Browsing by Author "Pitt, Henry A."

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    Adipocytes enhance murine pancreatic cancer growth via a hepatocyte growth factor (HGF)-mediated mechanism
    (Elsevier, 2016-04) Ziegler, Kathryn M.; Considine, Robert V.; True, Eben; Swartz-Basile, Deborah A.; Pitt, Henry A.; Zyromski, Nicholas J.; Department of Surgery, IU School of Medicine
    INTRODUCTION: Obesity accelerates the development and progression of pancreatic cancer, though the mechanisms underlying this association are unclear. Adipocytes are biologically active, producing factors such as hepatocyte growth factor (HGF) that may influence tumor progression. We therefore sought to test the hypothesis that adipocyte-secreted factors including HGF accelerate pancreatic cancer cell proliferation. MATERIAL AND METHODS: Murine pancreatic cancer cells (Pan02 and TGP-47) were grown in a) conditioned medium (CM) from murine F442A preadipocytes, b) HGF-knockdown preadipocyte CM, c) recombinant murine HGF at increasing doses, and d) CM plus HGF-receptor (c-met) inhibitor. Cell proliferation was measured using the MTT assay. ANOVA and t-test were applied; p < 0.05 considered significant. RESULTS: Wild-type preadipocyte CM accelerated Pan02 and TGP-47 cell proliferation relative to control (59 ± 12% and 34 ± 12%, p < 0.01, respectively). Knockdown of preadipocyte HGF resulted in attenuated proliferation vs. wild type CM in Pan02 cells (35 ± 5% vs. 68 ± 14% greater than control; p < 0.05), but proliferation in TGP-47 cells remained unchanged. Recombinant HGF dose-dependently increased Pan02, but not TGP-47, proliferation (p < 0.05). Inhibition of HGF receptor, c-met, resulted in attenuated proliferation versus control in Pan02 cells, but not TGP-47 cells. CONCLUSIONS: These experiments demonstrate that adipocyte-derived factors accelerate murine pancreatic cancer proliferation. In the case of Pan02 cells, HGF is responsible, in part, for this proliferation.
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    Is American College of Surgeons NSQIP organ space infection a surrogate for pancreatic fistula?
    (Elsevier, 2014-12) Parikh, Janak Atul; Beane, Joal D.; Kilbane, E. Molly; Milgrom, Daniel P.; Pitt, Henry A.; Department of Surgery, IU School of Medicine
    BACKGROUND: In the American College of Surgeons National Surgical Quality Improvement Program (ACS NSQIP), pancreatic fistula has not been monitored, although organ space infection (OSI) data are collected. Therefore, the purpose of this analysis was to determine the relationship between ACS NSQIP organ space infection and pancreatic fistulas. STUDY DESIGN: From 2007 to 2011, 976 pancreatic resection patients were monitored via ACS NSQIP at our institution. From this database, 250 patients were randomly chosen for further analysis. Four patients were excluded because they underwent total pancreatectomy. Data on OSI were gathered prospectively. Data on pancreatic fistulas and other intra-abdominal complications were determined retrospectively. RESULTS: Organ space infections (OSIs) were documented in 22 patients (8.9%). Grades B (n = 26) and C (n = 5) pancreatic fistulas occurred in 31 patients (12.4%); grade A fistulas were observed in 38 patients (15.2%). Bile leaks and gastrointestinal (GI) anastomotic leaks each developed in 5 (2.0%) patients. Only 17 of 31 grade B and C pancreatic fistulas (55%), and none of 38 grade A fistulas were classified as OSIs in ACS NSQIP. In addition, only 2 of 5 bile leaks (40%) and 2 of 5 GI anastomotic leaks (40%) were OSIs. Moreover, 3 OSIs were due to bacterial peritonitis, a chyle leak, and an ischemic bowel. CONCLUSIONS: This analysis suggests that the sensitivity (55%) and specificity (45%) of organ space infection (OSI) in ACS NSQIP are too low for OSI to be a surrogate for grade B and C pancreatic fistulas. We concluded that procedure-specific variables will be required for ACS NSQIP to improve outcomes after pancreatectomy.
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    Prevention of Gallstone Formation After Gastrectomy
    (AMA, 2020-06) Pitt, Henry A.; Nakeeb, Attila; Surgery, School of Medicine
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    Surgical Outcome After Distal Pancreatectomy With and Without Portomesenteric Venous Resection in Patients with Pancreatic Adenocarcinoma: A Transatlantic Evaluation of Patients in North America, Germany, Sweden, and The Netherlands (GAPASURG)
    (Springer, 2024) Stoop, Thomas F.; Augustinus, Simone; Björnsson, Bergthor; Tingstedt, Bobby; Andersson, Bodil; Wolfgang, Christopher L.; Werner, Jens; Johansen, Karin; Stommel, Martijn W. J.; Katz, Matthew H. G.; Ghadimi, Michael; House, Michael G.; Ghorbani, Poya; Molenaar, I. Quintus; de Wilde, Roeland F.; Mieog, J. Sven D.; Keck, Tobias; Wellner, Ulrich F.; Uhl, Waldemar; Besselink, Marc G.; Pitt, Henry A.; Del Chiaro, Marco; Global Audits on Pancreatic Surgery Group (GAPASURG); Surgery, School of Medicine
    Background: Pancreatic adenocarcinoma located in the pancreatic body might require a portomesenteric venous resection (PVR), but data regarding surgical risks after distal pancreatectomy (DP) with PVR are sparse. Insight into additional surgical risks of DP-PVR could support preoperative counseling and intraoperative decision making. This study aimed to provide insight into the surgical outcome of DP-PVR, including its potential risk elevation over standard DP. Methods: We conducted a retrospective, multicenter study including all patients with pancreatic adenocarcinoma who underwent DP ± PVR (2018-2020), registered in four audits for pancreatic surgery from North America, Germany, Sweden, and The Netherlands. Patients who underwent concomitant arterial and/or multivisceral resection(s) were excluded. Predictors for in-hospital/30-day major morbidity and mortality were investigated by logistic regression, correcting for each audit. Results: Overall, 2924 patients after DP were included, of whom 241 patients (8.2%) underwent DP-PVR. Rates of major morbidity (24% vs. 18%; p = 0.024) and post-pancreatectomy hemorrhage grade B/C (10% vs. 3%; p = 0.041) were higher after DP-PVR compared with standard DP. Mortality after DP-PVR and standard DP did not differ significantly (2% vs. 1%; p = 0.542). Predictors for major morbidity were PVR (odds ratio [OR] 1.500, 95% confidence interval [CI] 1.086-2.071) and conversion from minimally invasive to open surgery (OR 1.420, 95% CI 1.032-1.970). Predictors for mortality were higher age (OR 1.087, 95% CI 1.045-1.132), chronic obstructive pulmonary disease (OR 4.167, 95% CI 1.852-9.374), and conversion from minimally invasive to open surgery (OR 2.919, 95% CI 1.197-7.118), whereas concomitant PVR was not associated with mortality. Conclusions: PVR during DP for pancreatic adenocarcinoma in the pancreatic body is associated with increased morbidity, but can be performed safely in terms of mortality.