Systemic inflammation and symptomatology in patients with prostate cancer treated with androgen deprivation therapy: Preliminary findings

Autor: Paul B. Jacobsen, Aasha I. Hoogland, Brent J. Small, Danielle L. Gilvary, Elizabeth C. Breen, Babu Zachariah, Heather S.L. Jim, Mayer Fishman, Brian D. Gonzalez, Julienne E. Bower
Rok vydání: 2020
Předmět:
Male
Oncology
Cancer Research
medicine.medical_specialty
Antineoplastic Agents
Hormonal

Population
Neuropsychological Tests
Systemic inflammation
Androgen deprivation therapy
03 medical and health sciences
Prostate cancer
0302 clinical medicine
Internal medicine
medicine
Humans
Receptors
Tumor Necrosis Factor
Type II

030212 general & internal medicine
education
Interleukin 6
Fatigue
Testosterone
Depression (differential diagnoses)
Aged
Inflammation
education.field_of_study
biology
Depression
Interleukin-6
business.industry
Prostatic Neoplasms
Cancer
Androgen Antagonists
medicine.disease
Interleukin 1 Receptor Antagonist Protein
C-Reactive Protein
030220 oncology & carcinogenesis
biology.protein
Inflammation Mediators
Symptom Assessment
medicine.symptom
Cognition Disorders
business
Preliminary Data
Zdroj: Cancer. 127:1476-1482
ISSN: 1097-0142
0008-543X
DOI: 10.1002/cncr.33397
Popis: 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.
Databáze: OpenAIRE