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Los insulinomas son tumores neuroendocrinos que se manifiestan por episodios de hipoglucemia de ayuno. El diagnostico se basa en la sospecha clinica, que debe ir seguida de la demostracion de hiperinsulinismo y la localizacion tumoral. Sin embargo, la localizacion no siempre es posible con las tecnicas de imagen habituales, por lo que se debe recurrir a otras mas complejas. Presentamos 2 casos de insulinomas cuya localizacion tumoral no fue posible con tecnicas de imagen convencionales, pero si con ultrasonografia endoscopica.

Flavonoids are polyphenols that help the maintenance of health, aiding the prevention of diseases. In this work, CdTe QDs coated with 3-mercaptopropionic acid (3MPA), with an average size of 2.7nm, were used as photoluminescence probe for flavonoids in different conditions. The interaction between 14 flavonoids and QDs was evaluated in aqueous dispersions in the absence and in the presence of cetyltrimethylammonium bromide (CTAB). To establish a relationship between photoluminescence quenching and the concentration of flavonoids, the Stern-Volmer model was used. In the absence of CTAB, the linear ranges for quercetin, morin and rutin were from 5.0×10-6molL-1 to 6.0×10-5molL-1 and from 1.0×10-5molL-1 to 6.0×10-4molL-1 for kaempferol. The sensibility of the Stern-Volmer curves (Ks) indicated that quercetin interacts more strongly with the probe: Ks quercetin>Ks kaempferol>Ks rutin>Ks morin. The conjugation extension in the 3 rings, and the acidic hydroxyl groups (positions 3'and 4') in the B-ring enhanced the interaction with 3MPA-CdTe QDs. The other flavonoids do not interact with the probe at 10-5molL-1 level. In CTAB organized dispersions, Ks 3-hydroxyflavone>Ks 7-hydroxyflavone>Ks flavona>Ks rutin in the range from 1.0×10-6molL-1 to 1.2×10-5molL-1 for flavones and of 1.0×10-6molL-1 to 1.0×10-5molL-1 for rutin. Dynamic light scattering, conductometric measurements and microenvironment polarity studies were employed to elucidate the QDs-flavonoids interaction in systems containing CTAB. The quenching can be attributed to the preferential solubility of hydrophobic flavonoid in the palisade layer of the CTAB aggregates adsorbed on the surface of the 3MPA CdTe QDs.

Familial hypercholesterolemia (FH) is associated with higher levels of inflammatory mediators such as chemokines, which contribute to an increased risk of premature atherosclerosis in these patients. We studied the response of chemokines related to early atherosclerotic processes during an oral unsaturated fat load test (OFLT) in patients with heterozygous FH and compared this response to normolipidemic and normoglycemic subjects.Blood samples were taken from 12 FH patients and 20 healthy controls with a similar age, gender distribution, and body mass index. Plasma chemokine levels were determined in both groups in a fasting state and at 2, 4, 6, and 8 h after an OFLT using human cytokine multiplex kits (Linco) and a Luminex LABScan™100 system.In the fasting state MIP-1β, MIP-1α, IP-10, IFN-γ, MCP-1, and IL-8 were significantly increased in the FH group compared to the healthy controls (p0.05). In addition, a significant decrease in postprandial chemokine plasma values were found in the FH group compared to fasting values after the OFLT. In normolipidemic nondiabetic controls no significant changes were found in the postprandial state.There was a postprandial decrease in chemokines related to early atherosclerotic processes after an OFLT in FH patients. These results confirm the influence of dietary patterns in this group of patients.

Atherosclerosis is an inflammatory chronic disease influenced by multiple factors. Different prospective studies have shown that plasmatic levels of inflammatory markers were related to atherosclerosis and cardiovascular disease.To evaluate whether plasmatic levels of interleukin 18 (IL-18) are modulated by SNPs (single nucleotide polymorphisms) of the IL 18 gene and its possible association with insulin levels and other cardiovascular risk factors.746 individuals were studied for a period of two years by opportunistic selection in the metropolitan area of Valencia. Parameters of lipid and glucose metabolism were analyzed by standard methodology. IL-18 was measured by ELISA.Individuals with insulin resistance showed significant higher levels of IL-18. IL 18 was significantly correlated with insulin levels and other cardiovascular risk factors. The CC genotype of the rs1834481 SNP was significantly associated with lower levels of IL-18. However, the GG genotype of the rs7559479 was associated with significant higher levels of IL-18.IL-18 is associated with insulin resistance and other cardiovascular risk factors, being those levels genetically regulated.

Se estudia la relacion entre sindrome metabolico (SM) e infarto agudo de miocardio (IAM) en la hiperlipidemia familiar combinada (HFC). Se comparan 20 sujetos varones con HFC supervivientes a IAM con otras 2 series de sujetos emparejados por edad e indice de masa corporal (IMC): 20 individuos con HFC que no han presentado IAM y 20 controles sanos. Se determinaron los lipidos, la glucosa y la insulina en plasma y la presencia de SM definido por criterios de la Organizacion Mundial de la Salud (OMS) y National Cholesterol Education Program-Adults Treatment Panel (NCEP-ATP-III). El SM definido por criterios OMS se encontro en 19 sujetos con HFC e IAM, en 11 sujetos con HFC sin IAM y en 6 controles (p

Fundamento y objetivo Averiguar si el diagnostico de sindrome metabolico (SM) definido por los criterios de la International Diabetes Federation (IDF) en 2005 identifica a un mayor numero de sujetos con dislipemia aterogenica de elevado riesgo cardiovascular que los criterios del National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATP-III). Pacientes y metodo Estudiamos a una poblacion de 344 sujetos no diabeticos (158 varones y 186 mujeres), de edades comprendidas entre 20 y 70 anos, seleccionados por un metodo de muestreo simple aleatorio entre los que consultaron durante un ano en un centro de salud en el area metropolitana de Valencia (metodo de busqueda oportunista). Se estudiaron parametros antropometricos, cifras de presion arterial, de lipidos plasmaticos –entre ellos, colesterol no unido a lipoproteinas de alta densidad (c-no-HDL), indice colesterol total:colesterol unido a lipoproteinas de alta densidad (CT:cHDL)–, de glucosa e insulina plasmatica y el valor del indice HOMA (Homeostasis Model Assessment). Resultados Al separar a los sujetos basandonos en la definicion del SM segun criterios IDF o ATP-III, identificamos a un grupo con importantes alteraciones lipidicas de riesgo cardiovascular: aumento del c-no-HDL, del CT:cHDL y de la apolipoproteina B. El indice CT:cHDL fue mayor o igual a 6 en el 28,6% de los sujetos con SM-IDF y solo en el 9,4% de los sujetos sin SM-IDF (p Conclusiones La definicion del SM segun los criterios IDF o ATP-III identifica por igual a los sujetos con dislipemia aterogenica, con aumento del c-no-HDL, del indice CT:cHDL y de la apolipoproteina B, y que por ello presentan un elevado riesgo cardiovascular.

