Epidural Steroid Injection-Induced Pancreatitis: A Case Report.

BACKGROUND Degenerative disc disease of the lumbar spine can be associated with spinal canal and neuroforaminal stenosis, resulting in severe pain. Conservative approaches to treatment are generally recommended initially, especially in the elderly. Epidural corticosteroid injections can provide significant but temporary pain relief and are a commonly performed procedure in pain management. Pancreatitis caused by corticosteroids is unusual and the prognosis typically is good. CASE REPORT A 73-year-old woman presented with severe intractable back pain 1 week after lumbar epidural steroid injection for symptomatic spinal stenosis. Imaging confirmed severe multi-level degenerative disc disease of the lumbar spine resulting in severe canal and bilateral neuroforaminal stenosis. Because of abdominal pain and nausea, an abdominal CT and labs were performed, revealing evidence of pancreatic inflammation. CONCLUSIONS Lumbar epidural steroid injection may be a risk factor for developing steroid-induced pancreatitis.

Sarcoidosis-Like Granulomatous Lymphadenopathy Mistaken for Neoplastic Disease on Positron Emission Tomography.

This is a rare case of sarcoidosis-like granulomatous lymphadenopathy that was initially mistaken for a neoplastic process due to the degree of hypermetabolic changes observed on positron emission tomography (PET) scan. Sarcoid-like granulomatous pulmonary disease is a disorder that has been described in WTC (World Trade Center) Rescue Workers, and also known as post 9/11 sarcoidosis. We present an interesting case of a man who presented with several months of progressive dyspnea and was later discovered to have significant bilateral hilar adenopathy, which was PET avid. Even more interesting, this patient's symptoms completely resolved without the use of systemic steroids or immune suppressants. This is a condition that requires awareness in order to avoid repeating unnecessary tests of performing interventions on a benign condition that may resolve on its own.

Preferential PPAR-α activation reduces neuroinflammation, and blocks neurodegeneration in vivo.

Neuroinflammation, immune reactivity and mitochondrial abnormalities are considered as causes and/or contributors to neuronal degeneration. Peroxisome proliferator-activated receptors (PPARs) regulate both inflammatory and multiple other pathways that are implicated in neurodegeneration. In the present study, we investigated the efficacy of fenofibrate (Tricor), a pan-PPAR agonist that activates PPAR-α as well as other PPARs. We administered fenofibrate to superoxide dismutase 1 (SOD1(G93A)) mice daily prior to any detectable phenotypes and then animal behavior, pathology and longevity were assessed. Treated animals showed a significant slowing of the progression of disease with weight loss attenuation, enhanced motor performance, delayed onset and survival extension. Histopathological analysis of the spinal cords showed that neuronal loss was significantly attenuated in fenofibrate-treated mice. Mitochondria were preserved as indicated by Cytochrome c immunostaining in the spinal cord, which maybe partly due to increased expression of the PPAR-γ co-activator 1-α. The total mRNA analysis revealed that neuroprotective and anti-inflammatory genes were elevated, while neuroinflammatory genes were down-regulated. This study demonstrates that the activation of PPAR-α action via fenofibrate leads to neuroprotection by both reducing neuroinflammation and protecting mitochondria, which leads to a significant increase in survival in SOD1(G93A) mice. Therefore, the development of therapeutic strategies to activate PPAR-α as well as other PPARs may lead to new therapeutic agents to slow or halt the progression of amyotrophic lateral sclerosis.