Alterations of blood coagulation are thought to be involved in malaria pathogenesis. This study had the aim to investigate changes of blood coagulation under the standardized conditions of controlled human malaria infection. In a clinical trial aseptic, purified, cryopreserved Plasmodium falciparum sporozoites were intravenously (n = 24) or intradermally (n = 6) injected into 30 healthy volunteers. Twenty-two participants developed parasitaemia. Serial blood samples before and during prepatent period and at parasitaemia, diagnosed by microscopic assessment of thick blood smear, were obtained. Biomarkers of blood coagulation (thrombin generation potential, D-dimer, prothrombin fragment 1 + 2, von Willebrand factor, ADAMTS13 activity and soluble P-selectin) were determined. At first detection of P. falciparum parasitaemia, 72.7 % of volunteers had peak thrombin generation 10 % above their baseline. Overall, peak thrombin generation was 17.7 % higher at parasitaemia compared to baseline [median (25th–75th percentile): 225.4 nM (168.1–295.6) vs. 191.5 nM (138.2–231.9); p = 0.026]. There were no significant changes of other coagulation parameters. The thrombin generation potential, an in vitro blood coagulation test, which reflects an individual´s global coagulation status, was increased by 17.7 % at very early stages of P. falciparum malaria, suggesting a hypercoagulable state may be induced, even when parasite density is low.

A tight interplay between inflammation and hemostasis has been described as a potential driver for developing venous thromboembolism (VTE). Here, we investigated the association of systemic cytokine levels and risk of VTE in patients with glioma. This analysis was conducted within the prospective, observational Vienna Cancer and Thrombosis Study. Patients with glioma were included at time of diagnosis or progression and were observed for a maximum of two years. Primary endpoint was objectively confirmed VTE. At study entry, a single blood draw was performed. A panel of nine cytokines was measured in serum samples with the xMAP technology developed by Luminex. Results: Overall, 76 glioma patients were included in this analysis, and 10 (13.2%) of them developed VTE during the follow-up. Chemokine C-C motif ligand 3 (CCL3) levels were inversely associated with risk of VTE (hazard ratio [HR] per double increase, 95% confidence interval [CI]: 0.385, 95% CI: 0.161–0.925, p = 0.033), while there was no association between the risk of VTE and serum levels of interleukin (IL)-1β, IL-4, IL-6, IL-8, IL-10, IL-11, tumor necrosis factor (TNF)-α and vascular endothelial growth factor (VEGF), respectively. In conclusion, low serum levels of CCL3 were associated with an increased risk of VTE. CCL3 might serve as a potential biomarker to predict VTE risk in patients with glioma.

Patients with high‐grade gliomas are at high risk of venous thromboembolism (VTE). MicroRNAs (miRNAs) are small non‐coding RNAs with multiple roles in tumour biology, haemostasis and platelet function. Their association with VTE risk in high‐grade glioma has not been comprehensively mapped so far. We thus conducted a nested case–control study within 152 patients with WHO grade IV glioma that had been part of a prospective cohort study on VTE risk factors. At inclusion a single blood draw was taken, and patients were thereafter followed for a maximum of 2 years. During that time, 24 patients (16%) developed VTE. Of the other 128 patients, we randomly selected 24 age‐ and sex‐matched controls. After quality control, the final group size was 21 patients with VTE during follow‐up and 23 without VTE. Small RNA next‐generation sequencing of plasma was performed. We observed that hsa‐miR‐451a was globally the most abundant miRNA. Notably, 51% of all miRNAs showed a correlation with platelet count. The analysis of miRNAs differentially regulated in VTE patients—with and without platelet adjustment—identified potential VTE biomarker candidates such as has‐miR‐221‐3p. Therewith, we here provide one of the largest and deepest peripheral blood miRNA datasets of high‐grade glioma patients so far, in which we identified first VTE biomarker candidates that can serve as the starting point for future research.

