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Systemic inflammation and symptomatology in patients with prostate cancer treated with androgen deprivation therapy: Preliminary findings
Author(s) -
Hoogland Aasha I.,
Jim Heather S. L.,
Gonzalez Brian D.,
Small Brent J.,
Gilvary Danielle,
Breen Elizabeth C.,
Bower Julienne E.,
Fishman Mayer,
Zachariah Babu,
Jacobsen Paul B.
Publication year - 2021
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/cncr.33397
Subject(s) - medicine , androgen deprivation therapy , prostate cancer , inflammation , depression (economics) , oncology , neuropsychology , major depressive disorder , cancer , systemic inflammation , cognition , psychiatry , amygdala , economics , macroeconomics
Background Increases in fatigue, depressive symptomatology, and cognitive impairment are common after the initiation of androgen deprivation therapy (ADT) for prostate cancer. To date, no studies have examined the potential role of inflammation in the development of these symptoms in ADT recipients. The goal of the current study was to examine circulating markers of inflammation as potential mediators of change in fatigue, depressive symptomatology, and cognitive impairment related to the receipt of ADT. Methods Patients treated with ADT for prostate cancer (ADT+; n = 47) were assessed around the time of the initiation of ADT and 6 and 12 months later. An age‐ and education‐matched group of men without a history of cancer (CA–; n = 82) was assessed at comparable time points. Fatigue, depressive symptomatology, and cognitive impairment were assessed with the Fatigue Symptom Inventory, the Center for Epidemiological Studies Depression Scale, and a battery of neuropsychological tests, respectively. Circulating markers of inflammation included interleukin 1 receptor antagonist (IL‐1RA), interleukin 6 (IL‐6), soluble tumor necrosis factor receptor II (sTNF‐RII), and C‐reactive protein (CRP). Results Fatigue, depressive symptomatology, and serum IL‐6 increased significantly over time in the ADT+ group versus the CA– group; rates of cognitive impairment also changed significantly between the groups. No significant changes in IL‐1RA, sTNF‐RII, or CRP over time were detected. Treatment‐related increases in IL‐6 were associated with worsening fatigue but not depressive symptomatology or cognitive impairment. Conclusions Results of this preliminary study suggest that increases in circulating IL‐6, perhaps due to testosterone inhibition, may play a role in fatigue secondary to receipt of ADT. Additional research is needed to determine whether interventions to reduce circulating inflammation improve fatigue in this population.