Paraneoplastic Hyperthyroidism in Advanced Testicular Non-Seminomatous Germ Cell Tumors: Prevalence and Clinical Management.

IF 2.5 3区医学 Q3 ONCOLOGY

Oncology Pub Date : 2024-05-06 DOI:10.1159/000538634

Markus Angerer, Bendix Hansen, Christian Wülfing, Klaus-Peter Dieckmann

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Abstract

Introduction: Paraneoplastic hyperthyroidism (PH) has been reported in patients with testicular germ cell tumors (GCTs), sporadically. This disorder is caused by extremely elevated serum levels of beta-human chorionic gonadotropin (bHCG). To date, little is known about the prevalence of PH, and its clinical features are poorly understood. The aim of the present study was to analyze the relative frequency and clinical features of PH in GCTs and evaluate their effects on therapeutic outcomes.

Methods: A cohort of 438 patients treated for testicular GCT from 2017 to 2023 was retrospectively analyzed for histology, age, clinical stage, and presence of PH. The clinical features of the patients with PH were evaluated descriptively. The relative frequency of PH was compared among the subgroups using descriptive statistical methods.

Results: Three patients with PH were identified; all had clinical symptoms of hyperthyroidism, suppressed serum levels of thyroid-stimulating hormone (TSH), and increased levels of tri-iodothyronin (fT3). All the patients had advanced, metastasized, and non-seminomatous GCTs. Serum bHCG levels ranged from 225,00 U/L to 1,520,000 U/L. The prevalence of PH was 0.7% in the entire GCT population and 60% in those with very high bHCG serum levels. All the patients received standard cisplatin-based chemotherapy along with thyrostatic treatment. The clinical symptoms of the hyperthyroidism rapidly disappeared. TSH levels normalized with decreasing bHCG levels. The PH treatment did not affect the therapeutic outcomes of the patients.

Conclusion: PH may occur in 0.7% of all patients with GCT but may be present in up to 60% of patients with very high levels of bHCG. Measuring serum levels of TSH and fT3 should be performed in addition to routine diagnostic measures in all patients with poor prognosis GCTs. Thyrostatic medication is recommended for patients with the clinical symptoms of hyperthyroidism. Early recognition of hyperthyroidism and prompt intervention will reduce comorbidity and help optimize therapeutic outcomes.

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晚期睾丸非肉芽肿性生殖细胞肿瘤中的副肿瘤性甲状腺功能亢进症：发病率和临床管理。

导言：据报道，睾丸生殖细胞瘤（GCT）患者中偶尔会出现副肿瘤性甲状腺功能亢进症（PH）。这种疾病是由β-人绒毛膜促性腺激素（bHCG）血清水平极度升高引起的。迄今为止，人们对 PH 的发病率知之甚少，对其临床特征也知之甚少。本研究旨在分析 PH 在 GCT 中的相对发生率和临床特征，并评估其对治疗效果的影响。方法回顾性分析了2017-2023年间接受治疗的438例睾丸GCT患者的组织学、年龄、临床分期以及是否存在PH。对PH患者的临床特征进行了描述性评估。使用描述性统计方法比较了亚组之间 PH 的相对频率。结果发现了三名 PH 患者，他们都有甲状腺功能亢进的临床症状、血清促甲状腺激素（TSH）水平受抑制和三碘甲状腺原氨酸（fT3）水平升高。所有患者均为晚期、转移性和非肉芽肿性（GCT）甲状腺肿。血清 bHCG 水平从 225,00 U/l 到 1,520,000 U/l 不等。在所有GCT患者中，PH的发病率为0.7%，而在血清bHCG水平极高的患者中，PH的发病率为60%。所有患者都接受了标准的顺铂化疗和甲状腺治疗。甲亢的临床症状迅速消失。随着 bHCG 水平的降低，促甲状腺激素（TSH）水平也趋于正常。PH 治疗并未影响患者的治疗效果。结论在所有 GCT 患者中，PH 的发生率为 0.7%，但在 bHCG 水平非常高的患者中，PH 的发生率可能高达 60%。对于所有预后不良的 GCT 患者，除常规诊断措施外，还应检测血清 TSH 和 fT3 水平。建议对有甲状腺功能亢进临床症状的患者使用促甲状腺激素药物。早期识别甲状腺功能亢进症并及时干预将减少并发症，有助于优化治疗效果。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Oncology 医学-肿瘤学

CiteScore

6.00

自引率

2.90%

发文量

审稿时长

6-12 weeks

期刊介绍： Although laboratory and clinical cancer research need to be closely linked, observations at the basic level often remain removed from medical applications. This journal works to accelerate the translation of experimental results into the clinic, and back again into the laboratory for further investigation. The fundamental purpose of this effort is to advance clinically-relevant knowledge of cancer, and improve the outcome of prevention, diagnosis and treatment of malignant disease. The journal publishes significant clinical studies from cancer programs around the world, along with important translational laboratory findings, mini-reviews (invited and submitted) and in-depth discussions of evolving and controversial topics in the oncology arena. A unique feature of the journal is a new section which focuses on rapid peer-review and subsequent publication of short reports of phase 1 and phase 2 clinical cancer trials, with a goal of insuring that high-quality clinical cancer research quickly enters the public domain, regardless of the trial’s ultimate conclusions regarding efficacy or toxicity.

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