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Austin L Spitzer

Publications and source records attributed to Austin L Spitzer.

6 recordsLinked to original sources
PubMed2006

Statins attenuate sepsis.

HYPOTHESIS: If (1) 3-hydroxy-3-methylglutaryl-coenzyme reductase inhibitors (statins) block the rate-limiting step in cholesterol synthesis and promote the expression of low-density lipoprotein receptors, (2) "Gram-negative sepsis" results from an abundant systemic response to bacterial lipopolysaccharide (endotoxin), (3) triglyceride-rich lipoproteins can bind endotoxin and low-density lipoprotein receptors enhance the uptake of both of these molecules, and (4) low-density lipoprotein receptor internalization of lipoproteins and endotoxin co-opts a common transcriptional regulatory system (NF-kappaB) that results in reduced cell vulnerability to inflammation, then statins, in addition to their lipid-lowering capacity, enhance endotoxin clearance from the circulation and attenuate the septic response.

Cholesterol↗
PubMed2006

Applying Ockham's razor to pancreatitis prognostication: a four-variable predictive model.

OBJECTIVE: We sought to develop a simple yet accurate prognostic scoring system to determine the severity of acute pancreatitis at admission. SUMMARY BACKGROUND DATA: Because acute pancreatitis has a variable and frequently unpredictable course, identifying individuals at greatest risk for significant, life-threatening complications and stratifying their care appropriately remain a concern. Previous prognostic scoring systems predict severity reasonably well but are limited by time constraints, are unwieldy to use, or both. METHODS: Data from the international phase III trial of the platelet-activating factor receptor-antagonist Lexipafant were used to develop a 4-variable prognostic model. We then compared the model's ability to predict the severity of acute pancreatitis with the Ranson, Glasgow, and APACHE II systems. RESULTS: The model (BALI), which included BUN >or=25 mg/dL, Age >or=65 years, LDH >or=300 IU/L, and IL-6 >or=300 pg/mL, measured at admission, was similar to the Ranson, Glasgow, and APACHE II systems in its ability to identify increased mortality from acute pancreatitis. The receiver operating characteristic curve area for the BALI model was >or=0.82 +/- 0.03 (mean +/- SD) versus 0.75 +/- 0.04 (Ranson), 0.80 +/- 0.03 (Glasgow), and 0.79 +/- 0.03 (APACHE II). Furthermore, at a prevalence of 15%, the positive and negative predictive values for increased mortality were similar for all systems. CONCLUSION: The prognostic ability of the BALI 4-variable model was similar to the Ranson, Glasgow, and APACHE II systems but is unique in its simplicity and ability to accurately predict disease severity when used at admission or anytime during the first 48 hours of hospitalization.

APACHE↗
PubMed2005

Heat shock inhibits NF-kB activation in a dose- and time-dependent manner.

BACKGROUND: The heat shock response (HSR) attenuates NF-kappaB mediated activation of the acute inflammatory response by inhibiting IkB degradation. The HSR also confers a protective phenotype upon cells through production of heat shock proteins (HSP). However, the exact conditions that induce the HSR and stimulate the production of protective HSP are poorly defined. Consequently, we hypothesized that the inhibition of NF-kappaB activation through the HSR is dependent both on the degree of cellular injury and the length of the recovery period from the heat shock. METHODS: RAW 264.7 murine macrophages were heated to 43 degrees C for 15 (mild heat shock), 45 (moderate heat shock), or 90 min (severe heat shock), allowed to recover at 37 degrees C for 0 to 24 h, and then exposed to 100 ng/ml of Escherichia coli (055:B5) lipopolysaccharide (LPS). Cellular viability, HSP expression, and the activation of NF-kappaB after LPS exposure were determined by alamarBlue assay, immunoblot, and electrophoretic mobility shift assay, respectively. RESULTS: Transient attenuation of NF-kappaB activation and IkappaB preservation was observed only with moderate heat shock and 1 h of recovery. Mild heat shock had no effect on LPS-induced NF-kappaB activation or IkappaB degradation. Severe heat shock completely inhibited NF-kappaB activation and preserved IkappaB protein levels. Heat shock proteins were detectable 30 min after moderate heat shock, with maximal and sustained levels 2 to 24 h after heat shock. CONCLUSION: The attenuation of NF-kappaB activation after heat shock is both dose- and time-dependent.

Animals↗
PubMed2004

Anatomic classification system for surgical management of paraspinal tumors.

HYPOTHESIS: An anatomic classification system for paraspinal tumors that identifies complexity of regional anatomy, morbidity in complete or partial resection of anatomic structures, and potential complications may assist surgeons in preoperative planning. DESIGN: Application of a 6-level anatomic classification system for paraspinal tumors by retrospective medical record analysis. The classification system is defined by the following divisions of the vertebral column: I (C3-T3), II (T3-T10), III (T10-L2), IV (L1-L5, anterior to spine), V (L2-L5, lateral to spine), and VI (S1-S5). PATIENTS: All patients seen by us who underwent paraspinal tumor resection between 1997 and 2002. SETTING: Tertiary referral facility. MAIN OUTCOME MEASURES: Level-specific preoperative and surgical procedures and expected and unexpected vascular and neurologic morbidity caused by surgical intervention. RESULTS: Twenty-six patients met the inclusion criteria, and each of the levels (I through VI) of the classification system was represented by at least 2 patients. Expected morbidity that occurred because of surgical intervention included laryngeal paralysis in 1 patient with a level I tumor, femoral nerve palsy in 1 patient with a level V tumor, and neurogenic bladder and rectal dysfunction in 2 patients with level VI tumors. No unexpected neurologic deficit developed in any patient. Unanticipated intestinal ischemia and infarction occurred in 1 patient, who died after undergoing level IV surgery. Follow-up period ranged from 3 months to more than 5 years. CONCLUSION: Application of this 6-level anatomic classification system based on paraspinal tumor location may allow surgeons to anticipate specific surgical problems and to evaluate risks of resection and potential complications on the basis of regional anatomy.

Adult↗
PubMedDate not supplied

Early nonenhanced abdominal computed tomography can predict mortality in severe acute pancreatitis.

We wondered whether nonenhanced computed tomography (CT) within 48 hours of admission could identify individuals at risk for higher mortality from acute pancreatitis. Data from the international phase III study of the platelet-activating factor-inhibitor Lexipafant was used to analyze noncontrast CT versus acute pancreatitis mortality. Nonenhanced CT examinations of the abdomen from the trial were classified by disease severity (Balthazar grades A-E) and then correlated with patient survival. Among the 477 individuals who underwent CT within 48 hours of admission and 220 individuals who did so over the subsequent 6 days, higher CT grades were associated with increased mortality. Each unit increase in Balthazar grade during the initial 48 hours was associated with an estimated increase in the risk of mortality of 33%, and this trend increased to 50% if pancreatic enlargement and peripancreatic stranding (grades B and C) were combined (P<0.05). CT grade correlated minimally with Ranson, Glasgow, or APACHE II score during the initial 48 hours; however, this correlation improved over 3-8 days. Early nonenhanced abdominal CT in patients with acute pancreatitis is a valuable prognostic indicator of mortality in acute pancreatitis, even among patients without clinical features of severe acute pancreatitis.

APACHE↗