Abstract: Introduction: While the presence of HIV portends a poor prognosis in many malignancies, its clinical association with MDS and AML has not been well studied, and is known primarily from small case reports and case series. We evaluated the prevalence and clinical course of unexplained cytopenias and clinically proven MDS/AML in a large cohort of HIV-positive (HIV+) patients (pts) seen at a single center, and compared their clinical course to MDS/AML in non-HIV (HIV-) pts. Methods: Data from 15,120 HIV+ pts seen between 1/1/1997 to 6/1/2016 was analyzed for hematologic parameters, HIV status (CD4 count, HIV viral load), chronic disease status and nutrient deficiencies. Anemia was defined as hemoglobin 〈 10, thrombocytopenia as platelets 〈 100 and neutropenia as absolute neutrophil count of 〈 1800, as per the MDS IPSS criteria. Pts with no obvious causes for their cytopenias, such as advanced AIDS, opportunistic infections, chronic kidney disease or nutrient deficiency anemia were determined to have unexplained cytopenias. Furthermore, pts with multiple lineage cytopenias were assessed for evidence of primary bone marrow etiology. Results: Out of 13,277 HIV+ pts that had evaluable blood counts, 1075 pts (8.1%) had cytopenias affecting more than one lineage. 912 pts had bilineage cytopenias and 163 pts had a pancytopenia. This was significantly higher than the frequency of bi/trilineage cytopenias in a non-HIV elderly population that was recently analyzed; 8.1% in HIV+ pts vs 0.9% in non-HIV pts, p 〈 0.0001. Out of a total of 466 cytopenic pts that had all evaluable blood test results, including HIV parameters and chronic disease labs, 119 pts (25.6%) were found to have unexplained bi/trilineage cytopenias with a CD4 count of 〉 250 and HIV viral load 〈 100. Pts with unexplained bi/trilineage cytopenias also presented at relatively younger age (median age 47 years (yrs) (range 24-70 yrs), than pts presenting with MDS. We also identified 10 MDS and 9 AML pts in our HIV+ cohort. Mean CD4 count for these cases was 340 cells/mm3, with only 4 pts 〈 200 cells/mm3. Median time to MDS or AML diagnosis from date of HIV diagnosis was 15.6 and 13.7 yrs respectively. All pts were receiving anti-retroviral therapy at the time of MDS or AML diagnosis. Only 3 MDS pts and 1 AML patient had a history of prior exposure to chemotherapy. Clinical characteristics of the HIV+ MDS pts (n=10) were compared to HIV- MDS pts (n=135) from the same institution diagnosed between 1997-2011. HIV+ MDS pts presented at a younger age (59.5 vs 70.6 yrs, p = 0.001) and also had significantly higher risk (Int-2/High) disease by IPSS (87.5% vs 17.8%, p 〈 0.001). HIV+ AML pts also presented at a younger age compared with known historical data (56 vs 69 yrs, p = 0.002). Cytogenetic abnormalities were found in 6 of 7 (85.7%) evaluable HIV+ MDS pts, with monosomy 7 being the commonest alteration (71.4%). Six (60%) of the HIV+ MDS pts progressed to AML, with a mean time to progression of 10.4 months. Importantly, HIV+ MDS pts had significantly worse overall survival compared to controls (9.6 vs 58.2 mo, p 〈 0.001, Figure 1.). Univraiate analysis of MDS pts confirmed that HIV+ pts had statistically significant worse OS, higher risk cytogenetics and younger age at presentation. HIV+ AML pts exhibited poor overall survival of 9.5 mo (range 39-73 yrs). Conclusions: Anemia occurs in most HIV pts at some point in their course, however, bicytopenia and pancytopenia are generally thought to be uncommon, especially in pts with well-controlled disease. We demonstrated in our cohort an unexpectedly high prevalence of unexplained bi/trilieneage cytopenias, not associated with advanced HIV, chronic disease or nutrient deficiencies. This finding suggests the presence of an independent, HIV-specific, mechanism of hematopoietic suppression, acting either at the level of the stem cell, or the bone marrow milieu. We also report on the largest cohort of HIV+ MDS/AML cases in the literature and demonstrate that HIV+ pts who develop MDS and AML do so at a younger age, present with more advanced disease that is resistant to standard therapy, and have worse overall survival than a control cohort of HIV- pts. These data present evidence that suggests that MDS should be considered as a diagnosis early in HIV. Appropriate risk stratification and new therapeutic approaches are needed. Kaplan-Meier curve comparing overall survival in HIV infected and non-HIV infected MDS patients. Kaplan-Meier curve comparing overall survival in HIV infected and non-HIV infected MDS patients. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

