Evolution of interconsultal activity to endocrinology and nutrition in hospitalization floor in a third level hospital.

INTRODUCTION: Endocrinology and Nutrition (EyN) is an outpatient and hospital medical specialty. This study aims to understand the evolution of the activity of interdepartmental consultation (IC) carried out by EyN in hospitalization floor of a third level hospital, comparing its evolution with other medical specialties, and comparing endocrine IC with nutritional IC. MATERIAL AND METHODS: Longitudinal and retrospective study which analyzes IC notes of EyN and other medical specialties between 01-01-2013 and 31-12-2022. RESULTS: A total of 76093 IC notes (12623 patients) were performed by the EyN service (average age 65.4 years; 59% male) with an average of 4.8 notes per patient. Average annual growth was 7% in notes and 4% in patients (versus 6% and 3% of all other medical services, differences statistically significant). Of all patients hospitalized for 4 or more days, EyN went from attending 7.9% (2013) to 12.3% (2022). 66% of the IC performed by EyN was for nutritional cause and 34% for other pathologies. CONCLUSIONS: The EyN service is the one that most patients attend in hospital IC activity, with growth over the last few years greater than other medical specialties. Nutritional pathology is the main reason for IC.

Repercusión de la pérdida ponderal tras cirugía bariátrica en la estructura y función cardiaca / Impact of ponderal loss after bariatric surgery on the cardiac structure and function

Introducción y objetivoEl exceso de peso puede inducir modificaciones en la estructura y función del miocardio. La presencia de hipertrofia ventricular izquierda es un predictor independiente de morbimortalidad cardiovascular.El objetivo principal del estudio ha sido conocer la prevalencia de alteraciones morfofuncionales cardiacas en pacientes con obesidad y su modificación tras la pérdida de peso después de una cirugía bariátrica (CB).Pacientes y métodosEstudio de cohortes prospectivo de 75 pacientes con obesidad y sin cardiopatía conocida a los que se les realizó un bypass gástrico. Se midieron parámetros antropométricos, analíticos y ecocardiográficos antes, a los 6 y 12 meses de la intervención.ResultadosSe incluyeron 75 pacientes (66,6% mujeres, edad media 39,3 [9,7] años e índice de masa corporal [IMC] 47,8 [7,1] kg/m2). A los 6 y 12 meses de la CB se produjo una reducción significativa del peso corporal, una mejora en los parámetros metabólicos, inflamatorios y protrombóticos, así como en los factores de riesgo cardiovascular asociados a la obesidad (hipertensión arterial [HTA], diabetes mellitus tipo 2 [DM2], dislipemia [DLP] y síndrome de apnea-hipopnea del sueño [SAHOS]).Antes de la intervención, el 62,7% de los pacientes presentaba alteración en la geometría del ventrículo izquierdo, siendo el remodelado concéntrico la más frecuente (38,7%). Además, el 50,7% presentaba disfunción diastólica. Al año de la CB, el patrón ventricular fue normal en el 92% de los casos y la función diastólica mejoró significativamente.ConclusionesNuestros resultados corroboran el efecto negativo de la obesidad sobre el miocardio, así como la potencial reversibilidad de estas alteraciones tras una pérdida significativa de peso después de una CB. (AU)

