头发皮质醇浓度与成人患者癌症相关结局之间的关联：一项系统综述

摘要(中文译文)

慢性应激通过持续激活下丘脑-垂体-肾上腺（HPA）轴，被认为与癌症进展有关。头发皮质醇浓度（HCC）为累积皮质醇暴露提供了一个独特的回顾性观察窗口，但其与癌症结局的关系从未被系统研究。旨在批判性评价HCC与成人癌症相关结局之间关联的证据，并识别目前限制这一新兴领域的方法学缺口。检索了四个数据库（PubMed、Embase、Scopus、Web of Science）和两个试验注册平台（ClinicalTrials.gov、WHO ICTRP），检索时间自建库至2026年3月。纳入标准为确诊癌症的成人，且HCC通过任何经验证的方法测定。根据研究设计，分别采用Cochrane RoB 2、纽卡斯尔-渥太华量表和JBI清单评估偏倚风险。叙述性综合遵循SWiM指南。PROSPERO注册号：CRD420261328214。从2313条初始记录中，六项研究（两项随机试验、两项队列研究、两项横断面研究）符合纳入标准，涵盖七个国家、6683名参与者。在根治性肝细胞癌治疗后，HCC升高可预测较短的无病生存期和总生存期。在一个基于人群的队列中，调整年龄和性别后，头发可的松（而非皮质醇）与癌症发病率相关。乳腺癌幸存者的HCC显著高于匹配对照。一项干预试验表明，心理社会干预项目后HCC显著降低，而另一项试验未发现效果。各研究报告的HCC差异很大，基于LC-MS/MS的测定值范围从低于3至约60 pg/mg，而一项基于ELISA的研究报告均值为1751 pg/mg，这一差异主要由分析平台不同所致。方法学质量参差不齐，混杂因素调整和生物学数据缺失是反复出现的问题。有限证据提示，慢性皮质醇暴露升高可能与已确诊恶性肿瘤患者的不良生存结局相关，而关于癌症发病率的发现仍无定论。分析异质性、混杂因素控制有限以及乳腺癌研究占主导地位，限制了这些结论的强度。标准化测量方案和前瞻性纵向设计是必要的下一步。

Abstract

Chronic stress, through sustained hypothalamic-pituitary-adrenal (HPA) axis activation, has been implicated in cancer progression. Hair cortisol concentration (HCC) offers a unique retrospective window into cumulative cortisol exposure, yet its relationship with cancer outcomes has never been systematically examined. To critically appraise the evidence linking HCC to cancer-related outcomes in adults and to identify the methodological gaps that currently limit this emerging field. Four databases (PubMed, Embase, Scopus, Web of Science) and two trial registries (ClinicalTrials.gov, WHO ICTRP) were searched from inception to March 2026. Adults with confirmed cancer and HCC measured by any validated method were eligible. Risk of bias was assessed using Cochrane RoB 2, the Newcastle-Ottawa Scale, and the JBI checklist according to study design. Narrative synthesis followed SWiM guidelines. PROSPERO registration: CRD420261328214. From 2313 initial records, six studies (two randomised trials, two cohorts, two cross-sectional) met the inclusion criteria, spanning seven countries with 6683 participants. Elevated HCC predicted shorter disease-free and overall survival following curative hepatocellular carcinoma treatment. Hair cortisone, but not cortisol, was associated with cancer incidence in a population-based cohort after adjustment for age and gender. Breast cancer survivors showed significantly higher HCC than matched controls. One intervention trial demonstrated a significant reduction in HCC following a psychosocial programme, while another found no effect. Reported HCC varied widely across studies, with LC-MS/MS-based measurements ranging from below 3 to approximately 60 pg/mg, while a single ELISA-based study reported a mean of 1751 pg/mg, a discrepancy largely driven by analytical platform differences. Methodological quality was variable, with confounder adjustment and missing biological data representing recurring concerns. Limited evidence suggests that elevated chronic cortisol exposure may be associated with adverse survival outcomes in patients with established malignancies, while findings regarding cancer incidence remain inconclusive. Analytical heterogeneity, limited confounder control, and the predominance of breast cancer studies constrain the strength of these conclusions. Standardised measurement protocols and prospective longitudinal designs are essential next steps.

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