posted on 2016-10-11, 00:00authored byYA Nyame, AB Murphy, DK Bowen, G Jordan, K Batai, M Dixon, CM Hollowell, S Kielb, JJ Meeks, PH Gann, V Macias, A Kajdacsy-Balla, WJ Catalona, R Kittles
Purpose
Lower serum vitamin D levels have been associated with an increased risk of aggressive prostate
cancer. Among men with localized prostate cancer, especially with low- or intermediate-risk disease,
vitamin D may serve as an important biomarker of disease aggression. The aim of this study was to
assess the relationship between adverse pathology at the time of radical prostatectomy and serum
25-hydroxyvitamin D (25-OH D) levels.
Methods
This cross-sectional study was carried out from 2009 to 2014, nested within a large epidemiologic
study of 1,760 healthy controls and men undergoing prostate cancer screening. In total, 190 men
underwent radical prostatectomy in the cohort. Adverse pathology was defined as the presence of
primary Gleason 4 or any Gleason 5 disease, or extraprostatic extension. Descriptive and multivariate
analyses were performed to assess the relationship between 25-OH D and adverse
pathology at the time of prostatectomy.
Results
Eighty-seven men (45.8%) in this cohort demonstrated adverse pathology at radical prostatectomy.
The median age in the cohort was 64.0 years (interquartile range, 59.0 to 67.0). On univariate analysis, men
with adverse pathology at radical prostatectomy demonstrated lower median serum 25-OH D (22.7 v
27.0 ng/mL, P = .007) compared with their counterparts. On multivariate analysis, controlling for age, serum
prostate specific antigen, and abnormal digital rectal examination, serum 25-OH D less than 30 ng/mL was
associated with increased odds of adverse pathology (odds ratio, 2.64; 95% CI, 1.25 to 5.59; P = .01).
Conclusion
Insufficiency/deficiency of serum 25-OH D is associated with increased odds of adverse pathology
in men with localized disease undergoing radical prostatectomy. Serum 25-OH D may serve as a
useful biomarker in prostate cancer aggressiveness, which deserves continued study.
Funding
Supported by a grant from the US
Department of Defense W81XWH-10-1-
0532 pd22E (A.B.M.), and the following
National Institutes of Health grants:
1R01MD007105-01 (R.K.); IK2CX000926-01
(A.B.M.), and P50 CA090386-10S1 (W.J.C.).