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1.
Clin Endocrinol (Oxf) ; 84(3): 361-71, 2016 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-26464129

RESUMEN

OBJECTIVES: To estimate the prevalence of central precocious puberty (CPP) after treatment for tumours and malignancies involving the central nervous system (CNS) and examine repercussions on growth and pubertal outcomes. DESIGN: Retrospective study of patients with tumours near and/or exposed to radiotherapy to the hypothalamus/pituitary axis (HPA). PATIENTS AND MEASUREMENTS: Patients with CPP were evaluated at puberty onset, completion of GnRH agonist treatment (GnRHa) and last follow-up. Multivariable analysis was used to test associations between tumour location, sex, age at CPP, GnRHa duration and a diagnosis of CPP with final height <-2SD score (SDS), gonadotropin deficiency (LH/FSHD) and obesity, respectively. RESULTS: Eighty patients (47 females) had CPP and were followed for 11·4 ± 5·0 years (mean ± SD). The prevalence of CPP was 15·2% overall, 29·2% following HPA tumours and 6·6% after radiotherapy for non-HPA tumours. Height <-2SDS was more common at the last follow-up than at the puberty onset (21·4% vs 2·4%, P = 0·005). Obesity was more prevalent at the last follow-up than at the completion of GnRHa or the puberty onset (37·7%, 22·6% and 20·8%, respectively, P = 0·03). Longer duration of GnRHa was associated with increased odds of final height <-2SDS (OR = 2·1, 95% CI 1·0-4·3) and longer follow-up with obesity (OR = 1·3, 95% CI 1·1-1·6). LH/FSHD was diagnosed in 32·6%. There was no independent association between CPP and final height <-2SDS, and LH/FSHD and obesity in the subset of patients with HPA low-grade gliomas. CONCLUSIONS: Patients with organic CPP experience an incomplete recovery of growth and a high prevalence of LH/FSHD and obesity. Early diagnosis and treatment of CPP may limit further deterioration of final height prospects.


Asunto(s)
Neoplasias del Sistema Nervioso Central/diagnóstico , Neoplasias del Sistema Nervioso Central/radioterapia , Pubertad Precoz/diagnóstico , Estatura , Niño , Preescolar , Femenino , Hormona Folículo Estimulante/deficiencia , Estudios de Seguimiento , Trastornos del Crecimiento/etiología , Humanos , Hipotálamo/efectos de la radiación , Lactante , Hormona Luteinizante/deficiencia , Masculino , Obesidad/etiología , Evaluación de Resultado en la Atención de Salud/métodos , Evaluación de Resultado en la Atención de Salud/estadística & datos numéricos , Irradiación Hipofisaria/efectos adversos , Pubertad Precoz/etiología , Radioterapia/efectos adversos , Estudios Retrospectivos , Factores de Tiempo
2.
Pituitary ; 18(4): 561-7, 2015 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-25315032

RESUMEN

BACKGROUND: Children initially diagnosed with isolated GH deficiency (IGHD) have a variable rate to progress to combined pituitary hormone deficiency (CPHD) during follow-up. OBJECTIVE: To evaluate the development of CPHD in a group of childhood-onset IGHD followed at a single tertiary center over a long period of time. PATIENTS AND METHODS: We retrospectively analyzed data from 83 patients initially diagnosed as IGHD with a mean follow-up of 15.2 years. The Kaplan-Meier method and Cox regression analysis was used to estimate the temporal progression and to identify risk factors to development of CPHD over time. RESULTS: From 83 patients initially with IGHD, 37 (45%) developed CPHD after a median time of follow up of 5.4 years (range from 1.2 to 21 years). LH and FSH deficiencies were the most common pituitary hormone (38%) deficiencies developed followed by TSH (31%), ACTH (12%) and ADH deficiency (5%). ADH deficiency (3.1 ± 1 years from GHD diagnosis) presented earlier and ACTH deficiency (9.3 ± 3.5 years) presented later during follow up compared to LH/FSH (8.3 ± 4 years) and TSH (7.5 ± 5.6 years) deficiencies. In a Cox regression model, pituitary stalk abnormalities was the strongest risk factor for the development of CPHD (hazard ratio of 3.28; p = 0.002). CONCLUSION: Our study indicated a high frequency of development of CPHD in patients initially diagnosed as IGHD at childhood. Half of our patients with IGHD developed the second hormone deficiency after 5 years of diagnosis, reinforcing the need for lifelong monitoring of pituitary function in these patients.


