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. 2023 Jul 31;12(7):1079-1089.
doi: 10.21037/tau-22-684. Epub 2023 Jul 28.

Retrospective study of testosterone deficiency and symptom burden in patients with pancreatic cancer

Affiliations

Retrospective study of testosterone deficiency and symptom burden in patients with pancreatic cancer

Austin G Kazarian et al. Transl Androl Urol. .

Abstract

Background: Pancreatic cancer patients have poor quality of life. Testosterone deficiency is associated with constitutional symptoms and sexual dysfunction which may contribute to poor quality of life. We investigated the prevalence of screening for and presence of testosterone deficiency in male pancreatic cancer patients.

Methods: To determine the frequency of screening for testosterone deficiency in pancreatic cancer patients, our institution's electronic medical record system was queried for male patients diagnosed with a pancreatic mass between 2006 and 2020 and an available testosterone level. In a separate analysis, total testosterone was measured in serum samples from a cohort of 89 male pancreatic ductal adenocarcinoma (PDAC) patients. Low serum testosterone was defined as <300 ng/dL.

Results: One thousand five hundred and sixty-six male patients were identified with a pancreatic mass, and 35 (2.2%) also had a testosterone level. In our analysis cohort, 44 of 89 patients (49.4%) were found to have low serum testosterone. Symptoms consistent with testosterone deficiency were documented for 70% of these patients, with fatigue being the most common. Testosterone level had no significant association with progression-free survival (PFS) (P=0.66) or overall survival (OS) (P=0.95).

Conclusions: Testosterone deficiency is common but rarely assessed in male patients with pancreatic cancer. Further studies are warranted to explore the possibility of testosterone supplementation to improve quality of life in this patient population.

Keywords: Pancreatic neoplasms; hypogonadism; testosterone.

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Conflict of interest statement

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tau.amegroups.com/article/view/10.21037/tau-22-684/coif). AGK receives support from the National Heart, Lung, and Blood Institute of the National Institutes of Health T35 (No. HL007485). AMP receives grant funding from and is a consultant for Boston Scientific. She also is a consultant for Endo Pharmaceuticals and she is on the medical advisory board for FirmTech. After the conclusion of data collection but prior to publication, AMP co-founded the PRIME institute, a for-profit company. EET has received salary support provided by NIH (No. NIH R00AR071508) and Institutional NIH support for core resources (No. NIH P30CA086862). She has also received grants from NIH (No. NIH R21 CA257972), lecture honoraria from the University of Kentucky and West Virginia University, travel costs for AACR Annual Meeting 2023 (Invited Speaker) from the American Association for Cancer Research, travel costs for the seminar from West Virginia University, Travel costs for 18th International Biochemistry of Exercise Conference (Invited Speaker) from International Research Group on Biochemistry of Exercise, and travel costs for Journées de la Société Française de Myologie (Invited Speaker) from Société Française de Myologie. EET was also the Co-chair of the education committee of Cancer Cachexia Society. The other authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Univariate analysis of PFS by low testosterone status for the serum sample cohort. PFS was not significantly different between patients with low or normal testosterone levels (P=0.56). PFS, progression-free survival.
Figure 2
Figure 2
Univariate analysis of OS by low testosterone status for the serum sample cohort. OS was not significantly different between patients with low or normal testosterone levels (P=0.81). OS, overall survival.

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