Activation of platelets and fibrinolysis induced by saturated air dives.

INTRODUCTION: The Doppler technique is currently the usual method for detection of bubbles in the circulation following decompression. However, cases of decompression sickness (DCS) frequently occur in the absence of detectable bubbles, so that other markers for increasing risk of DCS would be welcome. This study assessed the hemostatic effects of compressed-air saturation dives that conformed to the "safe" limits of accepted decompression tables. METHODS: We measured coagulation times, thrombin generation, platelets, and fibrinolysis in 21 male divers who were subjected to saturated hyperbaric exposures to 0.28-0.3 MPa (corresponds to 18-20 msw). Each diver did one dive. RESULTS: Pooled before- and after-dive data for all exposures showed after decompression, statistically significant changes included decrease of the mean platelet count after, increased induced platelet aggregation and number of platelet aggregates, increased number of P-selectin (CD62P) positive platelets and CD62P density on platelets, increase of platelet derived microparticles in the blood of the divers, decrease of factor XII, X, and fibrinogen concentrations, and marked increase of plasmin-antiplasmin complex concentration. Thrombin activation markers and coagulation times did not change significantly. CONCLUSIONS: Saturated hyperbaric exposures followed by nominally safe decompression led to activation of platelets and the fibrinolytic system. The probable mechanism for the activation of platelets and fibrinolysis is contact with the surface of evolved bubbles in the divers' circulation.

On the prophylactic and therapeutic use of danaparoid sodium (Orgaran) in patients with heparin-induced thrombocytopenia.

Heparin-induced thrombocytopenia (HIT) is a rare but dangerous complication of heparin prophylaxis or treatment. The present laboratory tests to measure heparin-associated antibodies are not specific. The diagnosis of HIT mainly depends on the decrease in platelet count and on clinical symptoms. To evaluate clinical outcome, bleeding complications and platelet counts were evaluated in 45 patients with HIT type II (HIT II) treated prophylactically (subcutaneous injections) or therapeutically (intravenous infusion) with danaparoid. Group I included 24 patients with HIT II without thromboembolic complications who received danaparoid twice daily subcutaneously (10 IU/kg) for a mean of 16 days. Group II included 21 patients with thromboembolic complications. They were treated with intravenous danaparoid (2.6 IU/kg/h +/- 1.1) for a mean of 17 days. During subcutaneous prophylaxis, mean anti-Xa levels of 0.2 U/mL and during intravenous treatment, mean anti-Xa levels of 0.4 U/mL were reached. No deaths, amputations, or serious bleeding complications occurred, and no new thromboses were observed in both patient groups. Treatment with danaparoid led to a fast normalization of the platelet counts. This normalization occurred earlier and the concentration of platelets was higher in patients treated with intravenous doses. Danaparoid with subsequent vitamin K-antagonist treatment effectively prevents thromboembolic complications in patients with HIT.

[Tissue factor (TF) and inhibitor (TFPI) concentrations in patients with urinary tract tumors and haematological malignancies]. / Stezenie czynnika tkankowego i jego inhibitora u chorych na guzy ukladu moczowego i choroby rozrostowe ukladu krwiotwórczego.

The aim of study was to evaluate TF activity and TFPI concentration in patients with haematological malignancies and urinary tract tumors. TFPI concentration and activity and TF concentration were measured in 20 patients suffering from acute myeloblastic leukaemia (AML), 21 patients with chronic myelogenous leukaemia (CML), 17 patients with chronic lymphatic leukaemia (CLL), 16 patients with multiple myeloma (MM) and 65 healthy adults. TFPI and TF concentrations were measured also in patients with renal cell carcinoma (n = 12) and bladder cancer (n = 17) and patients with benign prostatic hyperplasia (BPH) (n = 15). Patients with AML, CML, CLL, and cancer revealed elevated TFPI concentrations. Patients with AML, CML, CLL, MM showed decreased TFPI activity. However TFPI concentration correlated inversely with TFPI activity only in the AML group. No significant changes were observed in TF concentrations in all investigated groups.