Limits...
Emerging potential of parenteral estrogen as androgen deprivation therapy for prostate cancer.

Ali Shah SI - South Asian J Cancer (2015 Apr-Jun)

Bottom Line: Androgen deprivation therapy (ADT) is a key management strategy for prostate cancer (PC), achieved commonly by administration of luteinizing hormone-releasing hormone agonist (LHRHa), ADT markedly suppresses both male and female sex hormones which results in "castration syndrome", a constellation of adverse events such as muscle weakness, impairment of glucose and lipid metabolism, impotence, osteoporosis, and fractures.Recent evidence suggests that estrogen, in the parenteral form, may emerge as an alternative to LHRHa as it offers potential benefits of arresting PC growth as well as avoiding some of the estrogen deficiency related toxicities of LHRHa by maintaining endogenous levels of estrogen.

View Article: PubMed Central - PubMed

Affiliation: Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, London W12 ONN, United Kingdom.

ABSTRACT
Androgen deprivation therapy (ADT) is a key management strategy for prostate cancer (PC), achieved commonly by administration of luteinizing hormone-releasing hormone agonist (LHRHa), ADT markedly suppresses both male and female sex hormones which results in "castration syndrome", a constellation of adverse events such as muscle weakness, impairment of glucose and lipid metabolism, impotence, osteoporosis, and fractures. Recent evidence suggests that estrogen, in the parenteral form, may emerge as an alternative to LHRHa as it offers potential benefits of arresting PC growth as well as avoiding some of the estrogen deficiency related toxicities of LHRHa by maintaining endogenous levels of estrogen.

No MeSH data available.


Related in: MedlinePlus

Inhibition of hypothalamic-pituitary-gonadal axis; estrogen inhibits testicular androgen production by negative feedback, luteinizing hormone-releasing hormone agonist down-regulates anterior pituitary receptors and suppresses release of luteinizing hormone and follicle-stimulating hormone, subsequently diminishing androgen formation in testes
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4418092&req=5

Figure 1: Inhibition of hypothalamic-pituitary-gonadal axis; estrogen inhibits testicular androgen production by negative feedback, luteinizing hormone-releasing hormone agonist down-regulates anterior pituitary receptors and suppresses release of luteinizing hormone and follicle-stimulating hormone, subsequently diminishing androgen formation in testes

Mentions: Introduced in the 1980s, LHRHa acts by down-regulating gonadotrophin receptors in the pituitary, thereby causing central hypogonadism [Figure 1]. However, initial exposure to LHRHa leads to a “testosterone flare”, which can exacerbate symptoms in a few patients like worsening bone pain from skeletal metastasis. The flare phenomenon is blocked by giving anti-androgens, a week before administering LHRHa.[4] Contemporary LHRHa as ADT delivers up to a 95% reduction in endogenous testosterone levels, which in turn results in suppression of endogenous estrogen (by about 80%) as it is derived from testosterone.[5]


Emerging potential of parenteral estrogen as androgen deprivation therapy for prostate cancer.

Ali Shah SI - South Asian J Cancer (2015 Apr-Jun)

Inhibition of hypothalamic-pituitary-gonadal axis; estrogen inhibits testicular androgen production by negative feedback, luteinizing hormone-releasing hormone agonist down-regulates anterior pituitary receptors and suppresses release of luteinizing hormone and follicle-stimulating hormone, subsequently diminishing androgen formation in testes
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4418092&req=5

Figure 1: Inhibition of hypothalamic-pituitary-gonadal axis; estrogen inhibits testicular androgen production by negative feedback, luteinizing hormone-releasing hormone agonist down-regulates anterior pituitary receptors and suppresses release of luteinizing hormone and follicle-stimulating hormone, subsequently diminishing androgen formation in testes
Mentions: Introduced in the 1980s, LHRHa acts by down-regulating gonadotrophin receptors in the pituitary, thereby causing central hypogonadism [Figure 1]. However, initial exposure to LHRHa leads to a “testosterone flare”, which can exacerbate symptoms in a few patients like worsening bone pain from skeletal metastasis. The flare phenomenon is blocked by giving anti-androgens, a week before administering LHRHa.[4] Contemporary LHRHa as ADT delivers up to a 95% reduction in endogenous testosterone levels, which in turn results in suppression of endogenous estrogen (by about 80%) as it is derived from testosterone.[5]

Bottom Line: Androgen deprivation therapy (ADT) is a key management strategy for prostate cancer (PC), achieved commonly by administration of luteinizing hormone-releasing hormone agonist (LHRHa), ADT markedly suppresses both male and female sex hormones which results in "castration syndrome", a constellation of adverse events such as muscle weakness, impairment of glucose and lipid metabolism, impotence, osteoporosis, and fractures.Recent evidence suggests that estrogen, in the parenteral form, may emerge as an alternative to LHRHa as it offers potential benefits of arresting PC growth as well as avoiding some of the estrogen deficiency related toxicities of LHRHa by maintaining endogenous levels of estrogen.

View Article: PubMed Central - PubMed

Affiliation: Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, London W12 ONN, United Kingdom.

ABSTRACT
Androgen deprivation therapy (ADT) is a key management strategy for prostate cancer (PC), achieved commonly by administration of luteinizing hormone-releasing hormone agonist (LHRHa), ADT markedly suppresses both male and female sex hormones which results in "castration syndrome", a constellation of adverse events such as muscle weakness, impairment of glucose and lipid metabolism, impotence, osteoporosis, and fractures. Recent evidence suggests that estrogen, in the parenteral form, may emerge as an alternative to LHRHa as it offers potential benefits of arresting PC growth as well as avoiding some of the estrogen deficiency related toxicities of LHRHa by maintaining endogenous levels of estrogen.

No MeSH data available.


Related in: MedlinePlus