BAD on the Runs: Improved Diagnosis of Idiopathic Bile Acid Diarrhea

Camilleri, Michael

doi:10.1007/s10620-021-07044-9

Cited by 1 publication

(2 citation statements)

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“…The strongest evidence regarding the mechanism of idiopathic BAD is the reduced production of FGF‐19 by ileal enterocytes, leading to increased hepatic synthesis of BAs, 20 which is accompanied by increased serum 7α‐C4. The low FGF‐19 may result from reduced FGF‐19 and ASBT mRNA expression in ileal biopsies from patients with BAD, 21 and this has also been confirmed by studies of FGF‐19 protein expression based on immunohistochemistry 22,23 . A second mechanism that probably accounts for <1% of idiopathic BAD results from a mutation in the gene ( SLC10A2 ) for the ileal BA transporter protein, ASBT 24 .…”

Section: Introductionmentioning

confidence: 82%

“…The low FGF-19 may result from reduced FGF-19 and ASBT mRNA expression in ileal biopsies from patients with BAD, 21 and this has also been confirmed by studies of FGF-19 protein expression based on immunohistochemistry. 22,23 A second mechanism that probably accounts for <1% of idiopathic BAD results from a mutation in the gene (SLC10A2) for the ileal BA transporter protein, ASBT. 24 A third potential mechanism is based on associations of genetic variants in GPBAR1 rs11554825, klotho β rs17618244, and FGFR4 rs351855, with acceleration of colonic transit (as a surrogate of diarrhea) in patients presenting with IBS-D or functional diarrhea.…”

Section: Potential Mechanisms Underpinning Idiopathic Bile Acid Diarrheamentioning

confidence: 99%

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Bile Acid Diarrhea in Adults and Adolescents

Camilleri

Nurko

2021

Neurogastroenterology Motil

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Background Bile acids are central to enterohepatic signaling pathways activated through natural receptors, farnesoid X receptor [FXR mediates synthesis of fibroblast growth factor‐19 (FGF‐19)], and G protein‐coupled bile acid receptor 1 (GPBAR1, also known as TGR5). Although bile acid diarrhea (BAD) is more commonly encountered in ileal resection or disease, there is evidence documenting “idiopathic” BAD in about 20% of adolescents and 30% of adults presenting with chronic, non‐bloody diarrhea often attributed to irritable bowel syndrome. Mechanism(s) leading to increased hepatic synthesis and colonic bile acid levels in “idiopathic” BAD include reduced synthesis of FGF‐19 by the ileal mucosa, or genetic variation in hepatocyte proteins klotho β and FGF receptor 4 (FGFR4) that mediate negative feedback of bile acid synthesis. Purpose: The objective of this review is to summarize the diagnosis of BAD in adults and adolescents. In addition to 75SeHCAT retention for diagnosis of BAD, studies have validated fasting serum 7αC4 and FGF‐19, respectively, by‐product and inhibitor of hepatic bile acid synthesis, as well as fecal bile acid measurements. These assays are widely available through reference laboratories, and they are being simplified (eg, measurement of primary fecal bile acids in a random stool sample). BAD has also been identified as a co‐factor contributing to persistent diarrhea in other diseases in remission including inflammatory bowel disease, microscopic colitis, celiac disease, and neuroendocrine tumors. In summary, advances in diagnosis of BAD provide opportunities for generalists and pediatric and adult gastroenterologists to provide targeted treatment for BAD presenting as chronic non‐bloody diarrhea.

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Section: Introductionmentioning

confidence: 82%