Changes In Prostate-specific Antigen Concentrations Research Articles

Immunomagnetic Assay Using Photon-Upconversion Nanoparticles for the Detection of Cancer Biomarkers

Prostatic carcinoma is the most frequently diagnosed type of cancer within the male population worldwide. The most important prostate cancer biomarker is the prostate-specific antigen (PSA). Changes in PSA concentration may occur in very narrow ranges, making ultrasensitive analytical methods necessary. Enzyme-linked immunosorbent assay (ELISA) is considered the gold standard of analytical methods. It utilizes microtiter plates as solid phase and enzyme-based labels. However, ELISAs are often not sensitive enough for early-stage detection of subclinical levels of PSA. To enhance the sensitivity, it is possible to introduce suitable alternatives for both the solid phase and the label. Our work focuses on the use of magnetic microparticles (MBs) and photon-upconversion nanoparticles (MBs) as alternatives for solid phase and the label, respectively. The superparamagnetic properties and higher specific surface of MBs allows for analyte preconcentration and simple magnetic separation of the immunocomplex. UCNPs, on the other hand, are nanocrystals exhibiting anti-Stokes luminescence (converting light in the NIR region to visible light). After surface modification, it is possible to utilize UCNPs as labels in the upconversion-linked immunosorbent assay (ULISA), significantly enhancing the sensitivity. We have developed and optimized ELISA and ULISA assays for the detection of PSA and compared their parameters with the equivalent assays utilizing MBs as solid phase. Moreover, we have developed a novel ULISA method with an additional magnetic preconcentration step to further enhance sensitivity, providing a limit of detection of 0.46 pg mL–1.

Capacitive label-free ultrasensitive detection of PSA on a covalently attached monoclonal anti-PSA antibody gold surface

• The design of an ultrasensitive label-free detection of prostate specific antigen (PSA) was achieved. • The fabricated immunosensor used monoclonal anti-PSA antibody as capture probe on an electrografted isophthalic thin fim. • Capacitance signals were deconvoluted from the impedance plots and were sensitive to PSA concentrations. • The detection of PSA could be achieved in fg.ml -1 . A rapid, low-cost, and accurate point-of-care analytical device for the determination of prostate-specific antigen (PSA) is required for the early diagnosis and prognosis of prostate cancer (PCa). In this work, an electrochemical capacitive immunosensor was developed for the label-free detection of PSA. The immunosensor was based on the covalent immobilization of monoclonal anti -PSA antibody via carbodiimide chemistry onto gold electrode pre-modified with a thin monolayer film of isophthalic acid (IPA). A methodology based on the steric hindrance of 1,3-substituted aryldiazonium salt was adopted to control the growth of the IPA thin film on the gold electrode. The non-specific binding sites were blocked with bovine serum albumin (BSA) to afford an AuE-IPA- anti -PSA-mAb|BSA immunosensor. The immunosensor was characterized by X-ray photoelectron spectroscopy (XPS), cyclic voltammetry (CV), and electrochemical impedance spectroscopy (EIS). The analytical performance of the developed sensor was evaluated using the capacitance Nyquist plots generated from the complex impedance data. In addition, complex capacitance was also calculated from the imaginary part of the impedance and plotted against the log of frequency. The double layer capacitance from the circuit fitting (R S C) was also used and compared the sensitive capacitance signals to the changes in PSA concentrations. The LOD values were in fg.mL -1 and distinguishable from the blank (PBS) for the Nyquist plots of capacitance, complex capacitance, and double layer capacitance signals. The developed immunosensor exhibited good stability, selectivity, low detection limits, and a wide linear range which was suitable for screening of prostate cancer using prostate-specific antigen.

The risk of prostate cancer for men on aspirin, statin or antidiabetic medications

