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2.
Article in Spanish | LILACS, CUMED | ID: biblio-1138901

ABSTRACT

RESUMEN Introducción: El uso de la terapia de reemplazo con testosterona en hombres mayores se ha incrementado en los últimos años, lo que ha generado múltiples controversias aún no resueltas acerca de sus beneficios y riesgos potenciales, sobre todo los relacionados con el desarrollo o agravamiento de la enfermedad prostática o cardiovascular. Métodos: Se realizó una revisión bibliográfica con el objetivo de ofrecer un estado de la cuestión que ayude a los médicos a tomar decisiones al considerar el tratamiento con testosterona en pacientes con hipogonadismo de inicio tardío. La búsqueda de información se realizó en las bases de datos Google Académico, Medline y Pubmed. Conclusiones: El tratamiento con testosterona en el hipogonadismo de inicio tardío es seguro, racional y basado en evidencia, pero no se recomienda ofrecerlo a todos los hombres mayores con niveles bajos de testosterona sérica. Se aconseja en aquellos con síntomas manifiestos de deficiencia androgénica, sin cáncer de próstata activo, de mama o hígado, hematocrito elevado, hiperplasia prostática benigna con síntomas obstructivos graves, nódulo o induración prostática no evaluada, antígeno prostático específico > 4 ng/mL (o > 3 ng/mL en pacientes con alto riesgo), apnea obstructiva del sueño severa no tratada, deseos de fertilidad a corto plazo, insuficiencia cardiaca no controlada, infarto agudo de miocardio o accidente cerebrovascular en los últimos SEIS meses o trombofilia. Se recomienda realizar monitoreo trimestral durante el primer año y luego según cada caso, que incluya evaluación de la respuesta clínica, de condiciones que pueden agravarse con el tratamiento y de parámetros de laboratorio(AU)


ABSTRACT Introduction: The use of testosterone replacement therapy in older men has increased in recent years, which has generated multiple controversies not yet resolved about its benefits and potential risks, especially those related to the development or worsening of the prostate or cardiovascular disease. Methods: A literature review was conducted with the aim of offering a state of the art that helps clinicians make decisions when considering testosterone treatment in patients with late-onset hypogonadism. The information search was carried out with the Google Scholar, Medline and Pubmed search engines. Conclusions: Testosterone treatment in late-onset hypogonadism is safe, rational, and evidence-based, but it is not recommended to offer it to all older men with low serum testosterone levels. It is advised in those with overt symptoms of androgen deficiency, without active prostate, breast or liver cancer, elevated hematocrit, benign prostatic hyperplasia with severe obstructive symptoms, untested prostate nodule or induration, prostate specific antigen > 4 ng / mL (or > 3 ng / mL in high-risk patients), severe untreated obstructive sleep apnea, short-term fertility wishes, uncontrolled heart failure, acute myocardial infarction or stroke in the last SIX months, or thrombophilia. It is recommended to carry out quarterly monitoring during the first year and then according to each case, which includes evaluation of the clinical response, of conditions that can be aggravated by treatment, and of laboratory parameters(AU)


Subject(s)
Humans , Male , Aged , Testosterone/therapeutic use , Hypogonadism/etiology
3.
Arch. endocrinol. metab. (Online) ; 64(3): 223-234, May-June 2020. tab
Article in English | LILACS | ID: biblio-1131088

ABSTRACT

ABSTRACT Prader-Willi syndrome (PWS) is a genetic disorder caused by the absence of gene expression in the 15q11.2-q13 paternal chromosome. Patients with PWS develop hypothalamic dysfunction that can lead to various endocrine changes such as: obesity, growth hormone deficiency, hypogonadism, hypothyroidism, adrenal insufficiency and low bone mineral density. In addition, individuals with PWS have increased risk of developing type 2 diabetes mellitus. This review summarizes and updates the current knowledge about the prevention, diagnosis and treatment of endocrine manifestations associated with Prader Willi syndrome, especially diagnosis of growth hormone deficiency, management and monitoring of adverse effects; diagnosis of central adrenal insufficiency and management in stressful situations; screening for central hypothyroidism; research and treatment of hypogonadism; prevention and treatment of disorders of glucose metabolism. Careful attention to the endocrine aspects of PWS contributes significantly to the health of these individuals. Arch Endocrinol Metab. 2020;64(3):223-34


Subject(s)
Humans , Prader-Willi Syndrome/complications , Prader-Willi Syndrome/diagnosis , Prader-Willi Syndrome/genetics , Diabetes Mellitus/etiology , Hypogonadism/etiology , Hypothyroidism/etiology , Obesity/etiology
4.
Rev. chil. endocrinol. diabetes ; 13(1): 11-13, 2020.
Article in Spanish | LILACS | ID: biblio-1048794

ABSTRACT

El término disgenesia gonadal pura hace referencia a mujeres fenotípicas con infantilismo sexual, amenorrea primaria, hábito eunucoide y un cariotipo 46, XX o 46, XY sin anomalías cromosómicas. Puede asociarse a complicaciones como osteoporosis y síndrome metabólico, elevando el riesgo cardiovascular. Se presenta una paciente femenina de 16 años y 8 meses de edad que acude a consulta de endocrinología por presentar amenorrea primaria.