Introduccion Un nuevo metodo basado en la autodeterminacion de trigliceridos (TG) capilares permite un mejor conocimiento de la lipemia posprandial (LP). Los objetivos de nuestro estudio son analizar el efecto del genero y la obesidad sobre la LP valorada por medicion capilar de TG diurnos mediante Accutrend GCT® en sujetos sanos y sujetos con hiperlipemia familiar combinada (HFC). Material y metodos Hemos estudiado a 23 sujetos con HFC no relacionados entre si (10 hombres) y a 45 sujetos (29 hombres) normolipidemicos no diabeticos. Todos ellos realizaron tres perfiles diarios de TG capilares durante una semana. Resultados En los sujetos sanos normolipidemicos no diabeticos encontramos valores significativamente elevados en el perfil de TG capilares y area bajo la curva de TG capilares (ABCTGc) (25,25±9,09 frente a 19,71±6,16 mmolh/l) en el grupo de hombres frente al de las mujeres. En sujetos con HFC no se hallaron estas diferencias y el ABCTGc se correlaciono con el indice de masa corporal (IMC) (r=0,510; p Discusion Las mujeres sanas normolipidemicas no diabeticas presentaron una menor lipemia posprandial que los hombres, probablemente por el efecto de los estrogenos sobre el metabolismo lipidico. La obesidad ejercia un efecto negativo sobre la lipemia posprandial, tanto en sujetos sanos como en sujetos con HFC.

Our aim was to investigate the relationship between metabolic syndrome and cardiovascular disease (i.e., survivors of myocardial infarction) in patients with familial combined hyperlipidemia (FCH). We compared a group of 20 male patients with FCH who had survived a myocardial infarction with two other groups matched for age and body mass index, comprising 20 individuals with FCH who had not had a myocardial infraction and 20 control subjects. Plasma lipid, glucose, and insulin levels were determined. Metabolic syndrome was judged to present on the basis of World Health Organization (WHO) and National Cholesterol Education Program-Adult treatment panel (NCEP-ATPIII) criteria. Differences between the groups were evaluated using non-parametric tests and the association between ischemic coronary disease and other parameters was assessed by logistic regression analysis. According to WHO criteria, the metabolic syndrome was present in 19 FCH patients who had survived a myocardial infarction, in 11 individuals with FCH who had not had a myocardial infraction, and in six control subject (P

Methods presently employed for detection of large rearrangements have several drawbacks, such as the amount of sample and time required, technical difficulty, or the probability of false-negative carriers. Using the low-density-lipoprotein receptor (LDLR) gene, whose mutations are responsible for familial hypercholesterolemia (FH), we have developed a procedure to detect large rearrangements in this gene based on semiquantitative PCR, with important improvements as compared to previous methods. Our method covers the complete LDLR gene and introduces an internal control in the reaction. The procedure discriminates the four different large rearrangements (two deletions and two insertions) that we have used as positive mutation controls (Valencia-1 to -5). All altered exons from each rearrangement are identified. Furthermore, when families from probands carrying these large rearrangements (34 members) were analyzed, our results agreed with those obtained previously with Southern blot. We have also analyzed a sample of 110 unrelated FH probands and the method has correctly identified the two different large rearrangements present and insertions or deletions as small as 1 bp. In conclusion, the method we present allows the identification of large rearrangements affecting exons of the gene, including small insertions or deletions or complete gene deletion. In addition, it constitutes a first characterization step of rearrangements, and is easy to carry out fast, and can be applied to the analysis of any gene.

Fundamento y objetivo: Conocer los determinantes clinicos y biologicos de la lipemia posprandial, medida con la autodeterminacion diurna de trigliceridos en sangre capilar (TGc), en personas sin dislipemia ni diabetes. Pacientes y metodo: Hemos estudiado a 76 personas sanas (45 mujeres premenopausicas) con normolipemia y sin diabetes. La determinacion de los TGc se realizo mediante Accutrend® durante 3 dias en 6 puntos establecidos: ayunas, inmediatamente antes y 3 h despues de comer y de cenar, y antes de acostarse. Se midio el area bajo la curva de TGc (ABC-TGc) como expresion de la lipemia posprandial diurna. Resultados: El ABC-TGc fue significativamente mayor en los varones (26,20 [11,00]) que en las mujeres (19,12 [6,57]) (p < 0,001). Los obesos presentaron valores mayores de ABC-TGc (27,87 [12,47] frente a 20,05 [7,04]; p < 0,01). El ABC-TGc se correlaciono con la edad (r = 0,242; p < 0,05), el indice de masa corporal (r = 0,312; p < 0,01), el perimetro de la cintura (r = 0,394; p < 0,01), los trigliceridos plasmaticos en ayunas (r = 0,634; p < 0,001), la insulinemia en ayunas (r = 0,485; p < 0,001) y el indice HOMA en ayunas (r = 0,484; p < 0,001). El analisis del estudio multivariante mostro que el indice HOMA (coeficiente de regresion de 0,352; p = 0,02) y el perimetro de la cintura (coeficiente de regresion de 0,4; p = 0,05) predicen de forma independiente el ABC-TGc. Conclusiones: Los determinantes independientes de la lipemia posprandial en nuestra poblacion son el perimetro de la cintura y el HOMA.

Presentamos el caso de una mujer con sindrome de McCune-Albright como paradigma de afeccion tumoral en multiples glandulas endocrinas. El diagnostico de la enfermedad se baso en la presencia de la triada clasica (lesiones hiperpigmentadas cutaneas de color cafe con leche, pubertad precoz y displasia fibrosa). Durante su seguimiento presento hipertiroidismo secundario a bocio multinodular toxico, hiperparatiroidismo, probablemente secundario a hiperplasia paratiroidea, y acromegalia secundaria a adenoma hipofisario productor de hormona de crecimiento. Se comenta la base molecular de la enfermedad y su amplia expresion fenotipica.

Objetivos Comparar la lipidemia posprandial valorada por medicion de los trigliceridos capilares (TGc) diurnos mediante Accutrend GCT® entre sujetos sanos y sujetos con hiperlipidemia familiar combinada (HFC), y relacionarla con parametros antropometricos en una poblacion del sur de Europa. Sujetos y metodo Se ha analizado a 23 sujetos diagnosticados de HFC no relacionados entre si (13 mujeres) y 45 sujetos sanos (26 mujeres) normolipemicos no diabeticos. En todos ellos se midieron de forma estandarizada parametros antropometricos, perfil lipidico, insulinemia y HOMA (homeostasis model assessment) en ayunas. Ademas, se determinaron mediante Accutrend GCT® durante 3 dias los TGc en 6 momentos: en ayunas, al acostarse y antes y 3 h despues de la comida y cena. Resultados Los sujetos con HFC presentaron significativamente mayores concentraciones de insulinemia, HOMA, TGc diurnos y area bajo la curva de TGc que los controles. Tanto en sujetos sanos como en sujetos con HFC el area bajo la curva de TGc, como expresion de la lipidemia posprandial, se correlaciono de forma positiva con el tipo y grado de obesidad. Conclusiones La HFC es un modelo genetico de hiperlipidemia posprandial. La obesidad y el deposito de grasa abdominal se relacionan con la lipidemia posprandial, probablemente por medio de la resistencia a la insulina.