BackgroundA decreased risk of prostate cancer (PCa) has been suggested in men taking aspirin, statins and metformin, although the evidence has been conflicting. We estimated the association between prescribed medications, prostate specific antigen (PSA) levels and the risk of either any PCa or high-grade PCa. MethodsThis population-based cohort study included 185,667 men having a first recorded PSA test and 18,574 men having a first prostate biopsy in Stockholm County, Sweden for the period 2007–2012. Detailed clinical information including PSA levels, biopsy results, comorbidities and educational level were obtained from population-based registers. High-grade prostate cancer was defined as a Gleason score of seven or higher. Differences in PSA levels by medication status were estimated using linear regression on log PSA values. PCa risk was estimated using multivariate logistic regression. ResultsCompared with men who were not on medication, the PSA level at the first PSA test was lower among men using 75mg/dose aspirin (−3.9% change in PSA concentration; 95% confidence interval (CI): −5.8 to −2.1), statin (−4.6%; 95% CI: −6.2 to −2.9), metformin (−14%; 95% CI: −17 to −12) and insulin (−16%; 95% CI: −18 to −14). Men using any statins had an increased risk of both high-grade PCa (odds ratio (OR) 1.25; 95% CI: 1.10–1.42) and PCa of any grade (OR 1.16; 95% CI 1.04–1.29). There were no significant associations between aspirin or any antidiabetic medication and the risk of PCa. ConclusionWe found no protective effect of aspirin, statins or antidiabetics in terms of risk for any PCa or high-grade PCa. Use of any statins was associated with an elevated risk of being diagnosed with high-grade prostate cancer.

Racial Differences in Longitudinal Changes in Serum Prostate-specific Antigen Levels: The Olmsted County Study and the Flint Men's Health Study

To determine the distribution of, and racial differences in, changes in prostate-specific antigen (PSA) from a population-based sample of men. Data from 2 prospective cohort studies of a random sample of white men, aged 40-79 years in 1990, followed biennially through 2007, and African American men, aged 40-79 years in 1996, followed through 2000, were examined to assess the longitudinal changes in PSA concentrations. Serum PSA levels were determined at each examination for both cohorts and observations after a diagnosis of prostate cancer or treatment of benign prostatic hyperplasia were censored. The observed and estimated annual percentage of change in the serum PSA levels were examined by race. At baseline, the median PSA level in the white men did not differ from the median level observed in the African American men (white men 0.9 ng/mL; African American men 0.9 ng/mL; P= .48). However, African American men had a much more rapid increase in the PSA level over time compared with the white men (median annual percent change in PSA for white men 3.6%/y, African American men 7.9%/y; P<.001). These data suggest that African American men have more rapid rates of change in the PSA levelsover time. If the difference in the rate of changes between African American and white men is an early indicator of future prostate cancer diagnosis, earlier detection in African American men could help to alleviate the racial disparities in prostate cancer diagnosis and mortality.

Prostate‐specific antigen (PSA) concentrations in hypogonadal men during 6 years of transdermal testosterone treatment

WHAT'S KNOWN ON THE SUBJECT? AND WHAT DOES THE STUDY ADD?: Hypogonadism affects an estimated 2-4 million men in the USA, but only 5% receive treatment. Testosterone replacement therapy reduces the effects of testosterone deficiency on sexual function, mood and energy in hypogonadal patients. Long-term hypogonadism management requires testosterone treatment to restore serum concentrations of testosterone and its active metabolites, within physiological ranges; a testosterone preparation that achieves physiological plasma concentrations without supra-physiological escape is a preferred option. A previous 1-year study European clinical study showed the efficacy and safety of a transdermal testosterone patch (Testopatch(®) ). The present study shows the long-term (6-year) safety and efficacy of Testopatch in patients with primary or secondary hypogonadism. We show that, over the long-term, Testopatch was associated with no relevant changes in PSA concentration and PSA velocity, or any significant prostate risks (there were no cases of prostate cancer). To assess the change in prostate-specific antigen (PSA) concentrations in patients with primary or secondary hypogonadism, receiving transdermal testosterone. This was an interventional, 6-year study, conducted in Urology and Endocrinology centres in Belgium, France, Germany, the Netherlands and Spain. Participants were primary (48%) or secondary (52%) hypogonadal patients who received two 60 cm(2) testosterone patches (Testopatch(®) ), delivering 4.8 mg of testosterone per day, applied every 2 days. During treatment, total testosterone (TT), dihydrotestosterone, oestradiol and, PSA concentrations were measured in a centralised laboratory every 3 months during the first year, and every 6 months thereafter. In all, 200 patients [mean (sd) age 41.0 (12.5) years, body weight 82.5 (13.7) kg, height 177.2 (9.3) cm, body mass index 26.2 (3.4) kg/m(2) ] were treated with transdermal testosterone patches. In all, 161 patients completed the 1-year study and 115 entered into a 5-year study extension; 51 patients completed the sixth year of the study. The mean baseline concentrations of TT and PSA were 1.4 ng/mL and 0.47 ng/mL, respectively; TT serum concentrations >3 ng/mL were achieved in 85% of patients and fluctuated between 4.4 and 6.0 ng/mL. At each successive 6-month time point, mean the PSA values were 0.60, 0.67, 0.76, 0.70, 0.61, 0.68, 0.64, 0.71, 0.75, 0.74, 1.01, 0.78, 0.80 ng/mL, respectively. The mean PSA velocity was negligible (0.00-0.03 ng/mL/year) from 30 months to the end of the trial, except for a value of 0.08 at 60 months. Seven patients had a PSA concentration of >4 ng/mL due to a sharp PSA increase. Six of these patients had prostatitis and PSA concentrations returned to previous levels with appropriate treatment. No prostate cancer was reported during the trial. These data support a strong safety profile for Testopatch, even at the highest registered dosage.

