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)

Obesity, endothelial function and inflammation: the effects of weight loss after bariatric surgery / Obesidad, inflamación y función endotelial: efectos de la pérdida de peso tras cirugía bariatrica

Objective: Obesity is associated with a high risk for atherosclerotic cardiovascular disease. There is a causal association between obesity, inflammation, insulin resistance (IR) and endothelial dysfunction. The aim of this study was to evaluate changes in IR, proinflammatory state and markers of endothelial dysfunction in morbidly obese patients after weight loss following bariatric surgery. Methods: In this study, we measured the levels of soluble intracellular adhesion molecule-1 (sICAM1), plasminogen activator inhibitor 1 (PAI-1), high-sensitivity C-reactive protein (hs-CRP), and interleukin-6 (IL-6) in 79 morbidly obese patients at baseline and 3, 6 and 12 months after gastric bypass. Also, we evaluated changes in IR. Results: Twelve months after surgery, there was a significant decrease in plasma levels of sICAM1 (p < 0.001), PAI-1 (p < 0.05), hs-CRP (p < 0.001), IL-6 (p < 0.001) and homeostasis model assessment (HOMA) (p < 0.001) and a significant increase of McAuley index (McAuley) (p < 0.001). Baseline levels of hs-PCR were positively correlated with sICAM-1 (r = 0.450, p < 0.01) and IL-6 (r = 0.451, p < 0.01). Significant correlations were also found between the decrease of PAI-1 and the decrease of hs-PCR (r = 0.425, p < 0.01) and tryglicerides (r = 0.351, p < 0.01). Conclusions: In patients with morbid obesity, substantial surgically induced weight loss is followed by a significant improvement in the endothelial function, inflammatory state and insulin sensitivity, that may reduce their cardiovascular risk. A relationship exists between improved inflammatory profile and endothelial function (AU)

Objetivo: la obesidad está asociada con un aumento del riesgo de enfermedad cardiovascular. Se ha propuesto una relación causal entre obesidad, inflamación, resistencia a la insulina, y disfunción endotelial. El objetivo de este estudio fue valorar marcadores de insulinorresistencia, infl amación y disfunción endotelial en pacientes con obesidad mórbida antes y después de la pérdida de peso por cirugía bariátrica. Métodos: se midieron las concentraciones séricas de moléculas solubles de adhesión intercelular tipo 1 (sICAM-1), inhibidor del activador del plasminógeno tipo 1 (PAI-1), proteína C reactiva de alta sensibilidad (hs-PCR) e interleucina 6 (IL-6) en 79 pacientes con obesidad mórbida antes y a los 3, 6 y 12 meses de la realización de un by-pass gástrico. También se evaluaron índices de resistencia a la insulina. Resultados: a los 12 meses de la cirugía disminuyeron los niveles de sICAM1 (p < 0,001), PAI-1 (p < 0,05), hs-CRP (p < 0,001), IL-6 (p < 0,001) y el índice homeostasis model assessment (HOMA) (p < 0,001) y aumentó el índice McAuley (p < 0,001). Los niveles basales de hs-PCR estaban correlacionados con los de sICAM-1 (r = 0,450, p < 0,01) y de IL-6 (r = 0,451, p < 0,01). También existía correlación entre el descenso de los niveles de PAI-1 y el descenso de hs-PCR (r = 0,425, p < 0,01) y triglicéridos (r = 0,351, p < 0,01). Conclusiones: en pacientes con obesidad mórbida una importante pérdida de peso por cirugía bariátrica se acompaña de una mejora significativa de marcadores inflamatorios, de función endotelial e insulinorresistencia, lo que puede suponer una disminución del riesgo cardiovascular. Existe una relación entre mejora del perfil inflamatorio y función endotelial (AU)

Obesity and inflammation: change in adiponectin, C-reactive protein, tumour necrosis factor-alpha and interleukin-6 after bariatric surgery.

BACKGROUND: Obesity is associated with a low-grade inflammatory state. A causal association between inflammation and atherosclerosis has been suggested. The aim of this study was to evaluate changes in the proinflammatory profile of morbidly obese patients after weight loss following bariatric surgery. METHODS: In this study, we measured levels of adiponectin, high-sensitivity C-reactive protein (hs-CRP), tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) and their relation to insulin resistance and lipid parameters in 60 morbidly obese women at baseline and 3, 6 and 12 months after gastric bypass. RESULTS: Twelve months after surgery, there was a significant increase in plasma levels of adiponectin (p < 0.001) and high-density lipoprotein cholesterol (p < 0.01) and a significant decrease in levels of IL-6 (p < 0.001), hs-CRP (p < 0.001), cholesterol (p < 0.001), triglycerides (p < 0.001), low-density lipoprotein cholesterol (p < 0.001), glucose (p < 0.001), insulin (p < 0.001) and homeostasis model assessment (HOMA; p < 0.001). At 12 months, correlations were seen between IL-6 levels and the following: body mass index (BMI) (r = 0.53, p < 0.001), insulin (r = 0.51, p < 0.001) and HOMA (r = 0.55, p < 0.001). Also, hs-CRP levels correlated with BMI (r = 0.40, p = 0. 004), triglycerides (r = 0.34, p = 0.017), insulin (r = 0.50, p = 0.001) and HOMA (r = 0.46, p = 0.002). CONCLUSIONS: In patients with morbid obesity, significant weight loss is followed by a significant improvement in the inflammatory state, insulin sensitivity and lipid profile. A relationship exists between improved inflammatory profile and insulin sensitivity.

[Soluble intercellular adhesion molecule-1 and C reactive protein after bariatric surgery]. / Moléculas solubles de adhesión intercelular tipo 1 y proteína C reactiva tras cirugía bariátrica.

