[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)

[Atorvastatin lowers C-reactive protein in dislipemic patients with type 2 diabetes mellitus]. / Descenso de proteína C reactiva tras tratamiento con atorvastatina en diabéticos tipo 2 con dislipemia.

BACKGROUND AND OBJECTIVE: Type 2 diabetes mellitus is associated with an augmented risk for cardiovascular disease. The levels of C-reactive protein (CRP), the prototypic marker of inflammation, are associated with an increased risk for cardiovascular events. The statins have direct anti-inflammatory effects. Thus, we tested the effects of atorvastatin on levels of CRP on patients with type 2 diabetes. PATIENTS AND METHOD: We evaluated CRP in baseline and 6 months after onset of 20 mg daily atorvastatin therapy of 30 patients with type 2 diabetes with hyperlipidemia. Clinical and biochemical data were obtained. RESULTS: CRP-levels were significantly decreased after treatment with atorvastatin compared with baseline (median change: -4,99 mg/l; p < 0.001). We observed an correlation between CRP baseline with body mass index (r = 0.429; p = 0.018), serum fibrinogen (r = 0.607; p = 0.001) and microalbuminuria (r = 0.470; p = 0.01). Conversely, there was no significant correlation between CRP baseline with LDL cholesterol. The CRP reduction was significantly correlated with fasting glucose (r = -0.457; p = 0.019) and glycosylated hemoglobin at 6 months (r = -0.421; p = 0.03). CONCLUSIONS: These results confirm findings from previous studies that atorvastatin reduce CRP levels in a largely LDL cholesterol independent manner.