Fundamento y objetivo Comparar las caracteristicas clinicobioquimicas del defecto familiar de union de la apolipoproteina B100 (DFB) con la hipercolesterolemia familiar (HF) heterocigota en una poblacion mediterranea del sur de Europa donde existen pocos datos al respecto, estudiar la prevalencia y el posible efecto fundador del DFB en una zona de la Comunidad Valenciana y conocer las caracteristicas clinicobioquimicas del DFB. Sujetos y metodo Hemos estudiado a 19 heterocigotos con DFB (8 varones) pertenecientes a 12 familias, portadores de la mutacion R3500Q del gen de la apolipoproteina B, y a 57 heterocigotos con HF (24 varones) geneticamente caracterizados, seleccionados de forma aleatoria entre 213 y apareados con los sujetos con DFB por edad y sexo. En todos los sujetos se determinaron de forma estandarizada las concentraciones de lipidos y apolipoproteinas B y A-I. Resultados Encontramos un efecto fundador en un area rural aislada de la Comunidad Valenciana para la mutacion R3500Q del gen de la apolipoproteina B, causante del DFB. La prevalencia del DFB en esta zona es de 4/350. Comparados con los casos de HF, los heterocigotos con DFB presentan menor prevalencia de xantomas tendinosos y de cardiopatia isquemica y concentraciones significativamente menores de colesterol total y unido a lipoproteinas de baja densidad y de alta densidad, asi como de apolipoproteinas B y A-I. Conclusiones Existe una zona geografica en la Comunidad Valenciana con una alta prevalencia del DFB por un efecto fundador. Ademas, en nuestra poblacion, el fenotipo lipoproteinico y la expresion clinica de la hipercolesterolemia en sujetos con DFB son menos graves que los de los sujetos con HF.

La neoplasia endocrina multiple tipo 1 (NEM 1) es una enfermedad rara, autosomica dominante, debida a mutaciones localizadas en el gen menin, que asocia hiperparatiroidismo primario, tumores gastroenteropancreaticos y adenomas hipofisarios. La mayoria de los tumores de los islotes pancreaticos se asocian a niveles plasmaticos elevados de polipeptido pancreatico (PP), siendo excepcional que unicamente produzcan este peptido. La paciente que presentamos tenia antecedentes de un macroprolactinoma intervenido y una hiperplasia adenomatosa de paratiroides con triple paratiroidectomia. De forma totalmente casual se descubrio en la paciente una tumoracion pancreatica que resulto ser un PPoma. Dado el curso silente inicial de estos tumores y su potencial malignidad, su diagnostico precoz es importante. La determinacion plasmatica de PP es de utilidad para el cribado de estos tumores en sujetos de riesgo, como son los familiares de primer grado en la NEM 1. Multiple endocrine neoplasia type-1 (MEN-1) is an infrequent autosomal dominant inherited disease, associated with primary hyperparathyroidism, and pancreatic and pituitary tumors, due to mutations in the menin-encoding gene. Most pancreatic islets tumors are associated with high plasma levels of pancreatic polypeptide (PP), although production of this hormone alone is uncommon. We present a 48-year-old woman with a history of surgically treated macroprolactinoma and adenomatous hyperplasia of the parathyroid gland with triple parathyroidectomy. A pancreatic tumor was incidentally detected and identified as a pancreatic polypeptide-producing tumor (ppoma). Early diagnosis of this silent tumor is important because of its malignant potential. PP measurement is a good biochemical marker for the screening of islet pancreatic tumors in high-risk individuals, such as first degree relatives of patients with MEN-1.

Few data are available on genotype-phenotype interactions among familial hypercholesterolemia (FH) patients in South European populations and there are no data about the influence of R3500Q mutation on lipoprotein phenotype compared to low-density lipoprotein receptor (LDLR) mutations. The objective of the study is to analyze the influence of mutations in the LDLR and apolipoprotein B (apoB) genes on lipoprotein phenotype among subjects clinically diagnosed of FH living in East Spain. In all, 113 FH index patients and 100 affected relatives were studied. Genetic diagnosis was carried out following a protocol based on Southern blot and PCR-SSCP analysis. A total of 118 FH subjects could be classified into three groups according to the type of LDLR mutations (null mutations, missense mutations affecting the ligand binding 3-5 repeat, and missense mutations outside this domain). In addition, the lipoprotein phenotype of these FH groups was compared with 19 heterozygous subjects with familial ligand-defective apoB (FDB), due to R3500Q mutation. FH patients carrying missense mutations affecting the ligand binding repeat 3-5 showed total and LDL cholesterol levels significantly higher than FH patients with missense mutations in other LDLR domains or FDB patients. FH subjects carrying null mutations showed lower high-density lipoprotein cholesterol plasma values compared to FH carrying missense mutations. FDB subjects showed the lowest total and LDL cholesterol plasma values. In conclusion, the type of LDLR gene mutation and R3500Q mutation influences the lipoprotein phenotype of FH population from East Spain.

Objetivo Analizar la influencia de parametros antropometricos (tipo y grado de obesidad) sobre el fenotipo lipoproteico y la respuesta terapeutica a atorvastatina en mujeres con Metodos Estudio de intervencion no controlado con 20 mg de atorvastatina al dia (dosis nocturna) en 34 mujeres con hipercolesterolemia familiar heterocigota seleccionadas de forma aleatoria. Resultados El deposito de grasa abdominal influye de forma estadisticamente significativa en los valores de presion arterial y concentraciones plasmaticas basales y postratamiento de los trigliceridos. Existe una interaccion negativa entre el deposito de grasa abdominal y la respuesta terapeutica de cLDL, siendo menores los descensos en mujeres con mayor deposito de grasa abdominal. El indice de masa corporal y la edad no influyen en los valores basales de lipidos y apo B ni en la respuesta terapeutica a atorvastatina. Conclusion El deposito de grasa abdominal en mujeres con hipercolesterolemia familiar y su correccion en los casos en que este aumentado debe realizarse para mejorar su perfil lipidico basal y evitar la interaccion negativa con atorvastatina.