Abstract: Myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) suppress normal hematopoietic activity in part by enabling a pathogenic inflammatory milieu in the bone marrow. In this report, we show that elevation of angiopoietin-1 in myelodysplastic CD34+ stem-like cells is associated with higher risk disease and reduced overall survival in MDS and AML patients. Increased angiopoietin-1 expression was associated with a transcriptomic signature similar to known MDS/AML stem-like cell profiles. In seeking a small-molecule inhibitor of this pathway, we discovered and validated pexmetinib (ARRY-614), an inhibitor of the angiopoietin-1 receptor Tie-2, which was also found to inhibit the proinflammatory kinase p38 MAPK (which is overactivated in MDS). Pexmetinib inhibited leukemic proliferation, prevented activation of downstream effector kinases, and abrogated the effects of TNFα on healthy hematopoietic stem cells. Notably, treatment of primary MDS specimens with this compound stimulated hematopoiesis. Our results provide preclinical proof of concept for pexmetinib as a Tie-2/p38 MAPK dual inhibitor applicable to the treatment of MDS/AML. Cancer Res; 76(16); 4841–9. ©2016 AACR.

Abstract: Background: Carfilzomib and Bendamustine are currently FDA approved for therapy of relapsed refractory multiple myeloma (MM). Bendamustine, in addition to interference with DNA replication, it can induce inhibition of mitotic checkpoints, inefficient DNA repair, and initiation of a p53-dependent DNA-damaging stress response leading to apoptosis of tumor cells (1). It has previously shown significant activity in relapsed myeloma (2). Carfilzomib is a second generation, irreversible proteasome inhibitor has demonstrated promising activity in first line therapy (3,4). we hypothesized that combining them will yield an effective induction regimen in the newly diagnosed MM. Study design: Inclusion criteria included newly diagnosed MM with measurable disease, age ≥18, ECOG PS 0-2, adequate renal (creatinine clearance 〉 30 mL/min), cardiac and hepatic function. Carfilzomib was given IV on days 1, 2, 8, 9, 15, 16. All patients received 20 mg/m2 on days 1 and 2 of cycle 1, after which their dose was escalated to one of the following levels: 27, 36, 45, or 56 mg/m2. Bendamustine IVPB on days 1, 2, at 70 (dose levels 1 and 2) or 90 mg/m2 (dose levels 3-5). Dexamethasone 20 mg PO or IV D 1, 2, 8, 9, 15, 16, 22, 23. Each cycle of therapy was 28 days, and a total of 8 cycles was given. Stem cell harvest was done after 4 cycles and eligible patients proceeded to ASCT after 8 cycles. Maintenance was recommended - either carfilzomib (36mg/m2 D 1,2, 15, 16 of a 28-day cycle for 2 years, or investigator's choice. Primary objective was to determine the recommended phase 2 dose (RP2D) and additional objectives assessed efficacy and safety. Results: Between February 2014 and May 2018, 20 patients with newly diagnosed MM pts were accrued onto study (5 pts in phase I and 15 in phase II). Median age was 65 (range 48-74), and 14 (70%) patients were male. 7 (35%) were of Hispanic ethnicity. 3 patients (15%) were R-ISS stage 3, and 1 (5%) had high-risk cytogenetics. We did not observe any DLTs with our study treatment and established the RP2D as: carfilzomib 56 mg/m2, bendamustine 90 mg/m2 and dexamethasone 20 mg on the dosing schedule given above. The most common and severe toxicities were hematologic. Grade 3/4 hematologic toxicities were lymphocytopenia in 90% of patients, neutropenia 40%, anemia 20% and thrombocytopenia 20%. Notable non-hematologic toxicities were grade 3/4 infection in 20% of patients (typically upper respiratory and pneumonia), grade 1/2 acute kidney injury in 45% of patients, and grade 1/2 diarrhea in 40% of patients. No treatment emergent hypertension or heart failure were noted. 