The term pure gonadal dysgenesis refers to phenotypic women with sexual infantilism, primary amenorrhea an d the eunucoid habit and a 46, XX or 46, XY karyotype without chromosomal abnormalities. It can be associated with complications such as osteoporosis and metabolic syndrome, increasing cardiovascular risk. We present a female patient of 16 years and 8 months of age who attended endocrinology clinic for presenting primary amenorrea.


Subject(s)
Humans , Female , Adolescent , Gonadal Dysgenesis, 46,XX/diagnosis , Hypogonadism/etiology , Gonadal Dysgenesis, 46,XX/complications , Amenorrhea/etiology , Infertility, Female
5.
Rev. chil. pediatr ; 90(6): 598-605, dic. 2019. tab
Article in Spanish | LILACS | ID: biblio-1058190

ABSTRACT

INTRODUCCIÓN: La radioterapia, quimioterapia y la cirugía empleada en el tratamiento de los tumores cerebrales tienen efectos en el eje hipotálamo-hipofisario y pueden resultar en disfunción endocrina hasta en el 96% de los casos. PACIENTES Y MÉTODO: Estudio retrospectivo y descriptivo en pacientes diagnos ticados de meduloblastoma sometidos a tratamiento con quimio y radioterapia en los últimos 20 años en un hospital terciario. Se analizan variables edad, sexo, peso, talla, índice de masa corporal (IMC) al final del seguimiento, estadio de maduración sexual, niveles séricos de TSH y T4 libre, ACTH/cortisol e IGF-1, FSH, LH, estradiol, testosterona, perfil lipídico (colesterol total) y prueba de función dinámica de hormona de crecimiento. RESULTADOS: Muestra total de 23 pacientes. El déficit de hormona de crecimiento es la secuela más frecuente (82 %) seguido de disfunción ti roidea (44,8%) y disfunción puberal (24,1%). Solo se diagnosticó un caso de diabetes insípida y 2 casos de déficit de corticotrofina. CONCLUSIONES: El seguimiento a largo plazo de los supervivientes de meduloblastoma tratados con quimio y radioterapia revela una prevalencia muy alta de disfun ción endocrina, particularmente de deficiencia de hormona del crecimiento y de hipotiroidismo. Creemos oportuna la monitorización y el seguimiento a largo plazo de estos pacientes con el fin de garantizar un manejo terapéutico adecuado de aquellas disfunciones tratables.


INTRODUCTION: Radiation therapy, chemotherapy, and surgery used to treat brain tumors have effects on the hy pothalamic-pituitary-adrenal axis and can result in endocrine dysfunction in up to 96% of cases. PATIENTS Y METHOD: Retrospective and descriptive study in patients diagnosed with medulloblasto ma who underwent treatment with chemo and radiotherapy in the last 20 years in a tertiary hospital. The variables analyzed were age, sex, weight, height, body mass index (BMI) at the end of follow-up, sexual maturity stage, serum levels of TSH and free T4, ACTH/cortisol and IGF-1, FSH, LH, estradiol, testosterone, lipid profile (total cholesterol), and growth hormone dynamic function test. RESULTS: Total sample of 23 patients. Growth hormone deficiency is the most frequent sequelae (82%) fo llowed by thyroid dysfunction (44.8%), and disorders of puberty (24.1%). Only one case of diabetes insipidus and two cases of corticotropin deficiency were diagnosed. CONCLUSIONS: Long-term follow- up of medulloblastoma survivors treated with chemo and radiotherapy reveals a very high prevalence of endocrine dysfunction, especially growth hormone deficiency and hypothyroidism. We believe that monitoring and long-term follow-up of these patients is necessary in order to ensure adequate therapeutic management of those treatable dysfunctions.


Subject(s)
Humans , Male , Female , Child, Preschool , Child , Cerebellar Neoplasms/therapy , Chemoradiotherapy/adverse effects , Medulloblastoma/therapy , Puberty, Precocious/etiology , Thyroid Diseases/etiology , Cerebellar Neoplasms/blood , Retrospective Studies , Adrenocorticotropic Hormone/deficiency , Human Growth Hormone/deficiency , Diabetes Insipidus/etiology , Endocrine System Diseases/etiology , Overweight/etiology , Cancer Survivors , Hypogonadism/etiology , Medulloblastoma/blood
6.
Clinics ; 68(supl.1): 81-88, 2013. ilus, tab
Article in English | LILACS | ID: lil-668040