Background/objectivesObesity has been linked to morbidity and mortality through increased risk for many chronic diseases. Endothelin (EDN) system has been related to endothelial function but it can be involved in lipid metabolism regulation: Receptor type A (EDNRA) activates lipolysis in adipocytes, the two endothelin receptors mediate arsenic-stimulated adipocyte dysfunction, and endothelin system can regulate adiposity by modulating adiponectin activity in different situations and, therefore, influence obesity development. The aim of the present study was to analyze if single nucleotide polymorphisms (SNPs) in the EDN system could be associated with human obesity.Subjects/methodsWe analyzed two samples of general-population-based studies from two different regions of Spain: the VALCAR Study, 468 subjects from the area of Valencia, and the Hortega Study, 1502 subjects from the area of Valladolid. Eighteen SNPs throughout five genes were analyzed using SNPlex.ResultsWe found associations for two polymorphisms of the EDNRB gene which codifies for EDN receptor type B. Genotypes AG and AA of the rs5351 were associated with a lower risk for obesity in the VALCAR sample (p=0.048, OR=0.63) and in the Hortega sample (p=0.001, OR=0.62). Moreover, in the rs3759475 polymorphism, genotypes CT and TT were also associated with lower risk for obesity in the Hortega sample (p=0.0037, OR=0.66) and in the VALCAR sample we found the same tendency (p=0.12, OR=0.70). Furthermore, upon studying the pooled population, we found a stronger association with obesity (p=0.0001, OR=0.61 and p=0.0008, OR=0.66 for rs5351 and rs3759475, respectively). Regarding plasma arsenic levels, we have found a positive association for the two SNPs studied with obesity risk in individuals with higher arsenic levels in plasma: rs5351 (p=0.0054, OR=0.51) and rs3759475 (p=0.009, OR=0.53).ConclusionsOur results support the hypothesis that polymorphisms of the EDNRB gene may influence the susceptibility to obesity and can interact with plasma arsenic levels.

ObjectivesTo investigate the association betweenIL18RAPand body mass index (BMI) and obesity and to verify the effect of a polymorphism in the microRNA136 (MIR136)IL18RAPbinding region.DesignWe analysed samples from two Spanish cross-sectional studies, VALCAR (Spanish Mediterranean coast) and Hortega (Spanish centre). These studies aimed at analysing cardiovascular risk and development of cardiovascular disease in the general population. Both populations correspond to regions with different characteristics.SettingFiveIL18RAPsingle nucleotide polymorphisms were selected using the SYSNPs web tool and analysed by oligonucleotide ligation assay (SNPlex). For the MIR136 functional study, cells were transfected with plasmids containing different rs7559479 polymorphism alleles and analysed by luciferase reporter assays.Participants1970 individuals (Caucasian, both genders): VALCAR (468) and Hortega (1502).Resultsrs2293225, rs2272127 and rs7559479 showed the following associations: rs7559479 G allele correlated with a higher obesity risk (P=0.01; OR=1.82; 95% CI 1.15 to 2.87 for the VALCAR group; P=0.033; OR=1.35; 95% CI 1.03 to 1.79 for the Hortega population) and higher body mass index (BMI) values (P=0.0045; P=0.1 for VALCAR and Hortega, respectively); a significant association with obesity (P=0.0024, OR=1.44, 95% CI 1.14 to 1.82) and increased BMI values (P=0.008) was found when considering both populations together. rs2293225 T allele was associated with lower obesity risk (P=0.036; OR=0.60; 95% CI 0.35 to 0.96) and lower BMI values (P=0.0038; OR=1.41) while the rs2272127 G allele was associated with lower obesity risk (P=0.028; OR=0.66; 95% CI 0.44 to 0.97) only in the VALCAR population. A reporter assay showed that the presence of the A allele in rs7559479 was associated with increased MIR136 binding toIL18RAP.ConclusionsOur results suggest that polymorphisms inIL18RAPinfluence susceptibility to obesity. We demonstrated that the A allele in rs7559479 increases MIR136 binding, which regulates IL-18 system activity.

Fundamento Evaluar la relacion de los lipidos, del genotipo de APOE y del tipo de mutacion delgen del receptor de LDL, clasificandolas en nulas y no nulas, sobre la prevalencia de infartoagudo de miocardio (IAM) en individuos heterocigotos con hipercolesterolemia familiar (HF) delsur de Europa, donde existen pocos datos al respecto. Pacientes y metodo Se trata de un estudio transversal que compara individuos con HF e IAM(n = 32) y a individuos con HF sin IAM (n = 76) mayores de 35 anos (41 varones y 67 mujeres).En 88 sujetos se establecio el diagnostico genetico, siendo divididos en portadores de mutacionesnulas o no nulas del gen del receptor de LDL. Se han comparado los factores clasicosde riesgo cardiovascular, concentraciones plasmaticas de lipidos y lipoproteinas, tipo de mutaciondel receptor de LDL y genotipo de APOE entre individuos con HF e IAM y sin IAM. Resultados Las variables relacionadas con el IAM fueron, en el analisis univariante, la edad, lapresencia de xantomas tendinosos o arco corneal, las concentraciones plasmaticas de colesteroltotal (CT) y colesterol unido a lipoproteinas de baja densidad (cLDL), el cociente CT/cHDL > de 5,3 y genotipo e4 de la APOE. Las odds ratio (OR) bipareadas para IAM fueron: la presenciade xantomas o arco corneal, 1,36 (intervalo de confianza [IC] del 95%, 1,08–1,71; p = 0,01);la edad > 54 anos (percentil 50 del total de individuos con HF) 1,56 (IC del 95%, 1,19–2,04;p = 0,001), y las concentraciones plasmaticas de CT > 332 mg/dl (percentil 50 del total de individuoscon HF), 1,34 (IC del 95%, 1,05–1,71; p = 0,019). En el analisis multivariante solola edad (p = 0,002) y el CT (p = 0,032) permanecieron en el modelo. Conclusiones El IAM en individuos con HF mayores de 35 anos de una poblacion del sur deEuropa se relaciona de forma univariante con la edad y las concentraciones plasmaticas de CTy cLDL, el cociente CT/cHDL y genotipo e4. El IAM se relaciona de forma independiente con laedad y las concentraciones plasmaticas de CT.

