RESUMO
A 58-year-old woman with acromegaly developed massive epistaxis 7 days following trans-sphenoidal resection of a growth hormone-secreting pituitary adenoma. At autopsy, it was determined that the source of the hemorrhage was a rupture of the intracavernous segment of the internal carotid artery secondary to a bacterial arteritis. We describe the gross dissection and histologic examination undertaken in this unusual case, discuss the possible etiology of the infection and review the potential complications of this surgical approach with a view to improving forensic examination of these patients.
Assuntos
Adenoma/cirurgia , Arterite/etiologia , Artéria Carótida Interna/cirurgia , Epistaxe/etiologia , Adenoma Hipofisário Secretor de Hormônio do Crescimento/cirurgia , Procedimentos Neurocirúrgicos/efeitos adversos , Hemorragia Pós-Operatória/etiologia , Adenoma/patologia , Arterite/microbiologia , Autopsia , Artéria Carótida Interna/microbiologia , Artéria Carótida Interna/patologia , Evolução Fatal , Feminino , Adenoma Hipofisário Secretor de Hormônio do Crescimento/patologia , Parada Cardíaca/etiologia , Humanos , Pessoa de Meia-Idade , Invasividade Neoplásica , Ruptura Espontânea , Resultado do TratamentoRESUMO
Carbon-13 nuclear magnetic resonance (NMR) spectroscopy was employed to investigate alterations in hepatic carbohydrate metabolism in Meriones unguiculatus infected with Echinococcus multilocularis. Following portal vein injections of an equimolar mixture of [1,2-13C2]acetate and [3-13C]lactate, perchloric acid extracts of the livers were prepared and NMR spectra obtained. Isotopomer analysis using glutamate resonances in these spectra showed that the relative contributions of endogenous and exogenous substrates to the acetyl-CoA entering the tricarboxylic acid cycle differed significantly between infected and control groups. The mole fraction of acetyl-CoA that was derived from endogenous, unlabelled sources (F(U)) was 0.50 +/- 0.10 in controls compared to 0.34 +/- 0.04 in infected animals. However, the fraction of acetyl-CoA derived from [3-13C]lactate (FLL) was larger in livers of infected animals than those from controls with values of 0.27 +/- 0.04 and 0.18 +/- 0.04, respectively. Similarly, the fraction of acetyl-CoA derived from [1,2-13C2]acetate (FLA) was larger in livers of infected animals compared to those in controls; the fractions were 0.38 +/- 0.01 and 0.32 +/- 0.07, respectively. The ratio of FLA:FLL was significantly smaller in the infected group with a value of 1.42 +/- 0.18 compared to 1.74 +/- 0.09 for the controls. These results indicate that alveolar hydatid disease has a pronounced effect on the partitioning of substrates within the pathways of carbohydrate metabolism in the host liver.
