18 F-PSMA-1007 is a novel prostate-specific membrane antigen (PSMA)-based radiopharmaceutical for imaging prostate cancer (PCa). The aim of this study was to compare the diagnostic accuracy of 18 F-PSMA-1007 with 68 Ga-PSMA-11 PET/CT in the same patients presenting with newly diagnosed intermediate-or high-risk PCa. Methods: Sixteen patients with intermediate-or high-risk PCa underwent 18 F-PSMA-1007 and 68 Ga-PSMA-11 PET/CT within 15 d. PET findings were compared between the 2 radiotracers and with reference-standard pathologic specimens obtained from radical prostatectomy. The Cohen κ-coefficient was used to assess the concordance between 18 F-PSMA-1007 and 68 Ga-PSMA-11 for detection of intraprostatic lesions. The McNemar test was used to assess agreement between intraprostatic PET/CT findings and histopathologic findings. Sensitivity, specificity, positive predictive value, and negative predictive value were reported for each radiotracer. SUV max was measured for all lesions, and tumor-to-background activity was calculated. Areas under receiver-operating-characteristic curves were calculated for discriminating diseased from nondiseased prostate segments, and optimal SUV cutoffs were calculated using the Youden index for each radiotracer. Results: PSMA-avid lesions in the prostate were identified in all 16 patients with an almost perfect concordance between the 2 tracers (κ ranged from 0.871 to 1). Aside from the dominant intraprostatic lesion, similarly detected by both radiotracers, a second less intense positive focus was detected in 4 patients only with 18 F-PSMA-1007. Three of these secondary foci were confirmed as Gleason grade 3 lesions, whereas the fourth was shown on pathologic examination to represent chronic prostatitis. Conclusion: This pilot study showed that both 18 F-PSMA-1007 and 68 Ga-PSMA-11 identify all dominant prostatic lesions in patients with intermediateor high-risk PCa at staging. 18 F-PSMA-1007, however, may detect additional low-grade lesions of limited clinical relevance.
Studies are emerging alluding to the role of intestinal microbiome in the pathogenesis of diseases. Intestinal microbiome is susceptible to the influence of environmental factors such as smoking, and recent studies have indicated microbiome alterations in smokers. The aim of the study was to review the literature regarding the impact of smoking on the intestinal microbiome. A literature review of publications in PUBMED was performed using combinations of the terms "Intestinal/Gut/Gastrointestinal/Colonic" with "Microbiome/Microbiota/Microbial/Flora" and "Smoking/Smoker/Tobacco". We selected studies that were published between the years 2000 and 2016 as our inclusion criteria. Observational and interventional studies suggest that the composition of intestinal microbiome is altered due to smoking. In these studies, Proteobacteria and Bacteroidetes phyla were increased, as well as the genera of Clostridium, Bacteroides and Prevotella. On the other hand, Actinobacteria and Firmicutes phyla as well as the genera Bifidobacteria and Lactococcus were decreased. Smoking also decreased the diversity of the intestinal microbiome. Mechanisms that have been suggested to explain the effect of smoking on intestinal microbiome include: oxidative stress enhancement, alterations of intestinal tight junctions and intestinal mucin composition, and changes in acid-base balance. Interestingly, some smoking-induced alterations of intestinal microbiome resemble those demonstrated in conditions such as inflammatory bowel disease and obesity. Further studies should be performed to investigate this connection. Smoking has an effect on intestinal microbiome and is suggested to alter its composition. This interaction may contribute to the development of intestinal and systemic diseases, particularly inflammatory bowel diseases.
Aim: To assess the precision of preoperative ultrasonography (US)-determined prostate volume and to propose formulas for improving it. Methods: This retrospective study comprised 155 consecutive men who underwent open prostatectomy for benign prostatic hyperplasia (BPH) between 2013 and 2019. Preoperative prostate volume was estimated by either abdominal US (AUS) ( n = 92) or transrectal US (TRUS) ( n = 63), and was compared with the weight of surgically enucleated tissue at a conversion rate of 1 ml (US) = 1 g tissue. Statistical analysis was conducted and a novel formula for prostate volume was constructed. Results: The median prostate volumes by AUS and TRUS were 140 ml [interquartile ratio (IQR) 111–182] and 108 ml (IQR 93–120), respectively. Enucleated tissue weight was lower than the AUS assessment by a median difference of 50 g (IQR 28.7–75.7; p < 0.001), and lower than the TRUS assessment by a median difference of 27 g, IQR 10–43, p < 0.001). Using a cutoff of 80 ml, 30 (33%) AUS patients and 23 (36%) TRUS patients underwent unneeded open procedures. Mathematical calculations revealed two formulas that significantly adjusted for the actual weight: 1.082*Age + 0.523*AUS − 53.845 for AUS and 0.138*age + 2.22*prostate-specific antigen + 0.453*TRUS + 11.682 for TRUS ( p < 0.001). These formulas increased the overall US prostate volume accuracy from 65% to 85%. Conclusion: Assessment of prostate volume by US is imprecise for decision-making of whether to perform open simple prostatectomy for BPH. Our novel formulas may enhance stratification of patients with prostatic enlargement to a more optimal surgical approach. Future studies in larger cohorts are needed to substantiate our results.
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