ABSTRACT

Impaired testicular function, i.e., hypogonadism, can result from a primary testicular disorder (hypergonadotropic) or occur secondary to hypothalamic-pituitary dysfunction (hypogonadotropic). Hypogonadotropic hypogonadism can be congenital or acquired. Congenital hypogonadotropic hypogonadism is divided into anosmic hypogonadotropic hypogonadism (Kallmann syndrome) and congenital normosmic isolated hypogonadotropic hypogonadism (idiopathic hypogonadotropic hypogonadism). The incidence of congenital hypogonadotropic hypogonadism is approximately 1-10:100,000 live births, and approximately 2/3 and 1/3 of cases are caused by Kallmann syndrome (KS) and idiopathic hypogonadotropic hypogonadism, respectively. Acquired hypogonadotropic hypogonadism can be caused by drugs, infiltrative or infectious pituitary lesions, hyperprolactinemia, encephalic trauma, pituitary/brain radiation, exhausting exercise, abusive alcohol or illicit drug intake, and systemic diseases such as hemochromatosis, sarcoidosis and histiocytosis X. The clinical characteristics of hypogonadotropic hypogonadism are androgen deficiency and a lack/delay/stop of pubertal sexual maturation. Low blood testosterone levels and low pituitary hormone levels confirm the hypogonadotropic hypogonadism diagnosis. A prolonged stimulated intravenous GnRH test can be useful. In Kallmann syndrome, cerebral MRI can show an anomalous morphology or even absence of the olfactory bulb. Therapy for hypogonadotropic hypogonadism depends on the patient's desire for future fertility. Hormone replacement with testosterone is the classic treatment for hypogonadism. Androgen replacement is indicated for men who already have children or have no desire to induce pregnancy, and testosterone therapy is used to reverse the symptoms and signs of hypogonadism. Conversely, GnRH or gonadotropin therapies are the best options for men wishing to have children. Hypogonadotropic hypogonadism is one of the rare conditions in which specific medical treatment can reverse infertility. When an unassisted pregnancy is not achieved, assisted reproductive techniques ranging from intrauterine insemination to in vitro fertilization to the acquisition of viable sperm from the ejaculate or directly from the testes through testicular sperm extraction or testicular microdissection can also be used, depending on the woman's potential for pregnancy and the quality and quantity of the sperm.


Subject(s)
Humans , Male , Hypogonadism , Endocrine System Diseases/etiology , Endocrine System Diseases/therapy , Gonadotropins/physiology , Hormone Replacement Therapy/methods , Hypogonadism/diagnosis , Hypogonadism/etiology , Hypogonadism/therapy , Infertility, Male/etiology , Infertility, Male/therapy , Treatment Outcome
7.
Biomédica (Bogotá) ; 32(1): 13-22, ene.-mar. 2012. ilus, tab
Article in Spanish | LILACS | ID: lil-639807

ABSTRACT

Introducción. La afección testicular es frecuente en la lepra lepromatosa, daño que se incrementa cuando cursa con eritema nudoso leproso. Objetivo. Presentar un paciente con lepra lepromatosa y eritema nudoso leproso con grave compromiso testicular. Materiales y métodos. Se estudió un hombre de 28 años con lepra lepromatosa desde los 22, que durante la poliquimioterapia para la lepra presentó eritema nudoso leproso crónico que afectó ambos testículos y no respondió al manejo convencional. El dolor persistente obligó a practicar orquidectomía izquierda. Resultados. Este testículo presentaba atrofia tubular y fibrosis notorias, conglomerados de macrófagos espumosos, sin bacilos, hiperplasia focal de células de Leydig, endarteritis y arteritis linfocitaria y granulomatosa de vasos pequeños y medianos; estos cambios también estaban presentes en el epidídimo. Un estudio llevado a cabo dos años después de terminar su tratamiento y de la orquidectomía izquierda, demostró azoospermia, testosterona total normal, testosterona libre discretamente disminuida y hormonas lutropina (luteinizante) y folitropina (estimulante del folículo) elevadas. No había disminución de la libido ni de su actividad sexual. Se revisaron los conceptos generales sobre el eritema nudoso leproso y las alteraciones que la lepra produce en el testículo. Conclusión. La lepra lepromatosa puede conducir a hipogonadismo. Los programas de lepra deben contemplar esta complicación para corregir y evitar sus secuelas.


Introduction. Damage of testicles is frequent in lepromatous leprosy and worsened by the presence of erythema nodosum leprosum. Objective. A patient is presented who developed lepromatous leprosy and erythema nodosum leprosum with major testicular compromise. Material and methods. The 28-year-old male patient had lepromatous leprosy since age 22. During a polychemotherapy treatment for the lepromatous leprosy, he presented chronic erythema nodosum leprosum that affected both testicles; he did not respond to the conventional treatment. A left orchidectomy was performed to treat the persistent pain. Results. The extracted testis evidenced the following: tubular atrophy, extensive fibrosis, cumulus of foamy macrophages without rods, focal Leydig cell hyperplasia, linfocitary and granulomatous arteritis and endarteritis of small and medium size vessels. These changes were also observed in the epididymis. Two years after the polychemoterapy and the orchidectomy, the patient exhibited azoospermy, normal total testosterone, slightly diminished free testosterone and elevated levels of luteinizing hormone and follicle-stimulating hormone. No loss of libido or sexual activity was reported. General concepts of erythema nodosum leprosum were reviewed, as well as the pathologic changes produced by leprosy in the testis. Conclusion. Lepromatous leprosy may lead to hypogonadism. This condition is recommended for inclusion in leprosy diagnostic programs in order to detect and treat the consequences of the possible hypogonadism.