Asunto(s)
Hormona Adrenocorticotrópica/deficiencia , Enanismo Hipofisario/epidemiología , Hormona Folículo Estimulante/deficiencia , Hormona de Crecimiento Humana/deficiencia , Hipopituitarismo/epidemiología , Hormona Luteinizante/deficiencia , Tirotropina/deficiencia , Vasopresinas/deficiencia , Adolescente , Adulto , Niño , Preescolar , Estudios de Cohortes , Progresión de la Enfermedad , Femenino , Estudios de Seguimiento , Humanos , Hipopituitarismo/patología , Hipotálamo/patología , Estimación de Kaplan-Meier , Estudios Longitudinales , Imagen por Resonancia Magnética , Masculino , Hipófisis/patología , Modelos de Riesgos Proporcionales , Estudios Retrospectivos , Factores de Tiempo , Adulto Joven
3.
Semin Reprod Med ; 31(4): 237-44, 2013 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-23775378

RESUMEN

Infertility is generally defined as a couple's inability to conceive after 1 year of unprotected intercourse. When infertile couples seek assistance, a male factor will be identified half of the time. Once the male has been evaluated, there are four main categories to describe his infertility: (1) idiopathic, (2) post-testicular/obstructive, (3) primary-where the Sertoli and/or Leydig cells of the testis fail, and (4) secondary-where there is a problem with the hypothalamus and/or pituitary. The last, hypogonadotropic hypogonadism (HH), accounts for up to 2% of infertile men. HH is either congenital or acquired and usually can be successfully treated by medical intervention. This review will focus on the hypothalamus-pituitary-gonadal axis, specific defects of this coordination center, and potential interventions for improving male-factor fertility.


Asunto(s)
Gonadotropinas/uso terapéutico , Terapia de Reemplazo de Hormonas , Infertilidad Masculina/prevención & control , Gonadotropina Coriónica/deficiencia , Gonadotropina Coriónica/genética , Gonadotropina Coriónica/metabolismo , Gonadotropina Coriónica/uso terapéutico , Hormona Folículo Estimulante/deficiencia , Hormona Folículo Estimulante/genética , Hormona Folículo Estimulante/metabolismo , Hormona Folículo Estimulante/uso terapéutico , Gonadotropinas/deficiencia , Gonadotropinas/genética , Gonadotropinas/metabolismo , Humanos , Hipogonadismo/tratamiento farmacológico , Hipogonadismo/metabolismo , Hipogonadismo/fisiopatología , Hipotálamo/efectos de los fármacos , Hipotálamo/metabolismo , Infertilidad Masculina/etiología , Hormona Luteinizante/deficiencia , Hormona Luteinizante/genética , Hormona Luteinizante/metabolismo , Hormona Luteinizante/uso terapéutico , Masculino , Menotropinas/deficiencia , Menotropinas/genética , Menotropinas/metabolismo , Menotropinas/uso terapéutico , Hipófisis/efectos de los fármacos , Hipófisis/metabolismo , Proteínas Recombinantes/uso terapéutico , Testículo/efectos de los fármacos , Testículo/metabolismo
4.
Hum Reprod ; 20(1): 101-7, 2005 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-15513979

RESUMEN

BACKGROUND: The purpose of this work was to revisit the gonadotrophin insufficiency of functional hypothalamic amenorrhoea (FHA) with the use of relevant ovarian markers. METHODS: Serum anti-Mullerian hormone (AMH), estradiol (E2), inhibin B, LH and FSH were immunoassayed in 31 women with FHA and in 30 healthy women in early follicular phase. The ovarian antral follicle number (FN) was determined within two distinct diameter ranges (2-5 and 6-9 mm) by ultrasound in real time, the same day as the blood sampling. RESULTS: The 2-5 mm FN was similar between the two groups, while the 6-9 mm FN was significantly less in FHA than in controls, in relation with lower serum FSH levels (r=0.428; P<0.024). Nine (29%) FHA patients had a low serum basal FSH level (i.e. <4.5 IU/l, 5th percentile of control values). In the 22 (71%) patients with apparently normal FSH, the mean 6-9 mm FN was similar to controls. However, in this sub-group, the mean AMH serum level and the AMH:2-5 mm FN ratio were significantly higher and the mean inhibin B serum level was significantly lower than in controls. No significant relationship was found between the serum LH levels and the FN, AMH or inhibin B values. CONCLUSION: Only a minority of patients with FHA have a low serum basal FSH level, and we show that this is associated with fewer 6-9 mm follicles at the ovarian level. Despite a normal serum FSH level and 6-9 mm FN in the majority of patients with FHA, the functional follicle markers are abnormal. This suggests that the FSH action on the ovary is incomplete and is not properly reflected by its serum level nor by FN at ultrasound.


