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1.
Psychoneuroendocrinology ; 24(2): 131-42, 1999 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-10101722

RESUMEN

When separated from groups, squirrel monkeys respond with significant increases in plasma cortisol and adrenocorticotropic hormone (ACTH). While cortisol remains elevated above pre-separation levels, significant reductions occur in ACTH. Monkeys that respond with greater increases in cortisol subsequently exhibit greater reductions in ACTH, which suggests that reductions in ACTH are mediated by corticosteroid feedback. Monkeys that respond with greater increases in cortisol also tend to exhibit greater cerebrospinal fluid levels of the dopamine metabolite HVA, but not the norepinephrine metabolite MHPG, or corticotropin-releasing factor (CRF). Attenuation of corticosteroid feedback with metyrapone results in significant increases in circulating ACTH, and in older monkeys increases plasma HVA. Similar findings in humans have been reported in clinical studies of hypercortisolism and major depression.


Asunto(s)
Glándulas Suprarrenales/fisiopatología , Hiperfunción de las Glándulas Suprarrenales/fisiopatología , Ansiedad de Separación/fisiopatología , Hidrocortisona/sangre , Hipotálamo/fisiopatología , Hipófisis/fisiopatología , Hormona Adrenocorticotrópica/sangre , Animales , Hormona Liberadora de Corticotropina/líquido cefalorraquídeo , Retroalimentación , Femenino , Ácido Homovanílico/sangre , Humanos , Masculino , Metirapona/farmacología , Saimiri/fisiología
2.
Bol. Hosp. San Juan de Dios ; 43(5): 265-70, sept.-oct. 1996.
Artículo en Español | LILACS | ID: lil-185234

RESUMEN

Se analiza la sintomatología y signología del hipercortisolismo que es un síndrome producido por la exposición prolongada del organismo a la acción de los glucocorticoides. Se revisan sus mecanismos patogénicos, destacando entre ellos las alteraciones primarias hipofisiarias y las corticosuprarrenales (hiperplasias y tumores). Hay también hipercortisolismos por producción ectópica de ATCH y por administración terapéutica de corticoesteroides. La clínica permite la sospecha diagnóstica pero el laboratorio la confirma a través de determinaciones hormonales (cortisol libre urinario) y localiza la lesión mediante expamens de imágenes. El tratamiento es básicamente quirúrgico


Asunto(s)
Humanos , Hiperfunción de las Glándulas Suprarrenales/fisiopatología , Síntomatología , Hormona Adrenocorticotrópica , Técnicas de Laboratorio Clínico , Glucocorticoides/efectos adversos , Hiperfunción de las Glándulas Suprarrenales/cirugía , Hiperfunción de las Glándulas Suprarrenales/diagnóstico , Hiperfunción de las Glándulas Suprarrenales/etiología
3.
J Clin Endocrinol Metab ; 80(8): 2336-41, 1995 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-7629226

RESUMEN

We present two patients with Cushing's syndrome due to ACTH-independent macronodular adrenal hyperplasia who showed marked plasma cortisol response to lysine-8-vasopressin (LVP) injection (from 930 and 731 pmol/L to 2177 and 1920 pmol/L, respectively), while plasma ACTH levels remained undetectable. The ACTH independence of cortisol secretion in the two patients was determined from the following endocrinological findings. Plasma cortisol levels were not increased by corticotropin-releasing hormone injections and were not suppressed by high dose (16 mg) dexamethasone administrations. The plasma ACTH levels, measured by two independent sensitive immunoassays, were persistently undetectable even after corticotropin-releasing hormone injection, metyrapone administration, and bilateral adrenalectomy. The particular pathological finding of the two cases, atrophic lesions in nonnodular parts of the adrenal cortexes, also indicated ACTH independence of the macronodular hyperplasia. In vitro examination revealed a direct effect of LVP on cortisol secretion from the adrenal cells of the macronodules. We also examined seven patients with Cushing's syndrome caused by adrenal adenoma and found a statistically significant plasma cortisol response to LVP injection. The direct effect of LVP was also demonstrated in cultured adenoma cells. In conclusion, we discovered a direct adrenal effect of LVP on cortisol secretion in patients with ACTH-independent macronodular hyperplasia and, to a lesser extent, in patients with cortisol-producing adrenal adenoma. The cortisol response to LVP may serve to facilitate their diagnosis and choice of therapy.