Subject(s)
Adult , Humans , Male , Erythema Nodosum/etiology , Hypogonadism/etiology , Leprosy, Lepromatous/complications , Testicular Diseases/etiology , Atrophy , Azoospermia/etiology , Clofazimine/therapeutic use , Dapsone/therapeutic use , Epididymis/pathology , Erythema Nodosum/pathology , Erythema Nodosum/surgery , Fibrosis , Foam Cells/pathology , Follicle Stimulating Hormone/blood , Hyperplasia , Hypogonadism/blood , Leprostatic Agents/therapeutic use , Leprosy, Lepromatous/classification , Leprosy, Lepromatous/drug therapy , Leprosy, Lepromatous/immunology , Leprosy, Lepromatous/pathology , Leydig Cells/pathology , Luteinizing Hormone/blood , Orchiectomy , Rifampin/therapeutic use , Testicular Diseases/pathology , Testicular Diseases/surgery , Testosterone/blood , Thalidomide/therapeutic use
8.
Rev. méd. Chile ; 138(10): 1294-1301, oct. 2010. ilus, tab
Article in Spanish | LILACS | ID: lil-572944

ABSTRACT

Adipose tissue not only stores fat, but secretes factors and hormones, which modify the regulation, metabolism and secretion of several other hormones. The objective of this review is to describe the hormonal disorders associated with increased adipose tissue, which acts as a modulator or disruptor of the endocrine physiology, with special reference to cortisol, androgens, growth hormone and thyroid axis, and discuss the implications for the management and treatment of these patients.


Subject(s)
Female , Humans , Male , Adipose Tissue/physiology , Androgens/metabolism , Endocrine System/physiology , Growth Hormone/metabolism , Obesity/metabolism , Thyroid Hormones/metabolism , Hypogonadism/etiology , Hypothyroidism/etiology , Obesity/physiopathology
9.
Rev. chil. endocrinol. diabetes ; 3(1): 11-14, ene. 2010. tab
Article in Spanish | LILACS | ID: lil-610300

ABSTRACT

Hypothalamic amenorrhea is secondary to the dysfunction of the hypothalamic pacemaker that regulates the pulsatile secretion of gonadotropin releasing hormone (GnRH). We report a 21 years old female with an isolated and persistent hypogonadotropic hypogonadism probably of congenital origin. The patient had a good olfactory function, did not have anatomical alterations and two GnRH stimulation tests showed a pre puberal pattern. Hormone replacement therapy allowed her to complete her puberal development.


Subject(s)
Humans , Female , Adult , Amenorrhea/etiology , Hypothalamic Diseases/complications , Amenorrhea/diagnosis , Amenorrhea/drug therapy , Estrogen Replacement Therapy , Hypothalamic Diseases/diagnosis , Hypogonadism/etiology , Gonadotropin-Releasing Hormone , Puberty
11.
Arq. bras. endocrinol. metab ; 53(8): 908-914, nov. 2009. tab
Article in English | LILACS | ID: lil-537026

ABSTRACT

Traumatic brain injury (TBI) is the most common cause of death and disability in young adults. Post-TBI neuroendocrine disorders have been increasingly acknowledged in recent years due to their potential contribution to morbidity and, probably, to mortality after trauma. Marked alterations of the hypothalamic-pituitary axis during the post-TBI acute and chronic phases have been reported. Prospective and longitudinal studies have shown that some abnormalities are transitory. On the other hand, there is a high frequency (15 percent to 68 percent) of pituitary hormone deficiency among TBI survivors in a long term setting. Post-TBI hypogonadism is a common finding after cranial trauma, and it is predicted to develop in 16 percent of the survivors in the long term. Post-TBI hypogonadism has been associated with adverse results in the acute and chronic phases after injury. These data reinforce the need for identification of hormonal deficiencies and their proper treatment, in order to optimize patient recovery, improve their life quality, and avoid the negative consequences of non-treated hypogonadism in the long term.