Asunto(s)
Amenorrea/sangre , Hormona Folículo Estimulante/deficiencia , Hipotálamo/fisiopatología , Ovario/fisiopatología , Adulto , Amenorrea/patología , Amenorrea/fisiopatología , Hormona Antimülleriana , Biomarcadores/sangre , Estudios de Casos y Controles , Femenino , Hormona Folículo Estimulante/sangre , Fase Folicular/sangre , Glicoproteínas/sangre , Humanos , Inhibinas/sangre , Hormona Luteinizante/sangre , Folículo Ovárico/diagnóstico por imagen , Folículo Ovárico/patología , Hormonas Testiculares/sangre , Ultrasonografía
6.
J Androl ; 4(6): 393-8, 1983.
Artículo en Inglés | MEDLINE | ID: mdl-6140252

RESUMEN

Previous reports concerning isolated follicle stimulating hormone (FSH) deficiency and its possible pathogenesis have been conflicting. Both "normal" and "abnormal" FSH response to luteinizing hormone releasing hormone (LHRH) infusion have been described. We studied a 22-year-old man with normal basal serum testosterone and luteinizing hormone (LH) levels but undetectable levels of serum FSH. His serum LH titers showed one secretory spike during a 40-hour sampling at 20-minute intervals, whereas his serum FSH titers remained undetectable (less than 0.4 IU/l). Infusion of LHRH, 0.2 microgram/minute for 4 hours, induced the expected rise in the serum LH levels, but serum FSH levels remained low and only at one point reached 0.9 IU/l (normal adult male basal range 0.9-10.3 IU/l). The patient received LHRH, 100 micrograms/day, for three days. A second LHRH infusion, 0.2 microgram/minute for 4 hours, induced a normal rise in both the serum LH and FSH titers. The serum sex steroid binding globulin level was 10.3 ng DHT bound/ml (normal adult male level 8.0 +/- 0.3 ng DHT bound/ml). Presence of circulating auto-antibodies to the serum FSH was excluded by determining the binding of [125I] FSH with the patient's serum and comparing it with sera obtained from two normal male adult volunteers. Pituitary function tests were otherwise intact. Presence of a pituitary tumor was excluded by computerized axial tomography and x-ray studies of the pituitary fossa and normal visual fields. Clinically, the patient demonstrated cryptorchidism, hypospadias, surgically repaired omphalocele, and bilateral hearing loss.(ABSTRACT TRUNCATED AT 250 WORDS)


Asunto(s)
Hormona Folículo Estimulante/deficiencia , Adulto , Criptorquidismo/complicaciones , Hormona Folículo Estimulante/sangre , Hormona Liberadora de Gonadotropina/administración & dosificación , Pérdida Auditiva Bilateral/complicaciones , Hernia Umbilical/complicaciones , Humanos , Hipospadias/complicaciones , Hipotálamo/fisiología , Hormona Luteinizante/sangre , Masculino , Hipófisis/fisiología , Globulina de Unión a Hormona Sexual/metabolismo , Testosterona/sangre
7.
Am J Med Genet ; 15(3): 405-16, 1983 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-6410916

RESUMEN

To date, familial idiopathic gonadotropin deficiency (FIGD) has not been delineated as either a hypothalamic or a pituitary form of hypogonadism. Leydig cell sensitivity to human chorionic gonadotropin (HCG) has also been suggested as subnormal in FIGD. Also, in a few previously reported families the Kallmann syndrome was not clearly ruled out. Data herewith reported on three sibs with FIGD supported the following conclusions: 1) FIGD is due to insufficient hypothalamic luteinizing hormone-releasing hormone (LRH) secretion, 2) the sensitivity of Leydig cells to HCG is normal, 3) LRH treatment may be helpful in these patients, 4) an associated hypothalamic-pituitary-prolactin (PRL) dysfunction may also be present, and 5) FIGD and the Kallmann syndrome are different entities having a similar pathophysiology but different cause and overall clinical picture.


Asunto(s)
Gonadotropinas/deficiencia , Hipogonadismo/genética , Hipotálamo/anomalías , Femenino , Hormona Folículo Estimulante/deficiencia , Hormona Liberadora de Gonadotropina/deficiencia , Humanos , Hormona Luteinizante/deficiencia , Masculino , Caracteres Sexuales , Síndrome
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