Gilbert syndrome
- Overview
- Theory
- Diagnosis
- Management
- Follow up
- Resources
Treatment algorithm
Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
all patients
patient education + avoidance or reversal of inciting agents
No treatment is necessary for Gilbert syndrome. Patient education is important. There are no dietary or activity restrictions. Patients must be informed that they may become jaundiced when under increased stress, such as fasting, dehydration, sleep deprivation, heavy physical exertion, surgery or concurrent illness, menstruation, or psychological stress.[1]Claridge LC, Armstrong MJ, Booth C, et al. Gilbert's syndrome. BMJ. 2011 Apr 19;342:d2293. http://www.ncbi.nlm.nih.gov/pubmed/21508045?tool=bestpractice.com They should be reminded that reversing the inciting agent is all that is necessary to treat the hyperbilirubinaemia. Medical follow-up and drug therapy are unnecessary.
However, patients should be advised to seek medical care if they have a prolonged or severe episode of jaundice or associated symptoms such as fever, severe abdominal pain or change in stool colour, as supervenient conditions may require investigation and specific treatment.
Patients should be encouraged to tell their doctor they have GS if a new medication is planned. There is a concern that suboptimal glucuronidation in drug metabolism may lead to accumulation of toxic drug metabolites, particularly during treatment with certain drugs (e.g., irinotecan, sorafenib, atazanavir, tocilizumab).[14]King D, Armstrong MJ. Overview of Gilbert's syndrome. Drug Ther Bull. 2019 Feb;57(2):27-31. http://www.ncbi.nlm.nih.gov/pubmed/30709860?tool=bestpractice.com [26]Lee JS, Wang J, Martin M, et al. Genetic variation in UGT1A1 typical of Gilbert syndrome is associated with unconjugated hyperbilirubinemia in patients receiving tocilizumab. Pharmacogenet Genomics. 2011 Jul;21(7):365-74. http://www.ncbi.nlm.nih.gov/pubmed/21412181?tool=bestpractice.com [27]Peer CJ, Sissung TM, Kim A, et al. Sorafenib is an inhibitor of UGT1A1 but is metabolized by UGT1A9: implications of genetic variants on pharmacokinetics and hyperbilirubinemia. Clin Cancer Res. 2012 Apr 1;18(7):2099-107. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6432766 http://www.ncbi.nlm.nih.gov/pubmed/22307138?tool=bestpractice.com
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Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups. See disclaimer
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