O traumatismo cranioencefálico (TCE) é a causa mais comum de morte e incapacidade em adultos jovens. Desordens neuroendócrinas pós-TCE vêm sendo reconhecidas cada vez mais nos últimos anos devido à sua potencial contribuição para a morbidade e, possivelmente, mortalidade após trauma. Alterações acentuadas do eixo hipotálamo-hipófise foram documentadas nas fases aguda e crônica pós-TCE. Estudos prospectivos e longitudinais têm mostrado que algumas anormalidades são transitórias. Por outro lado, existe uma elevada frequência de deficiências hormonais hipofisárias a longo prazo entre os sobreviventes de TCE, que varia de 15 por cento a 68 por cento. Hipogonadismo pós-TCE é um achado comum a longo prazo e estima-se que, em média, 16 por cento dos sobreviventes sejam afetados. Hipogonadismo pós-TCE tem sido associado a resultados adversos tanto na fase aguda quanto na fase crônica após a lesão. Esses dados reforçam a necessidade da identificação e adequado tratamento das deficiências hormonais, para otimizar a recuperação do paciente, melhorar a qualidade de vida e evitar as consequências negativas a longo prazo do hipogonadismo não tratado.


Subject(s)
Adult , Humans , Young Adult , Brain Injuries/complications , Hypogonadism/etiology , Hormone Replacement Therapy , Hypogonadism/physiopathology , Pituitary Gland/anatomy & histology , Pituitary Gland/physiopathology , Young Adult
12.
Arq. bras. endocrinol. metab ; 53(8): 983-988, nov. 2009.
Article in Portuguese | LILACS | ID: lil-537035

ABSTRACT

A disfunção do eixo gonadotrófico é frequentemente observada em pacientes infectados pelo HIV. A patogênese é multifatorial e está relacionada à duração da infecção pelo HIV, aos efeitos citopáticos diretos do vírus, ao uso de drogas gonadotóxicas, às infecções oportunistas, às neoplasias, à desnutrição, entre outros fatores. Em homens, a redução dos níveis de testosterona está associada à perda de massa e de força muscular, à redução da densidade mineral óssea, à lipodistrofia, à depressão, à astenia, à fadiga e à disfunção sexual. Em pacientes infectados pelo HIV com hipogonadismo, inúmeros estudos têm comprovado os efeitos benéficos da reposição de testosterona sobre o perfil metabólico e a distribuição da gordura corporal, com aumento da massa corporal magra, além de promover melhora da qualidade de vida, reduzir a perda de massa óssea e reduzir os índices de depressão. Assim, esta revisão teve como objetivo trazer uma breve atualização sobre o presente tema, abordando dados epidemiológicos, mecanismos fisiopatológicos e estratégias terapêuticas para as principais anormalidades do eixo gonadotrófico masculino associadas à infecção pelo HIV e ao seu tratamento.


Gonadotrophic axis dysfunction is commonly observed in HIV-infected patients. The pathogenesis is multifactorial and related to duration of HIV infection, direct cytopathic effects of viruses, use of drugs, opportunistic infections, malignancies, and malnutrition, among other factors. In men, reduced levels of testosterone is associated with loss of muscle mass and strength, decreased bone mineral density, lipodystrophy, depression, asthenia, fatigue and sexual dysfunction. In HIV-infected patients with hypogonadism, numerous studies have shown the beneficial effects of testosterone replacement on the metabolic profile and distribution of body fat, with increased body mass weight, and promote better quality of life, reduce the bone mass loss and the rates of depression. Thus, this review aimed to present a brief update of epidemiologic data, pathophysiology aspects and treatment strategies for the major abnormalities of male gonadotrophic axis associated with HIV infection and its treatment.


Subject(s)
Humans , Male , Gonadal Disorders/etiology , HIV Infections/complications , Androgens/therapeutic use , Gonadal Disorders/drug therapy , Gonadal Disorders/physiopathology , Gynecomastia/etiology , HIV Infections/physiopathology , HIV Infections/therapy , HIV-Associated Lipodystrophy Syndrome/complications , Hyperprolactinemia/etiology , Hypogonadism/drug therapy , Hypogonadism/etiology , Testosterone/therapeutic use
13.
Arq. bras. endocrinol. metab ; 53(8): 1005-1011, nov. 2009. tab, graf
Article in English | LILACS | ID: lil-537038

ABSTRACT

OBJECTIVE: To evaluate the incidence of hypogonadism in men with metabolic syndrome and its correlation with serum insulin levels. METHODS: Observational, transversal study with 80 men with metabolic syndrome. The individuals were divided into two groups: Group 1: 56 patients (70 percent) with total testosterone > 300 ng/dL (normal gonadal function); Group 2: 24 patients (30 percent) with total testosterone < 300 ng/dL (hypogonadic). RESULTS: The subjects from Group 2 compared to Group 1 presented higher body mass index (BMI), waist and hip circumferences, insulin, homeostasis model assessment insulin resistance index (Homa-IR) and beta cell (Homa-β), and triglycerides, but lower SHBG and free testosterone values. Inverse correlations between insulin levels and total testosterone and SHBG, as well as between Homa-IR and total testosterone were observed. CONCLUSION: In this series of men with metabolic syndrome, hypogonadism was associated with insulin resistance and may be a marker of metabolic abnormalities.


