Reversible elevation of creatine kinase and creatinine caused by sintilimab-induced hypothyroidism: A case report.

Abstract

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. A 63-year-old male patient with esophageal cancer who developed hypothyroidism accompanied by unexplained increases in CK and creatinine after sintilimab treatment. 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. As the patient's thyroid function improved with levothyroxine replacement therapy, the levels of CK and creatinine concomitantly returned to normal. 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.