Ademas, existe cierta tendencia a infrautilizar los recursos terapeuticos y preventivos en los ancianos. Las enfermedades tiroideas son muy prevalentes en el anciano, pero su diagnostico y tratamiento difiere de los estandares establecidos en la poblacion de mediana edad 5 , debido a las modificaciones que se producen con el envejecimiento, que conducen a cambios morfologicos y funcionales del tiroides que dificultan la interpretacion de las pruebas diagnosticas. A estos cambios se unen las alteraciones que sobre la funcion tiroidea tienen otras enfermedades intercurrentes, no tiroideas, muy frecuentes entre los ancianos, y las interacciones farmacologicas. Ademas, en el anciano debemos tener en cuenta que las manifestaciones clinicas de la enfermedad tiroidea son diferentes, generalmente atipicas, lo que dificulta su diagnostico. Por otra parte, tanto el hipertiroidismo como el hipotiroidismo no tratados aumentan la morbilidad por el agravamiento de enfermedades cardiovasculares coexistentes, muy prevalentes en la poblacion anciana6. Finalmente, el tratamiento de la enfermedad tiroidea puede aumentar el riesgo de complicaciones en el anciano. Todo esto destaca el interes que las enfermedades tiroideas tienen en el anciano.

Presentamos un paciente diagnosticado de feocromocitoma maligno silente que en su evolucion presento metastasis en cuerpos vertebrales, huesos iliacos, ambos pulmones e higado. El paciente solo referia lumbalgia intermitente y las determinaciones urinarias de catecolaminas y sus metabolitos fueron normales. Se realizo inicialmente suprarrenalectomia derecha y se aplico telecobaltoterapia externa en la region L4-S2 (dosis total de 20 Gy), para control del dolor y por inicio de compresion radicular. Posteriormente, de forma paliativa se administro una dosis unica de 200 mCi de 131-I metaiodobencilguanidina (MIBG), desarrollando al mes una pancitopenia con neutropenia grave, que preciso antibioticoterapia de amplio espectro, transfusion de concentrados de hematies y tratamiento con factor de crecimiento granulocitario. Se comprobo la ausencia de infiltracion de la medula osea por el tumor. Al tratarse de un feocromocitoma no secretor no se acompano de manifestaciones clinicas que permitiesen su diagnostico precoz. El tratamiento paliativo con 131-I MIBG provoco una importante toxicidad sistemica relacionada con irradiacion de la medula osea por el elevado numero de metastasis vertebrales captadoras. Este caso pone en evidencia la dificultad para determinar la dosis optima de esta terapia y los posibles efectos toxicos de la misma.

Objectives Familial hypercholesterolemia (FH) is characterized by increased oxidative stress (OS) levels. In the postprandial state, lipids and lipoproteins modulate OS status through their impact on pro-oxidant and antioxidant mechanisms. The objective of this study was to evaluate in patients with FH the response to an unsaturated oral fat load test (OFLT) by analyzing the mRNA levels of genes involved in the glutathione and thioredoxin antioxidant systems. Design and Methods We analyzed 14 FH patients and 20 normolipidemic and normoglycemic controls. In both groups, mRNA values of antioxidant enzyme genes (glutathione and thioredoxin systems) were determined at baseline and at 2, 4, 6, and 8 h after OFLT by real time PCR. Results In the fasting state the mRNA levels of antioxidant enzymes GPX4 and the GSR, GSS, and GCLC enzymes (involved in glutathione regeneration and synthesis) and thioredoxin (TXN), were significantly increased in the FH group compared to the healthy controls. Some genes (GPX1 and GPX4) were increased at 4 h in both groups, but values for the rest of the antioxidant enzyme mRNAs were decreased in FH patients after 4 h from unsaturated OFLT and were increased in controls. Conclusions We concluded that an OFLT with predominantly unsaturated fat has a different effect on postprandial antioxidant enzyme mRNA levels in controls than in FH patients. Increased antioxidant enzyme mRNA is not the main way to reduce postprandial oxidative stress in FH. This difference could determine the influence of dietary patterns in these patients.

Aims Insulin resistance (IR) is a major risk factor for cardiovascular disease and atherosclerosis. Life-threatening acute events are mainly due to rupture of unstable plaques, and the role of vascular smooth muscle cells (VSMCs) in this process in IR, Type 2 diabetes mellitus, and metabolic syndrome (T2DM/MetS) has not been fully addressed. Therefore, the role of VSMC survival in the generation of unstable plaques in T2DM/MetS and the involvement of inflammatory mediators was investigated. Methods and results Defective insulin receptor substrate 2 (IRS2)-mediated signalling produced insulin-resistant VSMCs with reduced survival, migration, and higher apoptosis than control cells. Silencing of IRS2 or inhibition of the V-akt murine thymomaviral oncogene homologue kinase (AKT)–extracellular signal-regulated kinase (ERK)-dependent pathway in VSMCs augmented expression of the inflammatory chemokine fractalkine (CX3CL1) and its receptor CX3CR1, previously involved in atheroma plaque vulnerability. Interestingly, treatment of VSMCs with CX3CL1 promoted apoptosis in the presence of other stimuli or when the AKT pathway was blocked. Analysis of a mouse model of IR–MetS and accelerated atherosclerosis, apoE − / − Irs2+/ − mice, showed reduced VSMC survival, unstable plaques, and up-regulation of CX3CL1/CX3CR1 axis compared with apoE −/− mice. Human studies showed augmented soluble CX3CL1 plasma levels and CX3CR1 expression in monocytes from IR–MetS subjects compared with controls. A positive correlation between insulin levels, homeostatic model assessment (HOMA) index, carotid atherosclerosis, and CX3CR1 mRNA levels was also found in all patients. Conclusion IR increases plaque vulnerability by augmenting the CX3CL1/CX3CR1 axis, which is mechanistically linked to reduced VSMC survival. Thus, modulation of IRS2-dependent signalling emerges as a potential therapeutic strategy to promote VSMC survival and atheroma plaque stability and to reduce inflammatory mediators in IR–MetS.

Objective: To study the influence of apo E phenotype in plasma lipids, especially in triglycerides levels, in menopausal women receiving hormonal replacement therapy (HRT). Methods: One hundred and ten postmenopausal women were studied. Plasma total cholesterol (TC), HDL-C and triglycerides (TG) were measured before and after 3 months of HRT and the apo E phenotype was determined. According to the apo E phenotype the sample was divided into three groups: E2/E3 (n=28), E3/E3 (n=96) and E4/E3 (n=25). Results: In the pre-treatment state, higher plasma levels of TC and TC/HDL-C ratio were observed in women with phenotype E3/E4 (P