1 patient died while on study, from septic shock due to pneumonia 7 weeks after completion of induction. The regimen was highly effective, with an ORR of 100%. Best responses were: 2 (11%) PR, 5 VGPR (26%), and 12 CR (63%) (Figure 2). Among the CRs, 4 were MRD-positive, 5 were MRD-negative, and 3 did not have MRD testing. With a median follow-up of 28 months (range 11-71), 2 patients have progressed - 1 with del(17p) at 19 months after diagnosis, and the other with standard cytogenetic risk disease at 56 months. 2 patients have died - the patient with del(17p) from refractory myeloma at 37 months after diagnosis, and the other from septic shock as discussed above. Median PFS was 56 months, and median OS has not been reached. Conclusion: Carfilzomib, Bendamustine and Dexamethasone is safe and highly effective for newly diagnosed transplant eligible MM and should be further explored in a larger prospective trial for this patient population. References: 1. Leoni LM, Hartley JA. Mechanism of action: the unique pattern of bendamustine-induced cytotoxicity. Seminars in hematology 2011;48 Suppl 1:S12-23. 2. Lentzsch S, O'Sullivan A, Kennedy RC, et al. Combination of bendamustine, lenalidomide, and dexamethasone (BLD) in patients with relapsed or refractory multiple myeloma is feasible and highly effective: results of phase 1/2 open-label, dose escalation study. Blood 2012;119:4608-13. 3. Dimopoulos MA, Goldschmidt H, Niesvizky R, et al. Carfilzomib or bortezomib in relapsed or refractory multiple myeloma (ENDEAVOR): an interim overall survival analysis of an open-label, randomised, phase 3 trial. The Lancet Oncology 2017;18:1327-37. 4. Jakubowiak AJ, Dytfeld D, Griffith KA, et al. A phase 1/2 study of carfilzomib in combination with lenalidomide and low-dose dexamethasone as a frontline treatment for multiple myeloma. Blood 2012;120:1801-9. Disclosures Bhutani: Sanofi: Membership on an entity's Board of Directors or advisory committees. Assal:Incyte corporation: Consultancy, Research Funding; boston biomedical: Consultancy. Lentzsch:Janssen: Consultancy; Takeda: Consultancy; BMS: Consultancy; Proclara: Consultancy; Abbvie: Consultancy; Clinical Care Options: Speakers Bureau; Sanofi: Consultancy, Research Funding; Multiple Myeloma Research Foundation: Honoraria; International Myeloma Foundation: Honoraria; Karyopharm: Research Funding; Columbia University: Patents & Royalties: 11-1F4mAb as anti-amyloid strategy; Caelum Biosciences: Equity Ownership, Membership on an entity's Board of Directors or advisory committees; Bayer: Consultancy. OffLabel Disclosure: Carfilzomib, Bendamustine and Dexamethasone for newly diagnosed multiple myeloma.

Abstract: Introduction: The only cure for sickle cell disease (SCD) is allogeneic hematopoietic stem cell transplant (HSCT) although autologous HSCT of genetically engineered hematopoietic stem cells is promising. Lack of suitable matched related donors (MRD) is a major limitation driving interest in improving outcomes using unrelated donors. While excellent outcomes are achieved with non-myeloablative MRD HSCT in adults (Hsieh et al, 2009 and 2014), results from matched unrelated donor (MUD) HSCT have been limited by excessive graft versus host disease (GVHD) and treatment-related mortality (Shenoy et al, 2016). Here we present updated follow up of our institutional experience using MUD and mismatched unrelated donors (MMUD) in comparison to patients with MRD. Methods: Eligibility for HSCT included frequent pain crises requiring hospitalization and evidence of end-organ damage. Non-myeloablative conditioning with alemtuzumab and 3 Gy total body irradiation (TBI) was used for MRD HSCT (n=7), whereas patients without an MRD were transplanted using MUD, MMUD or haploidentical grafts (n=6) on a previously reported institutional protocol after conditioning with alemtuzumab (54 mg/m2), fludarabine (180 mg/m2), and melphalan (140 mg/m2), using a CD34+ selected graft with CD3+ cell add back. MRD recipients received sirolimus as GVHD prophylaxis. Non-MRD recipients initially received tacrolimus as GVHD prophylaxis (n=1) but