Fat Oxidation Rate as a Function of Plasma Lipid and Hormone Response in Endurance Athletes.

Soria, M, Ansón, M, Lou-Bonafonte, JM, Andrés-Otero, MJ, Puente, JJ, and Escanero, J. Fat oxidation rate as a function of plasma lipid and hormone response in endurance athletes. J Strength Cond Res 34(1): 104-113, 2020-Plasma lipid changes during incremental exercise are not well known. The aim of this study was to investigate the relationship among fat oxidation rate, plasma lipids, and hormone concentrations in well-trained athletes. Twenty-six trained triathletes completed a graded cycle ergometer test to exhaustion increasing by 0.5 W·kg every 10 minutes. Fat oxidation rates were determined using indirect calorimetry. For each individual, maximal fat oxidation (MFO), the intensity at which MFO occurred (Fatmax), and the intensity at which fat oxidation became negligible (Fatmin) were determined. Blood samples for lipids and hormones analysis were collected at the end of each stage of the graded exercise test. All variables studied except insulin showed an increase at the end of incremental protocol with respect to basal levels. Free fatty acid reached significant increase at 60%VO2max and maximal levels at 70%VO2max. Low-density lipoprotein (LDL) and triglycerides (TG) decreased and showed lowest levels at 60%VO2max and reaching significant increases after 80%VO2max. High-density lipoprotein reached significant increase at 60%VO2max. Adrenaline and noradrenaline increased until the end of the incremental exercise, and significant differences were from 50%VO2max. These results suggest that exercise intensities are related to plasma lipids levels. In the zone when lipids oxidation is maximal, plasma LDL and TG variation differs from other lipids. These results may have application for the more adequate exercise intensity prescription to maximize the beneficial effects of exercise.

A Cross-Sectional Study Examining the Parametric Thyroid Feedback Quantile Index and Its Relationship with Metabolic and Cardiovascular Diseases.

Background: The usual inverse correlation between thyrotropin (TSH) and thyroid hormone disappears in syndromes of central resistance to thyroid hormone, where both are high. TSH and thyroid hormone are also simultaneously high when there is an elevation of the set point of the thyroid regulation axis. This can be estimated with indices, such as the Parametric Thyroid Feedback Quantile-based Index (PTFQI), which was designed for the general population. The PTFQI is positively associated with diabetes prevalence, but association with other pathologies has not been yet explored. The aim of this project was to explore the potential relationship of the PTFQI with metabolic and cardiovascular disease in a sample of ambulatory adult patients from Spain. Methods: A cross-sectional study was carried out among the patients who underwent thyroid hormones measurement (6434 measurements from September to November 2018 in a central laboratory in Spain). We retrospectively reviewed clinical records of a subgroup of adults aged >18 years with normal TSH and free thyroxine (fT4) belonging to groups that represent extreme PTFQI (n = 661). Individuals with known conditions interfering the thyroid axis were excluded (remaining n = 296). Logistic and linear regression models adjusted for age and sex were used to calculate odds ratio (OR) of diseases and differences of clinical parameters, and 95% confidence intervals [CI]. Results: Across levels with higher PTFQI, there was an increase in the prevalence of type 2 diabetes (High vs. Low PTFQI OR: 2.88 [CI: 1.14-7.86], p-Trend = 0.02), ischemic heart disease (16.4% vs. 0%, unadjusted Haldane-Anscombe corrected OR: 23.90 [CI: 1.36-21.48], adjusted p-Trend = 0.04), atrial fibrillation (OR: 8.13 [CI: 1.33-158.20], p-Trend = 0.05), and hypertension (OR: 3.19 [CI: 1.14-9.94], p-Trend = 0.05). While the prevalence of type 2 diabetes was similarly associated with TSH and fT4, ischemic heart disease, atrial fibrillation, and hypertension were more strongly associated with the differences in fT4 values. Conclusions: Type 2 diabetes, ischemic heart disease, atrial fibrillation, and hypertension may be associated with a higher central regulation set point for thyroid hormone. These findings should be confirmed in other populations.

Multiple approaches to assess fourteen non-invasive serum indexes for the diagnosis of liver fibrosis in chronic hepatitis C patients.

