Complejo Hospitalario Universitario Insular Materno Infantil

Las Palmas de Gran Canaria, Spain

Complejo Hospitalario Universitario Insular Materno Infantil

Las Palmas de Gran Canaria, Spain

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Fornell Perez R.,Complejo Hospitalario Universitario Insular Materno Infantil
Radiologia | Year: 2017

This critically appraised topic (CAT) study aims to evaluate the quality and extent of the scientific evidence that supports the use of focused assessment with sonography for trauma (FAST) versus multidetector computed tomography (MDCT) in hemodynamically stable trauma patients in the emergency room. An efficient search of the literature yielded several recent articles with a high level of evidence. The CAT study concludes that FAST is an acceptable initial imaging test in hemodynamically stable patients, although its performance is limited in certain circumstances. The decision whether to use MDCT should be determined by evaluating the patient's degree of instability and the distance to the MDCT scanner. Nevertheless, few articles address the question of the distance to MDCT scanners in emergency departments. © 2017 SERAM.


Isasi A.G.,Hospital Universitario Insular | Echeburua E.,University of the Basque Country | Liminana J.M.,Complejo Hospitalario Universitario Insular Materno Infantil | Gonzalez-Pinto A.,Hospital Santiago Apostol
Journal of Affective Disorders | Year: 2010

Background: The aim of this research was to evaluate the short-term and long-term efficacy of a combined treatment (pharmacological + psychoeducational and cognitive-behavioral therapy) as compared with a standard pharmacological treatment in patients with refractory bipolar disorder. Method: 40 patients were randomly assigned to one of the following: Experimental group under combined treatment, and Control group under pharmacological treatment. We used an analysis of variance (ANOVA), including one or two factors, with repeated measures at different evaluation times: baseline, post-treatment, 6-month follow-up and 12-month follow-up. Results: We found significant between-group differences at all evaluation times after the treatment. The experimental group showed less hospitalizations than the control group in the 12-month evaluation (p = 0.007) as well as lower rates of depression and anxiety in the 6-month valuation (p = 0.015; p = 0.027) and the 12-month evaluation (p = 0.001; p < 0.001). Significant differences in relation to mania and inadaptation emerged in the post-treatment evaluation (p = 0.004; p < 0.001) and were sustained throughout the study (p = 0.002, p < 0.001; p < 0.001, p < 0.001). Analysis of within-group differences in the Experimental group showed reduction of mania (p < 0.001), depression (p = 0.001), anxiety (p = 0.003) and inadaptation (p < 0.001) throughout the study; while in the Control group, it showed increased numbers of hospitalizations (p = 0.016), as well as higher rates of mania (p = 0.030), anxiety (p < 0.001) and inadaptation (p = 0.003). Conclusions: Our results suggest that a combined treatment is effective in patients with refractory bipolar disorder. Suggestions for future research are commented on. © 2009 Elsevier B.V. All rights reserved.


Gonzalez Isasi A.,Hospital Universitario Insular | Echeburua E.,University of the Basque Country | Liminana J.M.,Complejo Hospitalario Universitario Insular Materno Infantil | Gonzalez-Pinto A.,Santiago Apostol Hospital
European Psychiatry | Year: 2014

Objective: The aim of this research, which represents an additional and longer follow-up to a previous trial, was to evaluate a 5-year follow-up study of a combined treatment (pharmacological. +. psychoeducational and cognitive-behavioral therapy) as compared with a standard pharmacological treatment in patients with refractory bipolar disorder. Method: Forty patients were randomly assigned to either an Experimental group-under combined treatment-or a Control group-under pharmacological treatment. Data were analyzed by analysis of variance (ANOVA), with repeated measures at different evaluation time points. Results: Between-group differences were significant at all evaluation time points after treatment. Experimental group had less hospitalization events than Control group in the 12-month evaluation (P= 0.015). The Experimental group showed lower depression and anxiety in the 6-month (P= 0.006; P= 0.019), 12-month (P = 0.001; P < 0.001) and 5-year (P < 0.001, P < 0.001) evaluation time points. Significant differences emerged in mania and misadjustment already in the post-treatment evaluation (P = 0.009; P < 0.001) and were sustained throughout the study (6-month: P= 0.006, P < 0.001; 12-month: P < 0.001, P < 0.001; 5-year: P= 0.004, P < 0.001). After 5-year follow-up, 88.9% of patients in the Control group and 20% of patients in the Experimental group showed persistent affective symptoms and/or difficulties in social-occupational functioning. Conclusions: A combined therapy is long-term effective for patients with refractory bipolar disorder. Suggestions for future research are commented. © 2012.


