Antihaemorrhagics/corticosteroids

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Low-titre inhibitors against susoctocog-α and lack of efficacy: 2 case reports In a retrospective study of nine patients, two men aged 68–81 years were described, who developed low-titre inhibitors against susoctocog-α while being treated for acquired haemophilia-A (AHA). Additionally, one of the two men did not exhibit resolution of bleeding after treatment with factor-VIII inhibitor bypassing fraction and tranexamic acid for AHA [routes, times to reactions onset and outcomes not stated]. Case 1: A 68-year-old man, who had diabetes, arterial hypertension, previous myocardial infarction, chronic obstructive pulmonary disease (COPD), gastritis, iatrogen hypothyroidism and chronic renal failure, was hospitalised for due to lung adenocarcinoma. He was only treated with radiotherapy, and eventually, he was discharged. One month later, he presented to the emergency department (ED) with left shoulder and head trauma. Laboratory tests showed a haemoglobin level of 6.3 g/dL and activated partial thromboplastin time (aPTT) ratio of 1.44. He was discharged following one supportive RBC transfusion. One week later, he was admitted to the ED due to haematomas in the periorbital region, hemithorax, right face, periorbital region and the left shoulder, during which he was diagnosed with AHA. Human inhibitor titre was 55.0 BU/mL and plasmatic human factor-VIII level was 2. He started receiving treatment with factor-VIII inhibitor bypassing fraction [activated prothrombin complex concentrate] 80 IU/kg every 12 hours, tranexamic acid 10 mg/kg/day and unspecified corticosteroids 1.0 mg/kg/day. Despite the haemostatic treatment with factor-VIII inhibitor bypassing fraction and tranexamic acid, his bleeding did not resolve. An increase in the size of thoracic haematoma was also observed. Hence, factor-VIII inhibitor bypassing fraction was discontinued, and he started receiving susoctocog-α [Obizur; Takeda Pharmaceutical Co.] at a loading dose of 100 IU/kg followed by 50 IU/kg every 12 hours for 6 days to maintain a target factor-VIII level >70%. However, a low-titre inhibitor anti-rpFVIII of 1.0 BU/mL was observed against susoctocogα, which was confirmed when his treatment was stopped with no impact on his porcine factor-VIII levels. Thereafter, he started receiving short-term prophylaxis with low-dose factor-VIII inhibitor bypassing fraction to prevent bleeding reoccurrences, unitl eradication of human inhibitor. Case 2: An 81-year-old man, whose medical history was notable for breast cancer, rheumatoid arthritis and carotid vasculopathy, was admitted due to non-ST elevation myocardial infarction with severe anaemia (treated with supportive transfusions) and suspected AHA. Within a few days, large SC haematomas were observed in the upper and lower limbs and in the soft palate. Diagnosis of AHA was confirmed. He started receiving treatment with susoctocog-α 50.0 IU/kg three times a day to resolve the bleeding along with unspecified corticosteroids and cyclophosphamide to eradicate the inhibitors. Ten days later, the dose of susoct

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