Репозиторий Университета

© 2019, The Author(s). Introduction: This study examined the dynamics of 24-h electrocardiogram (ECG) monitoring parameters (Holter monitoring) in patients with ischemic heart disease (IHD) before and after conservative or surgical treatment of patients with voiding and storage lower urinary tract symptoms (LTS) due to benign prostatic hyperplasia (BPH). Methods: A total of eighty-three 57 to 81-year-old (mean age 70.4 ± 5.75 years) patients with LUTS/BPH and accompanying IHD were examined and treated at the Institute of Urology and Human Reproductive Health and Clinic of Cardiology of Sechenov University. All patients received recommended cardiac therapy at least 6 months before inclusion in the study. Results: Our study demonstrated that there is correlation between voiding and storage LUTS/BPH and Holter-detected cardiac impairments in patients with IHD/BPH. These data make it possible to consider LUTS/BPH (voiding and storage) as a factor in the additional functional and psychological load on the activity of patients with ischemic heart disease. Improvement of voiding and storage LUTS due to BPH and objective parameters of urination (Qmax) in patients treated with alpha-1 adrenoceptor blocker tamsulosin correlated with improvement of 24-h ECG monitoring parameters (Holter monitoring) in 72% of patients. Improvement of 24-h ECG monitoring parameters (Holter monitoring) 1 month after transurethral resection of the prostate (TURP) in IHD/BPH patients and indications for surgical treatment was observed in 65.7%. Negative dynamics of the Holter-based ECG was not registered in patients who were operated on. Conclusion: Holter monitoring helps to identify groups of patients in whom urinary impairments caused by prostatic hyperplasia negatively affect the course of IHD. Restored urination (either conservatively or operatively) in patients with BPH in 72% of cases decreased the number of fits of angina, thus influencing favourably the course of IHD. Trial Registration: ClinicalTrials.gov Identifier: NCT03856242.

© Mary Ann Liebert, Inc. Introduction: Endoscopic enucleation of the prostate (EEP) has been recognized as a viable treatment modality for men with benign prostatic hyperplasia (BPH). The aim of our study was to compare the efficacy and functional outcomes of three different techniques of EEP, including monopolar enucleation (MEP), holmium laser enucleation of the prostate (HoLEP), and thulium laser enucleation of the prostate (ThuLEP). Methods: The study consisted of a retrospective comparison of pre- and postoperative parameters in men undergoing three types of EEP: MEP, HoLEP, and ThuLEP. Functional parameters were evaluated before and 6 months after surgery, which included the International Prostate Symptom Score, maximum flow rate, postvoid residual volume, prostate volume, and sodium levels of all patients. Results: A total of 551 men with the mean age of 67.1 years were included in the study. Of these, MEP was performed on 95 patients, HoLEP was performed on 254 patients, and ThuLEP on 202 patients. The mean mass of morcellated tissue obtained during the three techniques did not differ significantly (p > 0.05). Mean procedure times of ThuLEP and HoLEP were shorter than MEP demonstrating 72, 76, and 86 minutes, respectively (p < 0.01). The mean catheterization time following laser EEPs was shorter than MEP as shown by 1.3, 1.3, and 3.8 days, respectively (p < 0.01). Hospital stay times of HoLEP and ThuLEP were shorter than MEP demonstrated by 3.3, 3.4, and 6.9 days, respectively (p < 0.01). Patients after MEP had significant decrease in postoperative hemoglobin and sodium levels. All the groups showed statistically significant improvement in the aforementioned parameters following treatment. Conclusions: Both techniques of laser enucleation proved to be efficacious in the management of BPH. MEP of the prostate seems to be a highly promising addition to the list of enucleation techniques and was determined to be an effective and acceptable procedure, despite a higher complication rate.

© 2018, Polish Urological Association. All rights reserved. Introduction In order to investigate the efficacy and safety of Afalaza in men with benign prostatic hyperplasia (BPH) at risk of progression, this multicenter, double-blind, placebo-controlled, randomized clinical trial was performed. Derived by technological treatment of antibodies to prostate-specific antigen (PSA) and endothelial nitric oxide synthase (eNOs), Afalaza was previously proved to modulate its molecular targets. The mechanism of action of the drug is associated with the modulating effect of the antibiodies (RA-Abs) on the molecular targets (PSA and eNOS) by way of conformational changes. Material and methods A total of 249 patients aged 45–60 years with BPH and moderate lower urinary tract symptoms (LUTS), total prostate volume (TPV) ≥30 cm3, Qmax 10–15 ml/s, and serum PSA<4 ng/ml were randomly assigned to receive either Afalaza (n = 125) or placebo (n = 124) for 12 months. Changes in BPH/LUTS symptoms (according to the International Prostate Symptom Score), Qmax, TPV, PSA, BPH clinical progression, occurrence of acure urinary retention (AUR) events or BPH-related surgery were estimated as the study endpoints. Results IPSS mean change was-3.7 ±3.0 (95% CI-4.3 to-3.2) after 12 months of Afalaza (vs.-2.9 ±2.4; 95% CI-3.3 to-2.4 in placebo; р = 0.02). Qmax growth was 2.5 ±4.3 ml/s (vs. 1.4 ±3.3 in placebo; p = 0.049), TPV reduced by 11.8 ±16.0% (vs. 6.5 ±14.7%; p = 0.01, and PSA remained unchanged. Afalaza therapy resulted in a significant decrease in the total sum of BPH progression symptoms (p = 0.01). The maximum effect of Afalaza was registered after 12 months without a tendency to form a ‘plateau’. During the study, no patients experienced AUR or BPH-related surgery. Conclusions A 12-month course of Afalaza therapy is effective and safe for patients with BPH. The results of end points measurements revealed asignificant advantage of Afalaza compared to placebo in the overall symptoms benefit and a decline in the risk of BPH progression. ClinicalTrials.gov: NCT01716104.