Asunto(s)
Adenoma/fisiopatología , Neoplasias de las Glándulas Suprarrenales/fisiopatología , Hiperfunción de las Glándulas Suprarrenales/fisiopatología , Hormona Adrenocorticotrópica/sangre , Síndrome de Cushing/fisiopatología , Hidrocortisona/metabolismo , Lipresina , 17-Hidroxicorticoesteroides/orina , 17-Cetosteroides/orina , Adenoma/patología , Neoplasias de las Glándulas Suprarrenales/patología , Hiperfunción de las Glándulas Suprarrenales/sangre , Hiperfunción de las Glándulas Suprarrenales/orina , Adulto , Análisis de Varianza , Hormona Liberadora de Corticotropina , Síndrome de Cushing/sangre , Síndrome de Cushing/orina , Dexametasona , Femenino , Humanos , Hidrocortisona/sangre , Hidrocortisona/orina , Ensayo Inmunorradiométrico , Masculino , Persona de Mediana Edad , Sensibilidad y Especificidad
4.
Magnes Res ; 6(4): 379-94, 1993 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-8155490

RESUMEN

Ageing constitutes a risk factor for magnesium deficit. Primary magnesium deficit originates from two aetiological mechanisms: deficiency and depletion. Primary magnesium deficiency is due to insufficient magnesium intake. Dietary amounts of magnesium are marginal in the whole population whatever the age. Nutritional deficiencies are more pronounced in institutionalized than in free-living ageing groups. Primary magnesium depletion is due to dysregulation of factors controlling magnesium status: intestinal magnesium hypoabsorption, reduced magnesium bone uptake and mobilization, sometimes urinary leakage, hyperadrenoglucocorticism by decreased adaptability to stress, insulin resistance and adrenergic hyporeceptivity. Secondary magnesium deficit in ageing largely results from various pathologies and treatments common to elderly persons, i.e., non-insulin dependent diabetes mellitus and use of hypermagnesuric diuretics. Magnesium deficit may participate in the clinical pattern of ageing, particularly in neuromuscular, cardiovascular and renal symptomatologies. The consequences of hyperadrenoglucocorticism-the simplest marker of which is non-response to the dexamethasone suppression test-may include immunosuppression, muscle atrophy, centralization of fat mass, osteoporosis, hyperglycaemia, hyperlipidaemia, atherosclerosis, and disturbances of mood and mental performance through accelerated hippocampal ageing particularly. It seems very important to point out that magnesium deficit and stress aggravate each other in a true 'pathogenic vicious circle', particularly in the stressful state of ageing. The importance of magnesium deficit in the aetiologies of insulin resistance, and the adrenergic, osseous, oncogenic, immune and oxidant disturbances of ageing is still uncertain. Oral physiological magnesium supplementation (5 mg Mg/kg/d) is the best diagnostic tool for establishing the importance of magnesium deficiency. Too few open and double blind studies on the effects of the treatment of magnesium deficiency and of magnesium depletion in geriatric populations have been done. Further study is necessary to assess the true place of magnesium deficit in the pathophysiology of ageing.


Asunto(s)
Envejecimiento/fisiología , Deficiencia de Magnesio/fisiopatología , Magnesio/fisiología , Hiperfunción de las Glándulas Suprarrenales/fisiopatología , Anciano , Humanos , Resistencia a la Insulina , Deficiencia de Magnesio/complicaciones
5.
AACN Clin Issues Crit Care Nurs ; 3(2): 331-49, 1992 May.
Artículo en Inglés | MEDLINE | ID: mdl-1576032

