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1.
High Blood Press Cardiovasc Prev ; 31(2): 167-175, 2024 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-38530573

RESUMEN

INTRODUCTION: Although a number of pathophysiological aspects of childhood obesity have been reported, few information are available on obesity-related cardiac organ damage. AIM: The present study was aimed at assessing the impact of anthropometric, blood pressure (BP) and metabolic variable on cardiac structure and function in youth. METHODS: In 78 subjects aged 5-16 years attending the outpatient clinic of cardiovascular risk (Valencia, Spain) anthropometric and metabolic variables, clinic and ambulatory BP and echocardiographic parameters were assessed. Subjects were also classified according to the presence of insulin resistance. RESULTS: Subjects mean age (± SD) amounted to 12.03 ± 2.4 years and males to 53.8%. Ten subjects were normoweight, 11 overweight, 39 obese, and 18 severely obese. No significant difference in office and ambulatory BP was detected among different bodyweight groups. A significant direct correlation was observed between left ventricular mass index (LVMI) and obesity markers [body mass index (BMI): r = 0.38, waist circumference (WC): r = 0.46, P < 0.04 for both]. Left ventricular hypertrophy, relative wall thickness and left atrial diameter were significantly related to BMI and WC. In contrast, office and ambulatory BP were unrelated to other variables, and differences in LVMI among different BP phenotypes were not significant. When partitioning the population by insulin resistance, LVMI, adjusted for confounders, was significantly greater in the insulin-resistant group. CONCLUSIONS: In children and adolescents characterized by different body weight patterns, weight factors "per se" and the related insulin resistance state appear to represent the main determinants of LVMI and left ventricular hypertrophy, independently on BP values and BP phenotypes.


Asunto(s)
Presión Sanguínea , Índice de Masa Corporal , Hipertrofia Ventricular Izquierda , Resistencia a la Insulina , Obesidad Infantil , Humanos , Masculino , Niño , Adolescente , Femenino , Obesidad Infantil/fisiopatología , Obesidad Infantil/diagnóstico , Obesidad Infantil/epidemiología , Obesidad Infantil/complicaciones , Hipertrofia Ventricular Izquierda/fisiopatología , Hipertrofia Ventricular Izquierda/diagnóstico por imagen , Hipertrofia Ventricular Izquierda/etiología , Preescolar , Factores de Edad , España/epidemiología , Función Ventricular Izquierda , Remodelación Ventricular , Circunferencia de la Cintura , Medición de Riesgo , Factores de Riesgo , Estudios Transversales
2.
Medicine (Baltimore) ; 101(21): e29416, 2022 May 27.
Artículo en Inglés | MEDLINE | ID: mdl-35623073

RESUMEN

RATIONALE: Whereas metronidazole-induced hepatotoxicity is quite rare in the general population, in individuals carrying a nucleotide excision repair disorder, namely Cockayne syndrome, there is a high risk of developing this complication. PATIENT CONCERNS: We report the case of a 44-year-old man, affected by xeroderma pigmentosum, who was admitted to the hospital presenting aspiration pneumoniae caused by worsening dysphagia and with severe hepatotoxicity during the hospitalization. DIAGNOSES: Acute hepatitis, which was leading to acute liver failure, occurred during antibiotic treatment with metronidazole and ceftazidime with an elevation of liver enzymes consistent with hepatocellular damage pattern. INTERVENTIONS: Hydration with glucose 5% solution, pantoprazole and vitamin K were administered, meanwhile other causes of hepatitis were ruled out and the ongoing antibiotic treatment was stopped suspecting a drug-induced liver injury. OUTCOMES: Liver function nearly completely recovered 1 month later with a first rapid improvement, within few days, of aminotransferases and coagulation studies, and slower of cholestatic enzymes. LESSONS: We describe the first case available in the literature of hepatotoxicity associated with metronidazole treatment in a xeroderma pigmentosum patient. Clinicians therefore, based on this report and according to the possible underlying mechanism shared by other genetic diseases characterized by alterations in the pathway of DNA-repair, should consider such adverse event also in patients affected by this rare disease.


Asunto(s)
Enfermedad Hepática Inducida por Sustancias y Drogas , Xerodermia Pigmentosa , Adulto , Antibacterianos , Enfermedad Hepática Inducida por Sustancias y Drogas/complicaciones , Reparación del ADN , Humanos , Masculino , Metronidazol/efectos adversos , Xerodermia Pigmentosa/genética
3.
Sci Rep ; 11(1): 9150, 2021 04 28.
Artículo en Inglés | MEDLINE | ID: mdl-33911085

RESUMEN

We provide here a first-hand description of the coseismic surface effects caused by the Mw 6.4 Petrinja earthquake that hit central Croatia on 29 December 2020. This was one of the strongest seismic events that occurred in Croatia in the last two centuries. Field surveys in the epicentral area allowed us to observe and map primary coseismic effects, including geometry and kinematics of surface faulting, as well as secondary effects, such as liquefaction, sinkholes and landslides. The resulting dataset consists of homogeneous georeferenced records identifying 222 observation points, each of which contains a minimum of 5 to a maximum of 14 numeric and string fields of relevant information. The earthquake caused surface faulting defining a typical 'conjugate' fault pattern characterized by Y and X shears, tension cracks (T fractures), and compression structures (P shears) within a ca. 10 km wide (across strike), NW-SE striking right-lateral strike-slip shear zone (i.e., the Petrinja Fault Zone, PFZ). We believe that the results of the field survey provide fundamental information to improve the interpretation of seismological, GPS and InSAR data of this earthquake. Moreover, the data related to the surface faulting may impact future studies focused on earthquake processes in active strike-slip settings, integrating the estimates of slip amount and distribution in assessing the hazard associated with capable transcurrent faults.

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