madman
Super Moderator
Abstract
Context: Clinical guidelines recommend measurement of the serum prostate-specific antigen (PSA) concentration during testosterone treatment of hypogonadal men to determine whether the increase is sufficiently high to warrant urologic referral. Prior studies of the effect of testosterone treatment on PSA concentrations have been conducted in men who were mild to moderately hypogonadal.
Objective: The objective of this work is to determine the PSA response to testosterone treatment of men who are severely hypogonadal.
Design and Setting: This retrospective cohort study was conducted at a single academic medical center.
Participants: Eighty-five men participated who were severely hypogonadal as a result of the hypothalamic-pituitary or testicular disease.
Main Outcome Measure: Changes in serum PSA concentrations were measured during testosterone treatment for up to 18 months. Results: Testosterone treatment increased the median serum testosterone concentration from 36 ng/dL (interquartile range [IQR], 20-91 ng/dL) at baseline to 395 ng/dL (IQR, 266-542 ng/dL) at 6 to 18 months. This treatment resulted in a median increment in PSA above the baseline of 0.70 ng/mL (IQR, 0.10-1.85 ng/mL) at 6 to 18 months. Apropos current Endocrine Society clinical guidelines, 31% of the men experienced a PSA increase above baseline greater than 1.4 ng/ml, and 13% reached an absolute PSA concentration of greater than 4.0 ng/mL. Four men were diagnosed with prostate cancer.
Conclusions: The PSA response to testosterone replacement in men who are severely hypogonadal as a result of pituitary or testicular disease is greater than that previously reported in men with mild to moderate hypogonadism. These results suggest the magnitude of the PSA response to testosterone replacement is related to the degree of hypogonadism.
Testosterone stimulates the growth and function of the prostate gland, including production of the enzyme prostate-specific antigen (PSA). Testosterone treatment of hypogonadal men has long been known to increase their serum PSA concentrations.
Prostate cancer also causes an increase in the serum PSA concentration [1], so it is common practice to monitor the PSA concentration in a man treated with testosterone to determine whether an increase is within the range expected or sufficiently high to warrant urological referral to evaluate for prostate cancer. Endocrine Society clinical guidelines recommend measuring serum PSA in hypogonadal men older than 50 years 3 and 12 months after initiating testosterone therapy and referring men for urologic evaluation if the serum PSA increases more than 1.4 ng/mL above baseline or to an absolute value of more than 4.0 ng/mL [2]. Neither of these criteria, however, are based on testosterone treatment of hypogonadal men.
A. Strength and Limitations
These findings demonstrate the degree to which serum PSA can be expected to increase in a relatively large number of men who meet the FDA indication for testosterone treatment of classical hypogonadism [5]. Some limitations of this study are the result of its retrospective nature—a review of patients in clinical practice—although that could also make the results more generally applicable to clinical practice. Because the study was retrospective, there was no prespecified protocol for referral for urologic evaluation, which would have influenced the number of biopsies and the diagnosis of prostate cancer. Other limitations are the lack of a control group, lack of data on lower urinary tract symptoms, and incomplete PSA results in about 20% of the men. Because most men in this study were using transdermal testosterone preparations, the results apply primarily to these preparations. This study examined the effect of testosterone treatment on PSA concentrations for up to 18 months, so we do not know the effect afterward
4. Conclusions
The results presented here demonstrate that the PSA responses to testosterone replacement in men who are severely hypogonadal as a result of hypothalamic-pituitary or testicular causes are greater than previously reported in men with mild to moderate hypogonadism primarily due to normal aging. These results suggest that the magnitude of the PSA response to testosterone replacement is related to the degree of hypogonadism. These results also suggest that testosterone treatment of severely hypogonadal men often increases PSA above the commonly accepted thresholds for a urologic referral.
Context: Clinical guidelines recommend measurement of the serum prostate-specific antigen (PSA) concentration during testosterone treatment of hypogonadal men to determine whether the increase is sufficiently high to warrant urologic referral. Prior studies of the effect of testosterone treatment on PSA concentrations have been conducted in men who were mild to moderately hypogonadal.
Objective: The objective of this work is to determine the PSA response to testosterone treatment of men who are severely hypogonadal.
Design and Setting: This retrospective cohort study was conducted at a single academic medical center.
Participants: Eighty-five men participated who were severely hypogonadal as a result of the hypothalamic-pituitary or testicular disease.
Main Outcome Measure: Changes in serum PSA concentrations were measured during testosterone treatment for up to 18 months. Results: Testosterone treatment increased the median serum testosterone concentration from 36 ng/dL (interquartile range [IQR], 20-91 ng/dL) at baseline to 395 ng/dL (IQR, 266-542 ng/dL) at 6 to 18 months. This treatment resulted in a median increment in PSA above the baseline of 0.70 ng/mL (IQR, 0.10-1.85 ng/mL) at 6 to 18 months. Apropos current Endocrine Society clinical guidelines, 31% of the men experienced a PSA increase above baseline greater than 1.4 ng/ml, and 13% reached an absolute PSA concentration of greater than 4.0 ng/mL. Four men were diagnosed with prostate cancer.
Conclusions: The PSA response to testosterone replacement in men who are severely hypogonadal as a result of pituitary or testicular disease is greater than that previously reported in men with mild to moderate hypogonadism. These results suggest the magnitude of the PSA response to testosterone replacement is related to the degree of hypogonadism.
Testosterone stimulates the growth and function of the prostate gland, including production of the enzyme prostate-specific antigen (PSA). Testosterone treatment of hypogonadal men has long been known to increase their serum PSA concentrations.
Prostate cancer also causes an increase in the serum PSA concentration [1], so it is common practice to monitor the PSA concentration in a man treated with testosterone to determine whether an increase is within the range expected or sufficiently high to warrant urological referral to evaluate for prostate cancer. Endocrine Society clinical guidelines recommend measuring serum PSA in hypogonadal men older than 50 years 3 and 12 months after initiating testosterone therapy and referring men for urologic evaluation if the serum PSA increases more than 1.4 ng/mL above baseline or to an absolute value of more than 4.0 ng/mL [2]. Neither of these criteria, however, are based on testosterone treatment of hypogonadal men.
A. Strength and Limitations
These findings demonstrate the degree to which serum PSA can be expected to increase in a relatively large number of men who meet the FDA indication for testosterone treatment of classical hypogonadism [5]. Some limitations of this study are the result of its retrospective nature—a review of patients in clinical practice—although that could also make the results more generally applicable to clinical practice. Because the study was retrospective, there was no prespecified protocol for referral for urologic evaluation, which would have influenced the number of biopsies and the diagnosis of prostate cancer. Other limitations are the lack of a control group, lack of data on lower urinary tract symptoms, and incomplete PSA results in about 20% of the men. Because most men in this study were using transdermal testosterone preparations, the results apply primarily to these preparations. This study examined the effect of testosterone treatment on PSA concentrations for up to 18 months, so we do not know the effect afterward
4. Conclusions
The results presented here demonstrate that the PSA responses to testosterone replacement in men who are severely hypogonadal as a result of hypothalamic-pituitary or testicular causes are greater than previously reported in men with mild to moderate hypogonadism primarily due to normal aging. These results suggest that the magnitude of the PSA response to testosterone replacement is related to the degree of hypogonadism. These results also suggest that testosterone treatment of severely hypogonadal men often increases PSA above the commonly accepted thresholds for a urologic referral.
