Histological and Functional Changes of the Testis Tissue During GnRH Agonist Treatment of Prostatic Cancer

Huhtaniemi, Ilpo; Nikula, Hannu; Parvinen, Martti; Rannikko, S.

doi:10.1097/00000421-198812001-00003

Cited by 22 publications

(17 citation statements)

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“…Huhtaniemi et al. [16,17] reported on histological changes in the orchidectomised testis after 6 months of LHRHa therapy, showing that the seminiferous tubules and Sertoli cells were affected with no obvious changes in the number of Leydig cells; moreover, the testicular FSH receptor content was reduced by 80% while the LH receptor content was unchanged. This might lead to a stronger negative‐feedback mechanism for FSH.…”

Section: Discussionmentioning

confidence: 99%

Recovery of serum testosterone after neoadjuvant androgen deprivation therapy and radical radiotherapy in localized prostate cancer

et al. 2006

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before treatment (baseline), during LHRHa treatment, and at 6, 12, 18, 24 and > 40 weeks after the last LHRHa injection. RESULTSThe median (range) time from the first to last LHRHa injection was 116 (54-194) days. The mean (95% confidence interval) testosterone levels (in nmol/L) at baseline, during treatment and at 6, 12, 18, 24 and > 40 weeks afterward were 12.0 (10.8-13.1), 0.6 (0.5-0.7), 1.4 (0.6-2.2), 11.4 (9.7-13), 12.2 (10.5-14), 10.4 (8.9-12) and 11.7 (10.5-13). Four men had low baseline testosterone levels ( < 6.1 nmol/L). At 6 weeks after the last LHRHa injection, no men had testosterone levels in the 'normal' range; 35% were in the normal range at 12 weeks, 85% at 18 weeks, 89% at 24 weeks, and 96% at 1 year. CONCLUSIONAfter LHRHa treatment and radiotherapy, the testosterone levels of most men had recovered to normal by 18-24 weeks after the last LHRHa injection.

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Section: Discussionmentioning

confidence: 99%

Recovery of serum testosterone after neoadjuvant androgen deprivation therapy and radical radiotherapy in localized prostate cancer

et al. 2006

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“…This implies dissociation between inhibin B and AMH secretion following long-term exposure to GnRHa. Huhtaniemi et al (14) observed a reduction in testicular FSH receptors by 80% without a change in LH receptors following 6 months of GnRHa treatment. This may explain our findings, since in contrast to AMH, inhibin B secretion is FSH dependent.…”

Section: Discussionmentioning

confidence: 99%

“…This is supported by the observation that in contrast to full LH and testosterone suppression, inhibin B levels were only partially suppressed. Nevertheless, severe SC morphological abnormalities (including tubular atrophy, SC degeneration, and interstitial fibrosis) have been observed during prolonged other GnRHa treatment (13,14). There is still controversy as regards the reversibility of these changes (5, 13, 15).…”

Section: Discussionmentioning

confidence: 99%

Relationships between FSH, inhibin B, anti-Mullerian hormone, and testosterone during long-term treatment with the GnRH-agonist histrelin in patients with prostate cancer

Eldar‐Geva

Liberty

Chertin

et al. 2010

European Journal of Endocrinology

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Objectives: Medical castration with long-acting GnRH-agonist (GnRHa) is a well-established treatment for metastatic prostate cancer. Our aim was to explore the relationships between FSH, inhibin B, antiMullerian hormone (AMH), and testosterone during treatment with an implant releasing GnRHa. Design: Analysis of hormone levels in frozen serum samples. Methods: Ten patients aged 77G7 (meansGS.E.M.) years with prostate cancer were treated with the GnRHa histrelin for at least a year. Two weeks prior to insertion and for 3-4 months following removal the patients were treated with the antiandrogen flutamide. Serum inhibin B, FSH, testosterone, and AMH levels were measured retrospectively. Results: FSH, inhibin B, and testosterone increased during antiandrogen administration and levels fell after implant insertion. Four weeks post insertion, FSH gradually increased while inhibin B and testosterone remained fully suppressed. AMH levels did not change during antiandrogen treatment, but increased following implant insertion and remained elevated for the duration of implant use. Following removal, FSH and testosterone increased, inhibin B remained low, while AMH decreased. Conclusions: The secondary increase in FSH following initial suppression with the implant is probably related to impaired inhibin B secretion. The lack of inhibin B response to the secondary increase in FSH suggests that long-term exposure of Sertoli-cells to GnRHa impairs their function. This effect appears to be selective since unlike inhibin B, AMH increased. In the absence of testosterone, FSH has a role in AMH regulation.

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“…Long‐term treatment with LHRH agonists is associated with testicular atrophy and impaired spermatogenesis. History of testicular specimens obtained following 6 months of ADT demonstrate severe atrophy of the seminiferous tubules/seminiferous epithelium and a Sertoli only pattern compared with controls . No changes were noted in the number of Leydig cells between groups, and subsequent human chorionic gonadotropin (HCG) stimulation of the specimen revealed preserved ability to produce testosterone.…”

Section: Adverse Effects Of Adtmentioning

confidence: 96%

Androgen Deprivation Therapy Impact on Quality of Life and Cardiovascular Health, Monitoring Therapeutic Replacement

Trost

Şerefoğlu

Gökçe

et al. 2013

The Journal of Sexual Medicine

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Introduction Androgen deprivation therapy (ADT) is commonly utilized in the management of both localized and advanced adenocarcinoma of the prostate. The use of ADT is associated with several adverse events, physical changes, and development of medical comorbidities/mortality. Aim The current article reviews known adverse events associated with ADT as well as treatment options, where available. Current recommendations and guidelines are cited for ongoing monitoring of patients receiving ADT. Methods A PubMed search of topics relating to ADT and adverse outcomes was performed, with select articles highlighted and reviewed based on level of evidence and overall contribution. Main Outcome Measures Reported outcomes of studies detailing adverse effects of ADT were reviewed and discussed. Where available, randomized trials and meta-analyses were reported. Results ADT may result in several adverse events including decreased libido, erectile dysfunction, vasomotor symptoms, cognitive, psychological and quality of life impairments, weight gain, sarcopenia, increased adiposity, gynecomastia, reduced penile/testicular size, hair changes, periodontal disease, osteoporosis, increased fracture risk, diabetes and insulin resistance, hyperlipidemia, and anemia. The definitive impact of ADT on lipid profiles, cardiovascular morbidity/mortality, and all-cause mortality is currently unknown with available data. Treatment options to reduce ADT-related adverse events include changing to an intermittent treatment schedule, biophysical therapy, counseling, and pharmacotherapy. Conclusions Patients treated with ADT are at increased risk of several adverse events and should be routinely monitored for the development of potentially significant morbidity/mortality. Where appropriate, physicians should reduce known risk factors and counsel patients as to known risks and benefits of therapy.

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Histological and Functional Changes of the Testis Tissue During GnRH Agonist Treatment of Prostatic Cancer

Cited by 22 publications

References 0 publications

Recovery of serum testosterone after neoadjuvant androgen deprivation therapy and radical radiotherapy in localized prostate cancer

Recovery of serum testosterone after neoadjuvant androgen deprivation therapy and radical radiotherapy in localized prostate cancer

Relationships between FSH, inhibin B, anti-Mullerian hormone, and testosterone during long-term treatment with the GnRH-agonist histrelin in patients with prostate cancer

Androgen Deprivation Therapy Impact on Quality of Life and Cardiovascular Health, Monitoring Therapeutic Replacement

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