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Objetivo: Determinar la incidencia de hipofosfatemia en pacientes con nutrición parenteral, la cantidad de fosfato necesaria para prevenir esta complicación y los factores de riesgo asociados. Ámbito: Estudio observacional no controlado en un hospital de nivel III. Pacientes: pacientes ingresados con nutrición parenteral a los que se les ha realizado como mínimo una analitica completa. Intervención: Se registran durante un año, los días de nutrición parenteral, el fosfato administrado y los niveles plasmáticos de calcio ionizado, γ-glutamiltranspeptidasa, glucosa, fosfato, prealbúmina, urea y leucocitos. Para el análisis se aplica una regresión múltiple stepwise y una regresión logistica. Resultados: Se incluyeron en el estudio 827 determinaciones correspondientes a 401 pacientes. Las variables significativas (p < 0,05) fueron: fosfato administrado y los niveles séricos de calcio ionizado, glucosa, prealbúmina y urea; los coeficientes de regresión fueron 0,004 (95% IC: 0,002-0,006), -0,156 (95% IC: -0,270-0,037), -0,014 (95% IC: -0,022-0,009), 0,005 (95% CI: 0,002-0,009) y 0,019 (95% IC: 0,016-0,022) respectivamente; la constante fue 1,0735 (95% IC: 0,939-1,2079). El riesgo de desarrollar hipofosfatemia disminuyó de 0,65 (95% IC: 0,33-1,26) a 0,16 (95% IC: 0,078-0.35) cuando el fosfato administrado variaba deL rango 7,5-17,5 mmol a valores superiores a 27,5 mmol. Conclusiones: es necesario suplementar rutinariamente las nutriciones con fosfato debido a que su contenido en las emulsiones lipídicas comercializadas no es suficiente para evitar la hipofosfatemia en la mayoría de pacientes con nutrición parenteral. El aporte de fosfato debe ser suficiente para restaurar el déficit de fosfato intracelular y compensar la caída de fosfato plasmático, con especial cuidado para los pacientes desnutridos, hiperglucémicos o con insuficiencia renal. Aportes de fosfato entre 27-37 mmol, disminuyen drásticamente la incidencia de hipofosfatemia en los pacientes estudiados, no registrándose ningún caso de hipofosfatemia severa.Aim: To determine the incidence of hypophosphatemia in parenterally fed patients, the phosphate amount necessary to prevent this complication and associated risks factors. Setting: Observational study, not controlled, in a third level hospital. Patients: In-patients with parenteral nutrition with at least a complete laboratory work-up. Intervention: For a complete year, days on parenteral nutrition, administered phosphate and plasmatic ionised calcium levels, γ-glutamiltranspeptidase, glucose, phosphate, pre-albumin, urea, and leukocytes were recorded. A multiple stepwise regression analysis and logistic regression are used for data analysis. Results: Eight hundred and twenty seven determinations, corresponding to 401 patients, were included. Significant variables (p < 0.05) were: administered phosphate and ionised calcium serum levels, glucose, pre-albumin, and urea; regression coefficients were 0.004 (95%CI: 0.002 to 0.006), -0.156 (95%CI: -0.270 to 0.037), -0.014 (95%IC: -0.022 to 0.009), 0.005 (95%CI: 0.002 to 0.009) and 0.019 (95%CI: 0.016 to 0.022), respectively; the constant was 1.0735 (95%CI: 0.939 to 1.2079). The risk for developing hypophosphatemia decreased from 0.65 (95%CI: 0.33 to 1.26) to 0.16 (95%CI: 0.078 to 0.35) when administered phosphate varied from the span 7.5-17.5 mmol to values higher than 27.5 mmol. Conclusions: It is necessary to routinely supplement nutrition with phosphate since its content in commercially available lipidic emulsions is not sufficient to prevent hypophosphatemia in the majority of patients with parenteral nutrition. Phosphate intake must be sufficient to restore the intracellular phosphate deficit and to compensate for the plasmatic phosphate fall, with special attention to poorly nourished, hyperglycaemic or with renal failure patients. Phosphate intakes around 27-37 mmol dramatically decrease the incidence of hypophosphatemia in studied patients, with no recorded cases of severe hypophosphatemia.

Background: Secondary hyperparathyroidism (SHPT) is a common complication of chronic kidney disease (CKD). Cinacalcet use is controversial in non-dialysis patients., Methods: This retrospective observational study recruited patients receiving cinacalcet (off-label use) in 2010 and 2011. Patients were followed for three years from the beginning of treatment using an intention-to-treat approach., Results: Forty-one patients were studied: 14 CKD stage 3 (34.1%), 21 CKD stage 4 (51.2%), and 6 CKD stage 5 (14.6%). Median baseline parathyroid hormone (PTH) was 396 (101-1,300) pg/mL. Upon cinacalcet treatment (22 ± 12 months), PTH levels decreased by ≥ 30% in 73.2% of patients ( P < 0.001; 95% confidence interval [CI], 59-87%), with a mean time for response of 18.7 months (95% CI, 15.4-22.1). Sixteen patients were followed for 36 months and treated for 32 ± 9 months. Mean reduction in their PTH levels was 50.1% ( P < 0.001; 95% CI, 33.8-66.4%) at 36 months, with 62.5% of patients ( P < 0.001; 95% CI, 35.9-89.1%) presenting reductions of ≥ 30%. Serum calcium levels decreased from 9.95 ± 0.62 mg/dL to 9.21 ± 0.83 and 9.12 ± 0.78 mg/dL at 12 and 36 months, respectively ( P < 0.001). Serum phosphorus levels increased from 3.59 ± 0.43 to 3.82 ± 0.84 at 12 months ( P = 0.180), remaining so at 36 months ( P = 0.324). At 12 and 36 months, 2 (12.5%) patients experienced hypocalcemia. Meanwhile, 1 (6.3%) and 4 (25.0%) patients reported hyperphosphatemia at 12 and 36 months, respectively., Conclusion: Cinacalcet remained effective for at least 36 months in non-dialysis patients with SHPT. Electrolytic disturbances were managed with concurrent use of vitamin D and its analogs or phosphate binders.