subsequently received sirolimus (n=5) due to the first patient developing posterior reversible encephalopathy syndrome (PRES). All grafts were G-CSF mobilized peripheral blood grafts and all patients underwent RBC exchange to achieve Hgb S 〈 30%. Data is reported using n (%) or median (range) and Wilcoxon rank-sum test was used for continuous variables. Results: Median follow up is 21.7 months (range 4.7 - 63.4). Median age for MRD recipients was 28.7 (21.4 - 35.5) years and 22.8 (18.5 - 34.6) for non-MRD recipients. Of note, the MRD group included one patient with a renal allograft from the same donor and another with stage V renal disease awaiting a kidney transplant. All patients where homozygous for hemoglobin S except one who had hemoglobin Sβo -thalassemia in the MRD group, and another heterozygous for hemoglobin S and C in the non-MRD group. Patients in the MRD group received unmanipulated grafts with a median of 14 (6.2 - 16.9) x 10E6 CD34+ cells/kg. Non-MRD recipients received CD34 - selected grafts with a median of 7.8 (4.1 - 15.1) x 10E6 CD34+ cells/kg with 2.2 x 10E5 (0.1 - 2.5) CD3+ cells add back. No growth factors were used post-transplant. All patient engrafted with no cases of graft failure. Median time to engraftment was significantly longer for the MRD group at 25 (22 - 30) vs 19 (13 - 21) days, p=0.003. Two patients in the MRD group developed acute/late acute GVHD (2 grade II), and 3 patients in the non-MRD group (1 grade II, 2 grade III), 2 of which developed in while switching immune suppression due to PRES. All GVHD cases were steroid responsive and resolved. Three patients in the non-MRD group developed PRES and none in the MRD group. There were no cases of treatment related mortality and all patients are alive and free of SCD. As both groups received alemtuzumab, and the non-MRD group received a CD34-selected graft, we examined lymphocyte subset reconstitution at day 100 and 1 year post-HSCT. The most striking difference was in median CD8+ T cell counts at day +100 which were lower in the non-MRD group approaching significance [101 (43 - 2995) vs 6.5 (3 - 2233) cells/uL, p=0.055, for the MRD and non-MRD respectively]. CD8+ T-cell counts were not significantly different at 1 year [402 (184 - 1066) vs 774 (143 - 1002) cells/uL, p 〈 0.99]. Results from other lymphocyte subsets including CD4+ T-cells, NK cells and B cells are shown in table 1 and were not significantly different between the 2 groups. Of note, early donor T-cell chimerism at D100 was not significantly different between MRD and non-MRD groups [27.0 (18.0 - 50.0) % vs 37.5 (3.0 - 80.0) %, p=0.83] whereas at 1-year, MRD group donor T cell chimerism was significantly lower [53.5 (17.0 - 65.0) % vs 82.7 (69 - 90), p=0.01]. Conclusion: We demonstrate excellent outcomes with 100% survival and no graft rejection following matched and mismatched unrelated donor HSCT for adult patients with severe SCD. Larger cohorts are needed to confirm these results and further delineate the impact of T-cell subset reconstitution on early-post transplant complications. Disclosures Assal: Incyte corporation: Consultancy, Research Funding; boston biomedical: Consultancy. Bhatia:BMS: Consultancy; Vertex Pharmaceuticals: Membership on an entity's Board of Directors or advisory committees. Bhutani:Sanofi: Membership on an entity's Board of Directors or advisory committees. Lentzsch:Abbvie: Consultancy; Clinical Care Options: Speakers Bureau; Sanofi: Consultancy, Research Funding; Multiple Myeloma Research Foundation: Honoraria; International Myeloma Foundation: Honoraria; Karyopharm: Research Funding; Columbia University: Patents & Royalties: 11-1F4mAb as anti-amyloid strategy; Caelum Biosciences: Equity Ownership, Membership on an entity's Board of Directors or advisory committees; Bayer: Consultancy; Janssen: Consultancy; Takeda: Consultancy; BMS: Consultancy; Proclara: Consultancy. Reshef:Magenta: Consultancy; Kite: Consultancy, Research Funding; Atara: Consultancy, Research Funding; Pfizer: Consultancy; BMS: Consultancy; Pharmacyclics: Consultancy, Research Funding; Incyte: Consultancy, Research Funding; Celgene: Research Funding; Shire: Research Funding.

