Dyslipidemias and hypothyroidism.

BACKGROUND: Abnormalities in plasma lipids are most frequently the result of the interaction between the individual and the environment; therefore, it is essential to look for secondary causes in all patients with dyslipidemia. AIM: To describe the pathogenesis of dyslipidemia and in particular the role of hypothyroidism as a secondary dyslipidemia. MAIN DATA: Overt hypothyroidism (OH) is associated to impairment of the lipid profile both quantitatively and qualitatively. Subclinical hypothyroidism (5CH) has been also related to lipid derangement albeit with milder impact. Moreover, the association between low thyroid function and lipid plasma levels has been also found to extend into the normal range of TSH. However, confounders such as age, gender and body weight may modify this association. The effects of treatment with levothyroxine for cholesterol reduction are warranted in OH while in SCH, larger interventional studies on lipid reduction with levothyroxine are lacking. CONCLUSION: Hypothyroidism should always be considered in the evaluation of patients with dyslipidemia.

Assessment of left ventricular diastolic function by radionuclide ventriculography at rest and exercise in subclinical hypothyroidism, and its response to L-thyroxine therapy.

Hypothyroidism is associated with intrinsic myocardial changes reflected by alterations in contractility and relaxation. Diastolic function, however, rather than systolic cardiac function, seems to be mostly impaired by thyroid hormone deprivation. Our aim was to evaluate diastolic function at rest and during maximal exercise by means of radionuclide ventriculography in subclinical hypothyroidism before and after restoration of euthyroidism. Ten subclinical hypothyroid patients (50 +/- 8.7 years) (thyroid-stimulating hormone 11 +/- 4.2 microUI/ml) without cardiac disease were studied before and 6 months after levothyroxine (L-T(4)) replacement (thyroid-stimulating hormone 1.9 +/- 1.1 microUI/ml). We compared the basal and post-therapy cardiac parameters with a control group of 14 euthyroid patients (52.5 +/- 10 years) (thyroid-stimulating hormone 2.5 +/- 1.2 microUI/ml). Multigated equilibrium radionuclide ventriculography was performed to assess systolic and diastolic ventricular function. Student's t and paired Student's t tests were applied for statistical analysis. We found a significant difference between the time to peak filling rate (TPFR) at rest before (0.241 +/- 0.002 ms) and after (0.190 +/- 0.012 ms) treatment with L-T(4). A significant difference that disappeared after restoration of euthyroidism was also observed between the basal TPFR values of the subclinical hypothyroid patients and the control group (0.189 +/- 0.01 ms). The same pattern was observed at maximal exercise. Thus, TPFR, a parameter of left ventricular (LV) diastolic function measured by radionuclide ventriculography, is impaired in subclinical hypothyroid patients both at rest and during exercise and returns to normal values after L-T(4) therapy.

Dislipidemia postprandial en diabetes tipo 2 / Postprandial dyslipidemia in type 2 diabetes

La magnitud de la prevalencia y la inusal progresión de la enfermedad ateroesclerótica propias de la diabetes tipo 2 se relacionan, al menos en parte, con alteraciones lipídicas frecuentemente coexistentes. En las dos últimas décadas se han reportado numerosos datos que asignan un rol clave al metabolismo postabsortivo de ciertas lipoproteinas y también en procesos vinculados a la disfunción endotelial. A pesar de la correlación encontrada entre hiperlipidemia de ayunas e hiperlipidemia postprandial, hay hallazgos recientes que avalan la existencia de disfunción vascular temprana en personas con diabetes con anormalidades lipídicas exclusivamente postprandiales. Todo esto sugiere que las posibilidades de intervención médica sobre la dislipidemia asociada con diabetes mellitus tipo 2 probablemente no se agotan con la evaluación del paciente en estado de ayunas, de forma análoga a la importancia de la hiperglucemia postprandial en la aparición y evolución de la macrovasculopatía diabética. En esta revisión se describen los principales procesos postabsortivos postulados como generadores de los trastornos lipídicos en la población de personas con diabetes tipo 2, y el posible impacto de las lipoproteínas en el estado postprandial como factores co-mórbidos en los procesos aterogénicos. Intencionalmente se analizan por separado la fisiopatología de las lipoproteínas ricas en triglicéridos y HDL, y luego las que transportan fundamentalmente colesterol, asumiendo la estrecha interrelación que en realidad existe entre ambas. Posteriormente se describe el papel crucial de la insulinorresistencia en los cambios lipídicos postabsortivos y cómo éstos, a su vez, pueden propiciar y perpetuar los defectos de la acción insulínica en los tejidos blanco. Finalmente, se enumeran posibles efectos patogénicos del estado postprandial sobre la función endotelial en el paciente con diabetes