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Danville, PA, United States

Kanner A.M.,University of Illinois at Chicago | Barry J.J.,Stanford University | Gilliam F.,Geisinger Clinic | Hermann B.,University of Wisconsin - Madison | Meador K.J.,Emory University
Epilepsia | Year: 2012

Purpose: To compare the effect of anxiety disorders, major depressive episodes (MDEs), and subsyndromic depressive episodes (SSDEs) on antiepileptic drug (AED)-related adverse events (AEs) in persons with epilepsy (PWE). Methods: The study included 188 consecutive PWE from five U.S. outpatient epilepsy clinics, all of whom underwent structured interviews (SCID) to identify current and past mood disorders and other current Axis I psychiatric diagnoses according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) criteria. A diagnosis of SSDE was made in patients with total Beck Depression Inventory-II (BDI-II) scores >12 or the Centers of Epidemiologic Studies-Depression (CES-D) > 16 (in the absence of any DSM diagnosis of mood disorder. The presence and severity of AEs was measured with the Adverse Event Profile (AEP). Key Findings: Compared to asymptomatic patients (n=103), the AEP scores of patients with SSDE (n=26), MDE only (n=10), anxiety disorders only (n=21), or mixed MDE/anxiety disorders (n=28) were significantly higher, suggesting more severe AED-related AEs. Univariate analyses revealed that having persistent seizures in the last 6months and taking antidepressants was associated with more severe AEs. Post hoc analyses, however, showed that these differences were accounted for by the presence of a depressive and/or anxiety disorders. Significance: Depressive and anxiety disorders worsen AED-related AEs even when presenting as a subsyndromic type. These data suggest that the presence of psychiatric comorbidities must be considered in their interpretation, both in clinical practice and AED drug trials. Wiley Periodicals, Inc. © 2012 International League Against Epilepsy. Source

Benotti P.,Geisinger Obesity Research Institute | Wood G.C.,Geisinger Obesity Research Institute | Winegar D.A.,Surgical Review Corporation | Petrick A.T.,Geisinger Clinic | And 3 more authors.
Annals of Surgery | Year: 2014

OBJECTIVE: We sought to identify the major risk factors associated with mortality in Roux-en-Y gastric bypass (RYGB) surgery. BACKGROUND: Bariatric surgery has become an established treatment for extreme obesity. Bariatric surgery mortality has steadily declined with current rates of less than 0.5%. However, significant variation in the mortality rates has been reported for specific patient cohorts and among bariatric centers. METHODS: Clinical outcome data from 185,315 bariatric surgery patients from the Bariatric Outcome Longitudinal Database were reviewed. Of these, 157,559 patients had either documented 30 or more day follow-up data, including mortality. Multiple demographic, socioeconomic, and clinical factors were analyzed by univariate analysis for their association with 30-day mortality after gastric bypass. Variables found to be significant were entered into a multiple logistic regression model to identify factors independently associated with 30-day mortality. On the basis of these results, a RYGB mortality risk score was developed. RESULTS: The overall 30-day mortality rate for the entire bariatric surgery cohort was 0.1%. Of the 81,751 RYGB patients, the mortality rate was 0.15%. Factors significantly associated with 30-day gastric bypass mortality included increasing body mass index (BMI) (P < 0.0001), increasing age (P < 0.005), male gender (P < 0.001), pulmonary hypertension (P < 0.0001), congestive heart failure (P = 0.0008), and liver disease (P = 0.038). When the RYGB risk score was applied, a significant trend (P < 0.0001) between increasing risk score and mortality rate is found. CONCLUSIONS: Increasing BMI, increasing age, male gender, pulmonary hypertension, congestive heart failure, and liver disease are risk factors for 30-day mortality after RYGB. The RYGB risk score can be used to determine patients at greater risk for mortality after RYGB surgery. Copyright © 2013 by Lippincott Williams & Wilkins. Source

Faxon D.P.,Brigham and Womens Hospital | Eikelboom J.W.,Hamilton Health Sciences | Berger P.B.,Geisinger Clinic | Holmes Jr. D.R.,Mayo Medical School | And 4 more authors.
Circulation: Cardiovascular Interventions | Year: 2011