Cholesteryl ester transfer protein (CETP) facilitates the exchange of triglycerides (TG) and cholesteryl ester between lipoprotein particles. Subjects with familial hypercholesterolemia (FH) have been reported to have higher CETP activities, which could contribute to the lower high-density lipoprotein-cholesterol (HDL-C) levels and increased cardiovascular risk observed in some of these patients. Several polymorphisms have been reported in the CETP locus; the common TaqlB polymorphism is associated, in normolipidemic subjects, with decreased CETP activity and levels and with increased HDL-C levels. No data is available on the influence of this polymorphism in FH subjects. We have examined the TaqIB polymorphism in a group of 101 FH heterozygotes from Valencia, Spain. We have observed a frequency of 0.43 for the B2 allele, similar to those reported in the general population. Based on analysis of variance (ANOVA), we found significant associations between the presence of the B2 allele and increased plasma HDL-C (P [lt ] .04) and apolipoprotein A-I (apoA-I) levels (P [lt ] .01). An opposite association was observed for low-density lipoprotein-cholesterol (LDL-C) levels, with the B2/B2 subjects having lower levels than B1/B1 and B1/B2 subjects. The plasma apoB levels followed the same trend as those for LDL-C. In addition, the response to a National Cholesterol Education Program (NCEP)-I diet was studied in 77 of these subjects. The TaqlB polymorphism did not have a significant effect over the individual dietary response for any of the variables examined, as demonstrated by the lack of significant gene by diet interactions. In summary, the CETP TaqlB polymorphism is associated with a less atherogenic lipid profile, consisting of lower LDL-C, higher HDL-C levels, and a lower LDL-C/HDL-C ratio in heterozygous FH subjects. Moreover, the B2 allele was associated with a lower appearance of arcus cornealis, xanthomata, and clinical arteriosclerotic disease in these subjects.

Background Familial hypercholesterolemia (FH) is an autosomal dominant disease caused by mutations in the low-density lipoprotein receptor (LDLR) gene. To date, there has not been a systematic survey of the frequency of gross mutations in the LDLR gene in the Spanish population. The objective of our study was to investigate large rearrangements in the Spanish FH population and the relation between the kind of large rearrangement and the phenotype in carrier families. Material and methods The LDLR gene was screened to detect major rearrangements in a sample of 89 probands. Southern blot, long polymerase chain reaction (PCR), reverse transcription (RT) -PCR and DNA sequencing were used to detect and characterize the mutations. Results Five large rearrangements were found in six probands. Two mutations were due to duplications of internal regions of the gene, whereas the rest were caused by partial deletions, which eliminated the promoter region in two cases. The internal rearrangements, two duplications and one deletion, were apparently caused by recombination between ALU sequences and the study of their mRNA indicated that the reading frame was maintained. The analysis of the lipid profile between patients with similar characteristics (age, sex, body mass index, etc.) but carrying mutations that either eliminated the promoter region or produced internal rearrangements showed significant differences (total cholesterol: 366·6 ± 81·8 vs. 304·6 ± 25·1 P = 0·023, and LDL cholesterol: 317·7 ± 65·1 vs. 249·2 ± 27·4 P = 0·003). Conclusions The frequency of large mutations in a Spanish FH sample was close to 7% and at least four of the mutations found had not been described in other populations. Mutations that eliminate the promoter region originate more severe hypercholesterolemia than defective mutations, which suggests that the absence of the promoter region and transcription of the LDLR gene is worse compensated than the synthesis of a defective LDL receptor.

Aims To assess the relationship of the lipid profile to coronary heart disease in a group of heterozygous familial hypercholesterolaemic subjects with similar age, sex, body mass index, prevalence of angiotensin converting enzyme DD genotype and type of low density lipoprotein receptor mutation. Methods and Results A total of 66 molecularly defined heterozygous familial hypercholesterolaemic subjects, 33 of whom had coronary heart disease, were studied. Clinical features, cardiovascular risk factors and lipid parameters were compared in both groups. Familial hypercholesterolaemic patients with coronary heart disease showed significantly lower values of mean plasma HDL cholesterol and a higher total/HDL cholesterol ratio as compared with familial hypercholesterolaemic subjects free of coronary heart disease. Total and LDL cholesterol concentrations were higher in patients with coronary heart disease, without reaching statistical significance. No differences in plasma lipoprotein(a) levels on absolute and log-transformed values were observed between the two groups. In the whole familial hypercholesterolaemia group, plasma HDL cholesterol levels were related to plasma triglyceride values and to LDL receptor gene ‘null mutations’. Conclusions In familial hypercholesterolaemic subjects of similar age, gender, body mass index, systolic and diastolic blood pressure, and genetic factors that could influence coronary heart disease risk, plasma HDL cholesterol values and total/HDL cholesterol ratios are two important coronary risk factors. Hence, treatment of familial hypercholesterolaemia should focus not only on lowering total and LDL cholesterol levels, but also on increasing HDL cholesterol values for coronary heart disease prevention. More prospective and intervention trials should be conducted to establish the relationship of HDL cholesterol levels and coronary heart disease in familial hypercholesterolaemia.

Fundamento Analizar si el diagnostico molecular de la hipercolesterolemia familiar (HF) ayuda apredecir la respuesta terapeutica a simvastatina, en una poblacion mediterranea del sur de Europa. Sujetos y metodo Hemos estudiado la respuesta terapeutica en 27 sujetos con diagnostico genetico de HF (11 varones) pertenecientes a 8 familias con HF, seleccionadas por muestreo aleatorio entre 30 familias con HF con diagnostico molecular, en un estudio de intervencion sin grupo control con 20 mg/dia de simvastatina. Comparamos las caracteristicas clinicobiologicas entre sujetos clasificados como HF mutaciones nulas (HF Valencia 1 y Valencia 2; n = 11) o HF mutaciones no nulas (n = 16) en situacion basal y tras 6 semanas de tratamiento con simvastatina. Resultados Los sujetos con mutaciones nulas (HF Valencia 1 y 2) que no expresan ARNmy, por tanto, no sintetizan rLDL a partir del alelo mutado, responden menos al tratamiento con simvastatina que los pacientes con HF con mutaciones no nulas. La media del porcentaje de reduccion del cLDL fue significativamente inferior en el grupo con mutaciones nulas (32,6% [9,5] frente a 42,8% [12,2], p = 0,03). Ademas, los valores plasmaticos del cHDL en situacion basal y postratamiento fueron menores en los sujetos con HF con mutaciones nulas. No encontramos diferencias estadisticamente significativas en los parametros clinicos y lipidicos en situacion basal ni tras tratamiento entre varones y mujeres. Conclusion La respuesta terapeutica a simvastatina en sujetos con HF molecularmente caracterizados es significativamente menor en los sujetos con HF con mutaciones nulas (HF Valencia1 y 2). La aplicacion de estos resultados ayudara a predecir la respuesta al tratamiento con estatinas y permitira disenar terapeuticas individualizadas en este grupo de sujetos con alto riesgo cardiovascular.

