DESPUES DE LA INTERESANTE PERO VOLATIL INTERVENCION DEL USUARIO STEINKILL EN EL POST DE OSCAR_25 SOBRE SU DISFUNCION ERECTIL, ME COMENZÓ A INTERESAR EL INDAGAR UN POCO MÁS EN LA RELACIÓN DE LOS NIVELES DE ESTRADIOL CON ESTA SINTOMATOLOGÍA. CURIOSAMENTE ENCONTRE LO SIGUIENTE:
Relevance of oestradiol-testosterone balance in erectile dysfunction patients' prognosis.
Srilatha B, Adaikan PG, Chong YS.
Department of Obstetrics and Gynaecology, National University Hospital, 5 Lower Kent Ridge Road, Singapore 119074.
INTRODUCTION: The ageing process in man is accompanied by a number of endocrine changes including decline in testosterone (T), physiological imbalance between androgen and oestradiol (E2) and changes in the E2-T ratio. In this study, hormone profile data from a group of erectile dysfunction (ED) patients were reviewed to evaluate its impact on ED, with emphasis on oestradiol derangement. METHODS: 30 ED patient case notes with a record of hormone profiles were retrospectively reviewed. Laboratory investigation included levels of total testosterone, total oestradiol, prolactin, luteinising and follicle stimulating hormones, in addition to lipid profile and glucose, based on specific history. These patients were divided into two groups based on the history of presence (Group A) or absence (Group B) of adequate sexual desire. RESULTS: In Group B patients, the E2-T derangement with increasing age was statistically significant with lower serum T level (2.6 ng/ml; range, 1.6-3.7 ng/ml) and elevated E2 level (60 pg/ml; range, 40-120 pg/ml). CONCLUSION: In this preliminary report, although low total testosterone level is seen together with impaired libido and erectile impairment, the accompanying significant increase in E2 indicates the possible role for oestrogen in causation and/or persistence of ED in this group of patients.
LO QUE VIENE A DECIR MÁS O MENOS ES QUE EN PACIENTES VARONES QUE VAN ENVEJENCIENDO SE OBSERVA UNA CAÍDA EN LOS NIVELES DE TESTOSTERONA JUNTO CON ALTERACIONES EN LA LÍBIDO Y PROBLEMAS DE ERECCIÓN, Y TODO ESTO VA ACOMPAÑADO DE UN AUMENTO SIGNIFICATIVO DEL ESTRADIOL, LO QUE INDICA EL POSIBLE PAPEL DE LOS ESTRÓGENOS EN LA CAUSALIDAD Y / O PERSISTENCIA DE LA DISFUNCIÓN ERÉCTIL EN ESTOS PACIENTES. CURIOSO DATO QUE NO CONOCÍA
Oestrogen-mediated hormonal imbalance precipitates erectile dysfunction.
Adaikan PG, Srilatha B.
Department of Obstetrics & Gynaecology, National University Hospital, National University of Singapore, Singapore. obgadaik@nus.edu.sg
Declining testosterone (T) in an aging male offsets the equilibrium between androgen and oestrogen (oestradiol, E(2)) with a resultant increase in E(2)-T ratio. Similar functional hormone imbalance is existent in clinical states of hypogonadism and is likely to arise from exposure of males to environmental oestrogens. The pathophysiological significance of this derangement on erectile function, hitherto unknown, was estimated in sexually mature male rats following acute and chronic treatment with oestrogen. A total of 60 male Sprague-Dawley rats (200-250 g) were divided into control and two treatment groups, administered 0.01 and 0.1 mg of oestradiol through oral gavage daily for 1 week (n=30, acute study) and 12 weeks (n=30, long-term study), respectively. Sexual activity in the presence of hormonally primed female rats and intracavernous pressure (ICP) response to electrical stimulation estimated treatment-induced changes, which were correlated with hormone levels and penile morphology at 12 weeks. Following two to five-fold elevation in serum E(2) levels (and simultaneous reduction in testosterone), there was a significant prolongation of mount, intromission, ejaculation latencies and some decrease in frequencies. The ICP response to nerve stimulation was also impaired in all the treated groups. Histologically, trichrome staining highlighted the cavernosal connective tissue hyperplasia in the long-term study groups. Results of this investigation indicate that oestradiol causes pathophysiological changes in erectile function. These observations provide an indirect evidence for the possible sexual health hazards in man upon inadvertent exposure to environmental oestrogens, ageing and derangement of E(2)-T ratio.
