Azithromycin/enoxaparin sodium/hydroxychloroquineGastrointestinal bleeding, ischaemic stroke due to off-label use, and lack of efficacy: case report A 75-year-old man exhibited lack of efficacy during treatment with enoxaparin sodium for vascular thromboembolism prophylaxis. Additionally, he developed ischaemic stroke during off-label treatment with azithromycin and hydroxychloroquine for COVID-19, and severe GI bleeding during prophylactic treatment with enoxaparin sodium [not all routes stated].The man was hospitalised with dyspnoea and fever in March 2020. His medical history was significant for hypertension treated with irbesartan and amlodipine, stage 5 nondialysis chronic kidney disease, gout and ischaemic stroke treated by aspirin. Also, he had been receiving unspecified antidepressants and anxiolytics. On presentation, his vital signs were as follows: body temperature 38.2°C, RR was 20 breaths/min, BP 140/90 mmHg, HR 80 beats/min and oxygen saturation 92%. Subsequently, his RT-PCR test was positive for COVID-19. Therefore, he started receiving off-label azithromycin 500 mg/day on the first day followed by 250mg daily along with off-label hydroxychloroquine 600mg daily. He also received omeprazole as an antacid along with potassium supplements, and prophylaxis therapy for vascular thromboembolism with SC injection of enoxaparin sodium [enoxaparin] 20mg daily. However, 20 hours later, his consciousness deteriorated along with dyspnoea. Therefore, he was shifted to the ICU and started on hyperbaric oxygen therapy. Subsequently, the dose of enoxaparin sodium was increased to 40mg daily. Thereafter, a brain MRI revealed hypersignal fluid-attenuated inversion recovery and diffusion in the right frontal lobe with a decrease of the apparent diffusion coefficient in favour of a recent ischaemic stroke despite prophylactic enoxaparin sodium administration. After 7 days, his laboratory tests showed increased CRP, reduced Hb and lymphocyte count with elevated ferritin and LDH levels. Subsequently, he developed acute renal function deterioration. His other laboratory tests were as follows: prolonged prothrombin time (14.5 sec), prolonged activated partial thromboplastin time, D-dimer was 2195.72 ng/mL, fibrinogen was 7.91 g/L, NT-Pro-BNP was 19250 pg/mL. Subsequently, he developed severe sepsis of pulmonary origin. For his renal deterioration, he haemodialysis was started.The man received intensive support and treatment, after which his condition improved. However, his consciousness disorders persisted with a Glasgow coma scale core of 9/15. On day 20, his condition suddenly deteriorated due to severe GI bleeding secondary to enoxaparin sodium use, and he died due to it.Hazim A, et al. SARS-CoV2 disease seen through the prism of acutely decompensated chronic kidney disease and ischemic stroke: What lesson we have learned from using prophylaxis therapy of vascular thromboembolism?.