Thyroid–Liver Interplay: Early Recognition of Carbimazole-Induced Cholestasis Amid Thyrotoxicosis
https://doi.org/10.15605/jafes.041.S1
- Author:
Zhi Ling Ng
1
;
Siti Nabihah Hatta
2
;
Yohggesh Arumugam
1
;
Ooi Chuan Ng
1
Author Information
1. Faculty of Medicine and Health Sciences, Universiti Putra Malaysia
2. Department of Internal Medicine, Hospital Sultan Abdul Aziz Shah, Universiti Putra Malaysia
- Publication Type:Journal Article
- MeSH:
Thyrotoxicosis;
Cholestasis
- From:
Journal of the ASEAN Federation of Endocrine Societies
2026;41(S1):115-
- CountryPhilippines
- Language:English
-
Abstract:
Introduction:Carbimazole is a first-line therapy for thyrotoxicosis and is
generally well tolerated. Drug-induced liver injury is rare
(<1%) and typically presents as cholestatic hepatotoxicity,
in contrast to propylthiouracil, which more commonly
causes hepatocellular injury. Clinical presentation may
mimic obstructive jaundice, and delayed recognition can
lead to unnecessary investigations and interruption of
definitive thyroid management.
A 70-year-old female with toxic multinodular goiter
developed painless jaundice 4 weeks after starting
carbimazole 20 mg daily for thyrotoxicosis precipitated by
urinary tract infection. She had no prior liver disease or
alcohol exposure. Examination revealed isolated icterus
without features of chronic liver disease.
Initial thyroid function tests showed suppressed thyroidstimulating hormone (<0.01 mIU/L) with markedly elevated
free T4 (>100 pmol/L), improving after 4 weeks (free T4 29.1
pmol/L). She subsequently developed progressive jaundice
without abdominal pain, fever, pruritus, or encephalopathy.
Liver biochemistry demonstrated a cholestatic pattern (R factor 1.1) with conjugated hyperbilirubinemia (peak
bilirubin 227 µmol/L), mild transaminitis, and elevated
alkaline phosphatase.
Imaging, including hepatobiliary ultrasonography, contrast
computed tomography, and endoscopic ultrasound,
excluded biliary obstruction. Viral, autoimmune, and
structural causes were negative. Carbimazole-induced
cholestatic jaundice was diagnosed based on temporal
association and exclusion of alternatives. Carbimazole
was discontinued, ursodeoxycholic acid was initiated, and
radioactive iodine therapy was performed, followed by
gradual recovery.
Conclusion:Carbimazole-induced hepatotoxicity (0.1–0.2%) is likely
idiosyncratic and not dose dependent. Differentiating
drug-induced liver injury from thyrotoxicosis-related
liver dysfunction is critical, as restoration of euthyroidism
alone may normalize liver enzymes. Diagnosis relies
on the exclusion of obstruction and recognition of drug
chronology. Early drug withdrawal and multidisciplinary
management are essential to prevent progression while
ensuring timely definitive therapy.
- Full text:2026080509173449444EP_A171.pdf