The optimal regimen of the anticoagulant and antiplatelet therapies in patients with atrial fibrillation who have had a coronary stent is unclear. It is well recognized that "triple therapy" with aspirin, clopidogrel, and warfarin is associated with an increased risk of bleeding. National guidelines have not made specific recommendations, given the lack of adequate data. In choosing the best antithrombotic options for a patient, consideration needs to be given to the risks of stroke, stent thrombosis, and major bleeding. This executive summary describes these risks, provides specific recommendations concerning vascular access, stent choice, concomitant use of proton pump inhibitors, and the use and duration of triple therapy after stent placement, based on the risk assessment. © 2011 American Heart Association, Inc. Source

Alahmadi H.,University of Toronto | Dehdashti A.R.,Geisinger Clinic | Gentili F.,University of Toronto
World Neurosurgery | Year: 2012

Background: Despite the increasing interest in endoscopic techniques for pituitary surgery, little has been published on the endoscopic approach for recurrent and/or residual pituitary adenomas. We report the outcome of purely endoscopic endonasal surgery for a series of recurrent and/or residual pituitary tumors after a previous microscopic resection. Methods: We reviewed all of the patients in our institution who underwent endoscopic resection for recurrent and/or residual pituitary tumors after previous microscopic resection. All patients had clinical and magnetic resonance imaging follow-up of at least 3 months postoperatively. Careful attention was given to the operative reports documenting the degree of previous microscopic exposure. Our results were compared with published reports of surgery for recurrent and residual pituitary tumors. Results: Thirty-nine patients met our inclusion criteria. The mean follow-up was 21 months. Tumors were comprised of 19 nonfunctional, 10 adrenocorticotropic hormone, 9 growth hormone, and 1 prolactin-secreting adenoma. The endoscopic procedure revealed limited previous exposure of the sphenoidal and sellar structures in 30 cases (76%). Sphenoidotomy and sellar opening, in terms of working area and angle of view, were significantly restricted in 64% and 61% of the cases, respectively. Gross total removal was achieved in 46% of cases. Seventeen patients had frank cavernous sinus invasion. Conclusions: The restricted exposure of sphenoidal and sellar structures by the microscopic approach may be a contributing factor to incomplete tumor resection. The results observed in this setting make the endoscopic technique a valid option in recurrent and residual pituitary adenomas treated initially by microscopic surgery. © 2012 Elsevier Inc. All rights reserved. Source

Bieniek J.,Geisinger Clinic | Childress C.,00 N Academy | Swatski M.D.,00 N Academy | Yang W.,00 N Academy
Prostate | Year: 2014

BACKGROUND Previous studies have shown that COX-2 inhibitors inhibit cancer cell proliferation. However, the molecular mechanism remains elusive. METHODS Prostate cancer LNCaP, 22Rv1, and PC3 cells were cultured and treated with the COX-2 inhibitors celecoxib and CAY10404. Knockdown of COX-2 in LNCaP cells was carried out using lentiviral vector-loaded COX-2 shRNA. Cell cycle progression and cell proliferation were analyzed by flow cytometry, microscopy, cell counting, and the MTT assay. The antagonists of EP1, EP2, EP3, and EP4 were used to examine the effects of the PGE2 signaling. The effect of COX-2 inhibitors and COX-2 knockdown on expression of the kinetochore/centromere genes and proteins was determined by RT-PCR and immunoblotting. RESULTS Treatment with the COX-2 inhibitors celecoxib and CAY10404 or knockdown of COX-2 significantly inhibited prostate cancer cell proliferation. Flow-cytometric analysis and immunofluorescent staining confirmed the cell cycle arrested at the G2/M phase. Biochemical analysis showed that inhibition of COX-2 or suppression of COX-2 expression induced a dramatic down-regulation of key proteins in the kinetochore/centromere assembly, such as ZWINT, Cdc20, Ndc80, CENP-A, Bub1, and Plk1. Furthermore, the EP1 receptor antagonist SC51322, but not the EP2, EP3, and EP4 receptor antagonists, produced similar effects to the COX-2 inhibitors on cell proliferation and down-regulation of kinetochore/centromere proteins, suggesting that the effect of the COX-2 inhibition is through inactivation of the EP1 receptor signaling. CONCLUSIONS Our studies indicate that inhibition of COX-2 can arrest prostate cancer cell cycle progression through inactivation of the EP1 receptor signaling and down-regulation of kinetochore/centromere proteins. Prostate 74:999-1011, 2014. © 2014 Wiley Periodicals, Inc. Source

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