OBJETIVO: Avaliar a frequência de hipogonadismo em homens portadores da síndrome metabólica e a sua correlação com a concentração sérica de insulina. MÉTODOS: Estudo observacional e transversal com 80 homens portadores da síndrome metabólica. Os sujeitos foram estratificados em dois grupos: Grupo 1: 56 pacientes (70 por cento) com testosterona total > 300 ng/dL (função gonadal normal); Grupo 2: 24 pacientes (30 por cento) com testosterona < 300 ng/dL (hipogonádicos). RESULTADOS: Os sujeitos do Grupo 2 comparados ao Grupo 1 tinham maior índice de massa corporal (IMC), de circunferências do quadril e da cintura, insulina, Homa-IR, Homa-β e triglicerídeos, mas tinham valores menores de SHBG e testosterona livre. Observou-se correlação inversa da concentração de insulina com a de testosterona total e SHBG, e do Homa-IR com a concentração de testosterona total. CONCLUSÃO: Nos indivíduos estudados, a presença de hipogonadismo esteve associada à resistência à insulina, podendo ser um marcador de alterações metabólicas.


Subject(s)
Adolescent , Adult , Aged , Humans , Male , Middle Aged , Young Adult , Hypogonadism/etiology , Insulin/blood , Metabolic Syndrome/complications , Testosterone/blood , Body Mass Index , Biomarkers/blood , Brazil/epidemiology , Epidemiologic Methods , Hypogonadism/blood , Hypogonadism/epidemiology , Metabolic Syndrome/blood , Young Adult
14.
Arq. bras. endocrinol. metab ; 53(8): 1012-1019, nov. 2009. tab
Article in Portuguese | LILACS | ID: lil-537039

ABSTRACT

OBJETIVO: Avaliar a função hipofisária-gonadal nos pacientes vítimas de TCE graves ocorridos na Grande Florianópolis, entre 2000 e 2004. MÉTODOS: Foram estudados 30 pacientes, sendo 22 homens e 8 mulheres, submetidos à avaliação clínica e laboratorial em seguimento médio de 4 anos após a data do traumatismo. RESULTADOS: Os homens possuíam em média 38 anos no ano da avaliação, enquanto as mulheres, 42 anos. A maioria dos traumatismos está relacionada aos acidentes de trânsito (63,3 por cento). Três pacientes (10 por cento) estavam com valores de FSH abaixo do normal e apenas 1 paciente (3,3 por cento) apresentou LH alterado. Nas mulheres avaliadas, os níveis de estradiol foram normais. Na população masculina, foi evidenciado nível de testosterona baixo em 2 pacientes (9,1 por cento). Todos os pacientes apresentavam normoprolactinemia. CONCLUSÃO: Dois casos de hipogonadismo masculino (9,1 por cento) foram diagnosticados neste estudo. Isso indica a necessidade de atenção aos pacientes sobreviventes de TCE grave para realizar diagnóstico precoce de hipogonadismo.


OBJECTIVE: The purpose of this study is to evaluate pituitary function impairment in order to verify the prevalence of sex hormone deficiency and to analyze the profile of TBI population. METHODS: Thirty patients were studied, 22 were male and 8 were female. All patients had their gonadal function assessed and they were evaluated at a median of 4 years post-trauma. RESULTS: The average age of the men was 38 years at the time of the evaluation, while the mean age of women was 42 years. The majority of TBI was related to traffic accidents (63.3 percent). Three patients (10 percent) had low FSH and only 1 patient (3.3 percent) had low LH. There was no biochemical evidence of hypogonadism in women. Two male patients presented low testosterone (9.1 percent) and were diagnosed with hypogonadism. Prolactin levels were normal in all patients. CONCLUSION: Two cases of hypogonadism (9.1 percent) were diagnosed among men in this study. It is therefore necessary that medical professionals involved in the management of TBI patients are aware of hypogonadism as a complication of TBI, in order to diagnose it early.


Subject(s)
Adolescent , Adult , Aged , Female , Humans , Male , Middle Aged , Young Adult , Brain Injuries/complications , Gonadotropins, Pituitary/blood , Hypogonadism/etiology , Hypothalamo-Hypophyseal System/physiopathology , Pituitary-Adrenal System/physiopathology , Survivors , Accidents, Traffic , Brain Injuries/blood , Brain Injuries/physiopathology , Epidemiologic Methods , Gonads/physiopathology , Hypogonadism/blood , Pituitary Gland/physiopathology , Testosterone/blood , Young Adult
15.
The Medical Journal of Malaysia ; : 242-3, 2009.
Article in English | WPRIM | ID: wpr-630023

ABSTRACT

We report a case of a 16 years old girl who presented sequentially with primary amenorrhoea, hypertension and hypokalaemia. Eight years later, she was finally diagnosed with 17alpha-hydroxylase deficiency congenital adrenal hyperplasia. Previous antihypertensive medications were stopped. Hydrocortisone alone successfully maintained normotension and normokalaemia.


