ABSTRACT
El diagnostico precoz de la enfermedad metastásica vertebral es importante, porque la evolución clínica depende de la situación neurológica en el momento del diagnóstico. La metástasis epidural del sarcoma de Ewing en la médula espinal es poco común. A pesar de que se ha descrito en pocos casos de sarcoma de Ewing primario extraesquelético, la afectación epidural es extraordinariamente rara. Incluso es más rara la afectación metastásica epidural secundaria a sarcoma de Ewing. Con el rápido incremento en la utilización y la aceptación de la PET/TC en oncología, la técnica está desempeñando un papel creciente en la detección de metástasis en localizaciones anatómicas inesperadas. A la luz de nuestro conocimiento, este trabajo presenta la primera descripción de los hallazgos de la PET/TC en esta entidad clínica extremadamente rara(AU)
Early diagnosis of metastatic spinal disease is important because functional outcome depends on neurologic condition at the time of diagnosis. Epidural metastasis to the spine from Ewing's sarcoma is very uncommon. Despite the fact that epidural involvement has been described in a few cases of primary extraskeletal Ewing's sarcoma, it is considerably rare. Metastatic epidural involvement secondary to Ewing's sarcoma is even rarer. With the rapid increase in the utilization and acceptance of PET/CT imaging in oncological practice, it is playing an ever-increasing role in detecting malignant spread to several unexpected sites. This report is, to the best of our knowledge, the first description of the PET/CT findings of this extremely rare entity(AU)
Subject(s)
Humans , Male , Child , Epidural Neoplasms/diagnosis , Nuclear Medicine/trends , Sarcoma, Ewing/diagnosis , Sarcoma, Ewing/radiotherapy , Sarcoma, Ewing , Positron-Emission Tomography/methods , Positron-Emission Tomography , Early Diagnosis , Nuclear Medicine/methodsABSTRACT
We measured beta-endorphin concentrations in the anterior and neurointermediate lobes of the pituitary gland and in microdissected brain regions of moderate-seizure genetically epilepsy-prone rats (GEPR-3), severe-seizure GEPR-9s and Sprague-Dawley non-epileptic control rats. Plasma concentrations of beta-endorphin and beta-melanocyte-stimulating hormone (alpha-MSH) were also measured as indicators of pituitary POMC-peptide secretion. Concentrations of beta-endorphin in the anterior lobe of GEPR-3s were 53% higher compared to controls and 57% higher compared to GEPR-9s. There were no differences in neurointermediate lobe beta-endorphin concentrations between control and either GEPR strain. Plasma beta-endorphin concentrations were significantly lower in GEPR-9s than controls. Plasma levels of alpha-MSH did not differ between control and GEPRs. In the hypothalamus of GEPR-9s beta-endorphin concentrations in the arcuate nucleus were significantly greater than in GEPR-3s. Concentrations of beta-endorphin in the central amygdala of GEPR-9s were two- to threefold greater than in control or GEPR-3s. Beta-Endorphin concentrations in the central gray of GEPR-3s were 58% lower than control or GEPR-9s. These data suggest that anterior lobe beta-endorphin secretion is reduced in GEPR-9s. Furthermore, brain endorphinergic pathways appear to be differentially altered in GEPR-3s and GEPR-9s. Alterations in pituitary beta-endorphin secretion and brain endorphinergic systems may contribute to seizure susceptibility in GEPRs and to differences in seizure severity between GEPR-3s and GEPR-9s.
Subject(s)
Brain Chemistry , Epilepsy/genetics , Pituitary Gland, Anterior/chemistry , Pituitary Gland/chemistry , beta-Endorphin/analysis , Animals , Epilepsy/metabolism , Radioimmunoassay , Rats , Rats, Sprague-Dawley , alpha-MSH/blood , beta-Endorphin/bloodABSTRACT
[125I]beta-endorphin bound to high affinity (Kd = 0.25 nM) receptors in the caudal dorsomedial medulla of rats with a Bmax of 97 fmol/mg protein. The relative potency for displacement of [125I]beta-endorphin binding was: beta-endorphin(1-31) > beta-endorphin(1-27) > DAMGO > naloxone > N-acetyl-beta-endorphin(1-31) > U50488 > DPDPE. The Bmax for [3H]DAMGO binding was 81 fmol/mg protein, indicating that most [125I]beta-endorphin binding corresponds to mu-opioid receptors. [3H]DAMGO binding was not influenced by lesioning noradrenergic nerve terminals in the caudal dorsomedial medulla. Our findings indicate that beta-endorphin interacts primarily with mu-opioid receptors in the caudal dorsomedial medulla. These receptors are not affected by noradrenergic denervation.
