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Stool osmotic gap

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(Redirected fromStool osmolal gap)

Stool osmotic gap is a measurement of the difference in solute types betweenserum andfeces, used to distinguish among different causes ofdiarrhea.

Feces is normally in osmotic equilibrium with blood serum, which the human body maintains between 290–300 mOsm/kg.[1] However, the solutes contributing to this total differ. Serum is mostlysodium andpotassium salts (as reflected in the formulas for serumosmol gap andanion gap), while the digestive tract contains significant amounts of othercompounds. Stool osmotic gap is a measure of the concentration of those other compounds.[citation needed]

Stool osmotic gap is calculated as 290 mOsm/kg − 2 × (stool Na + stool K).[2] 290 mOsm/kg is the presumed stool osmolality, and the measured concentration of sodium and potassiumcations is doubled to account for the correspondinganions which must be present.[citation needed]

A normal gap is between 50 and 100 mOsm/kg,[3] corresponding to the concentration of other solutes such asmagnesium salts and sugars.[citation needed]

A low stool osmotic gap suggests secretory diarrhea, wherein the digestive tract is hyperpermeable and losing electrolytes, while a high gap suggests osmotic diarrhea, wherein the digestive tract is unable to absorb solutes from thechyme, either because the digestive tract is hypopermeable (e.g. due toinflammation), or non-absorbable compounds (e.g.Epsom salt) are present.[4] The reason for this is that secreted sodium and potassium ions make up a greater percentage of the stool osmolality in secretory diarrhea, whereas in osmotic diarrhea, other molecules such as unabsorbed carbohydrates are more significant contributors to stool osmolality.[citation needed]

High osmotic gap (>100 mOsm/kg) causes of osmotic diarrhea include celiac sprue, chronic pancreatitis, lactase deficiency,lactulose, osmotic laxative use/abuse, andWhipple's disease.[citation needed]

Low osmotic gap (<50 mOsm/kg) causes of secretory diarrhea include toxin-mediated causes (cholera, enterotoxigenic strains ofE. coli) and secretagogues such asvasoactive intestinal peptide (from aVIPoma, for example). Uncommon causes includegastrinoma,medullary thyroid carcinoma (which produces excesscalcitonin),factitious diarrhea from non-osmoticlaxative abuse[5] andvillous adenoma.[citation needed]

References

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  1. ^Topazian M, Binder HJ (May 1994)."Brief report: factitious diarrhea detected by measurement of stool osmolality".N. Engl. J. Med.330 (20):1418–9.doi:10.1056/NEJM199405193302004.PMID 8159195.
  2. ^Greenberger, Norton J."Diarrhea: Approach to the Patient With Lower GI Complaints".Merck Manual Professional. Retrieved2009-04-10.
  3. ^Ghosh, Amit K.; Habermann, Thomas (2007).Mayo Clinic Internal Medicine Concise Textbook. Informa Healthcare. p. 228.ISBN 978-1-4200-6749-1.
  4. ^Shiau YF, Feldman GM, Resnick MA, Coff PM (June 1985). "Stool electrolyte and osmolality measurements in the evaluation of diarrheal disorders".Ann. Intern. Med.102 (6):773–5.doi:10.7326/0003-4819-102-6-773.PMID 3994188.
  5. ^Oster, JR; Materson, BJ; Rogers, AI (1980). "Laxative abuse syndrome".The American Journal of Gastroenterology.74 (5):451–8.PMID 7234824.

Further reading

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  • Duncan, A; Robertson, C; Russell, RI (April 1992). "The fecal osmotic gap: technical aspects regarding its calculation".The Journal of Laboratory and Clinical Medicine.119 (4):359–63.PMID 1583385.
  • Eherer, Andreas J.; Fordtran, John S. (August 1992). "Fecal osmotic gap and pH in experimental diarrhea of various causes".Gastroenterology.103 (2):545–551.doi:10.1016/0016-5085(92)90845-P.PMID 1634072.
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