Subject(s)
Adrenal Hyperplasia, Congenital/diagnosis , Adrenal Hyperplasia, Congenital/etiology , Diagnosis, Differential , Hypertension/etiology , Hypogonadism/etiology , Hypokalemia/etiology , Steroid Hydroxylases/deficiency
16.
Femina ; 36(11): 677-681, nov. 2008. tab
Article in Portuguese | LILACS | ID: lil-508549

ABSTRACT

O objetivo da indução da puberdade com estrogênio em meninas hipogonádicas é alcançar o desenvolvimento físico e psicológico semelhante ao que ocorre na puberdade natural. Neste trabalho, descrevem-se os principais protocolos para indução da puberdde e de terapia de reposição hormonal (TRH) utilizados na síndrome de Turner. Revisão da literatura, associada à experiência dos autores, serve de base para a elaboração deste artigo, que propõe diretrizes no manuseio dessas pacientes. Constatou-se na literatura que os tipos de estrogênio mais utilizados foram o etinilestradiol e os estrogênios eqüinos conjugados. O estrogênio percutâneo na forma de gel foi o tipo de reposição mais aceito pelas pacientes do nosso ambulatório de Endocrinologia. Considerando a importância do uso de estrogênio nas adolescentes com hipogonadismo, propõe-se um protocolo de indução de puberdade e de acompanhamento às pacientes com síndrome de Turner


The aim of pubertal induction with estrogen in hypogonadal girls is to achieve physical and psychological development similar to that in the natural puberty. In this study we describe the main protocols for puberty induction and hormonal replacement therapy (HRT) used in Turner syndrome. A review of the literature, associated with the authors'experience, is the basis of this paper which proposes guidelines for the treatment of these patients. We have observed in the literature that the estrogens most commonly used are ethinylestradiol and conjugated equine estrogens. Moreover, percutaneous estrogen gel was the type of replacement most frequently accepted by the patients in our Ambulatory of Endocrinology Clinic. Considering the importance of the use of estrogen for teenagers with hypogonadism, we propose a protocol for puberty induction and follow-up of patients with Turner syndrome


Subject(s)
Female , Administration, Cutaneous , Ethinyl Estradiol/therapeutic use , Hormone Replacement Therapy , Hypogonadism/etiology , Puberty , Turner Syndrome/complications , Turner Syndrome/drug therapy , Estrogens, Conjugated (USP)/therapeutic use
17.
Urol. colomb ; 16(3): 55-69, dic. 2007. ilus
Article in Spanish | LILACS | ID: lil-506205

ABSTRACT

Se espera que en el año 2050 la población de Latinoamericanos mayores de 65 años, sea de 184 millones, aumentando el número de incapacitados e inválidos por las enfermedades relacionadas con la edad, provocando un desastre social y económico si no se toman medidas preventivas urgentes y adecuadas. Se discuten las manifestaciones clínicas y bioquímicas del Hipogonadismo de Inicio Tardío (LOH), los efectos de la testosterona y otras hormonas (hormona de crecimiento, tiroxina, leptinas, etc.), su relación con la hiperplasia prostática y el cáncer de próstata (CaP), Osteoporosis, Síndrome Metabólico y la Obesidad. El uso de la testosterona mejora la calidad de vida de los hombres con LOH, alejando los efectos de las enfermedades degenerativas y las incapacidades relacionadas. El manejo del LOH es eminentemente multidisciplinario, tomando como referencia la seguridad prostática y la consulta urológica cuando se requiera, con un seguimiento por el médico de primer contacto, y la participación activa de las especialidades afines. Se emiten recomendaciones de diagnostico, tratamiento, monitoreo y prevención del LOH en el hombre Latino Americano, que deben ser adaptadas a cada caso.


Subject(s)
Male , Erectile Dysfunction , Aging/pathology , Hypogonadism/etiology , Infertility, Male/classification , Men's Health , Testosterone/deficiency
18.
Braz. j. med. biol. res ; 40(10): 1383-1388, Oct. 2007. tab
Article in English | LILACS | ID: lil-461355

ABSTRACT

Liver cirrhosis, a highly prevalent chronic disease, is frequently associated with endocrine dysfunctions, notably in the gonadal axis. We evaluated lactotroph population by immunohistochemistry, gonadotropins and prolactin by immunoradiometric assay and testosterone and estradiol by radioimmunoassay in adult male Wistar rats with cirrhosis induced by carbon tetrachloride. No significant difference in mean ± SEM percentages of lactotrophs was found between cirrhotic animals and controls (N = 12, mean 18.95 ± 1.29 percent). Although there was no significant difference between groups in mean serum levels of prolactin (control: 19.2 ± 4 ng/mL), luteinizing hormone (control: 1.58 ± 0.43 ng/mL), follicle-stimulating hormone (control: 19.11 ± 2.28 ng/mL), estradiol (control: 14.65 ± 3.22 pg/mL), and total testosterone (control: 138.41 ± 20.07 ng/dL), 5 of the cirrhotic animals presented a hormonal profile consistent with hypogonadism, all of them pointing to a central origin of this dysfunction. Four of these animals presented high levels of estradiol and/or prolactin, with a significant correlation between these two hormones in both groups (r = 0.54; P = 0.013). It was possible to detect the presence of central hypogonadism in this model of cirrhotic animals. The hyperestrogenemia and hyperprolactinemia found in some hypogonadal animals suggest a role in the genesis of hypogonadism, and in the present study they were not associated with lactotroph hyperplasia.


