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Clinical Trial
. 1999 Jun;83(9):990-5.
doi: 10.1046/j.1464-410x.1999.00100.x.

Bleeding and activation of coagulation during and after transurethral prostatectomy: importance of the acute-phase response and prostate specific antigen?

Affiliations
Clinical Trial

Bleeding and activation of coagulation during and after transurethral prostatectomy: importance of the acute-phase response and prostate specific antigen?

J D Nielsen et al. BJU Int. 1999 Jun.

Abstract

Objective: To evaluate the importance of coagulation activation in patients with benign prostatic hyperplasia, undergoing transurethral prostatic resection (TURP) and to examine whether changes in activity are related to blood loss, the circulatory entry of prostate specific antigen (PSA), operative trauma (resected tissue weight) and the inflammatory response, as assessed by C-reactive protein (CRP).

Patients and methods: TURP was performed in 24 men and the weight of resected tissue and blood loss determined. The activation of coagulation was followed using new sensitive and specific assays, and the changes related to blood loss, the release of PSA, operative trauma and the acute-phase response. The area under the curve (AUC) for the measured quantities was used in correlation analysis.

Results: TURP was followed by a marked activation in coagulation. There was no correlation between the markers of coagulation and the operative blood loss, but the latter correlated with the weight of resected tissue (P=0.001). Postoperatively, the blood loss correlated with prothrombin fragment (F1+2; P=0.010), with thrombin-antithrombin complexes (TAT; P=0.024), and with the PSA concentrations (P=0.016) but not with fibrinogen. Serum concentrations of PSA increased significantly and the AUC in the operative period correlated with F1+2 (P=0.003) and TAT (P<0. 005), but postoperatively only with F1+2 (P=0.013). The weight of resected tissue correlated operatively with PSA (P=0.012) but not with the concentrations of F1+2 or TAT. Postoperatively, there was a correlation with the acute-phase proteins, CRP (P=0.005), fibrinogen (P=0.012) and with PSA (P=0.020).

Conclusion: The operative blood loss is caused by surgical factors and the observed postoperative hypercoagulable state can be explained as a physiological response to bleeding, i.e. to secure haemostasis. The activity of coagulation was unrelated to operative trauma, but the acute-phase proteins were. The release of PSA into the circulation probably has an effect on blood coagulation.

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