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ABSTRACT We report a 27 -year-old male referred because of hypergonadotropic hypogonadism with low testosterone and azoospermia. At 23 years of age, he underwent an excision of a hypoechoic 0.7 cm nodule of the left testicle. The pathological diagnosis was a Leydig cell tumor. In the right testicle, there were three nodules at ultrasound, the biggest measuring 0.6 cm. Four years later, the nodules in the right testicle were still present and the larger nodule was excised. The biopsy showed tubules with only Sertoli cells in the perinodular zone. Diffuse and nodular hyperplasia of the Leydig cells was found in the interstitium. The pathological diagnosis was Sertoli syndrome with severe hyperplasia of the Leydig cells. With testosterone therapy, LH decreased, and the nodules disappeared. Thereafter, upon interrupting therapy, LH increased, and the nodules reappeared in two occasions. Resuming testosterone treatment, the nodules disappeared again, suggesting a Leydig cell hyperplasia dependent on chronic LH stimulation.

Presentamos un varón de 27 años referido por hipogonadismo hipergonadotrófico con testosterona baja y azoospermia. El paciente tenía el antecedente de un nódulo sólido hipoecogénico de 0,7 cm en el testículo izquierdo, extirpado los 23 años de edad en el año 2002 y diagnosticado patológicamente como tumor de células de Leydig. En ese año se encontraron tres nódulos en el testículo derecho por ultrasonografía, el mayor de 0,6 cm. Cuatro años después, en 2007, los micronódulos del testículo derecho seguían presentes. El mayor de ellos fue extirpado. En la biopsia, había túbulos con solo células de Sertoli en la zona perinodular. En el intersticio había hiperplasia difusa y nodular de las células de Leydig. El diagnóstico patológico fue un síndrome de Sertoli con severa hiperplasia de células de Leydig. La terapia con testosterona disminuyó la LH y los nódulos inesperadamente desaparecieron. En dos ocasiones, al interrumpir esta terapia, la LH aumentó y los nódulos reaparecieron. Este proceso revirtió nuevamente con el uso de testosterona, sugiriendo una hiperplasia de células de Leydig dependiente del estímulo crónico de LH.

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RESUMO

We report a 27 -year-old male referred because of hypergonadotropic hypogonadism with low testosterone and azoospermia. At 23 years of age, he underwent an excision of a hypoechoic 0.7 cm nodule of the left testicle. The pathological diagnosis was a Leydig cell tumor. In the right testicle, there were three nodules at ultrasound, the biggest measuring 0.6 cm. Four years later, the nodules in the right testicle were still present and the larger nodule was excised. The biopsy showed tubules with only Sertoli cells in the perinodular zone. Diffuse and nodular hyperplasia of the Leydig cells was found in the interstitium. The pathological diagnosis was Sertoli syndrome with severe hyperplasia of the Leydig cells. With testosterone therapy, LH decreased, and the nodules disappeared. Thereafter, upon interrupting therapy, LH increased, and the nodules reappeared in two occasions. Resuming testosterone treatment, the nodules disappeared again, suggesting a Leydig cell hyperplasia dependent on chronic LH stimulation.

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Históricamente la sociedad ha rechazado el abuso sexual de menores de 13 años, dictándose leyes al respecto. La justicia luego de un debido proceso condenaba al victimario con reclusión incluso hasta la década del 70-80, con orquiectomía. Los adelantos en neurobiología, endocrinología, sicofarmacología y sicología se consideraron las bases para tratar al pedófilo y someterlo a libertad condicional, ahorrándose el costo financiero de la reclusión de por vida. Diversos países dictaron leyes contra la conducta pedófila. En dicha legislación ejerció gran influencia la promulgación en EE.UU. (estado de Washington "sobre el ofensor sexual" y el dictamen de la Corte Suprema en 1997 en el juicio de Kansas vs Hendricks). En Chile en los 90 el caso del pedófilo apodado "Zacarach" sacó a la luz pública el tema que no se quería ver. En esa fecha se presentó al parlamento un proyecto de Ley para "curar" la pedofilia con acetato de Medroxiprogesterona imitando legislación de EE.UU. Causó sorpresa en el medio endocrinológico que se usara terapia hormonal como "cura" de la pedofilia. Se ha utilizado en varios países la castración química producida por gestágenos o agonístas del GnRH más antiandrógenos (acetato de Ciproterona), para inhibir la secreción y acción de la testosterona disminuyendo líbido y erección. No se ha demostrado que exista curación de la orientación pedófila y existen dudas de la prevención primaria y secundaria de la pedofilia. Pese al adelanto tecnológico en neurociencias para estudio de las zonas vinculadas a la sexualidad, aún no existen marcadores que permitan diagnosticar o pronosticar futuros resultados de la terapia. El tratamiento médico de la pedofilia no garantiza curación ni prevención del delito pedofílico.

