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Background: Extended thromboprophylaxis after abdominal and pelvic cancer surgery to prevent venous thromboembolic events (VTE) is recommended but adherence is sub-optimal. Identifying patients at highest risk for post-discharge events may allow for selective extended thromboprophylaxis. The aim of our study was to identify the different risk factors of venous thromboembolism for in-hospital and post-discharge events.Methods: The American College of Surgeons-National Surgical Quality Improvement Program (ACS-NSQIP) 2012-2016 database was queried for all patients having colorectal resection. Primary outcome was postoperative VTE occurrence within 30 days. A multinomial logistic regression was performed to identify in-hospital and post-discharge predictors of VTE, adjusting for potential confounders.Results: Out of 260,258 patients, 5381 (2.1%) developed VTE. A total of 3442 (1.3%) were diagnosed during the initial hospital stay and 1929 (0.8%) post-discharge. Risk factors for in-hospital and post-discharge VTE were different as patients with an in-hospital event were more likely to be older, male, known for preoperative steroid use, have poor functional status, significant weight loss, preoperative sepsis, prolonged operative time, undergoing an emergency operation. In the post-discharge setting, steroid use, poor functional status, preoperative sepsis, and postoperative complications remained significant. Postoperative complications were the strongest predictor of in-hospital and post-discharge VTE. Patients with inflammatory bowel disease had a higher risk of VTE than patients with malignancy for both in-patient and post-discharge events.Conclusions: Patients at high-risk for post-discharge events have different characteristics than those who develop VTE in-hospital. Identifying this specific subset of patients at highest risk for post-discharge VTE may allow for the selective use of prolonged thromboprophylaxis. [ABSTRACT FROM AUTHOR]

Of the myeloproliferative neoplasms (MPNs), myelofibrosis (MF) is associated with the greatest symptom burden and poorest prognosis and is characterized by constitutional symptoms, cytopenias, splenomegaly and bone marrow fibrosis. A hallmark of MF is dysregulation of the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway that has led to the development of JAK inhibitors targeting this pathway. Calreticulin gene mutations have recently been identified in JAK2 mutation-negative patients with MF. Identification of JAK inhibitor resistance and broad contributions to MF disease pathogenesis from epigenetic deregulators, pathways that work in concert with JAK/STAT (that is, mammalian target of rapamycin/AKT/phosphoinositide 3-kinase, RAS/RAF/MEK, PIM kinase), fibrosis-promoting factors and the MF megakaryocyte, suggest that numerous options may be partnered with a JAK inhibitor. Therefore, we will discuss logical and potential partners for combination therapies for the treatment of patients with MF. [ABSTRACT FROM AUTHOR]

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