Antiplatelet therapy was discontinued and the patient was referred

to our centre. He was treated with HP-FVIII-VWF (FANHDI®) 120 U kg−1 as bolus, followed by 3.3 U kg−1 h−1 as c.i. for 9 days. IST with prednisone (1 mg kg−1 day−1) and cyclophosphamide (1 mg kg−1 day−1) was concomitantly RG7204 nmr started. FVIII activity was 102% and FVIII inhibitor disappeared in 8 days. No thromboembolic complications occurred during treatment. Cyclophosphamide was discontinued after 30 days; prednisone was tapered off and stopped after 90 days. Six months later, the patient had a relapse with reduction of FVIII (9.7%) and reappearance of the inhibitor (1.1 BU mL−1). Treatment with prednisone (1 mg kg−1 day−1) was restarted and is still ongoing. No bleeding recurred. A 78-year-old man was admitted with a 15-day

history of spontaneous haematomas on his upper limbs. Significant clinical history: in 1995, acute inferior myocardial infarction, ventricular tachycardia on antiarrhythmic prophylaxis and right carotid endarterectomy in 2002. The patient had been treated with acetylsalicylic acid therapy for many years. On admission, he had Hb levels of 109 g L−1, remarkably prolonged aPTT (97.3 s), FVIII activity levels 2.4% and presence of FVIII inhibitor (10.5 BU mL−1). On day 3, he was referred to our centre after a fall causing lumbar injury. An abdominal CT scan was urgently performed due to progressive anaemia and dorsal pain and a diagnosis of left retroperitoneal haematoma click here was made. The patient was transfused with 3 PRBC units. Haemostatic control was achieved through high-dose FVIII-VWF check details (HAEMOCTIN, Biotest®, Dreieich, Germany): 300 U Kg−1 as bolus followed by 15 U kg−1 h−1 as c.i on day 1. Dosage was adjusted to FVIII plasma values: 17 U kg−1 h−1 for 2 days; successively 13 U kg−1 h−1 for 2 days and later 11 U kg−1 h−1 for further 2 days, resulting in a 7-day therapy. Steroidal therapy with metilprednisolone 0.8 mg kg−1 day−1 was scheduled for 12 days, followed by prednisone

1 mg kg−1 day−1 and cyclophosphamide 0.6 mg kg−1 day−1 (reduced dosage because of chronic kidney failure) for 7 days. When therapy was stopped, FVIII was 177%. Due to the high cardiovascular risk, acetylsalicylic acid therapy was recommenced immediately after his discharge. Neither AHA nor thromboembolic events recurred in a 6-month follow-up. Overall data are shown in Table 2. The inhibitor was eradicated in 8.75 ± 3.59 days, whereas the treatment with FVIII lasted a median of 10.5 ± 2.63 days. A mean of 142250 ± 38887 U (total dose) of FVIII was administered. All of our cases have been treated following the suggested guidelines (high-dose factor VIII) and successively adjusting the doses to in vivo FVIII levels. Bleeding was stopped in all of the four patients and none of them relapsed into haemorrhage.