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Presenter: C. , Pollard1, ,
Authors: C. Pollard1, W.Y. Chung1, C. Stover2, A. Arshad1, M.S. Metcalfe1, A.R. Dennison1
P-186
Complement related pancreatic shock following total pancreatectomy for chronic pancreatitis
C. Pollard1, W.Y. Chung1, C. Stover2, A. Arshad1, M.S. Metcalfe1, A.R. Dennison1
1 University Hospitals of Leiceter NHS Trust, Leicester, U.K.; 2 University of Leicester, Leicester, U.K.
Objectives: Total pancreatectomy is a major surgical procedure which induces a systemic inflammatory response associated with significant morbidity. Our aim was to elucidate the mechanisms and time course of the resultant systemic inflammation by assessing complement and cytokine activity following total pancreatectomy.
Methods: Four patients underwent total pancreatectomy for chronic pancreatitis. Classical (CP), alternative (AP) and mannose-binding lectin (MBL) complement pathway activity was assessed during induction of anaesthesia, at the end of the surgical reconstruction, end of operation, 1 hour, 3 hours, 5 hours and days 1-7 postoperatively. GM-CSF, IFN-?, IL-10, IL-12p70, IL-1?, IL-2, IL-6, IL-8 and TNF-? were also assayed at the same time points.
Results: While patients (P3, P4 and P6) showed consumption and subsequent recovery of complement activity, one patient (P5) did not show this pattern: Baseline complement activities were recorded as normal, but between the end of surgical reconstruction and day 7 postoperatively there was no demonstrable MBL activity and no AP activity until day 3 when a minor recovery (up to 30%) was observed. Baseline concentration of IL-6, IL-8, IL-10 and IL-1? was <2.9 pg/ml in all markers. Peaks of IL-6, IL-8 and IL-10 concentrations were seen within the first 5 hours postoperatively (up to 300pg/ml). IL-1? concentration also increased to a lesser extent but with the same time profile.
Conclusions: Complement consumption occurs following total pancreatectomy and generally recovers rapidly. In one patient (P5) in this study, total pancreatectomy was associated with a massive activation and subsequent depletion of complement components, especially those of the alternative and MBL pathways, and a large concurrent cytokine response which did not recover over the usual time course. The frequency of this response is unknown but it may contribute to post-operative morbidity.
/P-186
Complement related pancreatic shock following total pancreatectomy for chronic pancreatitis
C. Pollard1, W.Y. Chung1, C. Stover2, A. Arshad1, M.S. Metcalfe1, A.R. Dennison1
1 University Hospitals of Leiceter NHS Trust, Leicester, U.K.; 2 University of Leicester, Leicester, U.K.
Objectives: Total pancreatectomy is a major surgical procedure which induces a systemic inflammatory response associated with significant morbidity. Our aim was to elucidate the mechanisms and time course of the resultant systemic inflammation by assessing complement and cytokine activity following total pancreatectomy.
Methods: Four patients underwent total pancreatectomy for chronic pancreatitis. Classical (CP), alternative (AP) and mannose-binding lectin (MBL) complement pathway activity was assessed during induction of anaesthesia, at the end of the surgical reconstruction, end of operation, 1 hour, 3 hours, 5 hours and days 1-7 postoperatively. GM-CSF, IFN-?, IL-10, IL-12p70, IL-1?, IL-2, IL-6, IL-8 and TNF-? were also assayed at the same time points.
Results: While patients (P3, P4 and P6) showed consumption and subsequent recovery of complement activity, one patient (P5) did not show this pattern: Baseline complement activities were recorded as normal, but between the end of surgical reconstruction and day 7 postoperatively there was no demonstrable MBL activity and no AP activity until day 3 when a minor recovery (up to 30%) was observed. Baseline concentration of IL-6, IL-8, IL-10 and IL-1? was <2.9 pg/ml in all markers. Peaks of IL-6, IL-8 and IL-10 concentrations were seen within the first 5 hours postoperatively (up to 300pg/ml). IL-1? concentration also increased to a lesser extent but with the same time profile.
Conclusions: Complement consumption occurs following total pancreatectomy and generally recovers rapidly. In one patient (P5) in this study, total pancreatectomy was associated with a massive activation and subsequent depletion of complement components, especially those of the alternative and MBL pathways, and a large concurrent cytokine response which did not recover over the usual time course. The frequency of this response is unknown but it may contribute to post-operative morbidity.
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