RESUMEN

Increased function of the adrenal cortex is a normal response in times of physiologic and psychologic stress. Adrenal cortical secretions (e.g., glucocorticoids, aldosterone) orchestrate a multitude of internal processes aimed at maintaining homeostasis and psychologic integrity. Many patients admitted to a critical care unit will manifest some increase, even minor, in adrenal function. However, excessive secretions of these hormones can have a lethal effect of fluid and electrolyte balance, energy metabolism, and immune function. Cushing's syndrome denotes a disorder characterized by increased circulating levels of glucocorticoids (primarily cortisol). An easily recognizable disorder, it may arise from pathology of the adrenal cortex or the anterior pituitary glands, ectopic secretions from a nonendocrine tumor, or from excessive doses of exogenously administered glucocorticoids. Cushing's syndrome is rarely an admitting diagnosis to critical care but is a disorder that can seriously affect recovery from coexisting illnesses if not treated. Aldosteronism, although rare, will often be diagnosed after admission to a critical care unit for management of troublesome hypertension, hypokalemia, congestive heart failure, and various dysrhythmias. Suspicion of the diagnosis should always arise when these manifestations occur, particularly when hypokalemia is refractory to potassium supplementation. Without timely diagnosis and treatment, these patients will succumb to lethal dysrhythmias.


Asunto(s)
Hiperfunción de las Glándulas Suprarrenales/fisiopatología , Síndrome de Cushing/fisiopatología , Hiperaldosteronismo/fisiopatología , Hiperfunción de las Glándulas Suprarrenales/diagnóstico , Hiperfunción de las Glándulas Suprarrenales/terapia , Adulto , Aldosterona/metabolismo , Andrógenos/metabolismo , Síndrome de Cushing/diagnóstico , Síndrome de Cushing/terapia , Humanos , Hidrocortisona/metabolismo , Masculino , Persona de Mediana Edad
6.
Brain Res ; 352(2): 296-301, 1985 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-2862962

RESUMEN

The ontogeny of the vasoactive intestinal peptide (VIP) and somatostatin (SRIF) was studied in various structures of the rat central nervous system (CNS), using specific radioimmunoassays. The effect of adrenal corticoids on the concentration of both peptides was investigated during the development of the rat from 3 days before birth to 2 months after birth. The evolution of both peptides was different since SRIF was found before birth in each structure tested while VIP appeared only after birth in the same structures. However, after birth the ontogeny of VIP and SRIF was quite similar and the maximum concentration of both peptides occurred between day 14 and day 21. Hypercorticism (implant of corticosterone) and hypocorticism (Metyrapone injections) modified the postnatal evolution of both peptides, suggesting that corticoids play an important role in the brain developmental patterns of VIP and SRIF.


Asunto(s)
Insuficiencia Suprarrenal/fisiopatología , Hiperfunción de las Glándulas Suprarrenales/fisiopatología , Química Encefálica , Somatostatina/análisis , Péptido Intestinal Vasoactivo/análisis , Amígdala del Cerebelo/análisis , Animales , Encéfalo/crecimiento & desarrollo , Hipocampo/análisis , Hipotálamo/análisis , Masculino , Bulbo Olfatorio/análisis , Lóbulo Parietal/análisis , Ratas , Ratas Endogámicas
7.
Endocrinologie ; 21(2): 123-9, 1983.
Artículo en Inglés | MEDLINE | ID: mdl-6867598

RESUMEN

The investigation was carried out on 66 patients with hypo- or hyperfunctional syndromes of adrenocorticism, hospitalized and treated by our team. The patients were grouped into 5 lots according to their diseases. Lot one consisted of 34 female patients with Cushing's syndrome, lot two of 10 males with Cushing's syndrome, lot three of 10 males with Addison's disease and lot four, of 6 females with androgenic hypercorticism. The morphofunctional disorders of reproduction were followed up clinically and by complex hormone assays, before and after treatment. The incidence of these disorders is very high, and the results of clinical observations and of laboratory data demonstrate that both the excess of adrenocortical hormones and the decrease in their circulating level have a negative influence on the reproduction function or represent a risk factor in cases of pregnancy. By the curative treatment of the adrenal cortex a preventive treatment of abortion and/or sterility is achieved.