Martinez-Quintana E.,Complejo Hospitalario Universitario Insular Materno Infantil | Rodriguez-Gonzalez F.,Complejo Hospitalario Universitario Insular Materno Infantil
Molecular Syndromology | Year: 2013

Mucopolysaccharidosis type II (MPS II), also known as Hunter syndrome, is a rare, X-linked disease caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase, which catalyses a step in the catabolism of glycosaminoglycans resulting in accumulation of heparan and dermatan sulfate in many organs and tissues. This accumulation favors the appearance of neurologic involvement, severe airway obstruction, skeletal deformities, and cardiomyopathy, especially mitral and aortic valve regurgitation. In severe cases, obstructive airway disease and cardiac failure due to valvular dysfunction are the most common causes of death within the second decade of life. However, in mild cases, intelligence remains normal, stature is almost normal and death usually occurs due to cardiac failure in the fourth decade of life. We report the presentation, diagnosis, management, and outcome of 2 siblings with MPS II and the G374sp mutation at the nucleotide c.1246 of the gene encoding for the iduronate-2-sulfatase. Copyright © 2013 S. Karger AG, Basel.


Martnez-Quintana E.,Complejo Hospitalario Universitario Insular Materno Infantil | Rodrguez-Gonzlez F.,Hospital Universitario Of Gran Canaria Dr Negrn
Molecular Syndromology | Year: 2012

The RAS/MAPK pathway proteins with germline mutations in their respective genes are associated with some disorders such as Noonan, LEOPARD (LS), neurofibromatosis type 1, Costello and cardio-facio-cutaneous syndromes. LEOPARD is an acronym, mnemonic for the major manifestations of this disorder, characterized by multiple lentigines, electrocardiographic abnormalities, ocular hypertelorism, pulmonic stenosis, abnormal genitalia, retardation of growth, and sensorineural deafness. Though it is not included in the acronym, hypertrophic cardiomyopathy is the most frequent cardiac anomaly observed, representing a potentially life-threatening problem in these patients. PTPN11, RAF1 and BRAF are the genes known to be associated with LS, identifying molecular genetic testing of the 3 gene mutations in about 95% of affected individuals. PTPN11 mutations are the most frequently found. Eleven different missense PTPN11 mutations (Tyr279Cys/Ser, Ala461Thr, Gly464Ala, Thr468Met/Pro, Arg498Trp/Leu, Gln506Pro, and Gln510Glu/Pro) have been reported so far in LS, 2 of which (Tyr279Cys and Thr468Met) occur in about 65% of the cases. Here, we provide an overview of clinical aspects of this disorder, the molecular mechanisms underlying pathogenesis and major genotype-phenotype correlations. © 2012 S. Karger AG, Basel.


Martinez-Quintana E.,Complejo Hospitalario Universitario Insular Materno Infantil | Miranda-Calderin G.,Complejo Hospitalario Universitario Insular Materno Infantil | Ugarte-Lopetegui A.,Complejo Hospitalario Universitario Insular Materno Infantil | Rodriguez-Gonzalez F.,Complejo Hospitalario Universitario Insular Materno Infantil
Congenital Heart Disease | Year: 2010

Introduction.: It is commonly believed that physical activity may have a negative impact on pulmonary hypertension patients. The object of this study is to determine the tolerability of a directed exercise program in congenital heart disease patients with pulmonary hypertension. Methods.: Eight congenital heart disease patients with pulmonary hypertension were studied and followed up during a 1-year period. Four of them were enrolled in a 3-month rehabilitation program. Results.: No significant changes in analytical data, hand and leg strength, or quality of life were seen at the end of the training program in rehabilitation and nonrehabilitation patients. However, patients in the rehabilitation group improved 6 minutes' walk test minimum hemoglobin oxygen saturation and functional class after ending the training program without having adverse events such as progression of symptoms or heart failure. Conclusions.: Cardiopulmonary rehabilitation appears to be a safe intervention in patients with congenital heart disease and pulmonary hypertension. © 2010 Copyright the Authors. Journal Compilation © 2010 Wiley Periodicals, Inc.


Martinez-Quintana E.,Complejo Hospitalario Universitario Insular Materno Infantil | Rodrguez-Gonzalez F.,Hospital Universitario Of Gran Canaria Dr Negrin
Molecular Syndromology | Year: 2011

LEOPARD syndrome (LS) is an acronym consisting of lentigines, electrocardiographic abnormalities, ocular hypertelorism, pulmonary valve stenosis, abnormal genitalia, retardation of growth and deafness. However, hypertrophic cardiomyopathy, the most frequent cause of sudden cardiac death in young people, is the most common cardiovascular manifestation in LS patients and the major determinant of mortality and morbidity. In approximately 85% of the patients with a definite diagnosis of LS, a missense mutation is found in the protein-tyrosine phosphatase non-receptor type 11 (PTPN11) gene located on chromosome 12q24.1. We report the case of an asymptomatic 17-year-old male with a missense mutation (c.836A>G) in exon 7 (Tyr279Cys) of the PTPN11 gene and a non-obstructive asymmetric anteroseptal hypertrophic cardiomyopathy. © 2012 S. Karger AG, Basel.


