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La expectativa de vida ha ido aumentando en Chile y en el mundo, lo que ha causado un gran impacto a nivel del número de cirugías que se realiza en la población añosa. El objetivo de este trabajo es describir la experiencia de nuestro centro en cirugías urológicas en pacientes mayores de 80 años y analizar que factores aumentan el riesgo de complicaciones postquirúrgicas.Materiales y método: Análisis retrospectivo de 138 cirugías urológicas realizadas en 120 pacientes mayores de 80 años, durante los años 2000 a 2012. Se obtuvo información sociodemográfica, riesgo quirúrgico (ASA), tipo y duración de cirugía realizada, complicaciones post-operatorias (escala de Clavien) y tiempo de hospitalización. Los datos obtenidos fueron analizados mediante el programa SPSS v17. Se realizó análisis multivariado y se estableció el riesgo relativo para el desarrollo de complicaciones. Se consideró signi ficativo p<0,05. Resultado: La edad promedio de los pacientes fue de 84+/-3.7 años, 86.2 por ciento fueron hombres. El 96.7 por ciento presentaba algún tipo de comorbilidad, con predominio de hipertensión arterial (60,84 por ciento) y diabetes mellitus tipo 2 (24,16 por ciento). La mayoría de las intervenciones fue de complejidad intermedia (77.27 por ciento), donde la anestesia regional (56,8 por ciento) y la vía endo urológica (84,78 por ciento) fueron las más utilizadas, con un tiempo operatorio promedio de 62+/-52.4 minutos. El riesgo quirúrgico prevalente fue ASA2 (62.7 por ciento). El promedio de hospitalización fue de 2,8+/-2.7 días. El 15.21 por ciento de los pacientes presentó algún tipo de complicación, con predominio de clasifi cación tipo 1 de Clavien (38 por ciento). En el análisis multivariado se evidenció como factores de riesgo signi ficativos para complicaciones, edad mayor a 90 años (p=0.03), presencia de insu ciencia renal (p=0.01), portar 4 o más comorbilidades (p=0.04), cirugía mayor a 3 horas (p=0.03) y tener riesgo quirúrgico ASA3 (p=0.04)...

Life expectancy has been increasing in Chile and in the World. This has caused a great impact over the number of surgeries being performed in the elderly population. The aim of this paper is to describe the experience of our center in urological surgery in patients older than 80 years and analyze which factors increase the risk of postoperative complications.Materials and methods: Retrospective analysis of 138 urological surgeries performed in 120 patients older than 80 years, during the years 2000-2012. Sociodemographic information, surgical risk (ASA), type and duration of surgery, postoperative complications (Clavien scale) and length of hospitalization was obtained. The data were analyzed using SPSS v17. Multivariate analysis was performed and the relative risk for developing complications was established. Signi cance was p <0.05. Average age of the patients was 84 +/- 3.7 years, 86.2percentwere men. The 96.7 percenct had some kind of comorbidity, with prevalence of hypertension (60.84 percent) and diabetes mellitus type 2 (24.16 percent). Most of the interventions was of intermediate complexity (77.27percent), where regional anesthesia (56.8 percent) and endourological aproach (84.78 percent) were the most used, with average operative time of 62 +/- 52.4 minutes. Most common Surgical risk was ASA2 (62.7 percent). Average hospital stay was 2.8 +/- 2.7 days. 15.21 percent of patients had some type of complication, with a predominance of type 1 Clavien classication (38 percent). The multivariate analysis showed signi cant risk factors for complications: age greater than 90 years (p = 0.03), renal failure (p = 0.01), carrying 4 or more comorbidities (p = 0.04), surgery Langer than 3 hours (p = 0.03) and ASA3 surgical risk (p =.04). No mortality was reported in our series. In this study, although most of our patients underwent endourological procedures, we evidence that surgery in patients older than 80 years is feasible...