The impact of HMG‐CoA reductase therapy on serum PSA

3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibitors, otherwise known as statins, inhibit the enzyme that controls the conversion of HMG-CoA to mevalonate, a precursor for cholesterol. Statins may be important to prostate cancer biology by inhibiting cell growth, inflammation, and oxidative stress. The purpose of this study was to assess the influence of statin therapy on serum prostate-specific antigen (PSA) levels. The computerized medical records at the University of Rochester Medical Center were used to identify men who filled statin prescriptions between May 31st, 2008 and September 30th, 2008. Men with at least one PSA assay performed within 2 years before and at least one PSA assay performed within 1 year after starting a statin medication were included. The primary endpoint was the change in PSA concentration computed as the difference between PSA levels before and after starting a statin medication. Paired t-tests were used to analyze the mean differences in PSA values. A total of 962 patients were identified. The mean difference in serum PSA level after statin administration was -0.29 ng/ml (-8.04%). Subgroup analyses for mean PSA concentration change before and after statin administration by age group revealed: 50-59 years old (-0.1609, 95% CI: -0.2444, -0.0775, P < 0.0002), 60-69 years old (-0.3393, 95% CI: -0.4641, -0.2145, P < 0.0001), and >70 years old (-0.351, 95% CI: -0.490, -0.212, P < 0.0001). These observations suggest a statistically significant reduction in serum PSA level that is associated with the onset of statin therapy.

The Influence of Statin Medications on Prostate-specific Antigen Levels

Recent data suggest that statin use may be associated with a reduced risk of advanced prostate cancer. However, the influence of statins on prostate-specific antigen (PSA) levels and what effect this could potentially have on prostate cancer diagnosis are unknown. We conducted a longitudinal study of 1214 men who were prescribed a statin between 1990 and 2006 at the Durham Veterans Affairs Medical Center who were free of prostate cancer, had not undergone prostate surgery or taken medications known to alter androgen levels and who had at least one PSA value within 2 years before and at least one PSA value within 1 year after starting a statin. The change in PSA from before to after statin treatment was analyzed as a continuous variable using the Wilcoxon signed rank test. The association between change in PSA and change in cholesterol parameters (low-density lipoprotein [LDL], high-density lipoprotein [HDL], and total cholesterol) was analyzed using multivariate linear regression. All statistical tests were two-sided. Mean (SD) age when starting statins was 60.3 (8.3) years; median prestatin PSA concentration was 0.9 (1.9) ng/mL; and mean prestatin LDL cholesterol concentration was 144 (34) mg/dL. After starting a statin, the median LDL decline was 27.5%, and the median PSA decline was 4.1% (P < .001, for both comparisons). Changes in PSA concentration were strongly associated with statin dose and changes in LDL levels. For every 10% decrease in LDL after starting a statin, PSA levels declined by 1.64 (95 % confidence interval [CI] = 0.64% to 2.65%, p = .001). Among men most likely to be under consideration for prostate biopsy (prestatin PSA levels > or =2.5 ng/mL, n = 188), those with >41% declines in LDL (highest quartile) after starting a statin experienced a 17.4% (95% CI = 10.0% to 24.9%) decline in serum PSA. PSA levels declined by a statistically significant extent after initiation of statin treatment. The reduction was most pronounced among men with the largest LDL declines and those with PSA levels that would make them candidates for prostate biopsy. By lowering PSA levels, statins may complicate cancer detection, although further studies are needed to quantify the clinical significance of this effect.

How sensitive is a prostate-specific antigen measurement? How sensitive does it need to be?