Sandoval-Usme M.C.,National University of Colombia | Umana-Perez A.,National University of Colombia | Guerra B.,University of Las Palmas de Gran Canaria | Hernandez-Perera O.,Complejo Hospitalario Universitario Insular Materno Infantil | And 3 more authors.
PLoS ONE | Year: 2014

Recent studies have demonstrated that statins reduce cell viability and induce apoptosis in various types of cancer cells. The molecular mechanisms underlying these effects are poorly understood. The JAK/STAT pathway plays an important role in the regulation of proliferation and apoptosis in many tissues, and its deregulation is believed to be involved in tumorigenesis and cancer. The physiological activation of STAT proteins by GH is rapid but transient in nature and its inactivation is regulated mainly by the expression of SOCS proteins. UMR-106 osteosarcoma cells express a GH-responsive JAK2/STAT5 signaling pathway, providing an experimental model to study the influence of statins on this system. In this study we investigated the actions of simvastatin on cell proliferation, migration, and invasion on UMR-106 cells and examined whether alterations in GH-stimulated JAK/STAT/SOCS signaling may be observed. Results showed that treatment of osteosarcoma cells with simvastatin at 3 to 10 μM doses decreases cell proliferation, migration, and invasion in a time-and dose-dependent manner. At the molecular level, although the mechanisms used by simvastatin are not entirely clear, the effect of the statin on the reduction of JAK2 and STAT5 phosphorylation levels may partially explain the decrease in the GH-stimulated STAT5 transcriptional activity. This effect correlated with a time- and dose-dependent increase of SOCS-3 expression levels in cells treated with simvastatin, a regulatory role that has not been previously described. Furthermore, the finding that simvastatin is capable of inducing SOCS-3 and CIS genes expression shows the potential of the JAK/STAT pathway as a therapeutic target, reinforcing the efficacy of simvastatin as chemotherapeutic drug for the treatment of osteosarcoma. © 2014 Sandoval-Usme et al.


Martinez-Quintana E.,Complejo Hospitalario Universitario Insular Materno Infantil | Tugores A.,Complejo Hospitalario Universitario Insular Materno Infantil
Journal of Clinical Pharmacology | Year: 2015

Clopidogrel has been the therapy of choice, combined with aspirin, against platelet aggregation in patients at risk of suffering a vascular thrombotic event. Not all patients respond equally to clopidogrel, an observation that has led to searching for a test that, in the clinical setting, could predict patients' "resistance" to therapy. The evidence reveals a complex pharmacokinetic profile for clopidogrel, with multiple players involved, including cytochromes, characteristics of the target tissue, and accompanying clinical conditions. Despite FDA black box warnings recommending CYP2C19 genotyping before clopidogrel use, no robust evidence indicates that CYP2C19 function determines clinical response to the drug, either based on the presence of loss of function alleles or drug interactions with CYP2C19 inhibitors, like omeprazole. A tailored anti-aggregation treatment based on ex vivo platelet reactivity also seems unlikely due to the lack of robustness of most assays. The identification of clinical conditions that are at higher risk of new cardiovascular events, such as diabetes, obesity, coronary artery disease, or specific stenting procedures, seems to be a prudent approach to tailor anti-platelet therapy with more powerful drugs, accompanied by careful counseling to promote patient compliance. © 2014, The American College of Clinical Pharmacology.


Martinez-Quintana E.,Complejo Hospitalario Universitario Insular Materno Infantil | Rodriguez-Gonzalez F.,University of Las Palmas de Gran Canaria | Garay-Sanchez P.,University of Las Palmas de Gran Canaria | Tugores A.,University of Las Palmas de Gran Canaria
Molecular Syndromology | Year: 2014

CHARGE syndrome is a rare congenital condition characterized by 6 cardinal features: coloboma, heart defect, atresia choanae, retarded growth and development, genital anomalies, and ear anomalies/deafness. Mutations of the chromodomain helicase DNA-binding protein gene CHD7 are reported to be a major cause of CHARGE syndrome. Herein, we report the case of a 27-year-old patient presenting with typical symptoms who bears a novel heterozygous insertion in exon 2 of the CHD7 gene (c.327dupC) resulting in an amino acid substitution and a frameshift (p.Val110Argfs*22) that leads to a 131-amino-acid truncated polypeptide, likely representing a null allele. Parental genetic screening confirmed the sporadic origin of the mutation. © 2013 S. Karger AG, Basel.

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