A Case of Acute-On-Chronic Liver Failure Promoted by Thyrotoxicosis Triggered Due to Iodinated Contrast Media Exposure
Acute-on-chronic liver failure (ACLF) is a severe syndrome observed in patients with chronic liver disease or cirrhosis, characterized by a sudden deterioration of liver function accompanied by one or more extrahepatic organ failures. This condition is associated with a high 28-day mortality rate, ranging from 23% to 74%. Common precipitating factors include viral infections, drug toxicity, alcohol abuse, sepsis, gastrointestinal hemorrhage, ischemia, surgery, and idiopathic insults. While these triggers are well-documented, there are few reported cases of ACLF promoted by thyrotoxicosis triggered by iodinated contrast media (ICM) exposure. This article presents a detailed account of such a case, highlighting the complexities and challenges in managing this rare clinical scenario.
The patient was a 30-year-old woman with a 2-year history of abnormal liver function but no prior symptoms. She was admitted to the hospital due to persistent jaundice, abdominal distension, and intermittent mild fever lasting for one month. Initial serologic tests ruled out hepatitis viruses A, B, C, and E, as well as Epstein-Barr virus, cytomegalovirus, and rubella virus. Autoimmune disease antibodies and alpha-fetoprotein (AFP) were also negative. There was no history of alcohol abuse, hepatotoxic medications, gastrointestinal hemorrhage, or recent surgery. One week before admission, an abdominal contrast-enhanced computed tomography (CT) scan revealed liver cirrhosis with moderate ascites and no space-occupying lesions in the liver.
Upon admission, the patient’s physical examination revealed a temperature of 38.1°C, a heart rate of 98 beats per minute (bpm), and normal breathing and blood pressure. She was fully conscious, and her thyroid was non-tender with no thyromegaly. However, she exhibited a bulging abdomen, positive ascites sign, pitting edema, and ecchymosis on both lower limbs. Blood tests showed a total leukocyte count of 3.19 × 10^9/L, neutrophil percentage of 63.3%, red blood cell count of 3.46 × 10^12/L, hemoglobin of 10.7 g/L, and platelets of 80 × 10^9/L. A bone marrow biopsy was normal, and no signs of infection were detected.
Despite these findings, the patient’s liver function continued to worsen, with increasing bilirubin levels and coagulopathy. Further investigations revealed a low serum ceruloplasmin level of 0.108 g/L (normal range [NR]: 0.210–0.530 g/L), elevated urinary copper at 5.5 mmol/L (NR: 0–1.6 mmol/L), and normal blood copper at 9.7 mmol/L (NR: 0–20.0 mmol/L). A Kayser-Fleischer ring was detected on her cornea using a slit lamp, and positive gene detection of ATP7B confirmed a diagnosis of Wilson’s disease (WD). The New Wilson Index score was 13, indicating a high probability of death without liver transplantation.
Thyroid function tests revealed severe thyrotoxicosis, with thyroid-stimulating hormone (TSH) levels below 0.005 mU/L (NR: 0.270–4.200 mU/L), free thyroxine (FT4) levels at 50.67 pmol/L (NR: 12.00–22.00 pmol/L), and thyrotrophin receptor antibodies at 4.52 IU/L (NR: <3.00 IU/L). Doppler ultrasound of the thyroid showed a non-uniform density with rich blood flow, consistent with hyperthyroidism. Given the patient’s severe liver dysfunction, anti-thyroid drugs were contraindicated, and radioactive iodine therapy was considered. However, her 24-hour thyroid iodine uptake was only 4.1%, far below the 30% required for effective treatment. Anti-copper therapy was also ineffective, leaving liver transplantation as the only viable option.
As a bridge to transplantation, the patient received several adjuvant medications, including polyene phosphatidyl choline, ademetionine 1,4-butanedisulfonate, diuretics, and infusions of albumin and plasma. Despite these interventions, her liver function continued to deteriorate, and she developed persistent mild fever. On day 16 of admission, she developed hepatic encephalopathy and progressed to a coma within two days. She was transferred to the intensive care unit, where she underwent plasma exchange, mechanical ventilation, and other supportive treatments. However, her condition remained critical, with increasing serum bilirubin levels and bleeding in the gastrointestinal, respiratory, and urinary tracts. Ultimately, her family decided to discontinue treatment, and she passed away at home.
This case highlights the Jod-Basedow phenomenon, where exogenous iodide exposure triggers thyrotoxicosis in patients with underlying thyroid disease. Abdominal contrast-enhanced CT is a common diagnostic tool for patients with chronic liver disease, but this case demonstrates the potential risks of ICM exposure in patients with WD and hyperthyroidism. Thyrotoxicosis can exacerbate liver damage, leading to severe ACLF. Managing patients with both thyrotoxicosis and liver failure is particularly challenging, as anti-thyroid medications, radioactive iodine ablation, and thyroidectomy are often contraindicated or ineffective.
The hepatic manifestations of WD are highly variable, ranging from asymptomatic liver test abnormalities to acute liver failure. This case underscores the importance of assessing thyroid function before administering ICM to patients with chronic liver disease to avoid triggering thyrotoxicosis and subsequent severe liver failure. The lessons learned from this case emphasize the need for careful evaluation and management of patients with complex, overlapping conditions to improve outcomes and prevent adverse events.
In conclusion, this case report illustrates the rare but potentially fatal consequences of ICM-induced thyrotoxicosis in a patient with WD and chronic liver disease. It highlights the critical need for thorough pre-procedural assessments and individualized treatment strategies in high-risk patients to mitigate the risk of ACLF and improve prognosis.
doi.org/10.1097/CM9.0000000000000700
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