scholarly journals Prostate-Specific Antigen Levels During Testosterone Treatment of Hypogonadal Older Men: Data from a Controlled Trial

2019 ◽  
Vol 104 (12) ◽  
pp. 6238-6246 ◽  
Author(s):  
Glenn R Cunningham ◽  
Susan S Ellenberg ◽  
Shalender Bhasin ◽  
Alvin M Matsumoto ◽  
J Kellogg Parsons ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Placebo Group ◽  
Prostate Specific Antigen ◽  
Controlled Trial ◽  
Specific Antigen ◽  
Older Men ◽  
Placebo Treatment ◽  
Testosterone Treatment ◽  
Testosterone Levels ◽  
Double Blinded

Abstract Context Prostate-specific antigen (PSA) changes during testosterone treatment of older hypogonadal men have not been rigorously evaluated. Design Double-blinded, placebo-controlled trial. Setting Twelve US academic medical centers. Participants Seven hundred ninety hypogonadal men ≥65 years of age with average testosterone levels ≤275 ng/dL. Men at high risk for prostate cancer were excluded. Interventions Testosterone or placebo gel for 12 months. Main Outcomes Percentile changes in PSA during testosterone treatment of 12 months. Results Testosterone treatment that increased testosterone levels from 232 ± 63 ng/dL to midnormal was associated with a small but substantially greater increase (P < 0.001) in PSA levels than placebo treatment. Serum PSA levels increased from 1.14 ± 0.86 ng/mL (mean ± SD) at baseline by 0.47 ± 1.1 ng/mL at 12 months in the testosterone group and from 1.25 ± 0.86 ng/mL by 0.06 ± 0.72 ng/mL in the placebo group. Five percent of men treated with testosterone had an increase ≥1.7 ng/mL and 2.5% of men had an increase of ≥3.4 ng/mL. A confirmed absolute PSA >4.0 ng/mL at 12 months was observed in 1.9% of men in the testosterone group and 0.3% in the placebo group. Four men were diagnosed with prostate cancer; two were Gleason 8. Conclusions When hypogonadal older men with normal baseline PSA are treated with testosterone, 5% had an increase in PSA ≥1.7 ng/mL, and 2.5% had an increase ≥3.4 ng/mL.

scholarly journals Prostate-specific antigen bounce after 125I-brachytherapy for prostate cancer is a favorable prognosticator in patients who are biochemical recurrence-free at 4 years and correlates with testosterone

2019 ◽  
Vol 50 (1) ◽  
pp. 58-65 ◽  
Author(s):  
Yasushi Nakai ◽  
Nobumichi Tanaka ◽  
Isao Asakawa ◽  
Satoshi Anai ◽  
Makito Miyake ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Prostate Specific Antigen ◽  
Biochemical Recurrence ◽  
Specific Antigen ◽  
Testosterone Levels ◽  
Psa Bounce ◽  
125I Brachytherapy ◽  
Psa Nadir ◽  
Free Rate

Abstract Background Because patients with prostate-specific antigen (PSA) bounce do not experience biochemical recurrence (BCR) until PSA bounce occurs, the period until PSA bounce ends can be considered the so-called lead-time bias. Therefore, we evaluated differences in BCR-free rate in prostate cancer patients who were BCR-free 4 years after 125I-brachytherapy alone. Furthermore, we evaluated predictors for PSA bounce and the correlation between testosterone and PSA bounce. Methods From 2004 to 2012, 256 patients with prostate adenocarcinoma underwent 125I-brachytherapy alone. PSA and testosterone levels were monitored prior to 125I-brachytherapy, at 1, 3, 6, 12, 18, 24, 30, 36, 42, 48, 54 and 60 months after 125I-brachytherapy and yearly after 5-year follow-up. PSA bounce was defined as ≥0.2 ng/ml increase above the interval PSA nadir, followed by a decrease to nadir or below. Results BCR-free rate in patients with PSA bounce (100% 7-year BCR-free rate) was significantly better (P &lt; 0.044) than that in patients without PSA bounce (95.7% 7-year BCR-free rate) in patients who were BCR-free 4 years after 125I-brachytherapy alone (n = 223). Age was the only predictor (odds ratio: 0.93, 95% confidence interval: 0.88–0.98, P = 0.004) for PSA bounce (n = 177). The testosterone level at PSA bounce was significantly higher (P = 0.036) than that at nadir before PSA bounce (87 cases). Conclusions Patients with PSA bounce had good BCR-free rate even in patients who were BCR-free 4 years after 125I-brachytherapy alone. Testosterone levels were higher at PSA bounce; increased testosterone levels may be a cause of PSA bounce.

