RESUMO
Meningiomas are slow growing, typically benign, tumors originating from arachnoid cap cells. Specifically, sphenoid wing or spheno-orbital meningiomas infiltrate the lesser wing of the sphenoid, lateral orbital wall, and orbital roof with occasional extension to the superior orbital fissure, optic canal, anterior clinoid process, and middle cranial fossa where neurologic and ophthalmologic functions are impaired by compressive injury. The extraocular muscles are rarely involved. The authors present a rare case of an spheno-orbital meningioma causing extraocular muscle enlargement mimicking idiopathic orbital inflammation and highlight important diagnostic clues to meningioma.
Assuntos
Inflamação/diagnóstico , Meningioma/diagnóstico , Músculos Oculomotores/patologia , Doenças Orbitárias/diagnóstico , Neoplasias Cranianas/diagnóstico , Osso Esfenoide , Biópsia , Craniotomia , Diagnóstico Diferencial , Feminino , Humanos , Imageamento por Ressonância Magnética , Meningioma/cirurgia , Pessoa de Meia-Idade , Invasividade Neoplásica , Neoplasias Cranianas/cirurgiaRESUMO
Previously, we reported that murine gammaherpesvirus-68 (M1-MHV-68) induces pulmonary artery (PA) neointimal lesions in S100A4-overexpressing, but not in wild-type (C57), mice. Lesions were associated with heightened lung elastase activity and PA elastin degradation. We now investigate a direct relationship between elastase and PA neointimal lesions, the nature and source of the enzyme, and its presence in clinical disease. We found an association exists between the percentage of PAs with neointimal lesions and elastin fragmentation in S100A4 mice 6 months after viral infection. Confocal microscopy documented the heightened susceptibility of S100A4 versus C57 PA elastin to degradation by elastase. A transient increase in lung elastase activity occurs in S100A4 mice, 7 days after M1-MHV-68, unrelated to inflammation or viral load and before neointimal lesions. Administration of recombinant elafin, an elastase-specific inhibitor, ameliorates early increases in serine elastase and attenuates later development of neointimal lesions. Neutrophils are the source of elevated elastase (NE) in the S100A4 lung, and NE mRNA and protein levels are greater in PA smooth muscle cells (SMC) from S100A4 mice than from C57 mice. Furthermore, elevated NE is observed in cultured PA SMC from idiopathic PA hypertension versus that in control lungs and localizes to neointimal lesions. Thus, PA SMC produce NE, and heightened production and activity of NE is linked to experimental and clinical pulmonary vascular disease.
