RESUMEN
Cerebral reperfusion following carotid endarterectomy occasionally causes cerebral hyperperfusion syndrome. This is a rare but important complication and this case report acted as a stimulus for a literature review of this problem. A 60-year-old businessman had a right carotid endarterectomy for a severe stenosis which had caused recurrent attacks of amaurosis fugax. The left internal carotid artery had occluded asymptomatically. The operation and his immediate postoperative recovery were entirely uneventful but he developed right-sided headaches and focal sensory motor seizures. He subsequently recovered. Hemodynamically compromised patients appear to be at greater risk and as the mortality of the operation is reduced and more complex patients are treated, it is likely that this unusual complication will increase in incidence.
Asunto(s)
Circulación Cerebrovascular/fisiología , Endarterectomía Carotidea/efectos adversos , Homeostasis , Encéfalo/irrigación sanguínea , Epilepsia Parcial Sensorial/etiología , Cefalea/etiología , Humanos , Masculino , Persona de Mediana Edad , Flujo Sanguíneo Regional , SíndromeRESUMEN
Links between a low vitamin D status and an increased risk of breast cancer have been observed in epidemiological studies. These links have been investigated in human tissue homogenates and cultured cell lines. We have used non-malignant, malignant and normal reduction mammoplasty breast tissues to investigate the biological and metabolic consequences of the application of vitamin D to intact ex vivo human breast tissue. Tissues were exposed to 1α,25(OH)(2)D(3) (1,25D; active metabolite) and 25(OH)D (25D; pre-metabolite). Changes in mRNA expression and protein expression after vitamin D exposure were analysed. Results indicate that while responses in normal and non-malignant breast tissues are similar between individuals, different tumour tissues are highly variable with regards to their gene expression and biological response. Collectively, malignant breast tissue responds well to active 1,25D, but not to the inactive pre-metabolite 25D. This may have consequences for the recommendation of vitamin D supplementation in breast cancer patients.