RESUMO
Physician and clinic charges for diagnosing growth hormone deficiency (GHD) in children are not generally known, whereas the charges for purchasing growth hormone (GH) are known. We recently surveyed the charges submitted to third-party payers for diagnosing GHD in five pediatric endocrine clinics throughout the United States: the Albert Einstein College of Medicine, Baylor College of Medicine, Health Science Schools of the State University of New York at Buffalo, Oregon Health Sciences University, and the University of Chicago. The financial data analyzed included charges for physician services and for GH testing. Different approaches to the medical examination of children with suspected GHD at these clinics prevented any comparison of physician or GH testing charges. However, the charges for diagnosing GHD could be determined for each pediatric endocrine clinic if the methods of examination were not considered. Contractual adjustments, net revenues, costs, and net margins were not surveyed. Subjective comments from the study sites suggest significantly reduced reimbursement amounts. We conclude that the total charges for diagnosing GHD submitted to third-party payers at these institutions averaged $1719.
Assuntos
Atenção à Saúde/economia , Transtornos do Crescimento/diagnóstico , Transtornos do Crescimento/tratamento farmacológico , Hormônio do Crescimento/deficiência , Hormônio do Crescimento/uso terapêutico , Criança , Pré-Escolar , Honorários Médicos/estatística & dados numéricos , Humanos , Seguro Saúde/economiaRESUMO
Because current concepts of growth hormone (GH) testing and GH treatment have become controversial, we investigated the GH secretory patterns in children with normal and short stature. Twenty-four-hour serum GH levels were evaluated in three groups of children. Group 1 was composed of children with normal height (mean height = 0.02 SD, n = 33); group 2 was composed of short children (less than 5th percentile, n = 63) with normal results on provocative GH testing; and group 3 was composed of short children (less than 5th percentile, n = 7) with subnormal results on provocative GH testing. Mean +/- SD (range) GH levels during 24-hour studies of GH secretion were 1.6 +/- 1.1 (0.5 to 5.6), 1.8 +/- 1.2 (0.6 to 6.3), and 0.9 +/- 0.4 (0.5 to 1.7) ng/ml in groups 1, 2, and 3, respectively. No statistical difference existed in mean GH levels between groups 1 and 2 or between groups 1 and 3. The mean GH concentration from 24-hour studies in group 2 children did not correlate with chronologic age, height standard deviation, growth rates, or insulin-like growth factor 1 levels. The linear growth rate of 26 of 28 children in group 2 who received GH therapy for 6 months improved by 2 cm/yr or more; the mean +/- SD growth rate was 4.0 +/- 1.3 and 8.8 +/- 2.0 cm/yr during control and treatment periods, respectively, for these 28 children. Mean GH levels from testing did not predict response to GH during 6 months of therapy. Children with slower growth rates responded better to GH therapy (p less than 0.05). We conclude that (1) in 24-hour studies, GH levels in normal children overlapped with those of short children, including those with classic GH deficiency, (2) in 24-hour studies, GH levels did not predict responses of linear growth to short-term GH treatment, nor did they correlate with children's heights or growth velocities, and (3) the majority of short children in group 2 treated with GH for 6 months had an increase in linear growth velocity, the mean +/- SD change being 4.8 +/- 2.0 cm/yr.
Assuntos
Transtornos do Crescimento/tratamento farmacológico , Hormônio do Crescimento/metabolismo , Criança , Ritmo Circadiano , Feminino , Hormônio do Crescimento/deficiência , Hormônio do Crescimento/uso terapêutico , Humanos , Fator de Crescimento Insulin-Like I/análise , MasculinoRESUMO
The agonistic analogues of luteinizing hormone releasing hormone decrease biochemical findings and clinical signs of gonadotropin-dependent precocious puberty. We tested a new analogue, nafarelin acetate, in 15 girls with gonadotropin-dependent precocious puberty. The hydrophobic nature and potency of this compound allow it to be administered by intranasal inhalation. Laboratory assessment of vaginal cytology, estradiol and urinary gonadotropin levels, and growth velocity revealed that nafarelin acetate 800 to 1200 micrograms/day diminished these values during a 6-month treatment period. These results suggest gonadotropin-dependent precocious puberty in girls can be treated with intranasal administration of nafarelin acetate.
Assuntos
Hormônio Liberador de Gonadotropina/análogos & derivados , Gonadotropinas Hipofisárias/fisiologia , Puberdade Precoce/tratamento farmacológico , Administração Intranasal , Criança , Pré-Escolar , Estradiol/sangue , Feminino , Hormônio Foliculoestimulante/sangue , Hormônio Liberador de Gonadotropina/administração & dosagem , Hormônio Liberador de Gonadotropina/uso terapêutico , Crescimento/efeitos dos fármacos , Humanos , Lactente , Hormônio Luteinizante/sangue , Nafarelina , Maturidade Sexual/efeitos dos fármacos , Vagina/citologiaRESUMO
Transient congenital hypoparathyroidism was observed in four neonates who also had congenital cardiac defects. Severe hypocalcemia and hyperphosphatemia were noted at 2 or 3 weeks of age, but resolved by 2 to 4 months of age with minimal treatment (oral calcium alone). Parathyroid hormone, measured with a highly sensitive, homologous antiserum, was initially borderline detectable and became easily detectable as the hypocalcemia resolved. Immune function was normal in each patient. The congenital cardiac defects in each case involved the pulmonary valve. These patients might be regarded as having either a partial form of the DiGeorge syndrome or a separate syndrome in which congenital pulmonary valve lesions are linked to delayed maturation of parathyroid function by an as yet obscure mechanism.