Objective: Dual PEGylated interferon-α (PEG-IFN) and ribavirin therapy has been the main hepatitis C virus (HCV) treatment of the last decade. Current direct-acting antiviral agents have improved the outcome of therapy but also have increased the cost and management complexity of treatment. The current study analyzes host genetics, viral and clinical predictors of sustained viral response (SVR) to dual PEG-IFN and ribavirin therapy in a representative Spanish population., Methods: Observational prospective multicentre pharmacogenetic cohort study conducted in 12 different hospitals of 12 different Spanish regions. A total of 98 patients with SVR and 106 with non-SVR in response to PEG-IFN and ribavirin therapy were included. 33 single nucleotide polymorphisms located in 24 different genes related with inflammatory, immune and virus response were selected. Clinical and viral data were also analyzed as candidate of SVR predictors., Results: IL-28B (rs12979860, rs7248668, rs8105790, rs8099917) and TNFRSF1B (rs1061622) genotypes, as well as TNFRSF1B/IL-10/TNFα (-308) non-TTG and TNFRSF1B/IL- 10/IL-4 non-TTC haplotypes together with lower age, lower basal HCV RNA load, higher basal serum LDL cholesterol values, VHC genotypes 2 and 3 and basal low grade fibrosis 0-2 were associated with a SVR in the univariate analysis. Independent predictors of SVR in the multivariate analysis were IL-28B rs12979860 CC, TNFRSF1B/IL-10/IL-4 non-TTC along with low baseline HCV RNA load and HCV genotypes 2 and 3., Conclusions: IL-28B rs12979860 CC, TNFRSF1B/ IL-10/ IL-4 non-TTC haplotype, low baseline HCV RNA load and HCV genotypes 2 and 3 may help to predict successful outcome to PEG-IFN/ribavirin therapy in Spanish population., (Copyright AULA MEDICA EDICIONES 2014. Published by AULA MEDICA. All rights reserved.)

Objective: To assess the efficacy and safety profile of omalizumab treatment. The conditions under which omalizumab was prescribed agreed with those in Xolair® drug information: age > 12 years old, severe uncontrolled asthma, FEV1 < 80%, IgE 30-700 UI/ml and positive test results for perennial allergens., Methods: Asthmatic patients treated with omalizumab between January 2010 and July 2011 were evaluated retrospectively. Age, sex, weight, IgE level, concomitant asthma medications, change in FEV1, emergency department visits, hospitalizations, asthma exacerbations and corticosteroids bursts were recorded before and after omalizumab initiation. A 1.5- year period was chosen., Results: A total of 22 patients were included. The mean weight of subjects was 73 Kg (range, 51-102). Mean IgE was 203 UI/ml (range, 30-992) and mean FEV1 60% (range, 30-93%) at baseline. Adverse events were observed in 4 patients. There were no significant changes in FEV1 values after omalizumab treatment but omalizumab was associated with a reduction in concomitant asthma medications use in 14 patients and improvements in global asthma control in 12., Conclusion: In these patients add-on therapy with omalizumab reduced asthma exacerbations and emergency visits or hospitalizations. Only 55% of patients significantly improved global asthma control and no significant changes in FEV1 were observed., (Copyright © 2013 SEFH. Published by AULA MEDICA. All rights reserved.)

Aim: To determine the incidence of hypophosphatemia in parenterally fed patients, the phosphate amount necessary to prevent this complication and associated risks factors., Setting: Observational study, not controlled, in a third level hospital., Patients: In-patients with parenteral nutrition with at least a complete laboratory work-up., Intervention: For a complete year, days on parenteral nutrition, administered phosphate and plasmatic ionised calcium levels, y-glutamiltranspeptidase, glucose, phosphate, pre-albumin, urea, and leukocytes were recorded. A multiple stepwise regression analysis and logistic regression are used for data analysis., Results: Eight hundred and twenty seven determinations, corresponding to 401 patients, were included. Significant variables (p < 0.05) were: administered phosphate and ionised calcium serum levels, glucose, pre-albumin, and urea; regression coefficients were 0.004 (95%CI: 0.002 to 0.006), -0.156 (95%CI: -0.270 to 0.037), -0.014 (95%IC: -0.022 to 0.009), 0.005 (95%CI: 0.002 to 0.009) and 0.019 (95%CI: 0.016 to 0.022), respectively; the constant was 1.0735 (95%CI: 0.939 to 1.2079). The risk for developing hypophosphatemia decreased from 0.65 (95%CI: 0.33 to 1.26) to 0.16 (95%CI: 0.078 to 0.35) when administered phosphate varied from the span 7.5-17.5 mmol to values higher than 27.5 mmol., Conclusions: It is necessary to routinely supplement nutrition with phosphate since its content in commercially available lipidic emulsions is not sufficient to prevent hypophosphatemia in the majority of patients with parenteral nutrition. Phosphate intake must be sufficient to restore the intracellular phosphate deficit and to compensate for the plasmatic phosphate fall, with special attention to poorly nourished, hyperglycaemic or with renal failure patients. Phosphate intakes around 27-37 mmol dramatically decrease the incidence of hypophosphatemia in studied patients, with no recorded cases of severe hypophosphatemia.