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IGF-I generation tests were developed over 20 yr ago and are currently used in differentiating GH insensitivity (GHI) from other disorders characterized by low serum IGF-I. Nevertheless, generation tests have never been adequately characterized, and insufficient normative data are available. One hundred and ninety-eight subjects [including normal subjects; subjects with GHI, GH deficiency (GHD), and idiopathic short stature (ISS); and heterozygotes for the E180 splice GH receptor mutation] were randomized to self-administration of either a high (0.05 mg/kg x d) or a low (0.025 mg/kg x d) dose of GH for 7 d. After a 2-wk washout period, they received the alternate dose. Samples were collected on d 1, 5, and 8 of each treatment period. In normal individuals, IGF-I generation was GH dependent at all ages, and little advantage was observed in using the higher dose of GH or extending beyond the d 5 sample. Some GHD patients had IGF-I levels, both baseline and stimulated, that overlapped levels in the verified GHI patients. Subjects heterozygous for the E180 GH receptor splice mutation did not show a decreased responsiveness to GH. ISS patients had low-normal IGF-I levels that did not stimulate beyond the baseline normative ranges for age. These data provide the first large scale effort to provide preliminary normative IGF generation data and evaluate the GH sensitivity of patients with GHI, GHD, and ISS.

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Although insulin-like growth factor binding proteins (IGFBPs) are known to be important modulators of the action of insulin-like growth factors (IGFs), regulation of their production in vivo is not completely understood. Serum concentrations of IGFBP-3, -4 and -5 and acid-labile subunit (ALS) were therefore examined in 20 children with growth hormone (GH) insensitivity before and after 6 months of therapy with recombinant human IGF-I (80 or 120 micrograms/kg twice daily). The IGFBP concentrations in these children were compared with those in 62 GH-deficient children receiving GH therapy for 3 months. Serum levels of IGFBP-3, -4 and -5 and ALS all increased significantly (p < 0.0001) in GH-deficient children in response to GH therapy, whereas no significant increases occurred in the children with GH insensitivity. These findings indicate that GH is responsible for the regulation of serum levels of IGFBP-3, -4 and -5 and ALS, and that IGF-I does not directly regulate the concentrations of these circulating IGFBPs.

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Growth hormone (GH) and insulin-like growth factor I (IGF-I) deficiencies have been associated with osteopenia in both children and adults. To examine the effects of growth hormone resistance on bone mineral and body composition, we studied 11 adults (mean age 30 years) with growth hormone receptor deficiency (GHRD, Laron syndrome) and 11 age- and gender-matched controls from Southern Ecuador. Bone mineral and body composition were determined by dual-energy X-ray absorptiometry. Bone physiology was assessed with biochemical markers of bone turnover and dynamic bone histomorphometry. Bone size and body composition differed markedly between subjects with GHRD and controls. Affected adults were 40 cm shorter than controls, had significantly less lean body mass, and had increased percent body fat. Bone mineral content and density (BMD) at the spine, femoral neck, and whole body were significantly lower in adults with GHRD than in controls. Mean BMD Z scores were -1.5 to -1.6 at all sites in affected women and -2.2 to -2.3 in men with GHRD. Estimated volumetric bone density (BMAD) at the spine and femoral neck, however, was not reduced in GHRD. Spine BMAD was 0.210 +/- 0.025 versus 0.177 +/- 0.021 for affected women versus controls (p < 0.05) and 0.173 +/- 0.018 versus 0.191 +/- 0.025 for men with GHRD versus normals (p = 0.31). Urinary pyridinoline concentrations were significantly greater in adults with GHRD than in controls, while type I collagen C-telopeptide breakdown products and markers of bone formation did not differ. Differences in histomorphometry were limited to a reduction in trabecular connectivity; bone volume and formation rate were similar to controls. These data confirm the importance of the GH/IGF axis in regulating bone size and body composition. The contribution of these peptides to the acquisition and maintenance of bone mineral is less certain since volumetric bone density was preserved despite low levels of IGF-I and IGFBP-3 associated with GH resistance.

