RESUMEN
The selection of short-statured children for growth hormone (GH) treatment has long been complicated by the requirement for provocative testing that is unphysiologic, difficult to administer, and potentially dangerous. The recent FDA approval of GH for the treatment of children with idiopathic short stature allows treatment decisions to be based more on the degree of short stature and the potential for attaining a normal adult height. Several studies conducted in children have shown that GH therapy can effectively and safely produce height outcomes within a normal adult range. The observed variability in height response associated with GH use in some of these studies has left the clinician with a difficult decision. Still, the availability of GH for this patient population provides a rational treatment option for patients who fail arbitrary and inaccurate assessments.
Asunto(s)
Estatura/efectos de los fármacos , Trastornos del Crecimiento/tratamiento farmacológico , Hormona de Crecimiento Humana/uso terapéutico , Ensayos Clínicos como Asunto , Trastornos del Crecimiento/diagnóstico , HumanosAsunto(s)
Cetoacidosis Diabética , Adolescente , Edema Encefálico/etiología , Edema Encefálico/fisiopatología , Edema Encefálico/terapia , Niño , Complicaciones de la Diabetes , Cetoacidosis Diabética/diagnóstico , Cetoacidosis Diabética/fisiopatología , Cetoacidosis Diabética/prevención & control , Cetoacidosis Diabética/terapia , Líquido Extracelular , Fluidoterapia , Humanos , Insulina/uso terapéutico , Factores de Riesgo , Cloruro de Sodio/uso terapéuticoRESUMEN
Growth hormone deficiency (GHD) diagnosed in childhood may persist into adult life. After attainment of final height, retesting of the patient's growth hormone-insulin-like growth factor (GH-IGF) axis using the adult GHD diagnostic criteria should be performed after an appropriate interval of 1-3 months off GH therapy. At the time of retesting, other pituitary hormones and serum IGF-I levels should also be measured. The opportunity should be taken to assess body composition, bone mineral density, and fasting lipid and insulin levels. Patients with severe, long-standing, multiple pituitary hormone deficiency, genetic defects, or severe organic GHD can be excluded from GH retesting. When the diagnosis of adult GHD is established, continuation of GH therapy can be recommended unless there is a known risk of diabetes mellitus or malignancy. The patient's transition to GH replacement in adulthood should be arranged as a close collaboration between the pediatric and adult endocrinologists, who should discuss the reinitiation of treatment with the patient.
Asunto(s)
Continuidad de la Atención al Paciente/tendencias , Hormona de Crecimiento Humana/deficiencia , Hipopituitarismo/diagnóstico , Reproducibilidad de los Resultados , Adulto , Factores de Edad , Niño , Hormona de Crecimiento Humana/sangre , Hormona de Crecimiento Humana/uso terapéutico , Humanos , Hipopituitarismo/sangre , Hipopituitarismo/tratamiento farmacológico , Factor I del Crecimiento Similar a la Insulina/química , Factor I del Crecimiento Similar a la Insulina/fisiología , Valor Predictivo de las PruebasAsunto(s)
Trastornos del Crecimiento/diagnóstico , Trastornos del Crecimiento/tratamiento farmacológico , Hormona de Crecimiento Humana/deficiencia , Hormona de Crecimiento Humana/uso terapéutico , Adolescente , Estatura/efectos de los fármacos , Niño , Relación Dosis-Respuesta a Droga , Femenino , Trastornos del Crecimiento/psicología , Hormona de Crecimiento Humana/administración & dosificación , Hormona de Crecimiento Humana/efectos adversos , Humanos , Masculino , Modelos Biológicos , Pubertad , Proteínas Recombinantes/administración & dosificación , Proteínas Recombinantes/efectos adversos , Proteínas Recombinantes/uso terapéuticoRESUMEN
Arginine stimulates growth hormone (GH) secretion, possibly by inhibiting hypothalamic somatostatin (SS) release. Insulin-like growth factor I (IGF-I) inhibits GH secretion via effects at the pituitary and/or hypothalamus. We hypothesized that if the dominant action of IGF-I is to suppress GH release at the level of the pituitary, then the arginine-induced net increase in GH concentration would be unaffected by an IGF-I infusion. Eight healthy young adults (3 women, 5 men) were studied on day 2 of a 47-h fast for 12 h (35th-47th h) on four occasions. Saline (Sal) or 10 microg. kg(-1). h(-1) recombinant human IGF-I was infused intravenously for 5 h from 37 to 42 h of the 47-h fast. Arginine (Arg) (30 g iv) or Sal was infused over 30 min during the IGF-I or Sal infusion from 40 to 40.5 h of the fast. Subjects received the following combinations of treatments in random order: 1) Sal + Sal; 2) Sal + Arg; 3) IGF-I + Sal; 4) IGF-I + Arg. Peak GH concentration on the IGF-I + Arg day was ~45% of that on the Sal + Arg day. The effect of arginine on net GH release was calculated as [(Sal + Arg) - (Sal + Sal)] - [(IGF-I + Arg) - (IGF-I + Sal)]. There was no significant effect of IGF-I on net arginine-induced GH release over control conditions. These findings suggest that the negative feedback effect of IGF-I on GH secretion is primarily mediated at the pituitary level and/or at the hypothalamus through a mechanism different from the stimulatory effect of arginine.