PDF(Pubmed)
Abstract：
UNASSIGNED: Immune checkpoint inhibitors (ICI), including Programmed Cell Death 1, Programmed Cell Death Ligand 1, and Cytotoxic T-lymphocyte Associated Antigen 4 inhibitors, upregulate T-cell responses against tumor cells and are becoming a cornerstone in the treatment of various advanced solid and hematological cancers. Mulvihill-Smith Syndrome (MSS) is a rare genetic syndrome that has been associated with metabolic abnormalities and early-onset tumors, including malignancies. We report the first known case of ICI-induced hyponatremia attributable to syndrome of inappropriate antidiuretic hormone ADH release (SIADH) in a patient with MSS.
UNASSIGNED: A 23-year-old female patient with MSS and hepatocellular carcinoma presented with recurrent hyponatremia. Assessment of fluid status and electrolytes revealed a euvolemic, hypotonic process consistent with SIADH shortly after initiating adjuvant therapy with atezolizumab, a Programmed Cell Death Ligand 1 inhibitor.
UNASSIGNED: Endocrine etiologies for euvolemic hypotonic hyponatremia, including adrenal insufficiency and hypothyroidism, were excluded. The diagnosis of SIADH was confirmed based on electrolyte and osmolality studies. Sodium levels normalized with fluid restriction. Given the onset of hyponatremia 30 days after atezolizumab initiation, we posit that atezolizumab triggered severe hyponatremia due to SIADH.
UNASSIGNED: With the expanding utilization of ICIs, including in patients predisposed to malignancies such as MSS, vigilant monitoring for ICI-mediated electrolyte imbalances is crucial. Monitoring for hyponatremia and SIADH in the setting of ICI therapy is recommended.
UNASSIGNED: A 23-year-old female patient with MSS and hepatocellular carcinoma presented with recurrent hyponatremia. Assessment of fluid status and electrolytes revealed a euvolemic, hypotonic process consistent with SIADH shortly after initiating adjuvant therapy with atezolizumab, a Programmed Cell Death Ligand 1 inhibitor.
UNASSIGNED: Endocrine etiologies for euvolemic hypotonic hyponatremia, including adrenal insufficiency and hypothyroidism, were excluded. The diagnosis of SIADH was confirmed based on electrolyte and osmolality studies. Sodium levels normalized with fluid restriction. Given the onset of hyponatremia 30 days after atezolizumab initiation, we posit that atezolizumab triggered severe hyponatremia due to SIADH.
UNASSIGNED: With the expanding utilization of ICIs, including in patients predisposed to malignancies such as MSS, vigilant monitoring for ICI-mediated electrolyte imbalances is crucial. Monitoring for hyponatremia and SIADH in the setting of ICI therapy is recommended.
摘要：
■免疫检查点抑制剂（ICI），包括程序性细胞死亡1，程序性细胞死亡配体1和细胞毒性T淋巴细胞相关抗原4抑制剂，上调T细胞对肿瘤细胞的反应，并成为治疗各种晚期实体和血液癌症的基石。Mulvihill-Smith综合征（MSS）是一种罕见的遗传综合征，与代谢异常和早发性肿瘤有关。包括恶性肿瘤.我们报告了第一例已知的MSS患者因抗利尿激素ADH释放不当（SIADH）综合征引起的ICI引起的低钠血症。
■一名23岁女性MSS合并肝细胞癌患者，表现为复发性低钠血症。对液体状态和电解质的评估显示，在开始阿特珠单抗辅助治疗后不久，低张过程与SIADH一致，程序性细胞死亡配体1抑制剂。
■等容量低渗性低钠血症的内分泌病因，包括肾上腺功能不全和甲状腺功能减退,被排除在外。根据电解质和渗透压研究证实了SIADH的诊断。钠水平在液体限制下正常化。鉴于阿特珠单抗开始后30天出现低钠血症，我们认为阿替珠单抗引发了SIADH引起的严重低钠血症.
■随着ICI利用率的扩大，包括易患恶性肿瘤的患者，如MSS，警惕监测ICI介导的电解质失衡至关重要.建议在ICI治疗中监测低钠血症和SIADH。
■一名23岁女性MSS合并肝细胞癌患者，表现为复发性低钠血症。对液体状态和电解质的评估显示，在开始阿特珠单抗辅助治疗后不久，低张过程与SIADH一致，程序性细胞死亡配体1抑制剂。
■等容量低渗性低钠血症的内分泌病因，包括肾上腺功能不全和甲状腺功能减退,被排除在外。根据电解质和渗透压研究证实了SIADH的诊断。钠水平在液体限制下正常化。鉴于阿特珠单抗开始后30天出现低钠血症，我们认为阿替珠单抗引发了SIADH引起的严重低钠血症.
■随着ICI利用率的扩大，包括易患恶性肿瘤的患者，如MSS，警惕监测ICI介导的电解质失衡至关重要.建议在ICI治疗中监测低钠血症和SIADH。