Introduction and objectiveExcess weight can cause structural and functional cardiac disorders. The presence of left ventricular hypertrophy in the obese patient is an independent predictor of cardiovascular morbidity and mortality.The major aim of the present study is to know the prevalence of cardiac morphofunctional disorders in obese patients, before and after weight loss due to bariatric surgery (BS).Patients and methodsProspective cohort study of 75 patients with obesity without known heart disease referred to gastric bypass. Anthropometric, analytical and echocardiographic parameters were measured before and after 6 and 12 months after BS.ResultsThe study included 75 patients (66.6% women, mean age 39.3 [9.7] years and BMI 47.8 [7.1] kg/m2). At 6 and 12 months after BS there was a significant reduction in body weight and an improvement in metabolic, inflammatory and prothrombotic parameters and in cardiovascular risk factors associated with obesity (hypertension, type 2 diabetes, dyslipidemia and obstructive sleep apnea−hypopnea syndrome).Before surgery, cardiac remodeling was present in 62.7%, most frequently in the form of concentric remodeling (38.7%). Diastolic dysfunction occurred in 50.7% of the patients.One year after surgery, the ventricular pattern was normal in 92% of cases and the diastolic function improved significantly.ConclusionsOur results support the negative effect of obesity on cardiac geometry and function and the potential reversibility of these cardiac alterations after marked weight loss due to BS. (AU)

Impact of ponderal loss after bariatric surgery on the cardiac structure and function. / Repercusión de la pérdida ponderal tras cirugía bariátrica en la estructura y función cardiaca.

INTRODUCTION AND OBJECTIVE: Excess weight can cause structural and functional cardiac disorders. The presence of left ventricular hypertrophy in the obese patient is an independent predictor of cardiovascular morbidity and mortality. The major aim of the present study is to know the prevalence of cardiac morphofunctional disorders in obese patients, before and after weight loss due to bariatric surgery (BS). PATIENTS AND METHODS: Prospective cohort study of 75 patients with obesity without known heart disease referred to gastric bypass. Anthropometric, analytical and echocardiographic parameters were measured before and after 6 and 12 months after BS. RESULTS: The study included 75 patients (66.6% women, mean age 39.3 [9.7] years and BMI 47.8 [7.1] kg/m2). At 6 and 12 months after BS there was a significant reduction in body weight and an improvement in metabolic, inflammatory and prothrombotic parameters and in cardiovascular risk factors associated with obesity (hypertension, type 2 diabetes, dyslipidemia and obstructive sleep apnea-hypopnea syndrome). Before surgery, cardiac remodeling was present in 62.7%, most frequently in the form of concentric remodeling (38.7%). Diastolic dysfunction occurred in 50.7% of the patients. One year after surgery, the ventricular pattern was normal in 92% of cases and the diastolic function improved significantly. CONCLUSIONS: Our results support the negative effect of obesity on cardiac geometry and function and the potential reversibility of these cardiac alterations after marked weight loss due to BS.

Resistin in morbidly obese patients before and after gastric bypass surgery.

BACKGROUND AND OBJECTIVES: Resistin was originally suggested to be a potential mediator of obesity-related insulin resistance in rodents. However, in humans, the role of resistin in obesity and insulin resistance has not yet been demonstrated. The present study investigates whether there are differences in resistin levels between patients with morbid obesity and lean subjects, and analyzes changes in resistin levels after significant weight loss secondary to bariatric surgery. METHODS: Sixty-eight patients with morbid obesity (body mass index [BMI] ≥ 40 kg/m2) and 31 lean subjects (BMI < 25 kg/m2) were selected. The study variables were: weight, height, BMI, waist-hip ratio (WHR), fat mass, family history of cardiovascular disease (CVD), type 2 diabetes mellitus (DM), hypertension, dyslipidemia, smoking, glucose, glycated hemoglobin (HbA1c), insulin, high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), adiponectin and resistin. Homoeostasis model assessment (HOMA) and quantitative insulin sensitivity check index (QUICKI) were calculated. The obese patients underwent gastric bypass surgery, and the above mentioned variables were reassessed after 12 months and major weight loss. RESULTS: There were no significant differences in resistin levels between morbidly obese patients and healthy subjects of normal weight, or between obese patients before and after weight loss. Resistin levels in morbidly obese patients were not correlated to adiposity anthropometric measures, insulin, glucose, HOMA, QUICKI, hsCRP, IL-6 or adiponectin. In the morbid obesity group, after one year of weight loss, the only study parameter correlated to resistin levels was IL-6. CONCLUSION: Our results do not support a relationship among resistin levels, obesity and insulin resistance in humans.