Abstract Assays are now available that can measure very low concentrations of prostate-specific antigen (PSA), but their analytic performance and clinical utility are not well defined. This brief article highlights some of the clinical issues related to the limited prognostic significance of small changes in PSA concentrations in men with prostate cancer who have been treated with prostate ablation therapy. College of American Pathologists proficiency survey data are presented, illustrating the performance of commercial PSA assays with low PSA concentration survey samples tested between 1998 and 2002. The performance of the assays appears to be improving, but many of the currently used assays have intralaboratory coefficients of variation greater than 20% for PSA concentrations less than 0.4 ng/mL. Also, there are major differences in the level of PSA reported by various assays in these low concentration samples. These level differences (if they are also seen in clinical samples) may cause clinical proble...

Postejaculation Serum Prostate-Specific Antigen Level

This study was carried out to determine whether ejaculation may modify the serum prostate-specific antigen (PSA) level and to investigate whether postejaculation serum PSA may play a role in male hypofertility work-up. Serum PSA concentration was determined before and 1 h after ejaculation in 18 healthy men (group A) and in 16 men with male-factor infertility (group B). PSA change (delta) was recorded and analyzed. Postejaculation serum PSA differed significantly from basal levels (p = 0.0037 by the Wilcoxon signed rank test). Following ejaculation, a rise was noticed in 74% of subjects. The median relative change in PSA concentration was 54%. No difference in respect to mean, median and relative change was observed between study groups. In two cases (6%), PSA rose from normal level to more than 4 ng/ml. A significant postejaculation serum PSA elevation does occur, it is thus recommended that men abstain from ejaculation for 24 h prior to PSA sampling. Postejaculation PSA was not found to significantly correlate with hypofertility.

Ejaculation increases the serum prostate-specific antigen concentration

To determine the effect of ejaculation on the serum prostate-specific antigen (PSA) concentration in men at risk for developing prostate cancer. A prospective, community-based study was conducted in which 64 men, aged 49 to 79 years, underwent a serum PSA determination immediately before ejaculation (baseline) and at 1 hour, 6 hours, and 24 hours following ejaculation. The serum PSA also was measured 48 hours and 1 week after ejaculation if the concentration had not returned to the baseline value by the previous time interval. All subjects abstained from ejaculation for a minimum of 7 days prior to the study and until the PSA concentration returned to the baseline level. Absolute and relative change in serum PSA concentration, as well as the time to return to baseline PSA concentration following ejaculation, were assessed. The serum PSA concentration increased following ejaculation in 87% of the subjects. The mean baseline PSA was 1.8 ng/mL (median, 0.7 ng/mL). The mean absolute PSA change +/- standard deviation 1 hour, 6 hours, 24 hours, and 48 hours after ejaculation was 0.8 +/- 1.32 ng/mL, 0.3 +/- 0.66 ng/mL, 0.2 +/- 0.33 ng/mL, and 0.4 +/- 0.40 ng/mL, respectively. The mean relative PSA change +/- standard error 1 hour, 6 hours, 24 hours, and 48 hours after ejaculation was 41 +/- 4%, 9 +/- 1.5%, 8 +/- 1.3%, and 10 +/- 2.3%, respectively. The absolute and relative changes in PSA concentration noted 1 hour, 6 hours, and 24 hours after ejaculation were statistically significant (P = 0.0001). A strong correlation was observed between absolute change in PSA and baseline serum PSA, at each time interval (1 hour: r = 0.68, 6 hours: r = 0.77, 24 hours: r = 0.70; P < 0.0001) after ejaculation. Similarly, a significant correlation was noted between absolute change in PSA and patient age at each time interval (1 hour: r = 0.37, 6 hours: r = 0.38; P = 0.002, 24 hours: r = 0.55; P < 0.0001). Ninety-two percent of subjects returned to baseline by 24 hours (95% confidence interval (Cl) = 83% to 97%), whereas 97% of subjects returned to baseline by 48 hours (95% Cl = 89% to 99%). Ejaculation causes a significant increase in the serum PSA concentration in men between 49 and 79 years of age that may persist for up to 48 hours. This change appears to correlate with age and baseline PSA. It is recommended that men abstain from ejaculation for 48 hours prior to having a serum PSA determination.

Abrupt changes in prostate-specific antigen concentration in acute renal failure

Journal Article Abrupt changes in prostate-specific antigen concentration in acute renal failure Get access A Price A Price Search for other works by this author on: Oxford Academic Google Scholar Clinical Chemistry, Volume 39, Issue 1, 1 January 1993, Pages 161–162, https://doi.org/10.1093/clinchem/39.1.161 Published: 01 January 1993