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Epistaxis and platelet function defect: case report A 71-year-old man developed epistaxis secondary to platelet function defect during treatment with sertraline for major depression. Subsequently, at an approximate age of 73 years, he developed platelet function defect during treatment with paroxetine for major depression [routes and durations of treatments to reactions onsets not stated; not all dosages and outcomes stated]. The man was admitted to emergency room in December 2015 due to nose bleeds (epistaxis) recurring for several days. He had medical history of an upper digestive tract ulcer, idiopathic thrombocytopenic purpura, cobalamin deficiency and major depression. For major depression he had been receiving sertraline 50 mg/day for several years. On admission, he was fond to have anaemia. The man was repeatedly treated with nose packing, which was ineffective. Therefore, he was treated with multiple transfusions (RBS and platelets) and ligation of the sphenopalatine artery. Consequently, nose bleeding resolved. Thereafter, bleeding did not recur till the time of this report writing. He was referred to the haematologist for further work-up. The first results obtained in December 2015 revealed a clear prolongation of the epinephrine (EPI) and adenosine diphosphate (ADP) closure times (PFA-100). First-line coagulation tests were normal. Platelet aggregometry showed decreased response to 2.5µM ADP. Without a clear explanation for the abnormal closure times, he was examined again in April 2016 and November 2016. Results revealed a very mild decrease in platelet aggregation despite recurrence of mild thrombocytopenia. However, ATP secretion was decreased after activation with 10µM ADP on the lumi-aggregometer. ATP secretion was normal for TRAP, collagen and thromboxane A2. These findings suggested an acquired thrombopathy (platelet function defect) which might have contributed to the nose bleeding. Mild thrombocytopenia was also considered as a risk factor for nose bleeding. Thrombopathy persisted, but bleeding did not recur. This suggested the possible contribution of other unidentified risk factors (like hidden NSAID self-medication, hypertensive flare-up, local inflammation etc.) in the epistaxis. Sertraline was presumed as a cause of platelet dysfunction. Owing to risk of haemorrhage, sertraline was stopped on 9 November 2017. Several weeks later, the EPI closure time normalized and ADP closure time was slight decreased. Unfortunately, his psychiatric status worsened. Therefore, at the end of 2017, he was started on paroxetine. Biological monitoring performed in February 2018 revealed slight increase in EPI and ADP closure times (compared to previous one), decreased ATP secretion after activation with 10µM ADP, collagen 3.3µg/mL and thromboxane A2 5µM and decreased response to 2.5µM ADP. These finding suggested platelet function defect (without bleeding) due to paroxetine. According to French imputability method, causality relationship between ADR (epistaxis secondary to platelet function defect) and se