Resistin in morbidly obese patients before and after gastric bypass surgery / Resistina en obesos mórbidos antes y después de un bypass gástrico

Background and objectives: Resistin was originally suggested to be a potential mediator of obesity-related insulin resistance in rodents. However, in humans, the role of resistin in obesity and insulin resistance has not yet been demonstrated. The present study investigates whether there are differences in resistin levels between patients with morbid obesity and lean subjects, and analyzes changes in resistin levels after significant weight loss secondary to bariatric surgery. Methods: Sixty-eight patients with morbid obesity (body mass index [BMI] ≥ 40 kg/m2) and 31 lean subjects (BMI < 25 kg/m2) were selected. The study variables were: weight, height, BMI, waist-hip ratio (WHR), fat mass, family history of cardiovascular disease (CVD), type 2 diabetes mellitus (DM), hypertension, dyslipidemia, smoking, glucose, glycated hemoglobin (HbA1c), insulin, high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), adiponectin and resistin. Homoeostasis model assessment (HOMA) and quantitative insulin sensitivity check index (QUICKI) were calculated. The obese patients underwent gastric bypass surgery, and the above mentioned variables were reassessed after 12 months and major weight loss. Results: There were no significant differences in resistin levels between morbidly obese patients and healthy subjects of normal weight, or between obese patients before and after weight loss. Resistin levels in morbidly obese patients were not correlated to adiposity anthropometric measures, insulin, glucose, HOMA, QUICKI, hsCRP, IL-6 or adiponectin. In the morbid obesity group, after one year of weight loss, the only study parameter correlated to resistin levels was IL-6. Conclusion: Our results do not support a relationship among resistin levels, obesity and insulin resistance in humans (AU)

Introducción y objetivos: inicialmente se sugirió que la resistina era un mediador potencial de la resistencia a la insulina relacionada con la obesidad en roedores. Sin embargo, en seres humanos, el papel de la resistina en la obesidad y la resistencia a la insulina aún no se ha demostrado. El presente estudio investiga si existen diferencias en los niveles de resistina entre pacientes con obesidad mórbida y sujetos con normopeso, y analiza los cambios en los niveles de resistina después de la pérdida significativa de peso debida a cirugía bariátrica. Métodos: se seleccionaron 68 pacientes con obesidad mórbida (IMC ≥ 40 kg/m2) y 31 sujetos normopeso (IMC < 25 kg/m2). Las variables del estudio fueron peso, talla, IMC, relación cintura-cadera (WHR), masa grasa, antecedentes familiares de enfermedad cardiovascular, diabetes mellitus tipo 2 (DM), hipertensión arterial, dislipidemia, tabaquismo, glucosa, hemoglobina glicosilada (HbA1c), insulina, proteína C reactiva de alta sensibilidad (hsCRP), interleucina-6 (IL-6), adiponectina y resistina. Se calcularon la evaluación del modelo de homeostasis (HOMA) y el índice cuantitativo de control de sensibilidad a la insulina (QUICKI). Los pacientes obesos se sometieron a un bypass gástrico, y las variables mencionadas fueron reevaluadas después de 12 meses y una pérdida de peso importante. Resultados: no hubo diferencias significativas en los niveles de resistina entre pacientes obesos mórbidos y sujetos sanos de peso normal, ni entre pacientes obesos antes y después de la pérdida de peso. Los niveles de resistina en pacientes obesos mórbidos no se correlacionaron con medidas antropométricas de adiposidad, insulina, glucosa, HOMA, QUICKI, hsCRP, IL-6 o adiponectina. En el grupo de obesos mórbidos, al año de la pérdida de peso experimentada, el único parámetro del estudio correlacionado con los niveles de resistina fue la IL-6. Conclusión: nuestros resultados no apoyan una relación entre los niveles de resistina, la obesidad y la resistencia a la insulina en los seres humanos (AU)