Abstract: Introduction: Sickle cell disease (SCD) affects 300,000 annual births globally, and about 100,000 individuals in the United States. Allogeneic hematopoietic stem cell transplant (HSCT) remains the only cure. HSCT risks necessitate a risk-benefit analysis in each case. Excellent long-term overall survival (OS) of 91-95% has been described with matched-sibling (SIB) HSCT, but fewer than 15% of SCD patients have a SIB donor. Matched unrelated donor (MUD) availability is limited for ethnic groups afflicted with SCD. Alternative donor HSCT from mismatched unrelated donors (MMUD) or haploidentical donors improves donor availability but increases toxicity and risk of graft failure. SCD-induced organ damage is another limitation to HSCT. In this study, we review our experience with HSCT for SCD and demonstrate that most patients can receive a curative HSCT despite lack of SIB donor and presence of significant co-morbidities. Methods: All adult SCD patients who received HSCT at our center since 2014 were included. Patients had at least 2 hospitalizations per year for pain crises despite hydroxyurea compliance and evidence of end-organ damage. Patients with a SIB donor (n=6) received conditioning with alemtuzumab and 3Gy TBI (per Hsieh et al, 2009). Patients with MUD/MMUD (n=4) or haploidentical (n=1) donors received conditioning with alemtuzumab, fludarabine, melphalan, and a CD34+ selected graft with CD3+ cell add back on an ongoing clinical trial for non-malignant hematologic diseases. One patient s/p kidney transplant and liver failure requiring TIPS procedure was conditioned with alemtuzumab and 4Gy TBI, received a 10/10 MUD graft, and given post-HSCT cyclophosphamide (50 mg/kg d+3) along with sirolimus continuation as GVHD prophylaxis. GVHD prophylaxis otherwise consisted of sirolimus (n=10) and tacrolimus (n=1). All patients received a G-CSF mobilized peripheral blood stem cell (PBSC) graft and underwent RBC exchange to achieve Hgb S 〈 30%. Results: Twelve patients are included in this analysis. Median age was 28.7 (18.5 - 44.2) years with 6 males and 6 females. Median follow up was 13.6 months (range 1.4 - 51.3). Two patients had stage V renal disease with one patient on active dialysis. Two patient were s/p kidney transplant with one patient awaiting a 2nd kidney transplant. Median CD34 cell dose in SIB and MUD/MMUD HSCT was 14.8 and 8.5 x 10e6 CD34/kg respectively. Median T cell add back in CD34-selected M/MMUD recipients was 2.5 x 10e5 CD3/kg. No G-CSF was used. All patient engrafted with no cases of graft failure or treatment related mortality (TRM). Median time to neutrophil engraftment for SIB and M/MMUD recipients was 24.5 and 19 days respectively. Median time to platelet engraftment was 19 days for M/MMUD recipients and 2 of 6 SIB recipients required only 1 platelet transfusion each. The patient s/p kidney allograft and TIPS for liver failure engrafted neutrophils and platelets on day +22 and +26 respectively. All patients are alive and free of SCD. Available chimerism analysis at 6 months (n=8) shows median myeloid chimerism to be the same in SIB and M/MMUD recipients (99.7%) where median T Cell chimerism was 35% and 65% for SIB and M/MMUD recipients respectively. Chimerism at 1 year shows stable myeloid engraftment and median T cell chimerism of 61.5% for SIB recipients. Two cases of PRES were noted after HSCT, one in a patient on tacrolimus after which the CD34-selected protocol was modified to include sirolimus as GVHD prophylaxis. Another case of PRES was noted on sirolimus which was switched to prednisone and mycophenolate mofetil. Two patients discontinued sirolimus due to myalgias and were switched to tacrolimus on days +44 and +58 with resolution of symptoms. Acute/Late acute GVHD occurred in 4 patients. Three cases were noted in patients treated on the CD34-selected protocol; two MMUD (Grade III and Grade I) and one haploidentical (Grade III) graft recipients. One case of late acute liver GVHD, evident in elevation of liver enzymes and alkaline phosphatase with evidence of hepatitis on biopsy, occurred in a SIB recipient (Grade I). All cases responded to corticosteroid therapy. Conclusion: SCD patients with or without a SIB donor can be offered a curative HSCT that is safe without TRM. SCD patients with severe SCD-related organ damage can also be offered HSCT however further research is warranted to identify optimal conditioning and GVHD prophylaxis regimens for these patients. Disclosures Reshef: Kite Pharma: Consultancy; Atara Biotherapeutics: Consultancy; Bristol-Myers Squibb: Consultancy; Takeda Pharmaceuticals: Consultancy; Pfizer: Consultancy; Incyte: Consultancy.

