Plessers Sam, Mebis Jeroen, De Moor Nina, Wessels Tim, Luyten Daisy, Requilé Annelies
Department of Medical Oncology, Jessa Ziekenhuis, Hasselt, Belgium.
Case Rep Oncol Med. 2025 Jul 10;2025:8600200. doi: 10.1155/crom/8600200. eCollection 2025.
Hypercalcemia of malignancy is a well-known phenomenon in cancer patients, often associated with poor prognosis. The discovery of immune checkpoint inhibitors has revolutionised cancer therapy by improving prognosis in numerous different cancer types. Unfortunately, immune-related adverse events frequently arise, particularly with dual checkpoint inhibition. We present a case of severe hypercalcemia in a 65-year-old woman undergoing treatment for metastasised malignant melanoma. Eleven weeks after initiating ipilimumab-nivolumab, the patient developed severe hypercalcemia, along with inflammation and hepatitis. This was initially presumed to be due to hypercalcemia of malignancy, given the clinical examination, imaging findings and laboratory values potentially consistent with progressive disease. The hypercalcemia responded well to bisphosphonates, intravenous saline and methylprednisolone. Interestingly, fluorodeoxyglucose-positron emission tomography/computed tomography (FDG-PET/CT) performed shortly after hospital discharge showed a complete metabolic remission, thereby making hypercalcemia of malignancy unlikely. Review of her medical history, imaging and laboratory revealed several features consistent with a sarcoid-like reaction. We hypothesise that this reaction led to elevated 1-alpha hydroxylase, thereby facilitating calcitriol-mediated hypercalcemia. In this report, we summarise previously published case reports on immune checkpoint inhibitor-induced hypercalcemia and discuss the various mechanisms that cause hypercalcemia in this rare immune-related adverse event. Immune checkpoint inhibitors can induce production of parathyroid hormone-related protein (PTHrP), calcitriol, and may cause hypocortisolaemia, all of which can disrupt calcium homeostasis. Through this case, we contribute to the growing body of evidence regarding hypercalcemia as an immune-related adverse event and aim to raise awareness among clinicians of this potential complication. Early recognition is critical for this life-threatening condition, as it can be refractory to conventional therapies and may necessitate corticosteroid therapy.
恶性肿瘤高钙血症是癌症患者中一种众所周知的现象,常与预后不良相关。免疫检查点抑制剂的发现彻底改变了癌症治疗方式,改善了多种不同癌症类型的预后。不幸的是,免疫相关不良事件经常出现,尤其是在双重检查点抑制治疗时。我们报告一例65岁接受转移性恶性黑色素瘤治疗的女性发生严重高钙血症的病例。在开始使用伊匹木单抗 - 纳武单抗治疗11周后,患者出现严重高钙血症,同时伴有炎症和肝炎。鉴于临床检查、影像学检查结果以及实验室值可能与疾病进展相符,最初推测这是由于恶性肿瘤高钙血症所致。高钙血症对双膦酸盐、静脉输注生理盐水和甲泼尼龙反应良好。有趣的是,出院后不久进行的氟脱氧葡萄糖 - 正电子发射断层扫描/计算机断层扫描(FDG - PET/CT)显示完全代谢缓解,因此恶性肿瘤高钙血症的可能性不大。回顾她的病史、影像学检查和实验室检查发现了一些与类肉瘤样反应相符的特征。我们推测这种反应导致1-α羟化酶升高,从而促进骨化三醇介导的高钙血症。在本报告中,我们总结了先前发表的关于免疫检查点抑制剂诱导高钙血症的病例报告,并讨论了在这种罕见的免疫相关不良事件中导致高钙血症的各种机制。免疫检查点抑制剂可诱导甲状旁腺激素相关蛋白(PTHrP)、骨化三醇的产生,并可能导致皮质醇减少,所有这些都可能破坏钙稳态。通过这个病例,我们为将高钙血症作为一种免疫相关不良事件的证据不断增加做出了贡献,并旨在提高临床医生对这种潜在并发症的认识。对于这种危及生命的疾病,早期识别至关重要,因为它可能对传统治疗无效,可能需要使用皮质类固醇治疗。