BACKGROUND AND OBJECTIVES: Obesity is associated with a state of chronic low-grade inflammation. A causal association between inflammatory processes and atherogenesis has been proposed. The aim of this study was to evaluate changes in the proinflammatory profile of morbidly obese patients who underwent bariatric surgery. Serum C-reactive protein (CRP) and soluble intercellular adhesion molecule-1 (sICAM-1) concentrations were measured before and after massive weight loss due to gastric bypass. METHODS: In this prospective study we measured CRP and sICAM-1 concentrations in 50 morbidly obese patients (19 men and 31 women) at baseline and 3, 6 and 12 months after gastric bypass. RESULTS: Body mass index (BMI), CRP, and sICAM-1 decreased significantly. BMI correlated with CRP but not with sICAM-1. CONCLUSIONS: The improvement in vascular risk profile after weight loss in morbidly obese patients could be partially explained by changes in inflammatory status.

Moléculas solubles de adhesión intercelular tipo 1 y proteína C reactiva tras cirugía bariátrica / Soluble intercellular adhesion molecule-1 and C reactive protein after bariatric surgery

Background and objectives Obesity is associated with a state of chronic low-grade inflammation. A causal association between inflammatory processes and atherogenesis has been proposed. The aim of this study was to evaluate changes in the proinflammatory profile of morbidly obese patients who underwent bariatric surgery. Serum C-reactive protein (CRP) and soluble intercellular adhesion molecule-1 (sICAM-1) concentrations were measured before and after massive weight loss due to gastric bypass. Methods In this prospective study we measured CRP and sICAM-1 concentrations in 50 morbidly obese patients (19 men and 31women) at baseline and 3, 6 and 12 months after gastric bypass. Results Body mass index (BMI), CRP, and sICAM-1 decreased significantly. BMI correlated with CRP but not with sICAM-1.ConclusionsThe improvement in vascular risk profile after weight loss in morbidly obese patients could be partially explained by changes in inflammatory status (AU)

Antecedentes y objetivos La obesidad se asocia a un desorden inflamatorio de bajo grado. Se ha propuesto una asociación causal entre inflamación y arteriosclerosis. El objetivo de este trabajo fue valorar el perfil inflamatorio en pacientes obesos mórbidos determinando las concentraciones de proteína C reactiva (PCR) y de moléculas solubles de adhesión intercelular tipo 1 (sICAM-1) antes y después de la pérdida de peso por cirugía bariátrica. Método Se realizó un estudio prospectivo en el que se midieron las concentraciones séricas de PCR y de sICAM-1 en 50 pacientes con obesidad mórbida (19 hombres y 31 mujeres) antes y a los 3, 6 y 12 meses de la realización de un by-pass gástrico. Resultados Se observó una disminución significativa de índice de masa corporal (IMC), PCR y sICAM-1. Se encontró correlación entre IMC y PCR, pero no entre IMC y sICAM-1.ConclusiónLa mejora del perfil de riesgo vascular en pacientes obesos tras la pérdida de peso podría atribuirse, en parte, a la mejora del estado inflamatorio (AU)

Tratamiento a largo plazo de un adenoma secretor de tirotropina con análogos de somatostatina / Long term treatment of a thyrotropin secreting adenoma with somatostatin analogues

Los tumores hipofisarios secretores de tirotropina (tirotropinomas) son menos del 1% de los adenomas hipofisarios y una causa rara de hipertiroidismo. La mayoría se diagnostica como macroadenoma, y los microadenomas son excepcionales. Debe hacerse el diagnóstico diferencial con la resistencia a las hormonas tiroideas. El tratamiento de elección es la adenomectomía transesfenoidal. Si fracasa, los análogos de somatostatina son una alternativa terapéutica. Presentamos a una paciente con un microadenoma productor de tirotropina en quien se practicó una adenomectomía transesfenoidal. Tras el fracaso de la cirugía, se inició tratamiento con un análogo de somatostatina. En laactualidad, después de 9 años, la paciente continúa el tratamiento y el hipertiroidismo y el crecimiento tumoral están controlados (AU)

Thyrotropin secreting adenomas (TSHomas)account for less than 1% of all pituitary adenomas and are a rare cause of hyperthyroidism. Most cases correspond to macroadenomas, microadenomas beingexceptional. Differential diagnosis should be made with resistance to thyroid hormones. The first line treatment is transphenoidal surgery. When surgery is unsuccessful, somatostatin analogues are a therapeutic alternative. We report a patient with a TSH-secreting microadenoma. The microadenoma was resected through the transsphenoidal route. Because surgery was unsuccessful, medical therapy with somatostatin analogue was initiated. Currently, 9 years later, the patient continues to be under treatment with somatostatin analogue therapy, which has controlled the hyperthyroidism and tumoral growth. We describe successful long-term treatment of a TSH-oma with somatostatin analogue therapy when surgery is unsuccessful (AU)

Long term treatment of a thyrotropin secreting adenoma with somatostatin analogues.

Thyrotropin secreting adenomas (TSH-omas) account for less than 1% of all pituitary adenomas and are a rare cause of hyperthyroidism. Most cases correspond to macroadenomas, microadenomas being exceptional. Differential diagnosis should be made with resistance to thyroid hormones. The first line treatment is transphenoidal surgery. When surgery is unsuccessful, somatostatin analogues are a therapeutic alternative. We report a patient with a TSH-secreting microadenoma. The microadenoma was resected through the transsphenoidal route. Because surgery was unsuccessful, medical therapy with somatostatin analogue was initiated. Currently, 9 years later, the patient continues to be under treatment with somatostatin analogue therapy, which has controlled the hyperthyroidism and tumoral growth. We describe successful long-term treatment of a TSH-oma with somatostatin analogue therapy when surgery is unsuccessful.