Enoxaparin-sodium/heparin
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Bullous haemorrhagic dermatosis: 3 case reports In a report, three patients (two women and one man) aged 45–72 years were described, who developed bullous haemorrhagic dermatosis during anticoagulation treatment with enoxaparin sodium or heparin [dosages not stated; not all time to reactions onset stated]. Case 1: A 72-year-old woman, who had history of bilateral pulmonary emboli and apixaban treatment, was admitted for the treatment of primary central nervous system lymphoma. Three weeks after the admission and initiation of SC enoxaparin sodium [enoxaparin], she was referred to the dermatology department of the hospital for evaluation of asymptomatic and bullous lesions on the legs, which had appeared 1 week prior. Examination revealed tense and irregularly scattered haemorrhagic bullae and vesicles, each present on a violaceous-erythematous base and were concentrated on the lower legs. A few eroded lesions were observed leaving trails of dried blood. A few similar isolated haemorrhagic vesicles were also observed on her upper extremities. On her abdomen several small ecchymoses were observed from her SC enoxaparin sodium injections. Laboratory tests revealed marginally low haemoglobin level of 11.8 g/dL, while her platelet count, prothrombin time (PT), partial thromboplastin time (PTT) and international normalised ratio (INR) were normal. She was diagnosed with enoxaparin-induced bullous haemorrhagic dermatosis, which was confirmed by punch biopsy. Histopathology demonstrated intraepidermal blisters containing RBCs and extravasated RBCs in the papillary dermis with no inflammatory infiltrate or vasculitis. During the following week, her lesions improved. Enoxaparin sodium treatment was continued with no new lesions. Case 2: A 52-year-old woman was inpatient with recurrent ventricular tachycardia (VT) due to nonischaemic cardiomyopathy with lamin A mutation and atrial fibrillation. She was referred to the dermatology department of the hospital due to new skin lesion on her face. Five months prior, she had been admitted due to VT leading to implantable cardioverterdefibrillator discharges and for evaluation for orthotopic heart transplant. Prior to the admission, she had been receiving warfarin for AF (diagnosed at the age of 30 years). Five days after the admission, warfarin was switched to continuous IV infusion of heparin [unfractionated heparin], which was maintained throughout her hospitalisation for AF and for intra-aortic balloon pump placed during hospital course. Her lesions appeared approximately 4 months after the initiation of heparin. At dermatology consultation, her medications included heparin, aspirin, amiodarone, metolazone, daratumumab, mexiletine, eplerenone and escitalopram. Examination showed asymptomatic and solitary haemorrhagic vesicle (4mm) with a background of uninvolved skin on the right malar aspect of the face. Similar asymptomatic discrete lesions (1–4mm) at different stage of healing were irregularly scattered on her lower abdomen, back, shoulders and left dorsal aspect of the h
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