Fundamento El defecto familiar de union de la apolipoproteina B-100 (DFB) es una enfermedad hereditaria autosomica dominante debida a mutaciones localizadas en el gen de la apolipoproteina B-100, clinicamente indistinguible de la hipercolesterolemia familiar. Describimos el primer homocigoto espanol para el DFB. Metodos Estudiamos por tecnica de PCR–SSCP la mutacion R3500Q en los familiares de primer y segundo grado de la familia con DFB previamente descrita por nuestro grupo. Ademas, analizamos la actividad del receptor de LDL en un ensayo con LDL conjugada con oro coloidal. Resultados El paciente presenta en ambos alelos la mutacion R3500Q causante de DFB. El estudio de la actividad del receptor de LDL es normal, lo que descarta que se trate de una hipercolesterolemia familiar. El grado de hipercolesterolemia es menor del esperado tratandose de un homocigoto (colesterol total, 415, y cLDL, 352 mg/dl), y presenta una buena respuesta terapeutica a estatinas y resins (descensos de hasta un 42% para el colesterol total y de un 51% para el cLDL). Conclusiones Hemos detectado y caracterizado el primer homocigoto espanol para el DFB (mutacion R3500Q), que presenta valores moderadamente elevados de colesterol total y cLDL a pesar de su situacion de homocigosis. Estos datos demuestran que el fenotipo lipoproteico de los homocigotos DFB es diferente de la situacion de homocigosis para la hipercolesterolemia familiar.

Fundamento Identificar y analizar los factores asociados con el ingreso hospitalario en diabeticos con ulceras en los pies, con el fin de identificar y tratar los pacientes de alto riesgo y evitar su ingreso hospitalario, que es la mayor fuente de gasto sanitario debido al pie diabetico. Sujetos y Metodo Hemos estudiado a 108 diabeticos (59 varones, edad media [DE] 68 [11] anos, 100 con diabetes tipo 2, con 16,4 [10,3] anos de evolucion) que acudieron a la unidad del pie diabetico desde enero 1996 hasta septiembre de 1997 con ulceras en los pies. En la primera visita se recogieron parametros clinicos y bioquimicos de riesgo en un protocolo clinico. Los sujetos fueron seguidos una media de 200,2 (121,3) dias, siendo necesario el ingreso hospitalario en 30 sujetos (28%). Resultados Los factores asociados con el ingreso hospitalario fueron mayor tamano de la ulceracion (1,9 [1,6] frente a 3,4 [2,3] cm; p Conclusiones Los factores de riesgo para ingreso hospitalario en pacientes diabeticos con ulceras en el pie se relacionan de forma independiente con el tamano de la ulcera y grado de retinopatia diabetica. Por tanto, en este grupo de diabeticos deben extremarse las medidas terapeuticas y preventivas.

Fundamento Calcular la prevalencia y definir el sindrome de insulinorresistencia mediante la determinacion de insulinemia basal y el indice HOMA, y estudiar su relacion con otros componentes del sindrome metabolico. Sujetos y metodo Estudiamos una poblacion de 292 sujetos no diabeticos, de ambos sexos y edades entre 20 y 65 anos, seleccionados por un metodo de muestreo simple aleatorio entre los que consultaron durante un ano en un centro de salud (en el area metropolitana de Valencia), mediante un metodo de busqueda oportunista. De ellos se selecciono a un subgrupo formado por 96 sujetos que no tenian caracteristicas clinicas ni analiticas del sindrome de insulinorresistencia, y se estudiaron los lipidos plasmaticos, parametros antropometricos, glucosa e insulina plasmatica y el valor del indice HOMA. Resultados El diagnostico de insulinorresistencia se ha establecido por los cortes del percentil 90 de la subpoblacion sin parametros clinicos ni analiticos del sindrome de insulinorresistencia, considerando una insulina plasmatica basal de 16,7 mU/l o superior, o indice HOMA de 3,8 o mayor. El indice HOMA es mas sensible que la insulina plasmatica para el diagnostico de insulinorresistencia. La prevalencia de insulinorresistencia (HOMA ≥ 3,8) en la poblacion estudiada por nosotros es elevada, 31,8%, siendo mas frecuente en hombres que en mujeres. Conclusion Ademas de los valores plasmaticos de insulina e indice HOMA, los mejores indicadores clinicobioquimicos de insulinorresistencia son los valores de glucemia en ayunas, el indice de masa corporal (IMC) y los trigliceridos plasmaticos. Asi, la razon de probabilidad de tener insulinorresistencia es de 5,9, 2,6 y 2,2, respectivamente para glucemia ≥ 110 mg/dl, IMC ≥ 25 kg/m2 y trigliceridos ≥ 150 mg/dl.

Abstract —Plasma lipid response to dietary fat and cholesterol is, in part, genetically controlled. The apolipoprotein A-IV (apoA-IV protein; APOA4, gene) has been shown to influence the response to dietary changes in normolipidemic individuals. The response to diet in subjects with familial hypercholesterolemia (FH) is also variable, and no studies are available on the influence of APOA4 mutations on dietary response in these subjects. We studied the effect of 2 common apoA-IV genetic variants (Gln 360 →His and Thr 347 →Ser) on the lipid response to the National Cholesterol Education Program type I (NCEP-I) diet in 67 FH heterozygotes (43 women and 24 men). Subjects were studied at baseline (after consuming for 1 month a diet with 35% fat [10% saturated] and 300 mg/d cholesterol) and after 3 months of consuming a low-fat diet. No sex-related differences were found, and results were combined for men and women. The APOA4-360 mutation was assessed in 67 subjects, 51 with genotype 1/1 and 16 with genotype 1/2. The APOA4-2 allele was associated with marginally significantly lower ( P =0.049) low density lipoprotein (LDL) cholesterol levels and significantly lower ( P =0.027) apoB levels independent of diet effects. After consuming an NCEP-I diet, carriers of the APOA4-2 allele showed a significantly lower reduction in apoB concentration (6.2%) than 1/1 subjects (14.1%; P =0.036); however, no significant differences in response were noted for LDL cholesterol. The APOA4-347 mutation was assessed in 63 individuals, 44 with the A/A allele and 19 with the A/T and T/T alleles. No significant differences were observed in baseline or post–NCEP-I diet values for these 2 groups in total, LDL, and high density lipoprotein cholesterol and plasma apoB levels. After dietary intervention, A/A individuals showed significant reductions in plasma triglyceride and very low density lipoprotein cholesterol levels; no changes were found in carriers of the T allele. Haplotype analysis suggested that in these FH subjects, the APOA4-360-2 allele was associated with lower plasma lipid levels during the NCEP-I diet period, whereas no significant effects were observed for the APOA4-347-T allele.

