RESUMEN
INTRODUCTION: Hormonal and metabolic factors related to pregnancy itself are considered to increase the likelihood of seizure recurrence. If so, we should expect a similar evolution of epilepsy in a subsequent pregnancy. We investigated differences in evolution of non-gestational epilepsy in each pregnancy of women suffering from epilepsy. METHODS: A prospective study was conducted in order to compare seizure frequency in two successive pregnancies of more than 36 weeks duration in 12 patients. Improvement/worsening is defined as a change of +/- 50 % in the number of seizures regarding that which occurred within the previous eleven months. RESULTS: Twelve epileptic women were studied during two subsequent pregnancies. Eight of them took the same antiepileptic treatment for both pregnancies and one took no antiepileptic drug. Three worsened in the first pregnancy and two in the second. Seven patients had the same seizure frequency during both pregnancies. The total plasma antiepileptic concentrations tended to decline with the same proportion in both pregnancies if the dose remained unchanged. We observed no differences in mean hormone plasma concentrations for each quarter, within subsequent pregnancies. CONCLUSION: Except for one case with drug-resistant epilepsy, we found that the reason for the discrepancy in the frequency of the seizure between two successive pregnancies in the same patient was a sharp or rapid change in antiepileptic drug dose or non-compliance. In well controlled epileptic women a consistent evolution of epilepsy should be expected in a subsequent pregnancy, if adequate treatment is maintained.
Asunto(s)
Epilepsia/epidemiología , Número de Embarazos , Complicaciones del Embarazo , Adulto , Anticonvulsivantes/uso terapéutico , Epilepsia/clasificación , Epilepsia/tratamiento farmacológico , Femenino , Humanos , Incidencia , Embarazo , Estudios ProspectivosRESUMEN
The article summarizes the endocrinology axis in relation to leptin in the obesity. There is a glucocorticoid hypothesis in the obesity origin. Human plasma leptin levels are elevated in Cushing's syndrome and there is a robust leptin secretory responses to dexamethasone. Obesity impacts on reproductive function in man and women. Leptin levels are higher in women than in men and a critical blood leptin level is necessary to trigger reproductive ability in women. The relationship between body mass index and circulating leptin varies during the course of spontaneous cycles in women, the best correlation occurring during the luteal phase when progesterone and leptin concentrations are highest. Obesity is associated with a decrease in growth hormone (GH) and reversible with weight loss. The influence of body composition on GH secretion in the obesity may be mediated through leptin, acting as a peripheral signal from adipose tissue. Thyroid dysfunction appear not associated with alterations in serum leptin levels. There is a significant relationship between insulin and leptin, but it is not immediate, since type 2 diabetics show similar leptin levels to those of nondiabetic humans of the same body mass index.
Asunto(s)
Leptina/fisiología , Obesidad/fisiopatología , Adulto , Animales , Índice de Masa Corporal , Síndrome de Cushing/sangre , Diabetes Mellitus Tipo 1/sangre , Diabetes Mellitus Tipo 2/sangre , Femenino , Hormona de Crecimiento Humana/sangre , Humanos , Hiperinsulinismo/fisiopatología , Hipertensión/sangre , Sistema Hipotálamo-Hipofisario/fisiología , Insulina/sangre , Leptina/sangre , Leptina/metabolismo , Masculino , Ciclo Menstrual/fisiología , Ratones , Ratones Obesos , Persona de Mediana Edad , Obesidad/sangre , Obesidad/etiología , Sistema Hipófiso-Suprarrenal/fisiología , Progesterona/sangre , Ratas , Reproducción/fisiología , Factores SexualesRESUMEN
El artículo revisa los diferentes ejes endocrinológicos en relación con los niveles plasmáticos de leptina del paciente obeso. Existe una hipótesis glucocorticoidea como causa de obesidad. Los niveles plasmáticos en humanos de leptina están elevados en el síndrome de Cushing y hay una respuesta secretora franca de leptina a la dexametasona. La obesidad altera la función reproductora tanto en el hombre como en la mujer. Los niveles de leptina son mayores en la mujer que en el hombre y se requiere un nivel crítico de leptina en plasma para desarrollar la capacidad reproductora femenina. La interrelación entre el índice de masa corporal y los niveles circulantes de leptina varían en el curso de los ciclos ováricos, la mejor correlación aparece en la fase luteal, cuando los niveles de leptina y progesterona están mas altos. La obesidad se asocia a disminución de los niveles plasmáticos de GH, situación que revierte con la pérdida de peso. La infuliencia de la composición corporal sobre la secreción de GH en la obesidad puede estar relacionada con la leptina, que acutaría como una señal periférica del tejido adiposo. La disfución tiroidea no parece producir alteraciones en los niveles de leptina. Existe una interrelación significativa entre los niveles de insulina y leptina, pero ésta no está clara ya que en el paciente con diabetes tipo 2 encontramos niveles similares de leptina a los de los controles con similar indice de masa corporal (AU)