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Contains fulltext : 291124.pdf (Publisher’s version ) (Open Access) BACKGROUND: In upper extremity thrombosis research, the occurrence of upper extremity postthrombotic syndrome (UE-PTS) is commonly used as the main outcome parameter. However, there is currently no reporting standard or a validated method to assess UE-PTS presence and severity. In a recent Delphi study, consensus was reached on a preliminary UE-PTS score, combining 5 symptoms, 3 signs, and the inclusion of a functional disability score. However, no consensus was reached on which functional disability score to be included. OBJECTIVES: The aim of the current Delphi consensus study was to determine the specific type of functional disability score to finalize UE-PTS score. METHODS: This Delphi project was designed as a three-round study using open text questions, statements with 7-point Likert scales, and multiple-choice questions. The CREDES recommendations for Delphi studies were applied. In this context, a systematic review was conducted before the start of the Delphi rounds to identify the available functional disability scores as available in the literature and present these to the expert panel. RESULTS: Thirty-five of 47 initially invited international experts from multiple disciplines completed all the Delphi rounds. In the second round, consensus was reached on the incorporation of the quick disabilities of the arm, shoulder, and hand (QuickDASH) in the UE-PTS score, rendering the third round obsolete. CONCLUSION: Consensus was reached that the QuickDASH should be incorporated in the UE-PTS score. The UE-PTS score will need to be validated in a large cohort of patients with upper extremity thrombosis before it can be used in clinical practice and future research. 01 januari 2023

We describe 2 renal transplant recipients with severe but reversible neurological manifestations related to Varicella zoster virus (VZV) cerebral vasculopathy. To the best of our knowledge, this is the first description of cerebral VZV vasculopathy in solid organ transplant recipients. We review the published literature on the clinical presentation, diagnosis and treatment. In solid organ transplant recipients presenting with neurological signs and symptoms, a diagnosis of VZV-associated vasculopathy should be considered.

3037 Background: Hypertension is the most common side effect in trials with inhibitors of vascular endothelial growth factor (VEGF) signaling, although the underlying pathophysiology is unclear. As the use of anti-VEGF therapy is increasing, hypertension and related serious adverse events are likely to become more important. Methods: To better understand this pathophysiology,blood pressure and vascular function parameters were assessed in this substudy of a phase I trial in patients with advanced solid tumours treated with BAY 57–9352, an oral VEGF receptor 2 (VEGFR2) inhibitor. Blood pressure, flow-mediated dilatation (FMD), nitroglycerin-mediated dilatation (NMD) and pulse-wave velocity (PWV) were measured at baseline and after 5 weeks of daily treatment in 10 patients. Patients were spread out over different cohorts, taking different dosages of study drug. Results: Mean systolic blood pressure increased from 129.0 mm Hg to 139.4 mm Hg after 5 weeks of treatment (difference 10.4 mm Hg; 95% confidence interval (CI) 5.0–15.7 mm Hg; p=0.002). Mean diastolic blood pressure increased from 80.9 to 87.4 mm Hg (difference 6.5 mm Hg; 95% CI 1.7–11.3; p=0.013). Endothelium-dependent vasodilatation (FMD) decreased from 5.6% to 3.0% (95% CI 1.1–3.9%; p=0.003). NMD, indicating endothelium-independent vasodilatation, also decreased from 12.9% to 7.7% (95% CI 2.7–7.6%; p=0.001). Arterial stiffness (PWV), increased from 9.4 m/s to 10.3 m/s (p=0.07). Conclusions: Inhibition of VEGFR2 significantly increases systolic and diastolic blood pressure. As VEGF enhances endothelial nitric oxide (NO) synthetase activity, the clear decrease in FMD could be explained by reduced bioavailability of NO. The decrease in NMD may be a direct effect of VEGFR2 inhibition on vascular smooth muscle cells. However, a more likely hypothesis for these profound vascular effects is a reduced number of microvessels (i.e. rarefaction). As the microcirculation is largely responsible for peripheral resistance, the rarefaction associated with VEGFR2 inhibition is likely to increase peripheral resistance and lead to hypertension. [Table: see text]