Abstract: Whether a complication of gynecologic surgeries or a peripartum event, ovarian vein thrombosis (OVT) remains poorly understood, with no consensus regarding its importance or treatment. In an effort to better understand the significance of OVT, we investigated the incidence, clinical features, predisposing factors, future thrombotic complications, and therapeutic patterns of this condition. Methods : We collected cases of OVT in adult women encountered over the 10 years. Data mining software was used to search the text of imaging reports for the terms ovarian or gonadal located within 5 words of the terms thrombus, thrombosis or thrombosed. Records were reviewed to confirm diagnosis and collect demographic data, presentation and features of OVT at baseline, past medical and surgical history, and future venous thromboembolism (VTE) events. Follow up period was defined as date of last EMR entry. All chart review were conducted by study authors and discrepancies reviewed by at least two authors. Data were analyzed using Chi-squared, t-testing for unpaired samples, and ANOVA. Results : 223 cases of confirmed OVT were identified and included in the analysis. Average follow-up time was 1163 (±977) days. The majority of cases were identified on computed tomography (CT) imaging (n=219). Mean age was 55 years (range 20 - 89 years). History of VTE was noted in 22 patients, diabetes in 44 patients and cancer in 134 patients, 64.3% of which were gynecologic. In a majority of patients, OVT was associated with a history of abdominal surgery; 60.5% of these were gynecologic procedures and 83.7% of those included a hysterectomy. Only 36.6% were noted to have otherwise unexplained abdominal pain. Chemotherapy was administered to 99 (44.4%) patients, 57 (57.6%) of which developed OVT during chemotherapy. Taxol was used in 61 patients (61.6%); 43 (70.5%) of which developed OVT during Taxol therapy. The incidence of right (R) or left (L) OVT was similar (44.6% vs. 41.4% respectively) with a high percentage of bilateral (B) thrombi (14%). Peripartum state was associated with an increase in ROVT (60.0% versus 43.1%, p=0.033); cancer patients had a higher incidence of LOVT and BOVT compared to non-cancer patients (46.6% and 18.8% vs. 33.7% and 6.7% respectively, p=0.0005). Gynecologic surgery was also associated with an increase in LOVT and B OVT (44.0% and 18.7% versus 37.5% and 6.8% p=0.007). Our cohort experienced 26 (11.7%) recurrent VTE events, 20 DVTs and 6 PEs (Table 1). Average time to recurrence was 393.5 (±400) days. Past VTE was associated with a higher risk of future DVT but not PE (22.0% and 0%, p=0.046 for VTE). No recurrent VTE events were noted in the peripartum group, however this did not reach statistical significance (p=0.089). Even when peripartum patients were excluded, LOVT and BOVT were associated with a higher VTE recurrence rate than ROVT (16.3% and 19.4%, p=0.01). Patients with cancer tended to have a higher VTE recurrence rate than non-cancer patients, but this did not reach statistical significance (14.2% versus 7.9%, p=0.15). However, recurrence was associated with greater mortality (p=0.002). Anticoagulation was initiated at the time of OVT diagnosis in only 21 (9.4%) patients, with 4 VTE recurrent events. Conclusion: This is the largest OVT study to date. We demonstrate that OVT can occur within either ovarian vein, but occurs predominantly on the right in peripartum patients. We show increased recurrent events in our cohort and an association of recurrence with mortality, which argues against a benign' nature of OVT in post-hysterectomy patients. We were not able to detect increased VTE recurrence in cancer patients, in the peripartum, in diabetics, or in patients with a history of VTE. Anticoagulation initiated at the time of OVT was not associated with decreased recurrence rates but this may be due to selection bias. This study provides evidence that a prospective study of patients is needed to determine the utility of therapy for OVT. Table 1 Subgroup analysis of the risk of future thrombotic events Variable (N) Recurrent VTE N (%) P Value Total (223) 26 (11.7%) Peripartum (20) 0 (0%) 0.089 Cancer (134) 19 (14.2%) 0.15 History of VTE (22) 5 (22.7%) 0.088 Laterality BOVT (31) 6 (19.4%) 0.07 LOVT (92) 15 (16.3%) ROVT (99) 5 (5.1%) Extension Present (17) 3 (17.6%) 0.42 Absent (206) 23 (11.2%) During chemotherapy (57) 9 (15.8) 0.65 Anticoagulated for OVT (21) 4 (19.0) 0.27 Disclosures No relevant conflicts of interest to declare.