Physical Therapy for Patellofemoral Pain

2002 ◽  
Vol 30 (6) ◽  
pp. 857-865 ◽  
Author(s):  
Kay Crossley ◽  
Kim Bennell ◽  
Sally Green ◽  
Sallie Cowan ◽  
Jenny McConnell
Keyword(s):  
Placebo Group ◽  
Physical Therapy ◽  
Therapy Group ◽  
Controlled Trial ◽  
Placebo Treatment ◽  
Quadriceps Muscle ◽  
Patellofemoral Pain ◽  
Therapy Regimen ◽  
Average Pain ◽  
Double Blinded

Background Although physical therapy forms the mainstay of nonoperative management for patellofemoral pain, its efficacy has not been established. Hypothesis Significantly more pain relief will be achieved from a 6-week regimen of physical therapy than from placebo treatment. Study Design Multicenter, randomized, double-blinded, placebo-controlled trial. Methods Seventy-one subjects, 40 years of age or younger with patellofemoral pain of 1 month or longer, were randomly allocated to a physical therapy or placebo group. A standardized treatment program consisted of six treatment sessions, once weekly. Physical therapy included quadriceps muscle retraining, patellofemoral joint mobilization, and patellar taping, and daily home exercises. The placebo treatment consisted of sham ultrasound, light application of a nontherapeutic gel, and placebo taping. Results Sixty-seven participants completed the trial. The physical therapy group (N = 33) demonstrated significantly greater reduction in the scores for average pain, worst pain, and disability than did the placebo group (N = 34). Conclusions A six-treatment, 6-week physical therapy regimen is efficacious for alleviation of patellofemoral pain.

Evaluation of Tamoxifen and Anastrozole in the Prevention of Gynecomastia and Breast Pain Induced by Bicalutamide Monotherapy of Prostate Cancer

2005 ◽  
Vol 23 (4) ◽  
pp. 808-815 ◽  
Author(s):  
F. Boccardo ◽  
A. Rubagotti ◽  
M. Battaglia ◽  
P. Di Tonno ◽  
F.P. Selvaggi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Adverse Events ◽  
Sexual Functioning ◽  
Controlled Trial ◽  
Locally Advanced ◽  
Specific Antigen ◽  
Sex Hormone Binding Globulin ◽  
Breast Pain ◽  
Testosterone Levels ◽  
Tamoxifen Group

Purpose To determine whether tamoxifen or anastrozole prevents gynecomastia and breast pain caused by bicalutamide (150 mg) without compromising efficacy, safety, or sexual functioning. Patients and Methods A double-blind, placebo-controlled trial was performed in patients with localized, locally advanced, or biochemically recurrent prostate cancer. Patients (N = 114) were randomly assigned to either bicalutamide (150 mg/d) plus placebo or in combination with tamoxifen (20 mg/d) or anastrozole (1 mg/d) for 48 weeks. Gynecomastia, breast pain, prostate-specific antigen (PSA), sexual functioning, and serum levels of hormones were assessed. Results Gynecomastia developed in 73% of patients in the bicalutamide group, 10% of patients in the bicalutamide-tamoxifen group, and 51% of patients in the bicalutamide-anastrozole group (P < .001); breast pain developed in 39%, 6%, and 27% of patients, respectively (P = .006). Baseline PSA level decreased by ≥ 50% in 97%, 97%, and 83% of patients in the bicalutamide, bicalutamide-tamoxifen, and bicalutamide-anastrozole groups, respectively (P = .07); and adverse events were reported in 37%, 35%, and 69% of patients, respectively (P = .004). There were no major differences among treatments in sexual functioning parameters from baseline to month 6. Elevated testosterone levels occurred in each group; however, free testosterone levels remained unchanged in the bicalutamide-tamoxifen group because of increased sex hormone–binding globulin levels. Conclusion Anastrozole did not significantly reduce the incidence of bicalutamide-induced gynecomastia and breast pain. In contrast, tamoxifen was effective, without increasing adverse events, at least in the short-term follow-up. These data support the need for a larger study to determine any effect on mortality.

scholarly journals Baseline Prostate-Specific Antigen Levels in Midlife Predict Lethal Prostate Cancer