Historically, society has rejected sexual abuse of children under 13, with there having been laws enacted in this regard. The judicial system, after a due process, condemned the perpetrator with reclusion and even up until the decades of the 70s and 80s with orchiectomy. Advances in neurobiology, endocrinology, psychopharmacology and psychology were considered the basis for treating the pedophile and putting them on probation, saving the financial cost of imprisonment for life. Multiple countries have enacted laws against pedophilic behaviour. Such legislation was greatly influenced by the enactment in the USA (state of Washington "on the sex offender" and the ruling of the Supreme Court in 1997 in the trial of Kansas against Hendricks). In Chile in the 90s, the case of a pedophile nicknamed "Zacarach" brought to light an issue that nobody wanted to see. Around that time, a bill was presented to Parliament to try and "cure" pedophilia with Medroxyprogesterone acetate, imitating US legislation. It was a surprise in the endocrinological world that hormonal therapy would be used as a "cure" for pedophilia. Chemical castration produced by gestagens or GnRH agonists plus antiandrogens (Cyproterone acetate) has been used in several countries to inhibit the secretion and action of testosterone, reducing libido and erection. It has not been proven that there is a cure for pedophile orientation and there are doubts about the primary and secondary prevention of pedophilia. Despite technological advances in neurosciences for the study of the zones pertaining to sexuality, there are still no indicators that allow for diagnosis or prediction of future results of therapy. The medical treatment of pedophilia does not guarantee cure or prevention of pedophilic crime.

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SOCHED debe preocuparse del desarrollo profesional de sus miembros y de alzar su voz ante temas endocrinológicos relevantes para la sociedad chilena. La invisibilidad a todo nivel del tema trans nos encontró mal posicionados, pues la nula formación en este aspecto cerraba el ciclo de su desconocimiento en pre y post grado. Las solicitudes de muchos años para discutir el tema en nuestros congresos había sido sistematicamente rechazadas o ignoradas. El desconcierto y alarma produjeron las consultas de personas trans que nos solicitaban la fase endocrinológica de la readecuación corporal, revelando la falta de preparación para comprenderlos y tratarlos. El proyecto de ley de identidad de género puso en evidencia además la falta de estructura de SOCHED para actuar en el campo político y parlamentario. Reseñamos la actuación de SOCHED en este proceso y las medidas sugeridas sobre cambios a realizar y puntos débiles a corregir. Se debe evitar su repetición , por ejemplo si se propusiera el tratamiento hormonal de la pedofilia.

SOCHED must worry about the professional development of its members and to raise its voice before the endocrinological issues for the Chilean society. The invisibility at all levels of the trans aspect found us bad positioned, as the null formation in this aspect closed the cycle of its disconnection in pre-and post-grade. The request of many years to discuss this topic in our congresses had been systematically rejected or ignored. The alarm and disconcerate caused by the questions of trans persons who requested us the endocrinological phase of body readjustment, revealing the failure of preparation to understand and treat them. The gender identity law project put evidence also the lack of SOCHED structure to act in the political and parliamentary field. We review the action of SOCHED in this process and the measures suggested about changes to be implemented and the weaknesses points to correct. their repetition must be avoided, for example if the hormone treatment of the pedophilia is proposed.

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Endocrinology step of transgender readjustment therapy is made according to previously published in the part 1 of article: “gender identity disorder in rev. chil. endocrinol. diabetes 2015, 8 (4): 167-173.During started puberty in Tanner stage 2-3, the persistence of the experience that their identity male or female gender is not coherent with its bodily, authorize to start the endocrinological therapy, as an important step of body readjusting. In the process of transition from male to female or female to male, should stop pubertal development, what we do with GNRH analogues: intramuscle leuprolideor triptorelin 11.25 mg. every 12 weeks or with medroxyprogesterone acetate 150 mg. monthly. This process continues until 16 years, adding antiandrogen, preferably spironolactone in the process of body readjusting of male to female. At 16 years old, starts the cross hormonal therapy to masculinizing or feminizing. Maintaining gonadotrophin suppression, female to male, testosterone undecanoate or other injectable testosterone esters is administered, customizing the date of administration and inMale to female, daily use of oral estradiol valerate or transdermal gel. Plasma levels of estradiol andtestosterone should not be located in high or supraphysiological range to avoid thromboembolism or polycythemia risk in those who receive testosterone. Should to be explained the time to obtain the bodily effects, achieving a realistic attitude of the goals and the need for regular checks. Attendance to emotional changes, mainly to meet the social gender role. The laboratory, metabolic, hormonal, hemogram and electrolytic changes are evaluated. To be indicated bone densitometry and study images of internal genitals and breasts are necesary...

