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Background: Romiplostim is a thrombopoietin‐mimetic peptibody for adult refractory chronic immune thrombocytopenia (ITP). We aimed to describe ITP patients receiving romiplostim, platelet counts and romiplostim usage in UK clinical practice. Methods: This was a retrospective cohort study of patients in the UKITP Registry who received romiplostim between October 2009 and January 2015, including data up to 6 months before romiplostim initiation through follow‐up. Results: Of 1440 patients in the UKITP Registry, 118 adults with primary ITP were eligible. Before romiplostim, 22% had splenectomy, 12% received platelet transfusion, 97% received ≥ 1 different ITP medication and 77% received ≥ 3. Most patients (73%) initiated romiplostim ≥ 1 year after ITP diagnosis (chronic phase). The mean duration of romiplostim treatment was 5.7 (SE 0.9) months, and the median was 1.4 months (IQR: 0.2, 6.5). Mean platelet count before romiplostim was 38 × 109/L, rising to 103 × 109/L within 1 month, and remaining 50‐150 × 109/L through up to 3 years of follow‐up. After romiplostim, 4% of patients had splenectomy, 6% received platelet transfusion, and 57% received just one ITP medication other than romiplostim. Conclusion: The study provides valuable insights into the real‐world use of romiplostim in primary ITP in routine practice and highlighted the timing of romiplostim initiation at different ITP disease phases. [ABSTRACT FROM AUTHOR]

Abstract Several adenosine receptor (AR) agonists have been shown in the past to possess anti-platelet potential; however, the adjunctive role of AR agonists in anti-platelet therapy with the use of P2Y 12 receptor inhibitors has not been elucidated so far. This in vitro aggregation-based study investigates whether the inhibition of platelet function mediated by cangrelor or prasugrel metabolite can be potentiated by AR agonists. It evaluates the effect of non-selective (2-chloroadenosine), A 2A -selective (UK 432097, MRE 0094, PSB 0777) and A 2B -selective AR agonists (BAY 60-6583) on platelet function in relation to their toxicity, specificity towards adenosine receptor subtypes, structure and solubility. UK 432097, 2-chloroadenosine, MRE 0094 and PSB 0777 were found to be more or less potent inhibitors of ADP-induced platelet aggregation when acting alone, and that they remained non-cytotoxic to the cells. These AR agonists were also effective in the potentiation of the effects exerted by P2Y 12 antagonists. Considering the estimated IC 50 value, UK 432097, showing a relatively high binding affinity to the A 2A adenosine receptor, has been identified as the most potent anti-aggregatory agent. This compound diminished platelet aggregation at nanomolar concentrations and further augmented platelet inhibition by P2Y 12 antagonists by approx. 60% (P <.01). Our results indicate the importance of adenosine receptors as therapeutic targets and point out challenges and potential benefits of therapeutic use of a combined therapy of P2Y 12 antagonist and AR agonist in cardioprotection. Our comparative analysis of the effects of AR agonists on platelet response in plasma and whole blood may indirectly suggest that other blood morphology elements contribute little to the inhibition of platelet function by AR agonists. Graphical abstract Unlabelled Image [ABSTRACT FROM AUTHOR]

What is known and objective In the management of anaemia associated with chronic kidney disease ( CKD), optimal use of intravenous (i.v.) iron has a central role. It minimizes reliance on erythropoiesis-stimulating agents ( ESAs) and may be beneficial in reducing overall cardiovascular risks through its effects on platelet counts ( PLT). We have examined the effects of i.v. iron on PLT in patients with CKD. Methods Two hundred and three patients with CKD, referred to a single teaching hospital in UK for i.v. iron therapy, received low molecular-weight iron dextran at a median dose of 1000 milligrams given over a median time of 2 h and 40 min. PLT at baseline were compared with the measurements taken during a 4-month follow-up period post-infusion. Results PLT were checked at various points following i.v. iron treatment. Compared with baseline, mean reduction in PLT ranged between 10·1 and 23·6 (×109/L) during consecutive 15-days intervals post-treatment. At the reference point of 90-days post-infusion, the drop in PLT was statistically significant ( P < 0·001). What is new and conclusion Low molecular-weight iron dextran in patients with CKD leads to reduction in PLT. This reduction appears soon after treatment and is maximal after 3 months. Prospective data are required to confirm these findings and examine whether this translates to a reduction in thrombotic episodes. [ABSTRACT FROM AUTHOR]