ArticlePloS one2015
A Population-Based Study on the Association between Benign Prostatic Enlargement and Rheumatoid Arthritis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- A genetic variant near GATA3 implicated in inherited susceptibility and etiology of benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS).The Prostate · 2017Trial
- The association between arthritis and the risk of lower urinary tract symptoms suggestive of benign prostate hyperplasia: evidence from the China Health and Retirement Longitudinal Study (CHARLS).Scientific reports · 2025Article
- Common salt aggravated pathology of testosterone-induced benign prostatic hyperplasia in adult male Wistar rat.BMC urology · 2023Article
- TNF is a potential therapeutic target to suppress prostatic inflammation and hyperplasia in autoimmune disease.Nature communications · 2022Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Benign prostatic hyperplasia is one of the chronic inflammatory conditions in ageing male populations. Rheumatoid arthritis (RA) is a major autoimmune disease and is also regarded as a chronic inflammatory disorder. Although RA and benign prostatic enlargement (BPE) may share the same underlying etiologies, almost no study has ever attempted to explore the relationship between RA and BPE. The aim of this study was to explore the relationship between RA and BPE using a population-based dataset. This case-control study used data retrieved from the Taiwan Longitudinal Health Insurance Database 2005. This study comprised 18,716 patients with BPE and 18,716 age-matched patients without BPE. Conditional logistic regression analyses were performed to calculate the odds ratio (OR) for having been previously diagnosed with RA between patients with BPE and comparison patients. In total, 485 of the 37,432 sampled patients (1.3%) had received a prior RA diagnosis. There was a significant difference in the prevalence of prior RA between cases and controls (1.6% vs. 1.0%, p<0.001). After adjusting for patient's urbanization level, monthly income, geographic region, and obesity, the adjusted OR was 1.54 (95% CI = 1.28~1.85) for patients with BPE compared to comparison patients. In addition, the sensitivity analysis showed that BPE was consistently and significantly associated with a prior RA diagnosis even after excluding subjects diagnosed with RA within 1, 2, or 3 years prior to the index date (the adjusted ORs were 1.46, 1.50, and 1.42, respectively). We concluded that there was a significant association between prior RA and BPE. Further large-scale longitudinal studies are suggested to clarify the causal relationship between RA and BPE.
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