Rotor Syndrome: Glucuronidated Bile Acidemia From Defective Reuptake by Hepatocytes-Reference-Cited by-同舟云学术

Rotor Syndrome: Glucuronidated Bile Acidemia From Defective Reuptake by Hepatocytes

Published:2020-12-31 Issue:4 Volume:5 Page:629-633
ISSN:2471-254X
Container-title:Hepatology Communications
language:en
Short-container-title:Hepatol Commun

Author:

Kimura Akihiko¹²,Kagawa Tatehiro³,Takei Hajime²,Maruo Yoshihiro⁴,Sakugawa Hiroshi⁵,Sasaki Takahiro⁶,Murai Tsuyoshi⁶,Naritaka Nakayuki²,Takikawa Hajime⁷,Nittono Hiroshi²

Affiliation:

1. Department of Pediatrics and Child Health Kurume University School of Medicine Kurume Japan

2. Junshin Clinic Bile Acid Institute Tokyo Japan

3. Division of Gastroenterology and Hepatology Department of Internal Medicine Tokai University School of Medicine Isehara Japan

4. Department of Pediatrics Shiga University of Medical Science Otsu Japan

5. Department of Internal Medicine Heartlife Hospital Nakagusuku Japan

6. Faculty of Pharmaceutical Science Health Science University of Hokkaido Ishikari‐Tobetsu Japan

7. Faculty of Medical Technology Teikyo University School of Medicine Tokyo Japan

Publisher

Wiley

Subject

General Medicine

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/hep4.1660

Reference7 articles.

1. Complete OATP1B1 and OATP1B3 deficiency causes human Rotor syndrome by interrupting conjugated bilirubin reuptake into the liver

2. Recessive Inheritance of Population-Specific Intronic LINE-1 Insertion Causes a Rotor Syndrome Phenotype

3. Detection of Δ4-3-oxo-steroid 5β-reductase deficiency by LC–ESI-MS/MS measurement of urinary bile acids

4. Loss of organic anion transporting polypeptide 1B3 function causes marked delay in indocyanine green clearance without any clinical symptoms

5. Profiling Serum Bile Acid Glucuronides in Humans: Gender Divergences, Genetic Determinants, and Response to Fenofibrate

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