Comprehensive analysis of serum chromogranin A and neuron-specific enolase levels in localized and castration-resistant prostate cancer.

OBJECTIVES: To assess chromogranin A (CGA) and neuron-specific enolase (NSE) levels and changes in these at different stages of prostatic adenocarcinoma (PCA). METHODS: Overall, 1095 serum samples from 395 patients, divided into three treatment groups, were analysed; the radical prostatectomy (RP) cohort (n = 157) included patients with clinically localized PCA, while the docetaxel (DOC) and the abiraterone (ABI)/enzalutamide (ENZA) cohorts included 95 and 143 patients, respectively, with metastatic castration-resistant prostate cancer. CGA, NSE and total PSA levels were measured using the KRYPTOR method. RESULTS: Baseline CGA and NSE levels were higher in castration-resistant (DOC and ABI/ENZA cohorts) than in hormone-naïve, clinically localized PCA (P < 0.001). High baseline CGA levels were independently associated with poor overall survival in both the DOC and the ABI/ENZA cohorts, with a stronger association in the ABI/ENZA cohort. In the ABI/ENZA cohort, a > 50% CGA increase at 3 months was associated with poor survival, especially in patients with high baseline CGA levels. CONCLUSIONS: The two- to threefold higher neuroendocrine marker levels in castration-resistant compared to hormone-naïve PCA support the presence of neuroendocrine transdifferentiation under androgen deprivation therapy. Our results showed patients with high baseline CGA levels who experienced a further CGA increase during ABI and ENZA treatment had the poorest prognosis. Serum CGA levels could help in tailoring and monitoring therapy in advanced PCA.

Our initial experiences with mpMRI-ultrasound fusion-guided prostate biopsy / Kezdeti tapasztalataink az mpMR fúziós ultrahangvezérelt prosztatabiopsziával

Introduction: The past decade has seen some major changes in the diagnostics of prostate cancer. Progress in MR imaging has allowed us to better visualise prostate cancer and thus perform targeted biopsies of tumour suspect lesions. mpMRI-ultrasound fusion-guided prostate biopsy is a precise and cost-effective method to diagnose prostate cancer. Objective: The purpose of this study was to summarise our results in mpMRI-ultrasound fusion biopsy between 2017 and 2019 and compare them with the findings in the current literature. Method: Between 2017 and 2019, fully 40, mpMRI-ultrasound fusion biopsies were performed transperineally using the BioJet fusion system at Semmelweis University Urology Clinic. The MRI evaluations were done in line with the PI-RADS v2 guidelines. It was analysed whether the PI-RADS score, the location of the tumour, lesion size, the signs of extraprostatic extension, PSA/PSAD density and prostate volume have an influence on the outcome of mpMRI-ultrasound fusion biopsy. Results: Prostate cancer was diagnosed in 80% of the cases during targeted biopsies. The detection rate was 91%, 85%, and 20% for PI-RADS 5, 4 and 3 lesions, respectively. The detection rate was significantly higher for lesions located at the peripheral zone compared to the ones in the transitional zone (khi2(1) = 6.555, p = 0.010, Fisher-exact p = 0.017, V = 0.355). Signs of extraprostatic extension and higher PSAD correlated with better detection rate (khi2(1)= 7.704, p = 0.006, Fisher-exact p = 0.004, V = 0.355; and 0.47 ± 0.50 ng/ml2 vs. 0.18 ± 0.17 ng/ml2; Z = 3.447, p<0.001, respectively). The size of the lesions did not influence the outcome. The analysis showed a significant correlation between large prostate volumes and negative biopsies (50.9 ± 18.8 ml vs. 119.6 ± 91.6 ml; Z= ­3.505, p<0.001). Conclusions: The detection rate of prostate cancer with targeted biopsies was higher than the data found in the international literature. The PI-RADS score, the location of the tumour, MRI signs of extraprostatic extension, PSAD and prostate volume had an influence on the detection rate. Our findings may promote a better selection of the best candidates for targeted biopsies in the future.

The presence of long and heavily calcified lesions predisposes for fracture in patients undergoing stenting of the first part of the subclavian artery.

OBJECTIVE: To determine the prevalence and risk factors of subclavian artery stent fractures and to investigate their impact on in-stent restenosis development. METHODS: One hundred eight patients (65 females; median age, 58.3 years [interquartile range, 53.4-65.5 years]) with steno-occlusive disease of the first part of the subclavian artery who underwent stenting (N = 108 stents; balloon-expandable, 83.3%; self-expandable, 16.7%) between 2005 and 2015 and returned for a fluoroscopic examination of the implanted stents in 2017 were included in our study. Fractures were type I (single strut fracture), type II (multiple strut fractures without deformation), type III (multiple strut fractures with deformation), type IV (multiple strut fractures with acquired transection but without gap), or type V (multiple strut fractures with acquired transection with gap in the stent body). Stent patency was monitored by duplex ultrasound imaging. The Mann-Whitney U and Fisher's exact tests; Kaplan-Meier, receiver operating characteristic, and logistic regression analyses; as well as a log-rank test were used as statistical methods. RESULTS: The median follow-up was 73.8 months (interquartile range, 35.6-104.2 months). Thirty-eight fractures (35.2%) were detected; fractures were type I in 13, type II in 12, type III in 6, type IV in 4, and type V in 3 cases. Multivariable logistic regression analysis revealed the presence of long (≥20 mm) lesions (odds ratio, 3.3; 95% confidence interval, 1.3-8.4; P = .012) and heavy calcification (odds ratio, 4.7; 95% confidence interval, 1.7-12.7; P = .002) to be significant independent predictors of stent fracture. The primary patency rates were significantly worse (P = .035) in patients with stent fracture compared with those without stent fracture. CONCLUSIONS: Stent fractures frequently occur. Patients with long and/or heavily calcified lesions require closer follow-up.