Subject(s)
Animals , Male , Rats , Gonadotropins, Pituitary/blood , Hypogonadism/etiology , Lactotrophs/pathology , Liver Cirrhosis/complications , Carbon Tetrachloride , Cell Count , Estradiol/blood , Follicle Stimulating Hormone/blood , Hyperplasia/blood , Hyperplasia/pathology , Hyperprolactinemia/etiology , Hypogonadism/blood , Liver Cirrhosis/blood , Luteinizing Hormone/blood , Prolactin/blood , Radioimmunoassay , Rats, Wistar , Testosterone/blood
19.
Arq. bras. endocrinol. metab ; 51(6): 920-929, ago. 2007. tab
Article in Portuguese | LILACS | ID: lil-464283

ABSTRACT

A falência ovariana prematura (FOP) acomete aproximadamente 1:1000 mulheres antes dos 30 anos, 1:250 em torno dos 35 anos e de 1:100 aos 40 anos. Manifesta-se como amenorréia primária ou amenorréia secundária, não podendo ser considerada definitiva em todas as pacientes, uma vez que a concepção espontânea pode ocorrer em até 5-10 por cento das FOP. Na maioria dos casos apresenta-se na forma esporádica, pois apenas 5 por cento apresentam história familial. Entre as causas conhecidas estão as alterações cromossômicas, dos genes ligados ao cromossomo X e cromossomos autossômicos, doenças autoimunes, alterações tóxicas e iatrogênicas. Com relativa freqüência, a causa etiológica não é obtida, sendo então denominada de idiopática. O diagnóstico da FOP é feito baseado na história clínica e níveis elevados do hormônio folículo estimulante (FSH), sendo posteriormente investigadas as causas mais específicas. O manejo clínico visa o suporte emocional, o tratamento hormonal com estrogênios e progestogênios, a abordagem da infertilidade e a prevenção de co-morbidades como a osteoporose e potencial maior risco cardiovascular.


Premature ovarian failure occurs in approximately 1:1000 women before 30 years, 1:250 by 35 years and 1:100 by the age of 40. It is characterized by primary or secondary amenorrhea and cannot be considered as definitive because spontaneous conception may occur in 5 to 10 percent of cases. In 95 percent of cases, premature ovarian failure is sporadic. The known causes of premature ovarian failure include chromosomal defects, autoimmune diseases, exposure to radiation or chemotherapy, surgical procedures, and certain drugs. Frequently, however, the etiology is not clear and these cases are considered to be idiopathic. Premature ovarian failure is defined by gonadal failure and high serum follicle-stimulating hormone (FSH) levels. Clinical approach includes emotional support, hormonal therapy with estrogens and progesterone or progestogens, infertility treatment, and prevention of osteoporosis and potential cardiovascular risk.


Subject(s)
Adult , Female , Humans , Autoimmune Diseases/complications , Follicular Atresia/genetics , Primary Ovarian Insufficiency/etiology , Amenorrhea/etiology , Biomarkers/blood , Estrogen Replacement Therapy , Estrogens/therapeutic use , Follicle Stimulating Hormone/blood , Hypogonadism/etiology , Infertility, Female/etiology , Mutation/genetics , Primary Ovarian Insufficiency/genetics , Primary Ovarian Insufficiency/therapy , Ovarian Follicle/abnormalities , Progesterone/therapeutic use , Progestins/therapeutic use , Receptors, FSH/genetics
20.
Indian J Dermatol Venereol Leprol ; 2007 Jul-Aug; 73(4): 280
Article in English | IMSEAR | ID: sea-52050

ABSTRACT

A sixteen year-old male patient with no history of consanguinity in the family, reported with patchy, thickened lichenified plaques over the whole body. Some areas had normal skin while some were Blaschkoid lesions. The child had delayed milestones along with hypogonadism. Digital contracture with palmoplantar keratoderma was present. Histopathology showed characteristic vacuolar degeneration of the upper epidermis and suprabasilar keratinocytes with hyperkeratosis.


Subject(s)
Adolescent , Contracture/etiology , Fingers/pathology , Humans , Hyperkeratosis, Epidermolytic/classification , Hypogonadism/etiology , Keratoderma, Palmoplantar/pathology , Male , Mosaicism , Skin/pathology
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