Letter to the editor regarding the article ‘association between asthma and risk of benign prostatic hyperplasia: a retrospective population-based study’

Sir,

We read with great interest the currently published manuscript by Peng et al. [1] on the possible association between asthma and benign prostate hyperplasia. Being one of the most common diseases disturbing aging males with lower urinary tract symptoms reducing the quality of life, BPH/LUTS is of keen interest to the researchers. Beyond the clinical relevance of BPH/LUTS, the studies for enhancing our understanding of the underlying pathophysiology is also precious, since the exact cause and effect mechanisms have not been elucidated yet. In this current manuscript, the authors evaluated the association between asthma and BPH. Being a retrospective cohort study, it yielded several significant outcomes of the cause-effect relationship between these two entities. From this point of view, we congratulate the authors, yet we want to make some inferences relating to the study.

The association of asthma and prostate cancer attracted the attention of the researchers in the last decades [2–4]. Although the results are controversial, the starting point of each of these studies is the fact that asthma, which is closely associated with altered immune system dynamics and inflammatory response could trigger the chronic cellular inflammation, thereby leading to the development of cancer. Given the immune system and inflammation pathways are also implicated in BPH pathogenesis according to the several studies [5,6], this study has a clear and sound background. However, the principal shortcoming of this study is the lack of BPH parameters including uroflowmetry, prostate volume, PSA, post-void residual volume. The authors found that the risk of undergoing TURP in the asthma group was 1.30-fold higher compared with the non-asthma group. This is an important finding, but this result would have been strengthened if the related BPH parameters had been captured. For instance, based on this outcome, we may propose that patients in the asthma group are more likely to have larger prostate volume, increased post void urine volume, and decreased Q max value. This result may lead us the plausible underlying pathophysiologic mechanisms of the BPH-asthma association, chronic inflammation, which is implicated in both two clinical entities. Upon the framework of all these inferences, further studies might focus on the inter-related conditions which have similar pathophysiologic mechanisms with BPH.

Consequently, the current study represents reliable data for the potential association of asthma with the most common benign neoplasm, BPH, in aging male. It is evident that further well-designed studies are needed to better understand the implication of inflammation-related conditions in underlying pathophysiological mechanisms of benign prostate hyperplasia.

Disclosure statement

No potential conflict of interest was reported by the authors.