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Bone loss following hypogonadism in men with prostate cancer treated with GnRH analogs
Daniella Mittan1, Shuko Lee, Elizabeth Miller
1Department of Medicine, University of Texas Health Science Center at San Antonio 78229, USA.
Abstract:
It is known that bone mineral density (BMD) is low in men who are hypogonadal. However, the rate and sites of bone loss following testosterone deficiency are not known. The resulting hypogonadism after GnRH analog therapy for the treatment of prostate cancer allows us to examine bone loss and bone resorption immediately after testosterone withdrawal. Therefore, we examined the effects of GnRH analog treatment on bone loss and bone resorption in men with prostate cancer. BMD and serum and urine concentrations of markers of bone turnover were determined in men with prostate cancer and in age-matched controls. Measurements were taken before GnRH therapy and 6 and 12 months after instituting therapy. After 12 months of GnRH therapy, the BMD of the total hip and ultra distal radius decreased significantly (P < 0.001) in men with prostate cancer compared with the controls. The mean bone loss was 3.3% and 5.3%, respectively. The observed reduction in BMD in the spine (2.8%) and the femoral neck (2.3%) did not reach statistical significance. No significant bone loss was observed in the control subjects. The concentration of the urine marker of bone resorption, N-telopeptide, was significantly increased from baseline and from controls at both 6 and 12 months in patients treated with GnRH analog therapy compared with control subjects (P < 0.05). The concentration of a serum marker of bone formation, bone-specific alkaline phosphatase, was not significantly different from baseline or from controls at 6 and 12 months. Thus, the decreased total hip and ultra distal radius BMD and increased urinary N-telopeptide concentration after testosterone withdrawal demonstrate an increase in trabecular bone loss and enhanced bone resorption. These findings demonstrate a significant loss of bone in men with prostate cancer after receiving GnRH therapy and suggest that the total hip and radius are the preferred sites for monitoring bone loss in older men. In addition, markers of bone resorption may be helpful.
Insights
Testosterone deficiency from GnRH analog therapy causes significant bone loss in prostate cancer patients, particularly at the total hip and radius. Bone resorption markers increased, indicating trabecular bone loss and enhanced resorption.
Area of Science:
- Endocrinology
- Oncology
- Bone Metabolism
Background:
- Hypogonadism is linked to low bone mineral density (BMD).
- The rate and specific sites of bone loss after testosterone deficiency are not well understood.
- GnRH analog therapy for prostate cancer induces hypogonadism, providing a model to study bone loss.
Purpose of the Study:
- To investigate the effects of GnRH analog therapy on bone loss and bone resorption in men with prostate cancer.
- To determine the rate and sites of bone loss following testosterone withdrawal.
Main Methods:
- Bone mineral density (BMD) was measured in prostate cancer patients and age-matched controls before and 12 months after GnRH analog therapy.
- Serum and urine markers of bone turnover, including N-telopeptide (resorption) and bone-specific alkaline phosphatase (formation), were analyzed.
Main Results:
- After 12 months, significant BMD decrease (3.3% hip, 5.3% radius) was observed in patients compared to controls (P < 0.001).
- Urinary N-telopeptide levels significantly increased, indicating enhanced bone resorption (P < 0.05).
- Bone-specific alkaline phosphatase levels showed no significant change.
Conclusions:
- Testosterone withdrawal via GnRH analog therapy leads to significant trabecular bone loss, particularly at the total hip and radius.
- Increased bone resorption markers suggest GnRH therapy accelerates bone loss in prostate cancer patients.
- The total hip and radius are recommended sites for monitoring bone loss in this population.
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