ABSTRACT
INTRODUCTION: Urethral stricture caused by fibrosis is a common medical condition, but top-line therapy for this pathology has a high recurrence rate. This study aimed to determine the efficacy of hyaluronic acid (HA) treatment in preventing the development of fibrosis in a rabbit model of urethral anastomosis. MATERIALS AND METHODS: This experimental study involved 20 rabbits. HA (0.5 mL, 25 µg/mL) was applied in the experimental group (n = 10) during an experimental urethral anastomosis, and sterile saline (0.9%) solution was applied in the control group (n = 10). Animals underwent reoperation 12 weeks later for urethral resection. Fibrosis, inflammation, and urethral diameter were measured by two blinded pathologists at the site of the anastomosis. RESULTS: The amount of inflammatory infiltrate was similar in both groups. The thicknesses of the collagen fiber band were 275.9 ± 62.3 and 373.4 ± 44.3 µm in the study and control groups (p = 0.001), respectively, and the urethral lumen diameters at the anastomosis site at follow-up were 2575 ± 167 and 2382 ± 214 µm, respectively (p = 0.04). CONCLUSION: HA treatment reduced fibrosis at the anastomosis site during this experiment; we suggest further research to corroborate its efficacy in the treatment of urethral stricture.
ABSTRACT
INTRODUCTION: Prostate cancer is one of the most common malignant neoplasias in developed countries. In 2003, 6,536 new cases and 4,602 related deaths were reported in Mexico. The renin-angiotensin system has been shown to play a role in prostate cancer pathology. Two previous studies investigated the association of prostate cancer with the insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene; both studies reported an association between prostate cancer and the DD genotype. The present study was aimed at searching for an association of prostate cancer and benign prostatic hyperplasia with the I/D polymorphism in the ACE gene and the A1166C polymorphism in the angiotensin type 1 receptor (AGT1R) gene and at comparing allele frequencies between both groups and the general population. MATERIALS AND METHODS: DNA was extracted from 20 samples from individuals with a prostate cancer diagnosis and from 20 samples from individuals with a benign prostatic hyperplasia diagnosis. Genotyping was performed by PCR-RFLP analysis. Polymorphism frequency results obtained for the test groups were compared with the frequencies in 66 individuals from the general population, which were previously obtained at the same molecular medicine laboratory in the context of other studies. RESULTS: The comparative analysis of the three groups revealed significant differences for allele frequencies in the two genes in patients groups (prostate cancer and benign prostatic hyperplasia) versus the general population. The D allele in the ACE gene was closely associated with a significant higher risk of developing both benign prostatic hyperplasia (odds ratio [OR]=21.87; 95% confidence interval [CI]=2.314-206.479) or prostate cancer (OR=31.66; 95% CI=0.091-1.272), and the AGT1R A1166 allele in the homozygote state was identified as a risk genotype for benign prostatic hyperplasia (OR=56.07). CONCLUSIONS: Genotypes in ACE and AGT1R polymorphisms could be considered as genetic risk markers for benign prostatic hyperplasia or prostate cancer.