BACKGROUND: The aim of this study was to compare fourteen non-invasive indexes/scores: AAR, APRI, Fibroindex, MODEL3, Forns index, FIB4, GUCI, FI, FCI, Pohl score, AP index, CDS, HGM-1 and HGM-2, in order to diagnose the hepatic fibrosis stage in a survey of patients with chronic hepatitis C. METHODS: 84 patients with chronic hepatitis C were studied. Liver fibrosis was staged according to the Scheuer scoring system. The diagnostic accuracy of these indexes/scores was evaluated by AUROC, contingency tables and logistic regression analysis. RESULTS: The best AUROCs (>0.9) to discriminate cirrhosis (F=4), were observed for CDS, FI, AAR, MODEL3, FIB4, HGM-2 and FCI. To discriminate at least advance fibrosis (F≥3), the best AUROCs (>0.89) were for CDS, FI, FIB4, HGM2-2, MODEL3 and FCI. To discriminate at least significant fibrosis (F≥2), the best AUROCs (>0.8) were for FIB4, GUCI, APRI, FI, Forns index, HGM-2 and FCI. Contingency tables and logistic regression analysis supported the results obtained by AUROC. CONCLUSIONS: This study compares the diagnostic performance of fourteen indexes for the diagnosis of liver fibrosis stage in the same group of CHC patients. These results allow the selection of the best indexes for further studies in larger populations, in order to build diagnostic algorithms as an alternative to liver biopsy for fibrosis staging in patients with chronic HCV infection. These algorithms would allow to take therapeutical decisions and the continuous follow-up of hepatic fibrosis in these patients.

Interferencia analítica en la determinación de troponina por anticuerpos heterófilos / Interference in the determination of Troponin due to heterophile antibodies

Resumen Por su elevada especificidad y sensibilidad, y a raíz de la tercera definición universal de infarto estas isoformas cardiacas han sido aceptadas en el ámbito internacional como los biomarcadaores de elección en la práctica clínica para el diagnóstico de síndrome coronario agudo, preferibles a la determinación de las enzimas creatina quinasa y su isoforma MB. Se presenta el caso de un varón de ochenta años, quien, de manera persistente, tuvo valores elevados de troponinas, pese a evolución clínica no compatible con síndrome coronario agudo ni otras causas de elevación de este biomarcador.

Abstract Due to its elevated specificity and sensitivity, and on being the third universal definition of myocardial infarction, these cardiac isoforms have been accepted internationally as the biomarkers of choice in clinical practice for the diagnosis of acute coronary syndrome, and are preferable to the determinations of creatine kinase and its MB isoform. A case is presented on an eighty year-old man, who persistently had elevated Troponin values, despite a clinical course that was incompatible with an acute coronary syndrome or any other causes of elevation of this biomarker.

Procedimiento para la interpretación de un cambio entre dos valores consecutivos de una magnitud biológica / Procedure for the interpretation of a change between two consecutive values of a biological quantity

Los intervalos de referencia biológicos no proporcionan información suficiente para la interpretación de un cambio entre dos valores medidos consecutivos debido a que, para la gran mayoría de las magnitudes, la variabilidad biológica intraindividual es menor que la variabilidad biológica interindividual. Teniendo en cuenta esta situación, el laboratorio podría proporcionar, conjuntamente con los intervalos de referencia, información adicional que permita estimar de manera objetiva la significación de un cambio en los valores de una magnitud biológica para un mismo individuo. En este sentido, la manera más adecuada para interpretar un cambio debe realizarse en función del concepto de incertidumbre, ya que permite considerar todas las posibles fuentes de variación a las que están sometidos los valores medidos. Este documento, basado en guías de ámbito nacional e internacional se describe un procedimiento para la interpretación de un cambio entre dos valores consecutivos de una magnitud biológica, basado en el estudio de las diversas fuentes de incertidumbre que le afectan

Biological reference intervals do not provide sufficient information for the interpretation of a change between two consecutive measured values of a biological quantity because, for the vast majority of quantities, the intra-individual biological variability is smaller than the inter-individual biological variability. Taking into account this situation, the laboratory could provide, in conjunction with the reference intervals, additional information to objectively estimate the significance of a change in the values of a biological quantity. In this sense, the most adequate way to interpret the change must be made on the basis of the uncertainty concept, since it allows taking into account all the possible sources of variation to which the measured values are subjected. This document, based on national and international guidelines, describes a procedure for the interpretation of a change between two consecutive values of a biological quantity, based on the study of the various sources of uncertainty that affect it

Síndrome de Gitelman en un paciente pediátrico: a propósito de un caso / Gitelman syndrome in a paediatric patient: a case report

