ORIGINAL ARTICLE   Free access

Minerva Urology and Nephrology 2021 October;73(5):631-7

DOI: 10.23736/S2724-6051.20.03992-2

Copyright © 2020 EDIZIONI MINERVA MEDICA

language: English

Impairment of autophagy may represent the molecular mechanism behind the relationship between obesity and inflammation in patients with BPH and LUTS

Cosimo DE NUNZIO ¹ ✉, Simona GIGLIO ², Valeria BALDASSARRI ¹, Roberto CIROMBELLA ², Giuseppe MALLEL ², Antonio NACCHIA ¹, Andrea TUBARO ¹, Andrea VECCHIONE ^{1, 2}

¹ Sant’Andrea Hospital, Sapienza University, Rome, Italy; ² Unit of Urology and Surgical Pathology, Department of Clinical and Molecular Medicine, Sant’Andrea Hospital, Sapienza University, Rome, Italy

BACKGROUND: Aim of this study was to evaluate the roles of inflammation and autophagy in obese patients with benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS).
METHODS: We analyzed 150 surgical specimens from patients underwent transurethral resection of the prostate (TURP) for LUTS/BPH (Median age 70.3±8.1 years, median BMI 25.7±4.0 kg/m² and median PSA 6.0±5.4 ng/mL). All surgical specimens were investigated for the presence inflammatory infiltrates, according to the standardized classification of chronic prostatitis of the National Institute of Health. The inflammatory score (IS Score) was calculated. High IS score was defined as ≥7. Each sample was stained for anti-LC3B (cell signaling) and for anti-P62/SQSTM1 (MBL) according to manufacturer’s suggestions and scored as follow: 0 (no dots); 1 (detectable dots in 5-25% of cells); 2 (readily detectable dots in 25-75% of cells); 3 (dots in >75% of cells). High percentage of p62 or LC3B was defined as >25%, whereas low percentage of p62 or LC3B was defined as <25% of cells with dots.
RESULTS: Overall 74/150 (49.3%) patients were overweight or obese (BMI >25 kg/m²). Obese patients presented a higher inflammatory score. Obese/overweight patients presented a lower percentage of LC3B (58/74; 78.4%) and higher of p62 (49/74; 66.2%) compared to those of normal weight, which it means a deactivated autophagy (P<0.05). At multivariate analysis LC3B (OR=0.22; CI: 0.069-0.70; P=0.01) percentage and BMI (OR=1.118; CI: 1.001-1.250; P=0.04) were independent risk factors of prostatic inflammation (IS≥7).
CONCLUSIONS: Here we confirm the association between obesity and prostatic inflammatory infiltrates and present the first evidence of autophagy deregulation in obese patients with LUTS/BPH. Further studies should better investigate this relationship and provide new possible therapeutic targets.

KEY WORDS: Autophagy; Inflammation; Prostate