Asunto(s)
Insuficiencia Suprarrenal/fisiopatología , Hiperfunción de las Glándulas Suprarrenales/fisiopatología , Reproducción , Adulto , Femenino , Hormonas Esteroides Gonadales/análisis , Gonadotropinas Hipofisarias/análisis , Humanos , Hipotálamo/fisiopatología , Masculino , Persona de Mediana Edad
8.
Am J Vet Res ; 42(11): 1881-3, 1981 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-7199880

RESUMEN

The plasma growth hormone response to the provocative agent, xylazine, was assessed in 4 dogs with spontaneous hyperadrenocorticism, before and after therapy. Before treatment of the hyperadrenocorticism, no significant increase in growth hormone concentration occurred in any of the dogs following the administration of xylazine. A significant increase in growth hormone concentrations following xylazine administration occurred in 2 of the 3 dogs with hypophysis (pituitary)-dependent hyperadrenocorticism after treatment with mitotane (o,p'-DDD) and in 1 dog after surgical removal of a hyperfunctional adrenal adenoma. Although the impaired growth hormone response persisted in 1 dog, the administration of xylazine was repeated in this animal after only 3 weeks of mitotane therapy; it is likely that growth hormone unresponsiveness would reverse if the hyperadrenocorticism were controlled for a longer period. These findings demonstrate that in dogs, as in persons, the excessive production of endogenous corticosteroids associated with either hypophysis-dependent hyperadrenocorticism or hyperfunctional adrenal tumor can induce suppression of growth hormone release which is reversible following treatment.


Asunto(s)
Hiperfunción de las Glándulas Suprarrenales/veterinaria , Enfermedades de los Perros/fisiopatología , Hormona del Crecimiento/metabolismo , Tiazinas/farmacología , Xilazina/farmacología , Adenoma/cirugía , Adenoma/veterinaria , Neoplasias de las Glándulas Suprarrenales/cirugía , Neoplasias de las Glándulas Suprarrenales/veterinaria , Hiperfunción de las Glándulas Suprarrenales/tratamiento farmacológico , Hiperfunción de las Glándulas Suprarrenales/fisiopatología , Animales , Síndrome de Cushing/fisiopatología , Enfermedades de los Perros/tratamiento farmacológico , Enfermedades de los Perros/cirugía , Perros , Femenino , Masculino , Hipófisis/fisiopatología
9.
Probl Endokrinol (Mosk) ; 23(2): 32-8, 1977.
Artículo en Ruso | MEDLINE | ID: mdl-198763

RESUMEN

Separate determination of hydrocortisone and corticosterone in the blood of patients with the hypercorticism symptom-complex showed that elevation of the corticosteroid concentration could occur on account of similar elevation of the concentration of both hormones, or one of the hormones alone. Analogous data were observed in patients after ACTH administration. Dexamethasone administration caused a reduction of the hydrocortisone and corticosterone concentration in patients with Itsenko-Cushing's disease, but to a lesser degree than in healthy individuals. Administration of the preparation to the patients with juvenile dyspituitrism decreased the cortizol level, but corticosterone chiefly; as to the patients with the hypothalamic syndrome--only the cortizol level was reduced, the level of corticosterone remaining unchanged. Thus, the evidence obtained before and after the administration of the ACTH preparations and dexamethasone permitted to assess the adrenal cortex function more fully and to defect disturbances of the corticosteroid secretion of interest of the understanding of the clinical symptoms of the disease.


Asunto(s)
Corteza Suprarrenal/fisiopatología , Hiperfunción de las Glándulas Suprarrenales/fisiopatología , Corticosterona/sangre , Hidrocortisona/sangre , 11-Hidroxicorticoesteroides/sangre , Adolescente , Hormona Adrenocorticotrópica , Adulto , Encefalopatías/fisiopatología , Enfermedad Crónica , Síndrome de Cushing/fisiopatología , Dexametasona , Diencéfalo , Humanos , Hipotálamo , Enfermedades de la Hipófisis/fisiopatología , Síndrome
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