Relationship of Gene Polymorphism to Pathogenesis of Benign Prostatic Hyperplasia: A Narrative Review

Benign Prostatic Hyperplasia (BPH) is a common pathological process that causes lower urinary tract symptoms (LUTS) in elderly males. The prevalence of BPH is currently increasing due to an increase in metabolic factors, such as obesity. The pathogenesis of BPH is very complex and includes various components such as the role of androgens, estrogens, stromal and epithelial interactions, growth factors, and neurotransmitters. Gene differences between individuals are one of the triggers in the development of BPH disease. Genetic polymorphisms are differences in DNA sequences between individuals, groups, or populations. The source of gene polymorphism can come from single nucleotide polymorphism (SNP), sequence repeat, insertion, deletion, and recombination. This gene recombination may be an individualized cause for the development of BPH disease. Gene polymorphisms are thought to play a significant role in the inflammatory process, one of the pathogenesis processes of BPH. In addition, some literature also suggests that differences in an individual's growth hormone levels may be one of the triggers in the process of BPH development, thereby increasing an individual's risk of developing BPH. Thus, summarized data for gene polymorphism is needed, which will correspond to individualized therapy for everyone.

کلیدواژه ها:

benign prostatic hyperplasia ، Pathogenesis ، gene polymorphism