Cardiovascular Prevention and Pharmacotherapy

Original Article

Correlation between metformin intake and prostate cancer: Raeun Kim, Minsun Song, Jiwon Shinn, Hun-Sung Kim; Cardiovasc Prev Pharmacother. 2023;5(3):91-97. Published online July 31, 2023; DOI: https://doi.org/10.36011/cpp.2023.5.e12

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Background
The relationship between metformin intake and prostate cancer incidence remains unclear. Therefore, we examined the correlation between prostate cancer and metformin use.
Methods
The subjects were diabetes patients aged ≥50 years who had been diagnosed with prostate cancer and had undergone surgery at Seoul St. Mary's Hospital. Groups taking metformin (MET(+) group) and not taking metformin (MET(–) group) were divided and compared.
Results
The mean preoperative prostate-specific antigen (PSA) levels in the MET(–) and MET(+) groups were 10.7±11.9 and 8.0±5.6 ng/mL, respectively, with no statistically significant difference between the two groups (P=0.387). The average prostate volume of the MET(–) group was 82.4±98.0 mL, and the average prostate volume of the MET(+) group was 55.4±20.1 mL, but there was no statistically significant difference between the two groups (P=0.226). The mean PSA velocity also did not show a significant difference between the two groups (0.025±0.102 ng/mL vs. 0.005±0.012 ng/mL, P=0.221).
Conclusions
We did not identify a significant positive correlation between metformin and prostate cancer. However, preoperational PSA and PSA velocity tended to be lower in the MET(+) group. A sophisticated prospective study with a large sample size should be planned.

Citations

Citations to this article as recorded by

Metformin: Beyond Type 2 Diabetes Mellitus
Rahnuma Ahmad, Mainul Haque
Cureus.2024;[Epub] CrossRef

Review Article

Diabetes mellitus and cancer: Jae Won Hong; Cardiovasc Prev Pharmacother. 2023;5(3):69-73. Published online July 27, 2023; DOI: https://doi.org/10.36011/cpp.2023.5.e9

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Abstract PDF

Diabetes mellitus and cancer are the most common life-threatening illnesses worldwide. Previous epidemiological studies have suggested a strong association between diabetes mellitus and an increased risk of cancer. Potential biological mechanisms underlying this relationship include obesity, hyperglycemia, hyperinsulinemia, chronic inflammation, and oxidative stress. The most common diabetes-related cancers are pancreatic, hepatocellular, breast, endometrial, and colorectal cancer. Special attention should be paid to patients with diabetes through careful cancer screening and preventive anticancer strategies.

Citations

Citations to this article as recorded by

Repurposing metabolic regulators: antidiabetic drugs as anticancer agents
Yogita Dhas, Nupur Biswas, Divyalakshmi M.R., Lawrence D. Jones, Shashaanka Ashili
Molecular Biomedicine.2024;[Epub] CrossRef

Original Article

Correlation analysis of cancer incidence after pravastatin treatment: Jin Yu, Raeun Kim, Jiwon Shinn, Man Young Park, Hun-Sung Kim; Cardiovasc Prev Pharmacother. 2023;5(2):61-68. Published online April 28, 2023; DOI: https://doi.org/10.36011/cpp.2023.5.e6

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Abstract PDF: Background
Few studies have investigated the cancer-preventive effects of statins, which are known to protect against cardio-cerebrovascular diseases. In this study, we analyzed the degree to which pravastatin, a low-potency statin, could prevent cancer.
Methods
This retrospective cohort study used data from the Korean National Health Insurance Service database. Patients diagnosed with diabetes after the age of 50 years were divided into a pravastatin group and a control group that did not receive any statin prescriptions.
Results
This study included 557 patients in the pravastatin group and 2,221 patients in the control (no statin) group. During the 5-year follow-up, the incidence of cancer was 16.7% (93 of 557 patients) in the pravastatin group and 19.9% (442 of 2,221 patients) in the control group. The incidence of cancer was 22% higher in the control group than in the pravastatin group (hazard ratio, 1.22; 95% confidence interval, 0.97–1.52; P=0.09). Death from various causes occurred at a 45% higher frequency in the control group than in the pravastatin group (hazard ratio, 1.45; 95% confidence interval, 0.99–2.12; P=0.06). However, neither of those relationships reached statistical significance.
Conclusions
Although pravastatin use did not show a significant causal relationship with cancer incidence, fewer cases of cancer occurred in pravastatin users than in controls. However, further large-scale studies are required to confirm these findings.

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