Symptomatic spinal epidural lipomatosis with severe obesity at a young age.

Symptomatic spinal epidural lipomatosis is a rare disorder characterized by overgrowth of fat in the extradural space. Most patients have an underlying endocrine disorder, such as Cushing's syndrome, or have taken exogenous steroids chronically. Although less common, obesity alone is thought to be a cause of spinal epidural lipomatosis, representing <25% of reported cases. Patients rarely become symptomatic before middle age without chronic exogenous steroid use. The usual clinical manifestations are similar to degenerative lumbar stenosis with neurogenic claudication, resulting in decreased walking and standing endurance with variable neurological deficits.This article describes 2 unique cases of spinal epidural lipomatosis, both in young patients with underlying morbid obesity who presented with acute progressive leg weakness and urinary retention. The patients had no underlying endocrinopathy, nor any history of exogenous steroid use. They underwent emergency laminectomy and removal of epidural fat, and histopathological examination confirmed the diagnosis of epidural lipomatosis. Postoperatively, the patients demonstrated significant improvement.We conducted a review of the available English literature and compared the age distribution in each group. Based on our review, our 2 patients are considerably younger than those in past reports, especially in the patient group to which the steroid was not administered. In addition, few cases exist of spinal epidural lipomatosis with acute sphincter dysfunction and paraparesis. Our cases suggest that morbid obesity can lead to juvenile spinal epidural lipomatosis with acute neurological changes.

Fetal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin induces expression of the chemokine genes Cxcl4 and Cxcl7 in the perinatal mouse brain.

Fetal exposure to dioxins affects brain development and influences behaviors in human and laboratory animals. However, the cellular target and mechanisms of the neurotoxic action of dioxins are largely unknown. To investigate the molecular basis for the neurotoxicity of dioxins, pregnant C57BL/6 mice were exposed to 5 µg kg(-1) body weight of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) by a single gavage on gestational day 12.5 (GD 12.5), and gene expression of the whole fetal brain at GD 18.5 was profiled by DNA microarray analysis. The analysis revealed that the expression of two chemokine genes, Cxcl4 and Cxcl7, was up-regulated by TCDD exposure. Real-time PCR analysis verified that they were up-regulated by TCDD in both male and female brains, while the mRNA levels of a majority of other chemokines and their receptor genes were not affected. The up-regulation was TCDD dose-dependent and peaked at GD 15.5-18.5. In situ hybridization analysis showed that the Cxcl4 mRNA expression was localized in part of the surface of cerebral cortex and that the level was increased by TCDD treatment. These results suggest that Cxcl4 and Cxcl7 play a role in the development of neurobehavioral alterations that are triggered by in utero TCDD exposure and later surface in adults.