title: Conjugated bile acid replacement therapy reduces urinary oxalate excretion in short bowel syndrome.
abstract: BACKGROUND
  Patients with short bowel syndrome (SBS) have steatorrhea, in part because of bile acid malabsorption that causes decreased bile acid secretion into the duodenum and consequent fat maldigestion. In SBS patients with colon in continuity, luminal calcium forms calcium fatty acid soaps rather than precipitating as insoluble calcium oxalate. Soluble oxalate is hyperabsorbed by the colon leading to hyperoxaluria and an increased risk for renal calcium oxalate stones and deposits. The authors hypothesized that oral ingestion of conjugated bile acids would increase fat absorption and thereby decrease calcium fatty acid soap formation and oxalate hyperabsorption.
  
  
  METHODS
  The effect of conjugated bile acid replacement therapy (9 g/d) on fecal fat excretion and urine oxalate excretion was measured in an appropriate patient, utilizing the metabolic balance technique. The effects of chronic bile acid replacement therapy on oxalate excretion and nutritional status also were measured in a 3-month outpatient study.
  
  
  RESULTS
  Natural conjugated bile acid replacement therapy reduced fecal fat excretion from 119 to 79 g/d (Delta40 g/d), and urinary oxalate excretion from 87 to 64 mg/d (966 to 710 micromol/d; Delta23 mg/d). Cholylsarcosine, a synthetic conjugated bile acid, had similar but less powerful effects. During a 3-month outpatient trial of natural conjugated bile acids (9 g/d), urine oxalate decreased to normal levels (27 mg/d) in association with weight gain, decreased hunger, and decreased hyperphagia.
  
  
  CONCLUSIONS
  Conjugated bile acid replacement therapy reduced fecal fat excretion, reduced urinary oxalate excretion, and improved nutritional status in a patient with SBS with colon in continuity, hyperoxaluria, and oxalate nephrolithiasis.
authors.affiliation: Department of Internal Medicine, Baylor University Medical Center, Dallas, TX 75246, USA. m.emmett@baylorhealth.edu
authors.forename: Michael
authors.initials: M
authors.lastname: Emmett
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Guirl
authors.forename: Carol A
authors.initials: CA
authors.lastname: Santa Ana
authors.forename: Jack L
authors.initials: JL
authors.lastname: Porter
authors.forename: Sidney
authors.initials: S
authors.lastname: Neimark
authors.forename: Alan F
authors.initials: AF
authors.lastname: Hofmann
authors.forename: John S
authors.initials: JS
authors.lastname: Fordtran
mesh_terms: D000284:Administration, Oral; D000368:Aged; D000818:Animals; D002129:Calcium Oxalate / Q000652:urine*; D002417:Cattle; D002446:Celiac Disease / Q000178:diet therapy / Q000188:drug therapy / Q000378:metabolism / Q000652:urine; D002793:Cholic Acids / Q000008:administration & dosage / Q000627:therapeutic use*; D005243:Feces / Q000737:chemistry; D006801:Humans; D006959:Hyperoxaluria / Q000178:diet therapy / Q000188:drug therapy*; D008297:Male; D010045:Outpatients; D012521:Sarcosine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use*; D012778:Short Bowel Syndrome / Q000178:diet therapy / Q000188:drug therapy* / Q000378:metabolism / Q000652:urine; D014556:Urine / Q000737:chemistry
chemical_list: D002793:Cholic Acids; D002129:Calcium Oxalate; C061997:cholylsarcosine; D012521:Sarcosine