LA CONCLUSIÓN DEL ESTUDIO VIENE A DECIR LO SIGUIENTE:
[LOS RESULTADOS DE ESTA INVESTIGACIÓN INDICAN QUE EL ESTRADIOL PROVOCA CAMBIOS FISIOPATOLÓGICOS EN LA FUNCIÓN ERÉCTIL. ESTAS OBSERVACIONES PROPORCIONAN UNA PRUEBA INDIRECTA DE LOS POSIBLES RIESGOS PARA LA SALUD SEXUAL EN EL HOMBRE CON LA EXPOSICIÓN INVOLUNTARIA A ESTRÓGENOS AMBIENTALES, EL ENVEJECIMIENTO AGENTES QUE GENEREN PERTURBACIONES DE LA RELACIÓN ESTRADIOL/TESTOSTERONA.
The role of estradiol in the maintenance of secondary hypogonadism in males in erectile dysfunction.
Cohen PG.
The Advanced Medical Group, Marietta, GA 30067-0059, USA.
The occurrence of secondary hypogonadism is a common finding in males who seek help with erectile dysfunction, although the relationship to diminished testosterone is unclear. Two possibilities exist regarding both the genesis and maintenance of the hypogonadotropic hypogonadal state. First, a defect in hypothalamic function, resulting in downregulation as well as in alterations of anterior pituitary function; second, estradiol inhibition of gonadotropin release, both of which result in decreased testosterone production. As testosterone levels decrease and estradiol levels increase, the ratio of free testosterone to estradiol reaches a critical point and the estrogenic gonadotropin suppressive effects predominate. This ratio may signal the biological point of no return and could become one of the criteria for defining the separation of the transitional hypogonadal state from the final 'end stage' hypogonadotropic hypogonadal state. As the aging process continues, there is a relative accumulation of fatty tissue, and aromatization accelerates the conversion of testosterone to estradiol. This additional secondary estradiol inhibition results in the maintenance of the testosterone deficient state, and the aging process continues uncontested.
EL ESTUDIO ANALIZA LA IMPLICACIÓN DEL ESTRADIOL EN LA APARICION Y MANTENIMIENTO DE HIPOGONADISMO EN HOMBRES CON DISFUNCIÓN ERÉCTIL. SE SUGIERE QUE EL ESTRADIOL EJERCE UN EFECTO INHIBITORIO EN LA LIBERACIÓN DE GONADOTROPINAS HIPOFISARIAS, LO QUE CAUSARÍA UNA BAJADA EN LOS NIVELES DE TESTOSTERONA. EL ESTRADIOL AUMENTARÍA Y LA TESTOSTERONA DISMINUIRÍA DE TAL MANERA QUE LA RELACION ESTRADIOL/TESTOSTERONA ALCANZARÍA UN PUNTO CRÍTICO QUE DARÍA LUGAR A UNA SEÑAL BIOLÓGICA DE PUNTO DE NO RETORNO HACIENDO ENTRAR AL ORGANISMO EN UN ESTADADO HIPOGONADAL HIPOGONADOTROPICO.
DESDE MI CRITERIO SEÑORES, ESTOS TRES ESTUDIOS SON UN PRUEBA BASTANTE CLARA DE QUE HAY OTRA HORMANA MÁS QUE EN VARONES GENERA DISFUNCIÓN ERÉCTIL Y QUE DEBEMOS VIGILAR, ESPECIALMENTE EN VARONES DE EDAD AVANZADA. CONCRETAMENTE MÁS QUE EL ESTRADIOL EN SÍ DE FORMA DIRECTA PARECE QUE ES LA RELACIÓN ESTRADIOL CON RESPECTO A TESTOSTERONA LA QUE LO CAUSA, Y NO SOLO CAUSA DISFUNCION ERÉCTIL SINO QUE PUEDE LLEGAR A CAUSAR HIPOGONADISMO SECUNDARIO CON PROBABLE ATROFIA TESTICULAR CON LA EDAD.
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