Plasma of patients with Tangier disease (TD) is devoid of alpha-LpA-I (apolipoprotein A-I-containing lipoprotein), which in normolipidemic plasma constitutes the majority of high density lipoprotein (HDL). The residual amounts of apolipoprotein A-I (apo A-I) in TD plasma have electrophoretic prebeta1-LpA-I mobility. We have previously demonstrated that TD plasma does not convert prebeta1-LpA-I into alpha-LpA-I. In this study we found that plasmas of normolipidemic controls, apo A-I-deficient patients and patients with fish-eye disease, but not plasmas of six TD patients, convert biotinylated lipid-free apo A-I into alpha-LpA-I. Supplementation of plasma with free oleic acid or fatty acid free albumin neither inhibited conversion activity in normal plasmas nor reconstituted it in TD plasma. In normal plasma the conversion activity was assessed in HDL and in the lipoprotein-free fraction. The latter fraction, however, generated larger particles only in the presence of exogenous phospholipid vesicles. To obtain particles with alpha-mobility, these vesicles had to contain phosphatidylinositol and/or cholesterol. Lipoprotein-depleted TD plasma did not convert lipid-free apo A-I into alpha-LpA-I even in the presence of exogenous vesicles with phospholipids or cholesterol. Taken together we conclude that disturbed transfer of glycerophospholipds onto apo A-I or prebeta1-LpA-I prevents maturation of HDL and thereby possibly causes deficiency of HDL cholesterol in patients with TD. Moreover, the lack of alpha-LpA-I in TD plasma together with its failure to convert exogenous apo A-I into an alpha-migrating particle provide specific tests for the diagnosis of TD.

Presentamos 2 casos clinicos con psoriasis extensa en los que el mal uso prolongado de corticoides topicos indujo la supresion del eje hipotalamohipofisario- suprarrenal y, como consecuencia, una insuficiencia suprarrenal secundaria. Se comentan los mecanismos y los factores que pueden dar lugar a dicha supresion.

Currently, reuse of solid waste from disused infrastructures is an important environmental issue to study. In this research, polymer concrete was developed by mixing orthophthalic unsaturated polyester resin, artificial microfillers (calcium carbonate), and waste aggregates (basalt and limestone) coming from the recycling process of concrete sleepers. The variation of the mechanical and physical properties of the polymer concrete (compressive strength, flexural strength, modulus of elasticity, density, and water absorption) was analyzed based on the modification of different variables: nature of the recycled aggregates, resin contents (11 wt%, 12 wt%, and 13 wt%), and particle-size distributions of microfillers used. The results show the influence of these variables on mechanical performance of polymer concrete. Compressive and flexural strength of recycled polymer concrete were improved by increasing amount of polyester resin and by optimizing the particle-size distribution of the microfillers. Besides, the results show the feasibility of developing a polymer concrete with excellent mechanical behavior.

The influence of obesity on blood pressure and plasma lipoproteins, glucose and insulin levels was investigated in patients with familial combined hyperlipidaemia (FCH). Sixty seven FCH patients mean age 49.0 +/- 8.9 y (45 male, 22 female) defined as obese (BMIor = 27 kg/m2, n = 39) or non-obese (BMI27 kg/m2, n = 28) were compared with control subjects matched for age, gender and body weight. Blood pressure, plasma lipoproteins, glucose and insulin were measured at baseline and following standard oral glucose load. The analysis indicate that FCH subjects with BMIor = 27 kg/m2 had significantly higher systolic and diastolic blood pressure, blood glucose and insulin levels following oral glucose tolerance test than those with BMI27 kg/m2. Fasting plasma insulin values were also significantly higher in the BMIor = 27kg/m2 subjects (138.5 +/- 66.6 vs 111.0 +/- 29.9 pmol/l, respectively, P0.05). Quantification of the area under the curve of the insulin secretion showed hyperinsulinaemia in 64.1% of patients with BMIor = 27kg/m2 compared to 28.5% in the group with BMI27 kg/m2 (P0.01). Plasma insulin values were positively related to triglyceridaemia. There were no differences in the plasma lipid values between the two FCH groups. We conclude that fasting and post-glucose stimulated plasma insulin levels are frequent findings in patients with FCH when compared with control subjects of similar age, gender and BMI. Moreover, obesity (BMIor = 27kg/m2) exacerbates the hyperglycaemia, hyperinsulinaemia and blood pressure values in these FCH subjects. These factors, together with lipid abnormalities, can predispose to the elevated risk of cardiovascular disease observed in FCH subjects.

Hospital malnutrition is a highly prevalent problem that affects patient morbidity and mortality resulting in longer hospital stays and increased healthcare costs. Although there is no single nutritional screening method, subjective global assessment (SGA) may be a useful, inexpensive, and easily reproducible tool.A cross-sectional, observational, randomized study was conducted in 197 patients in a tertiary hospital. SGA, anthropometric data, and biochemical parameters were used to assess the nutritional status of study patients.Fifty percent of subjects were malnourished according to SGA. A higher prevalence of malnutrition was found in medical (53%) as compared to surgical departments (47%). Half the subjects (50%) had malnutrition by SGA, but only 37.8% received nutritional treatment during their hospital stay. Mean hospital stay was longer for patients malnourished (13.5 days) or at risk of malnutrition (12.1 days) as compared to well nourished subjects (6.97 days). SGA significantly correlated (P.012) with anthropometric and biochemical malnutrition parameters.Prevalence of hospital malnutrition is very high in both medical and surgical departments and is inadequately treated. SGA is a useful tool for screening hospital malnutrition because of its high degree of correlation with anthropometric and biochemical parameters.

Low-density lipoprotein cholesterol (LDL-C) remains the primary target of therapy in most strategies of dyslipidaemia management focused on cardiovascular disease prevention. Different guidelines have identified specific LDL-C cut-off points as targets for therapeutic intervention. Many clinical situations characterised by dyslipidaemia and elevated triglycerides are common in our environment and in overall industrialised countries. Thus, lipid goals based only on LDL-C could misclassify an important percentage of subjects. The objective of the present study was to establish cut-off point values for apoB and non-HDL-C in relation to the identified LDL-C cut-off points for cardiovascular risk in a South European population.We performed a cross-sectional study including 1501 subjects (770 women and 731 men) between 18 and 80 years of age. Samples were collected after 12-14 h of fasting. Cholesterol, HDL-C, triglycerides and apoB levels were measured using direct methods. LDL-C was calculated by the Friedewald formula. Non-HDL-C was calculated as total cholesterol minus HDL-C.The Spearman's rank correlations between apoB and LDL-C (r 0.86, p 0.0001), and between apoB and non-HDL-C (r 0.91, p 0.0001) were both significant. The proposed cut-off points for apoB, according to LDL-C goals (70, 100, 130 and 160 mg/dl) in our population are 70, 80, 100 and 115 mg/dl respectively. The proposed cut-off values for non-HDL-C are 100, 120, 150 and 190 mg/dl respectively.The established LDL-C cut-off values could not be accurate to estimate cardiovascular risk in subjects with mild hypertriglyceridaemia, as frequently occurs in our Mediterranean population. To take into consideration the burden of atherogenic particles and better classify patients at risk we propose cut-off values for apoB or the equivalent for non-HDL-C. Prospective trials including cardiovascular variables are needed to validate our assumption.