Hypogonadism following prostate-bed radiation therapy for prostate carcinoma

Daniell, Henry; Clark, John C.; Pereira, Sharon; Niazi, Ziad; Ferguson, David W.; Dunn, Stephen; Figueroa, Michael L.; Stratte, P. Tryg

doi:10.1002/1097-0142(20010515)91:10<1889::aid-cncr1211>3.0.co;2-u

Cited by 69 publications

(43 citation statements)

References 25 publications

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“…The association between male hypogonadism and osteoporosis is further supported by reports of fractures occurring after external beam radiation therapy to the prostate bed for prostate cancer [89][90][91][92] (Table 2). In addition, pelvic or rib fracture can occur in relation with bone local irradiation [93,94].…”

Section: Sex Hormone Deprivation Therapy With Gnrh Agonists and Antagmentioning

confidence: 58%

Cancer-associated bone disease

Rizzoli

Body²,

Brandi³

et al. 2013

Osteoporos Int

128

103

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Bone is commonly affected in cancer. Cancer-induced bone disease results from the primary disease, or from therapies against the primary condition, causing bone fragility. Bone-modifying agents, such as bisphosphonates and denosumab, are efficacious in preventing and delaying cancer-related bone disease. With evidence-based care pathways, guidelines assist physicians in clinical decision-making. Of the 57 million deaths in 2008 worldwide, almost two thirds were due to non-communicable diseases, led by cardiovascular diseases and cancers. Bone is a commonly affected organ in cancer, and although the incidence of metastatic bone disease is not well defined, it is estimated that around half of patients who die from cancer in the USA each year have bone involvement. Furthermore, cancer-induced bone disease can result from the primary disease itself, either due to circulating bone resorbing substances or metastatic bone disease, such as commonly occurs with breast, lung and prostate cancer, or from therapies administered to treat the primary condition thus causing bone loss and fractures. Treatment-induced osteoporosis may occur in the setting of glucocorticoid therapy or oestrogen deprivation therapy, chemotherapy-induced ovarian failure and androgen deprivation therapy. Tumour skeletal-related events include pathologic fractures, spinal cord compression, surgery and radiotherapy to bone and may or may not include hypercalcaemia of malignancy while skeletal complication refers to pain and other symptoms. Some evidence demonstrates the efficacy of various interventions including bone-modifying agents, such as bisphosphonates and denosumab, in preventing or delaying cancer-related bone disease. The latter includes treatment of patients with metastatic skeletal lesions in general, adjuvant treatment of breast and prostate cancer in particular, and the prevention of cancerassociated bone disease. This has led to the development of guidelines by several societies and working groups to assist physicians in clinical decision making, providing them with evidencebased care pathways to prevent skeletal-related events and bone loss. The goal of this paper is to put forth an IOF position paper addressing bone diseases and cancer and summarizing the position papers of other organizations. Epidemiology of cancer-associated bone disease Bone metastasisCancer affects nearly 12.7 million people and is associated with over 7 million deaths in 2008 [1]. Cancer is a rising global health burden and it is estimated that in 2030, cancer deaths will be tallied at over 13 million (World Health Organization (WHO) 2010 Global Status Report [2]). Addressing the morbidity and mortality of cancer is an important public health concern. On purpose, we are limiting our analysis to cancer bone involvement in adults and do not discuss cancer in children.Metastases from cancer are associated with 90 % of cancer deaths [3]. It was estimated that one half of people who die from cancer in the USA have bone involvement [4][5][6]. Different tumou...

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Section: Sex Hormone Deprivation Therapy With Gnrh Agonists and Antagmentioning

confidence: 58%

Cancer-associated bone disease

Rizzoli

Body²,

Brandi³

et al. 2013

Osteoporos Int

128

103

View full text Add to dashboard Cite

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“…Daniell et al compared 33 patients who had received external-beam radiotherapy and 55 patients who had undergone prostatectomy without external-beam radiotherapy. After a follow-up of 3-8 years they found a significant decrease in testosterone levels, and an increase in LH and FSH levels for the irradiated group, indicating that prostate bed irradiation leads to a prominent and permanent testicular damage [7,8]. Older studies investigating the effect of prostate external-beam radiotherapy found similar results concerning FSH and LH serum levels, but on the other hand, the measured low testosterone levels returned to normal values within 2 years of follow-up [14,32].…”

Section: Discussionmentioning

confidence: 90%

“…Higher doses between 14 and 20 Gy can lead to a long-lasting impairment of the hormonal testicular function in humans [30]. On the other hand, there is evidence that external-beam radiotherapy of prostate cancer patients results in a significant and persistent change in hormone levels even after a follow-up of 3-8 years, which significantly increased the rate of hypogonadism and testicular atrophy [7,8]. In 52 men with paraaortic lymph node irradiation after operation for stage I seminoma, the calculated mean dose to the testicles was 22 cGy.…”

Section: Introductionmentioning

confidence: 99%

Testicular Dose in Prostate Cancer Radiotherapy

et al. 2005

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“…17,18 Recently, Zagars et al 19 demonstrated a statistically significant decrease in testosterone at 3 months after EBRT, and Daniell et al 20 reported lowered testosterone levels at 3-8 years after EBRT compared with patients treated with RP. Most previous studies which investigated testosterone recovery included patients treated by ADT combined with EBRT and did not set a control group receiving EBRT alone.…”

Section: Discussionmentioning

confidence: 99%

Kinetics of testosterone recovery in clinically localized prostate cancer patients treated with radical prostatectomy and subsequent short-term adjuvant androgen deprivation therapy

Dai¹,

Qu²,

Kong³

et al. 2013

Asian J Androl

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Androgen deprivation therapy (ADT) is a standard treatment for metastatic, recurrent and locally advanced prostate cancer (PCa). The aim of this study is to investigate the timing and extent of testosterone recovery in clinically localized PCa patients treated with radical prostatectomy (RP) and subsequent short-term adjuvant ADT. A total of 95 localized PCa patients underwent RP and 9-month adjuvant ADT were included in this prospective study. Serum testosterone level was measured before adjuvant ADT, at ADT cessation, and at 1, 3, 6, 9 and 12 months after cessation of ADT. A Cox proportional hazards model was used to assess variables associated with the time of testosterone normalization. The results showed that median patient age was 67 years and median testosterone level before adjuvant ADT was 361 (230-905) ng dl 21 . All patients finished 9-month adjuvant ADT and achieved castrate testosterone level. At 3 months after ADT cessation, testosterone recovered to supracastrate level in 97.9% patients and to normal level in 36.9% patients. The percentage of patients who recovered to normal testosterone level increased to 66.3%, 86.3% and 92.6% at 6, 9 and 12 months, respectively. Cox regression model found that higher baseline testosterone level (o300 ng dl 21 ) was the only variable associated with a shorter time to testosterone normalization (hazard ratio: 1.98; P 5 0.012). In conclusion, in most patients, testosterone recovered to supracastrate level at 3 months and to normal level at 12 months after 9-month adjuvant ADT cessation. Patients with higher baseline testosterone level need shorter time of testosterone normalization.

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Hypogonadism following prostate-bed radiation therapy for prostate carcinoma

Cited by 69 publications

References 25 publications

Cancer-associated bone disease

Cancer-associated bone disease

Testicular Dose in Prostate Cancer Radiotherapy

Kinetics of testosterone recovery in clinically localized prostate cancer patients treated with radical prostatectomy and subsequent short-term adjuvant androgen deprivation therapy

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