect primarily temporary losses of body water rather than energy (calorie) loss.[26][31][32]
Physicians warn against the chronic use of stimulant laxatives due to concern that chronic use could cause the colonic tissues to get worn out over time and not be able to expel feces due to long-term overstimulation.[33] A common finding in patients having used stimulant laxatives is a brown pigment deposited in the intestinal tissue, known asmelanosis coli.[citation needed]
^abcdef"Constipation"(PDF).www.digestive.niddk.nih.gov. National Digestive Diseases Information Clearinghouse. Archived fromthe original(PDF) on May 15, 2012. Retrieved3 November 2014.
^Bulk-forming agent entry in the public domain NCI Dictionary of Cancer Terms
^abcdefghBerardi M, Tietze KJ, Shimp LA, Rollins CJ, Popovich NG (2006).Handbook of Nonprescription Drugs (15th ed.). Washington, D.C.: American Pharmaceutical Association.ISBN978-1582120744.
^abc"The Facts About Fiber"(PDF).www.aicr.org. American Institute for Cancer Research. Archived fromthe original(PDF) on 3 November 2014. Retrieved3 November 2014.
^Stacewicz-Sapuntzakis M, Bowen PE, Hussain EA, Damayanti-Wood BI, Farnsworth NR (2001). "Chemical composition and potential health effects of prunes: a functional food?".Critical Reviews in Food Science and Nutrition.41 (4):251–86.doi:10.1080/20014091091814.PMID11401245.S2CID31159565.
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^Di Palma JA, Cleveland MV, McGowan J, Herrera JL (2007). "A randomized, multicenter comparison of polyethylene glycol laxative and tegaserod in treatment of patients with chronic constipation".Am. J. Gastroenterol.102 (9):1964–71.doi:10.1111/j.1572-0241.2007.01365.x.PMID17573794.S2CID32055676.
^Dipalma JA, Cleveland MV, McGowan J, Herrera JL (2007). "A randomized, multicenter, placebo-controlled trial of polyethylene glycol laxative for chronic treatment of chronic constipation".Am. J. Gastroenterol.102 (7):1436–41.doi:10.1111/j.1572-0241.2007.01199.x.PMID17403074.S2CID10946562.
^Lederle FA, Busch DL, Mattox KM, West MJ, Aske DM (1990). "Cost-effective treatment of constipation in the elderly: a randomized double-blind comparison of sorbitol and lactulose".Am J Med.89 (5):597–601.doi:10.1016/0002-9343(90)90177-F.PMID2122724.
^Oster JR, Materson BJ, Rogers AI (November 1980). "Laxative abuse syndrome".Am. J. Gastroenterol.74 (5):451–8.PMID7234824.
^Lacey JH, Gibson E (1985). "Controlling weight by purgation and vomiting: A comparative study of bulimics".Journal of Psychiatric Research.19 (2–3):337–341.doi:10.1016/0022-3956(85)90037-8.PMID3862833.
^Joo JS, Ehrenpreis ED, Gonzalez L, Kaye M, Breno S, Wexner SD, Zaitman D, Secrest K (June 1998). "Alterations in colonic anatomy induced by chronic stimulant laxatives: the cathartic colon revisited".Journal of Clinical Gastroenterology.26 (4):283–6.doi:10.1097/00004836-199806000-00014.PMID9649012.
^Stolberg, Michael (2003). "[The miraculous effects of taking laxatives. Success and failure of pre-modern medical treatment from the patients' perspective]".Wurzburger Medizinhistorische Mitteilungen.22:167–177.ISSN0177-5227.PMID15641192.