Biomedical subjects
Publications and source records attributed to M Komarnicki.
Bone marrow fibrosis appears with diverse extension in most neoplastic diseases of blood. It may cause difficulties in establishing a firm diagnosis. In some cases bone marrow fibrosis has a prognostic value.
We present a case of Hodgkin's disease first symptom of which was paraneoplastic syndrome in a form of myopathy. It caused a delay in putting forward an appropriate diagnosis.
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The authors present interactions between fibrinolysis and platelets. Platelets may exert both stimulatory and inhibitory effect on fibrinolysis. Also the problem of fibrinolysis activation on platelets function is considered.
The evaluation of both standard heparin (SH) and low molecular weight heparin (LMWH) (Fraxiparine) impact on spontaneous platelet aggregation assessed in the whole blood and in platelet-rich plasma (PRP). The results obtained reveal that SH enhance spontaneous aggregation in a similar degree both in the whole blood (34.5 +/- 3.0, control 21.3 +/- 4.1) and in PRP (33.5 +/- 2.7, control 13.8 +/- 3.2). LMWH significantly intensifies spontaneous aggregation in the whole blood (46.9 +/- 3.2, control 21.3 +/- 4.1) but not in PRP (19.4 +/- 4.3, control 13.8 +/- 3.2).
The influence of thrombin stimulated-blood platelets on plasma fibrinolytic activity was evaluated. Thrombin-activated blood platelets have been shown to significantly inhibit plasma fibrinolytic activity before and after venous stasis. This was expressed by a reduction of the digestion area of fibrin dish from 10.3 +/- 3.3 cm2 to 3.7 +/- 1.5 cm2 and from 15.6 +/- 6.8 cm2 to 3.7 +/- 1.7 cm2, respectively.
The influence of uremic serum on 125I-fibrinogen binding by normal blood platelets after induction with adenosine diphosphate was evaluated. The study was performed on 12 hemodialyzed uremic patients. The control group included 12 healthy subjects. It has been demonstrated that the uremic serum from the patients before hemodialysis significantly augmented fibrinogen binding by normal blood platelets (33.8 +/- 11.8%) in comparison with control subjects (14.4 +/- 8.9%). After hemodialysis, fibrinogen binding was comparable with the control group (14.9 +/- 10.1%). Uremic toxins removable during hemodialysis are probably responsible for the potentiation of 125I-fibrinogen binding by platelets.
Dense bodies are platelet organelles that store adenosine diphosphate. We have estimated the number of platelet dense bodies in patients with chronic uremia treated conservatively, by peritoneal dialysis and by hemodialysis. All groups of patients and control subjects were found to have similar mean numbers of platelet dense granules. Analysis of platelet distribution according to number of dense bodies has shown that patients undergoing hemodialysis have a decreased percent of platelets with a greater number of granules.
We have examined platelet aggregation in patients with chronic uremia using ADP, thrombin and calcium ionophore A23187 as inducers. The study was performed on patients treated conservatively, by hemodialysis and peritoneal dialysis. Platelet aggregation was most significantly depressed in patients treated conservatively and by hemodialysis. Different mechanisms are responsible for platelet dysfunction.
The binding of 125I-fibrinogen to blood platelets was assessed in 41 patients with chronic uraemia. The study was performed in three groups of subjects: treated conservatively, with haemodialysis and with peritoneal dialysis. Platelets from uraemic patients were shown to be more susceptible to fibrinogen binding than platelets from healthy subjects.
In 15 patients with chronic uraemia and 9 healthy subjects concentrations of platelets glycoproteins Ib, IIb, and IIIa were determined. There were no differences between patients and control group. The possible role of glycoproteins in disturbances of the platelets function is discussed.
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