In 1993-94, 15 high responders were treated in our centre according to the Malmo protocol which was modified as follows: serial plasmapheresis was performed instead of extracorporeal adsorbtion to protein A for reducing inhibitor levels and, after the bolus dose to neutralize the inhibitor, factor VIII concentrate was administered by a continuous infusion. Thus, this regimen included continuous infusion of factor VIII(FVIII) for 1-4 weeks, iv cyclophosphamide for 2 days and orally for 8-10 days, and intravenous immunoglobulin (IVIG) from the fourth day for 5 days. All patients had been qualified for the treatment when the antibody level was < 15 BU mL(-1) . Tolerance was induced in 10 patients (66.6% very good and good results). The treatment failed in five cases in which, due to a high inhibitor level, it was not possible to maintain a measurable factor VIII:C concentration throughout the whole period of infusion. We compared these results with results of our low-dose regimen: 25 IU FVIII kg(-1) b.w. twice a week (1985-89, 11 high responders). The modified Malmo Protocol is much shorter than the low-dose programme and this is a method of first choice in patients undergoing surgery in the near future.

Patients with hemophilia A and circulating anticoagulant (factor VIII inhibitor) present a difficult, even unsolvable problem, particularly if they require surgical treatment and the inhibitor titer is high. During the 1986-1995 period 29 surgical procedures on inhibitor hemophilia A patients were performed in our center. Each of the cases had an individual character, and all demanded special clinical treatment. Based on this experience we present the possibilities of hemostasis maintenance during the perioperative period with high doses of human or porcine factor VIII, aPCC, plasmapheresis, and extracorporeal antibody adsorption to protein A-Sepharose. In some patients hemostasis maintenance requires combined treatment. To induce immunotolerance in patients with inhibitor is the gold standard treatment because it is then possible to achieve proper hemostasis after factor VIII infusion. Various methods of immunotolerance induction have been discussed and compared with our experience with immunotolerance induction in 11 patients with small factor VIII doses (25 IU/kg twice a week) and the modified Malmö protocol in 15 patients.

The incidence and clinical significance of hepatitis G virus (HGV) is still not fully known. The aim of our study was to assess the frequency of HGV RNA and antibody to HGV E2 protein (anti-E2) in Polish blood donors and patients with hepatitis, and to compare the sequence of HGV clones with those reported by others. Two-hundred and nineteen blood donors and 83 patients with hepatitis were studied. HGV was detected in 3.2% and anti-E2 in 24.2% of blood donors and in 26.5% and 8.4% of patients with hepatitis, respectively. HGV was detected as a co-infection with HCV in four of 18 patients with chronic hepatitis, in four of 16 patients with acute hepatitis and in one of six patients with fulminant liver failure (FLF), and as a co-infection with HBV in one of six patients with FLF and in three of 10 patients with chronic hepatitis. In non-A-C hepatitis, eight of 23 patients with acute hepatitis and one of four patients with FLF were positive for HGV but all 10 patients with chronic cryptogenic hepatitis were negative. In the follow-up studies of patients with HGV alone, a correlation with viraemia and clinical symptoms was observed in two patients, but in three others HGV RNA was detected in spite of clinical resolution. Two HGV clones were sequenced, and the sequence of the HGV helicase region of the HGV isolates from donor and patient were homologous to those described by others. Hence, the frequency of HGV RNA in blood donors is similar to that obtained in other countries but the anti-E2 (marker of a past infection) frequency is higher. The incidence of HGV RNA and anti-E2 in hepatitis patients suggests that HGV plays a role in liver pathology, but careful analysis of individual cases does not confirm this.

From 1965 to 1985, 64 deep vein thrombosis (DVT) patients were treated with streptokinase (SK). In 26 cases 'high-dose SK' (IV 100,000 units/h for 4 days) was used and in 38 patients a 'low-dose SK' regime (IV 250,000 units every 12 h for 4 days) was employed. The clinical signs of DVT subsided in 78 per cent of treated patients within 30 days of completing SK treatment. A repeat phlebography was performed immediately after SK therapy in 29 patients (45 per cent) and a total recanalization or partial thrombolysis was achieved in 80 per cent of the studied cases. In 15 patients minor and major haemorrhagic complications occurred. There were five fatalities, all in the high-dose SK group (three intracranial haemorrhages and two major bleeds). Three patients developed pulmonary embolism and none of them died. The post-treatment clinical and phlebographic evaluation did not reveal any significant difference between the two methods of SK administration, but more haemorrhagic complications (P less than 0.02, chi=5.50825) occurred in the high-dose SK patients. This report emphasizes the risk of bleeding complications during thrombolytic therapy. If SK is to be used, therefore, careful selection of patients and meticulous monitoring are mandatory.

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