RESUMEN
A 73-year-old woman with a history of squamous cell carcinoma of the lung was referred for a follow-up metastatic bone survey. Focal extraosseous accumulation of Tc-99m MDP was identified in the right, paraspinal region, along the radiation therapy port.
Asunto(s)
Carcinoma de Células Escamosas/diagnóstico por imagen , Neoplasias Pulmonares/diagnóstico por imagen , Mediastino/diagnóstico por imagen , Recurrencia Local de Neoplasia/diagnóstico por imagen , Radiofármacos , Medronato de Tecnecio Tc 99m , Anciano , Carcinoma de Células Escamosas/radioterapia , Femenino , Fibrosis , Estudios de Seguimiento , Humanos , Neoplasias Pulmonares/radioterapia , Neumonectomía , Cintigrafía , Radiofármacos/farmacocinética , Radioterapia/instrumentación , Medronato de Tecnecio Tc 99m/farmacocinéticaRESUMEN
Stress activates the hypothalamic-pituitary-adrenal axis through release of corticotropin releasing hormone (CRH), leading to production of glucocorticoids that down-regulate immune responses. Acute stress, however, also has proinflammatory effects that seem to be mediated through the activation of mast cells. Stress and mast cells have been implicated in the pathophysiology of various inflammatory conditions, including some in the central nervous system, such as multiple sclerosis in which disruption of the blood-brain barrier (BBB) precedes clinical symptoms. We previously showed that acute restraint stress increases rat BBB permeability to intravenous 99Tc gluceptate and that administration of the "mast cell stabilizer" disodium cromoglycate (cromolyn) inhibits this effect. In this study, we show that the CRH-receptor antagonist Antalarmin blocks stress-induced 99Tc extravasation, whereas site-specific injection of CRH in the paraventricular nucleus (PVN) of the hypothalamus mimics acute stress. This latter effect is blocked by pretreatment of the PVN with cromolyn; moreover, restraint stress cannot disrupt the BBB in the diencephalon and cerebellum of W/W(v) mast cell-deficient mice. These results demonstrate that CRH and mast cells are involved in regulating BBB permeability and, possibly, brain inflammatory disorders exacerbated by acute stress.