The relationship between glucose homeostasis status and prostate size in aging Chinese males with benign prostatic hyperplasia.

ABSTRACT:

Purpose

Increasing evidence shows that many metabolic factors are involved in the progression of benign prostatic hyperplasia (BPH). We aimed to assess the relationship between the status of glucose homeostasis and prostate size in aging Chinese males undergoing transurethral resection of the prostate (TURP) for BPH.

Methods

A total of 1006 medical records of BPH patients undergoing TURP were reviewed. Prostate size was measured by transrectal ultrasound. Annual total prostate (TP) and transitional zone (TZ) growth rates were calculated. According to the American Diabetes Association criteria, the patients were categorized as normoglycemic, prediabetic, or diabetic. Levels of glucose homeostasis and other variables were considered independent variables in an effort to evaluate any potential correlations using non-adjusted and multivariate-adjusted regression models.

Results

A total of 659 individuals were included in the study. BPH patients < 70 years old and ≥ 70 years old in the normoglycemic group had a stable prostate growth rate. The change in prostate size in those younger than 70 years, however, was faster in the prediabetic and diabetic group. Further analysis revealed that abnormal glucose homeostasis was positively correlated with prostate size. In those younger than 70 years, compared with the normal glucose group, the adjusted odds ratio (OR) for TP and TZ enlargement in the prediabetic group was 2.27 (95%CI 1.29-4.00) and 3.19 (95%CI 1.78-5.72), respectively, and the adjusted ORs were 4.74 (95%CI 2.18-10.30) and 6.16 (95%CI 2.70-14.06), respectively, for men with diabetes. However there was no significant difference among men aged ≥ 70 years.

Conclusions

Among patients undergoing TURP, the prostate volume and growth rate were affected by different status of glucose homeostasis. Hyperglycemia may play an important role in prostate growth.

SUBMITTER: Wu Y 

PROVIDER: S-EPMC7644519 | biostudies-literature |

REPOSITORIES: biostudies-literature