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OBJECTIVE: To carry out a multicenter, prospective, randomized trial of human growth hormone (GH), alone or in combination with oxandrolone (OX), in patients with Turner's syndrome (TS). METHODS: In an initial phase lasting 12 to 24 months, 70 girls with TS, verified by karyotype, were randomly assigned to one of four groups: (1) observation, (2) OX, (3) GH, or (4) GH plus OX. After completion of the first phase, group 3 subjects continued to receive GH only. All other subjects were treated with GH plus OX. Subjects were followed up until attainment of adult height and/or cessation of treatment. Data from this trial were compared with growth characteristics of 25 American historical subjects with TS (matched for age, height, parental target height, and karyotype) who never received either GH or androgens. RESULTS: Of the 70 subjects enrolled, 60 completed the clinical trial. The 17 subjects receiving GH alone all completed the trial and reached a height of 150.4+/-5.5 cm (mean +/- SD), 8.4+/-4.5 cm taller than their mean projected adult height at enrollment (95% confidence interval [CI]: 6.3 to 10.6 cm). The 43 subjects receiving GH plus OX attained a mean height of 152.1+/-5.9 cm, 10.3+/-4.7 cm taller than their mean projected adult height (95% CI: 8.9 to 11.7 cm). The historical control subjects had a mean adult height of 144.2+/-6.0 cm, precisely matching their original projected adult height of 144.2+/-6.1 cm. CONCLUSIONS: GH, either alone or in combination with OX, is capable of stimulating short-term growth and augmenting adult height in girls with TS. With early diagnosis and initiation of treatment, an adult height of more than 150 cm is a reasonable goal for most girls with TS.

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We have reported 1-yr results of a double blind, placebo-controlled trial of recombinant human insulin-like growth factor I (rhIGF-I) replacement in 16 children from the Ecuadorian GH receptor-deficient (GHRD) population. This report extends observations of rhIGF-I efficacy at two dosage levels [120 micrograms/kg BW twice daily (n = 15) and 80 micrograms/kg twice daily (n = 7)] over 2 yr, compares biochemical responses [serum IGF-I and IGF-binding protein-3 (IGFBP-3)] and their relationship to growth effects, and compares treatment effects of rhIGF-I in GHRD to rhGH in idiopathic GH deficiency (GHD). There were no baseline differences between the low and high dose groups for growth velocity (GV), bone age (BA), SD score for height, or percent mean body weight for height (MBWH). Over 2 yr of rhIGF-I treatment, there were no differences in GV or in changes in height SD score, height age (HA), or BA between the two groups; a subgroup of six subjects at the higher dose followed for a third year continued at the second year GV. The higher dose resulted in a greater change in percent MBWH. GV in yr 1 and 2 for the entire group and in yr 3 for a subgroup were greater for GH-treated GHD (n = 11). The GHD group showed a greater change in SD score for height and HA, but did not differ from the rhIGF-I-treated GHRD group in the change in BA (delta BA) or delta HA/delta BA over 2 yr. There was a greater change in percent MBWH in GHRD. There were no differences between dosage groups for serum IGF-I levels at baseline or the near-normal trough levels 12 h after rhIGF-I injection; these individual levels correlated with HA gain in yr 1 and 2. IGFBP-3 levels were markedly low, with no changes of significance with treatment. Comparable growth responses to the two dosage levels and the biochemical changes indicate a plateau effect at or below 80 micrograms/kg BW twice daily. The growth response and favorable trough levels of IGF-I despite the overall lack of increase in circulating IGFBP-3 levels suggest an alternative mechanism for sustaining IGF-I levels and avoiding rapid clearance of rhIGF-I. The greater increase in MBWH with treatment of GHRD than with treatment of GHD may reflect comparable effects on lean body mass without the lipolytic effects of GH in the GHRD subjects. The difference in growth response between rhIGF-I-treated GHRD and rhGH-treated GHD groups is consistent with the hypothesis that 20% or more of GH-influenced growth is due to the direct effects of GH on bone. Nonetheless, the comparable delta HA/delta BA suggests similar long term effects of replacement therapy in the two conditions.

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