Introduction

Conflicting data exist on the association of obesity with the risk of prostate cancer (PCa) recurrence after radical prostatectomy (RP), due in part to underpowered cohorts and limited follow up. Herein, we evaluated the association between obesity and PCa recurrence after RP using a large institutional dataset with long-term follow-up.

Methods

We reviewed years 1987-2013 of the Mayo Clinic RP Registry to identify men with Body Mass Index (BMI) information available. Men who underwent PCa treatment prior to RP and men with metastatic disease at RP were excluded. Patients were grouped into four BMI categories: < 25, 25-29.9, 30-34.9, and > 35. BMI > 30 was defined as obese. Standard descriptive statistics compared baseline characteristics, while forced entry multivariable cox proportional hazard models assessed the association of BMI with metastasis and prostate cancer mortality (PCM). Multivariable models were adjusted for pre-RP PSA, pathologic Gleason Score, pT stage, pN stage, margin status, age, adjuvant hormone therapy, adjuvant radiation, year of surgery, and open vs robotic approach.

Results

In our cohort of 18,039 men (median follow-up 9.3 years after RP), 20.6% (3,707), 51.9% (9,348), 21.9% (3,936) and 5.6% (1,016) had a BMI < 25, 25-29.9, 30-34.9, and > 35, respectively. Higher BMI categories had higher rates of pathologic Gleason Score 7-10 disease: 38.7%, 40.7%, 46.1%, 54.0%, respectively (p<0.001). Obese patients also had higher positive margin rates: 23.4%, 26.3%, 30.1%, 31.9%, respectively (p<0.001). PSA, pT stage, pN stage, and adjuvant therapy did not significantly differ between BMI categories (p>0.05). Log Rank comparisons found higher Kaplan-Meier rates of metastasis and PCM for patients with a BMI of 30-34.9 and > 35 (p<0.05 for all). On multivariable cox regression for metastasis, patients with a BMI 30-34.9 (HR 1.307, 95% CI 1.073-1.592, p=0.008) and BMI > 35 (HR 1.421, 95% CI 1.071-1.886, p=0.015) had an increased risk of metastasis relative to patients with a BMI < 25. Similarly, patients with a BMI 30-34.9 (HR 1.323, 95% 1.010-1.733, p=0.042) and BMI > 35 (HR 1.620, 95% CI 1.098-2.392, p=0.015) had higher PCM rates relative to patients with BMI < 25 on multivariable analysis.

Conclusions

Our data supports an independent association between BMI and PCa metastasis and cancer-specific mortality after RP. There was a direct increase in the odds of metastasis and PCM between the BMI 30-34.9 and BMI > 35 groups, further strengthening this link. Further study is warranted to determine if weight loss can abrogate this effect of obesity on PCa recurrence after RP.

Funding

none