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Gender identity disorders (GID) or transsexuality have been a latent issue in Chile 20 years after the first sex reassignment treatment in 1973. Sexual minority groups have posed the problem and even present a bill for civil sexual change. Since the nineties, the number of consultants due to gender identity problems has increased steadily, including children and adolescents. The lack of medical expertise in the area, requires urgent training programs. The first part of this manuscript will deal with the definition, epidemiology, etiology and role of the endocrinologist in the process of sexual reassignment among patients with gender identity disorders. We review sexual differentiation, brain sexual dimorphism and Sexual Development Disorders (SDD) aiming to understand the neurobiological causes of GID and to perform a better differential diagnosis with Sexual Development Disorders. GID are not a psychiatric disease. However the suffering caused by stigmatization, exclusion andabuse generate emotional problems (gender dysphoria). SDD has a genetic and hormonal basis in most cases. Its clinical expression at birth can cause an erroneous civil sex assignation or a discordant civil sex with the sexual identity of the person when there is a surgical correction. GIS without gender dysphoria was excluded as a mental disease from DSM-V and it will also be excluded from the eleventh version of the international classification of diseases. It will maintained as a condition that should be differentiated from SDD and whose treatment should be financed by health systems.

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Hyperprolactinemic males usually have a hypoactive libido and less commonly, erectile dysfunction and disturbances of orgasm and ejaculation. Hyperprolactinemia alters the balance between neurotransmitters, neuropeptides and hormones involved in libido and erection, affecting dopaminergic tone. An imbalance between dopamine, that stimulates sexual function and serotonin that inhibits it, is generated. In the central nervous system, hyperprolactinemia inhibits centers controlling sexual desire and erection. At the neuroendocrine level, it decreases GnRH, LH and testosterone pulses, resulting in a hypogonadotrophic hypogonadism. Erection is also inhibited peripheral actions of low testosterone and high prolactin levels. There is a disturbance of penile smooth muscle relaxation and of the parasympathetic sacrum-penis reflex arch. In experimental animals, acute hyperprolactinemia hampers the central erection mechanism whereas in chronic conditions, peripheral disturbances also occur. Even correcting low testosterone levels, the adverse effects of hyperprolactinemia on sexual function persist. The use of dopaminergic agonists may achieve normal prolactin and testosterone levels resulting in normal sexual function. Chronic hyperprolactinemia results in progressive deterioration of sexual function and a higher hypothalamic damage that does not respond to clomiphene. In this situation and in the presence of sellar tumors that destroy gonadotrophic cells, there is indication of androgenic replacement maintaining the use of dopaminergic agonists...

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In males, congenital adrenal hyperplasia due to 21 hydroxylase deficiency is associated to normal fertility or infertility caused by a hypogonadotrophic hypogonadism (HH) or gonadal damage caused by intratesticular adrenal remnants. We report a 29-year-old male with azoospermia, without any important personal or family background. Physical examination was normal, his height was 150 cm and his testicular volume was 10 ml (normal 15 to 25 ml). Laboratory showed a normal testosterone and FSH and LH in the low normal limit. These results discarded a HH, whose diagnostic requirements are a low testosterone and inadequately normal or low gonadotrophins. A testicular biopsy was informed as compatible with HH. A 21 hydroxylase deficiency was suspected and confirmed with extremely high levels of 17 hydroxyprogesterone at baseline and after stimulation with fast acting ACTH. Clomiphene citrate did not increase testosterone or gonatrophin levels. Testicular ultrasound discarded the presence of adrenal nodules. Betametasone therapy resulted in a normal testicular development, normalization of sperm count, reduction of 17 hydroxyprogesterone and testosterone levels with an ulterior rise of the latter. Spontaneous paternity was achieved twice. It must be remembered that in cases of azoospermia due to congenital adrenal hyperplasia, testosterone produced by adrenal glands hinders the laboratory diagnosis of HH.

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RESUMO

In males, congenital adrenal hyperplasia due to 21 hydroxylase deficiency is associated to normal fertility or infertility caused by a hypogonadotrophic hypogonadism (HH) or gonadal damage caused by intratesticular adrenal remnants. We report a 29-year-old male with azoospermia, without any important personal or family background. Physical examination was normal, his height was 150 cm and his testicular volume was 10 ml (normal 15 to 25 ml). Laboratory showed a normal testosterone and FSH and LH in the low normal limit. These results discarded a HH, whose diagnostic requirements are a low testosterone and inadequately normal or low gonadotrophins. A testicular biopsy was informed as compatible with HH. A 21 hydroxylase deficiency was suspected and confirmed with extremely high levels of 17 hydroxyprogesterone at baseline and after stimulation with fast acting ACTH. Clomiphene citrate did not increase testosterone or gonatrophin levels. Testicular ultrasound discarded the presence of adrenal nodules. Betametasone therapy resulted in a normal testicular development, normalization of sperm count, reduction of 17 hydroxyprogesterone and testosterone levels with an ulterior rise of the latter. Spontaneous paternity was achieved twice. It must be remembered that in cases of azoospermia due to congenital adrenal hyperplasia, testosterone produced by adrenal glands hinders the laboratory diagnosis of HH.

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