Background: Lipedema is a subcutaneous adipose tissue disorder mainly affecting women. Its progressive nature often requires high-volume liposuction for efficient pain reduction. However, aspiration volumes of more than 5 L within a single session may lead to a variety of complications. Thus, we examined the effect of high-volume liposuctions on lipedema patients and the incidence of associated complications. Methods: We analyzed perioperative differences in lipedema patients undergoing low- or high-volume liposuctions. Statistical analyses were performed, investigating postoperative complications and the correlation of patients’ BMI, total amount of aspiration, duration of surgery, hospital stay and hemoglobin alterations. Complications were investigated according to the Clavien–Dindo Classification. Patients were divided in two groups based on the volume aspirated at liposuction (low-volume vs. high-volume liposuction). Results: Overall, 121 sessions were investigated. Mean total volume of aspiration was 8227.851 mL ± 3643.891. Mean preoperative hemoglobin levels were 13.646 g/dL ± 1.075 g/dL. Preoperatively, 7.44% of patients were anemic (Hb < 12 g/dL). Mean postoperative hemoglobin was 10.563 g/dL ± 1.230 g/dL. Postoperatively, 90.10% of patients showed Hb levels below 12 g/dL. Hemoglobin loss differed significantly between the two groups (p = 0.001). Significant correlations between pre- (p = 0.015) and postoperative (p < 0.001) hemoglobin levels and pre- (p < 0.001) and postoperative (p < 0.001) anemia with Class II complications were also seen. The total volume of aspiration did not correlate with complication rates (p = 0.176). Conclusions: Complication rates in high-volume liposuctions are hemoglobin-dependent rather than volume-associated. Preoperative anemia was the most influential for the occurrence of postoperative complications. To safely conduct high-volume liposuctions in lipedema patients, adequate patient selection and preoperative patient preparation are imperative.

Background: Belantamab mafodotin (belamaf) is a BCMA-targeting antibody–drug conjugate used in triple-class refractory multiple myeloma. Despite its efficacy, keratopathy remains a significant dose-limiting toxicity. Following its withdrawal from the U.S. market in 2022, its use in Austria is limited to clinical trials or compassionate use. Methods: In this real-world, retrospective study, we analyzed 36 relapsed/refractory, BCMA-naïve multiple myeloma patients treated at the University Hospital of Vienna (January 2020–June 2024); 42% received a reduced dose (1.9 mg/kg) throughout all treatment cycles. The primary objective was to assess adverse events, particularly keratopathy, and the impact of dose modifications on toxicity and efficacy. Results: The overall response rate was 64%, with responders having significantly fewer prior therapy lines (median 3 vs. 4.5, p = 0.015). Median PFS was 7.3 months, significantly longer in responders (11.1 vs. 1.6 months, p < 0.0001); median OS was 20.1 months, also longer in responders (not reached vs. 18 months, p = 0.031). Keratopathy occurred in 75% of patients; 33% experienced grade 3–4 events. Dose reduction significantly decreased grade 3–4 keratopathy (7% vs. 52%, p = 0.004) and thrombocytopenia (33% vs. 67%, p = 0.048) without compromising efficacy. Conclusions: Belamaf dose reductions improved tolerability without loss of efficacy, supporting reduced dosing in practice.

Background: Multiple mechanisms might lead to cancer-related hypercoagulability. In brain tumors, podoplanin, via its ability to activate platelets, seems to play a crucial role in developing venous thromboembolism (VTE). Different stimuli (including activated platelets) can trigger the release of prothrombotic neutrophil extracellular traps (NETs) by neutrophils. It remains to be elucidated whether podoplanin-induced platelet aggregates might also impact NET formation and subsequent hypercoagulability and thrombosis. Methods: Patients with glioma were enrolled in this prospective observational cohort study. The primary endpoint was VTE. Immunohistochemical staining of NETs (via citrullinated histone H3 [H3Cit]) and neutrophils (via myeloperoxidase [MPO]) was conducted in glioma specimens and correlated with intravascular platelet clusters (via CD61) and podoplanin. Results: In total, 154 patients were included. H3Cit+ tumor vessels were found in 45/154 cases. H3Cit were significantly associated with increased intravascular platelet clusters (CD61− vs. CD61+ vs. CD61++ vs. CD61+++: 3.7% (1/27) vs. 18.6% (11/59) vs. 39.4% (13/33) vs. 57.1% (20/35), p < 0.001) and podoplanin expression (PDPN− vs. PDPN+: 14.3% (7/49) vs. 36.2% (38/105), p = 0.007) in the tumor tissue. Furthermore, H3Cit+ tumor vessels were significantly associated with tumor-infiltrating MPO+ neutrophils (H3Cit− vs. H3Cit+, median [Q1-Q3]: 6.0 [3.3–12.3] vs. 12.5 [5.9–22.0] cells/mm², p < 0.001) and with D-dimer levels (H3Cit− vs. H3Cit+: 0.53 [0.32–1.10] vs. 0.84 [0.46–2.75] µg/mL, p = 0.034). The VTE risk was not linked to H3Cit+ tumor vessels (p = 0.613, log-rank). Conclusions: H3Cit in tumor vessels was not associated with VTE. However, H3Cit was linked to a local procoagulant phenotype in glioma, thereby potentially contributing to a systemic hypercoagulable state and thrombus formation.