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Procalcitonin following elective partial liver resection – origin from the liver? *
Author(s) -
Kretzschmar M.,
Krüger A.,
Schirrmeister W.
Publication year - 2001
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1034/j.1399-6576.2001.450918.x
Subject(s) - medicine , procalcitonin , venous blood , arterial blood , vein , oxygen saturation , gastroenterology , urology , anesthesia , oxygen , sepsis , chemistry , organic chemistry
Background: The origin of the inflammatory peptide procalcitonin (PCT) is still unknown. In the present study PCT concentrations in arterial and hepatic‐venous blood were examined in patients undergoing elective partial liver resection (LR) using a fiberoptic pulmonary arterial catheter placed in a liver vein to obtain further information on the origin of PCT. Methods: In 28 patients (21 male/7 female; average age of 58.8±8.8 years) undergoing LR, arterial and hepatic venous PCT concentrations were measured during 24 h perioperatively. The parallel blood withdrawals occurred immediately before the Pringle maneuver (Hx), 2 min, 1, 2, 6, 12, and 24 h after Hx. Over the whole period, the oxygen saturation in hepatic venous blood (ShvO 2 ) was monitored. PCT concentrations were assayed by immunoluminometry. Results: We observed a significant increase in PCT concentration already 6 h after Hx compared to the values before Hx. Twenty‐four hours after Hx we found the highest plasma concentrations. It was conspicuous that hepatic venous PCT concentrations were always higher than the arterial ones (significantly from the 6th hour after Hx). There was no correlation between the courses of ShvO 2 and PCT rise. A significant correlation was verified between Hx duration and PCT concentration measured 24 h after Hx both in the hepatic venous and arterial blood. Conclusions: The results of our investigation can be interpreted as evidence that liver (or the hepatosplanchnicus?) is a source of PCT. The mechanism of PCT induction cannot be clarified by our study: whether the induction of PCT was caused by an endotoxin translocation during the impeded splanchnic outflow or by the direct surgery‐induced lesion (hypoxia) of the liver remains unclear. However, the latter appears more probable because of the observed correlation between Hx duration and PCT concentration rise.