2016 ◽  
Vol 34 (23) ◽  
pp. 2705-2711 ◽  
Author(s):  
Mark A. Preston ◽  
Julie L. Batista ◽  
Kathryn M. Wilson ◽  
Sigrid V. Carlsson ◽  
Travis Gerke ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Prostate Specific Antigen ◽  
Controlled Trial ◽  
Conditional Logistic Regression ◽  
Characteristic Curve ◽  
Specific Antigen ◽  
Health Study ◽  
Opportunistic Screening ◽  
Odds Ratios ◽  
Baseline Psa

Purpose Prostate-specific antigen (PSA) level in midlife predicted future prostate cancer (PCa) mortality in an unscreened Swedish population. Our purpose was to determine if a baseline PSA level during midlife predicts lethal PCa in a US population with opportunistic screening. Materials and Methods We conducted a nested case-control study among men age 40 to 59 years who gave blood before random assignment in the Physicians’ Health Study, a randomized, placebo-controlled trial of aspirin and β-carotene among 22,071 US male physicians initiated in 1982 and then transitioned into a prospective cohort with 30 years of follow-up. Baseline PSA levels were available for 234 patients with PCa and 711 age-matched controls. Seventy-one participants who developed lethal PCa were rematched to 213 controls. Conditional logistic regression was used to estimate odds ratios and the area under the receiver operating characteristic curve, with 95% CIs, of the association between baseline PSA and risk of lethal PCa. Results Median PSA among controls was 0.68, 0.88, and 0.96 ng/mL for men age 40 to 49, 50 to 54, and 55 to 59 years, respectively. Risk of lethal PCa was strongly associated with baseline PSA in midlife: odds ratios (95% CIs) comparing PSA in the > 90th percentile versus less than or equal to median were 8.7 (1.0 to 78.2) at 40 to 49 years, 12.6 (1.4 to 110.4) at 50 to 54 years, and 6.9 (2.5 to 19.1) at 55 to 59 years. A total of 82%, 71%, and 86% of lethal cases occurred in men with PSA above the median at ages 40 to 49, 50 to 54, and 55 to 59 years, respectively. Conclusion PSA levels in midlife strongly predict future lethal PCa in a US cohort subject to opportunistic screening. Risk-stratified screening on the basis of midlife PSA should be considered in men age 45 to 59 years.

scholarly journals Denosumab and Bone Metastasis–Free Survival in Men With Nonmetastatic Castration-Resistant Prostate Cancer: Exploratory Analyses by Baseline Prostate-Specific Antigen Doubling Time

2013 ◽  
Vol 31 (30) ◽  
pp. 3800-3806 ◽  
Author(s):  
Matthew R. Smith ◽  
Fred Saad ◽  
Stephane Oudard ◽  
Neal Shore ◽  
Karim Fizazi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Placebo Group ◽  
Bone Metastasis ◽  
Prostate Specific Antigen ◽  
Doubling Time ◽  
Specific Antigen ◽  
Castration Resistant Prostate Cancer ◽  
Primary Analysis ◽  
Free Survival ◽  
Castration Resistant

Purpose Denosumab, an anti–RANK ligand monoclonal antibody, significantly increases bone metastasis–free survival (BMFS; hazard ratio [HR], 0.85; P = .028) and delays time to first bone metastasis in men with nonmetastatic castration-resistant prostate cancer (CRPC) and baseline prostate-specific antigen (PSA) ≥ 8.0 ng/mL and/or PSA doubling time (PSADT) ≤ 10.0 months. To identify men at greatest risk for bone metastasis or death, we evaluated relationships between PSA and PSADT with BMFS in the placebo group and the efficacy and safety of denosumab in men with PSADT ≤ 10, ≤ 6, and ≤ 4 months. Patients and Methods A total of 1,432 men with nonmetastatic CRPC were randomly assigned 1:1 to monthly subcutaneous denosumab 120 mg or placebo. Enrollment began February 2006; primary analysis cutoff was July 2010, when approximately 660 men were anticipated to have developed bone metastases or died. Results In the placebo group, shorter BMFS was observed as PSADT decreased below 8 months. In analyses by shorter baseline PSADT, denosumab consistently increased BMFS by a median of 6.0, 7.2, and 7.5 months among men with PSADT ≤ 10 (HR, 0.84; P = .042), ≤ 6 (HR, 0.77; P = .006), and ≤ 4 months (HR, 0.71; P = .004), respectively. Denosumab also consistently increased time to bone metastasis by PSADT subset. No difference in survival was observed between treatment groups for the overall study population or PSADT subsets. Conclusion Patients with shorter PSADT are at greater risk for bone metastasis or death. Denosumab consistently improves BMFS in men with shorter PSADT and seems to have the greatest treatment effects in men at high risk for progression.

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