El síndrome de Gitelman es una tubulopatía de herencia autosómica recesiva debida a mutaciones inactivantes en el gen SLC12A3 que codifica para el cotransportador sodio-cloro (NCC). El NCC es una proteína de membrana que pertenece a la familia de transportadores SLC12 cloro-catiónicos que constituye la principal vía de reabsorción de sodio y cloro (NaCl), determina la presión arterial y es el lugar de acción de los diuréticos tipo tiazida. El síndrome de Gitelman se caracteriza por hipopotasemia, hipomagnesemia, alcalosis metabólica, normocalcemia e hipocalciuria. El diagnóstico diferencial se realiza con el síndrome de Bartter tipoiii y la hipomagnesemia renal con hipocalciuria. Puede ser asintomático o expresarse con síntomas leves (calambres, fatiga o dolor articular) o con síntomas más graves (tetania, convulsiones). A pesar de considerarse benigno, la combinación de hipopotasemia con hipomagnesemia puede prolongar el intervalo QT y desencadenar arritmias que pueden amenazar la vida del paciente. Por todo ello resulta importante el diagnóstico diferencial y la confirmación mediante el estudio genético de cara al seguimiento de los pacientes y al asesoramiento genético (AU)

Gitelman syndrome, an autosomal recessive tubulopathy, is caused by inactivating mutations in SLC12A3 gene. This gene codes for the sodium chloride co-transporter (NCC), a membrane protein that belongs to the family of SLC12 chloride-cationic transporters. NCC constitutes the main route of sodium chloride (NaCl) reabsorption, determines blood pressure, and is the site of action of thiazide-type diuretics. Gitelman syndrome usually involves hypokalaemia, hypomagnesaemia, metabolic alkalosis, and hypocalciuria. The differential diagnosis for Gitelman syndrome includes Bartter syndrome typeiii and renal hypomagnesaemia. Symptoms reported in the literature range from asymptomatic, to mild symptoms of cramps and fatigue, to severe manifestations such as tetany and seizures. The prognosis is generally good, but a few patients with hypokalaemia and hypomagnesaemia may have a prolonged QT interval and trigger potentially life-threatening arrhythmias. Thus, genetic testing is important to confirm the diagnosis, as well as in the follow-up of patients (AU)

Biomarcadores, índices y algoritmos para el diagnóstico de fibrosis hepática en pacientes con hepatitis crónica por virus C / Biomarkers, indexes and algorithms for the detection of liver fibrosis in chronic hepatitis C patients

Determinar el estadio de fibrosis hepática es esencial en el manejo de la enfermedad hepática en pacientes con hepatitis crónica por virus C. La biopsia hepática ha sido considerada el gold standard para diagnosticar la enfermedad, la actividad necroinflamatoria y el estadio de fibrosis, pero tiene algunas limitaciones técnicas y riesgos. Teniendo en cuenta estas limitaciones, existe cierta exigencia en introducir biomarcadores séricos no invasivos para el diagnóstico de fibrosis que podrían ser capaces de reemplazar parcialmente a la biopsia hepática. El biomarcador sérico ideal debería ser específico para el hígado y fácil de determinar. Los marcadores séricos se dividen en directos e indirectos. Los directos reflejan el recambio de la matriz extracelular, mientras que los indirectos reflejan alteraciones en la función hepática. Aunque todavía está limitado el grado de implementación de los test no invasivos de fibrosis hepática, esta revisión es una visión de conjunto de los biomarcadores, índices y algoritmos diagnósticos de fibrosis hepática estudiados en hepatitis crónica C pero con un interés potencial en otras hepatopatías crónicas (AU)

Precise staging of liver fibrosis is essential in the management of liver disease activity in chronic hepatitis C patients. Liver biopsy has been considered the reference method for diagnosing disease, grading necroinflammatory activity, and staging fibrosis, but it has some technical limitations and risks. Taking into account these limitations, there is a need to introduce non-invasive serum markers for fibrosis that would be able to partially replace liver biopsy. Ideal serum markers should be specific for the liver and easy to perform. Serum markers of hepatic fibrosis are divided into direct and indirect. Direct markers reflect extracellular matrix turnover, whereas indirect markers reflect alterations in hepatic function. The degree of implementation of non-invasive diagnostic tests for liver fibrosis still remains limited. This review provides a current overview of biomarkers, indexes and algorithms for hepatic fibrosis diagnosis in chronic hepatitis C patients (AU)