Reversible elevation of creatine kinase and creatinine caused by sintilimab-induced hypothyroidism: A case report
Year: 2024
Type: article
Study design: Case Report
Abstract: RATIONALE: Programmed cell death (PD) -1 inhibitors has significantly improved the prognosis of cancer patients by enhancing antitumor immune responses. However, PD-1 inhibitors are associated with immune-related adverse events, some of which are rare and potentially life-threatening. Thus far, elevated creatine kinase (CK) and creatinine caused by a novel PD-1 inhibitor (sintilimab)-induced hypothyroidism has not yet been reported. PATIENT CONCERNS: A 63-year-old male patient with esophageal cancer who developed hypothyroidism accompanied by unexplained increases in CK and creatinine after sintilimab treatment. DIAGNOSIS: Since the increases in CK and creatinine paralleled the decrease in thyroxine, after excluding other potential conditions, we speculated that the muscular and renal dysfunction might be caused by sintilimab-induced hypothyroidism. INTERVENTIONS AND OUTCOMES: As the patient's thyroid function improved with levothyroxine replacement therapy, the levels of CK and creatinine concomitantly returned to normal. CONCLUSION AND LESSONS: The elevated CK and creatinine levels in this patient were caused by sintilimab-induced hypothyroidism. Our case highlights the importance of keeping PD-1 induced hypothyroidism in mind when patients present with unexplained increased levels of CK and creatinine. Hypothyroidism-related muscular and renal dysfunctions, which can be restored with thyroid hormone replacement, need to be identified early and treated promptly so that unnecessary examinations and treatments can be avoided in these patients.
Source: Medicine
Authors: Shu-Rong Liu, Zhen-Guang Zhao, Rui-Ren Zhai, Li-Juan Wang, Chen Yang, Quan-Bin Ma, Li Wang
Institution: People's Liberation Army 401 Hospital
Language: English
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $1,950
OpenAlex ID: W4403662850
