Metformin does not improve outcomes in diabetics after radical prostatectomy
MedWire News: Research results show that metformin use does not protect men with diabetes from the risk for biochemical recurrence (BCR) after radical prostatectomy (RP) for prostate cancer.
Regardless of metformin use, diabetic RP patients had a higher risk for BCR than non-diabetic RP patients, the researchers report.
Previous studies have indicated a potential antineoplastic role of metformin, which in turn has demonstrated growth inhibition of a number of cancer cell lines in clinical studies, including in prostate cancer cells, explain Trushar Patel from Columbia University in New York, USA, and colleagues.
“Metformin may have a role in cancer inhibition; however, its effects may be silent once cancer has already presented itself,” they suggest in the journal Urology.
The team examined incidence of BCR (defined as a prostate-specific antigen [PSA] level of 0.2 ng/ml after surgery) after RP in 210 men with diabetes, including 98 metformin-users.
Patients with diabetes were matched by pretreament PSA levels, biopsy Gleason score, and clinical disease stage to 406 prostate cancer patients without diabetes.
Univariate analysis showed a 53% increase in the risk for BCR among metformin users compared with diabetic patients not using metformin. However, this association was lost in adjusted analysis which only linked BCR to pre-operative PSA level, a Gleason score of 8 or higher, positive surgical margin, and diabetes.
The researchers estimated 5-year BCR-free survival to be markedly lower among diabetic non-metformin users than among metformin users and controls, at 59.3% versus 66.1% and 75.0%, respectively.
Of note, regardless of metformin use, diabetics had a 55% increased likelihood of developing BCR within 5 years compared with controls.
“Although intriguing, our results should be considered only hypothesis-generating, and should be followed with continued research to elucidate the metabolic pathways that affect the interaction between diabetes and prostate cancer biology,” conclude Patel and co-workers.
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By Sarah Guy