Heit, John A.

Abstract Background: Most trials of standard heparin and warfarin therapy used the 3- to 6-month cumulative incidence of venous thromboembolism (VTE) recurrence as the primary efficacy outcome. However, the independent effect of warfarin anticoagulation intensity on VTE recurrence after controlling for other predictors of recurrence (e.g., active cancer, neurological disease with extremity paresis) is uncertain. Objectives: To test warfarin anticoagulation intensity, using international normalized ratio (INR) data, as an independent predictor of 6-month VTE recurrence. Measurements: Using the resources of the Rochester Epidemiology Project, we identified all Olmsted County, MN residents with an incident deep vein thrombosis or pulmonary embolism over the 14-year period, 1984–1997 (n=1165). We followed each case (conditional on surviving 14 days without VTE recurrence) forward in time through their complete medical records in the community for first VTE recurrence. We collected date of incident VTE onset, start and stop dates of heparin and warfarin, and date, time and result of all INR values. Using these and other measures of standard warfarin therapy as time-dependent variables, we tested the intensity of warfarin anticoagulation (expressed as the cumulative percent of time with an INR at or above 2.0 [or at or above 1.5] while on warfarin) as an independent predictor of 6-month VTE recurrence while controlling for other baseline characteristics using Cox proportional hazards modeling. Results: Of the 1165 patients, 1026 (88%) and 989 (85%) received heparin and warfarin, respectively, and 254 (22%) developed recurrent VTE over 5461 person-years of follow-up; 52 recurred within 15–180 days. In the multivariate analysis, the independent predictor of 6-month recurrence was active cancer (HR=3.98, 95% CI: 2.12, 7.45; p<0.01); age, gender, body mass index and neurologic disease with extremity paresis were not predictors of VTE recurrence. In models that included presence or absence of warfarin therapy along with proportion of time with an INR ≥2, this latter intensity variable was protective (HR=0.16 for 100% versus 0% of time, p=0.02) against recurrence, while mere presence of warfarin therapy (HR =0.72, p= 0.56) was not. Similar results were obtained when intensity was represented as proportion of time with an INR ≥1.5 (HR=0.17, p=0.02). Interestingly, a therapeutic APTT within the first 24 hours of heparin therapy also was protective against 6-month recurrence (HR=0.45, p=0.02). Conclusions: Active cancer is an independent predictor of 6-month VTE recurrence. Warfarin therapy with a higher proportion of time with an INR ≥1.5 or ≥2 offers similar protection against recurrence. A rapid heparin-response (as reflected by a therapeutic APTT within 24 hours of heparin therapy) also is a predictor of reduced 6-month recurrence, possibly reflecting lower factor VIII activity at the acute incident VTE event. Gender is not a predictor of long-term recurrence.

Abstract Background Heparin-induced thrombocytopenia (HIT) is an immune-mediated drug reaction in which heparin-dependant IgG antibodies (HIT-IgG) to heparin-platelet factor 4 complexes form with the potential for platelet activation with resultant thrombocytopenia (HIT) and thrombosis (HITT). The frequency of HIT-IgG formation and clinically apparent HIT or HITT varies considerably, according to the patient population (surgical versus medical) and type of heparin (unfractionated [UFH] vs low molecular weight [LMWH]). One large prospective study showed a frequency of HIT-IgG formation of 7.5% with clinical HITT in 34.5% of these orthopedic patients receiving prophylactic LMWH and corresponding figures in cardiac surgery patients receiving UFH were 50% and 2%, respectively [Warkentin et al. Blood2000;96: 1703]. Due to daily exposure to heparin flushes (UFH) and prophylactic LMWH (to prevent venoocclusive disease) hematopoietic stem cell transplant (HSCT) recipients may be at risk for HIT/HITT. However, due to anticipated post-transplant thrombocytopenia, clinical cases of HIT/HITT may be overlooked. We retrospectively determined the incidence of HIT-IgG formation and its clinical significance in this population. Methods: HIT-IgG was measured retrospectively using a commercially available ELISA kit in samples collected from patients prior to conditioning therapy and on day 14 post-HSCT. Medical records were reviewed to in order to determine the clinical significance (development of clinical HIT/HITT) in those with detectable HIT-IgG. Patients Samples from a total of 103 HSCT recipients with hematologic malignancy (including 25 myeloma, 17 lymphoma, 16 AML, 14 amyloid, 10 MDS, 10 ALL, 8 CML and 3 CLL) were tested, of which 52 and 49 underwent allogeneic and autologous HSCT, respectively. All patients were exposed to UFH flushes during line care. In addition, all allogeneic recipients received prophylactic subcutaneous dalteparin 5000U daily beginning with conditioning until engraftment. Conditioning regimens included high dose melphalan (n=34), cyclophosphamide/TBI (n=30), carmustine, etoposide, cytarabine, melphalan (n=15), busulfan/cyclophosphamide (n=9), fludarabine/melphalan (n=10) and fludarabine/TBI (n=4). The median age was 51.5 years (20–72) and 68 were male. Results: The median platelet count prior to initiation of conditioning therapy and at day 14 was 157 × 109/L (range: 10–672) and 40 × 109/L (range: 9–289), respectively. Prior to conditioning, two of 103 (1.9%) patients had a positive HIT-IgG assay, that became negative in one and equivocal in the other by day 14 post-HSCT, and one patient had an equivocal HIT assay that became negative by day 14. All 3 were autologous recipients. None of the previously negative patients had a positive HIT-IgG assay at day 14, although 3 patients (2 autologous and one allogeneic) had an equivocal result of uncertain significance. No patients developed clinical or symptomatic thrombosis (HITT). Conclusion: In spite of frequent exposure to heparin, the frequency of seroconversion is low, and in those patients with preexisting HIT-IgG, no patient developed symptomatic thrombosis, including the 2 patients with positive HIT IgG assays prior to conditioning. The low frequency of HIT-IgG formation may reflect the profound immunosuppression of the conditioning regimens employed. Nevertheless, in this population, a high index of clinical suspicion must be maintained.

Abstract Background While consensus guidelines regarding VTE prophylaxis for hospital inpatients have been available for more than 15 years, the number of US inpatients who are potentially eligible for prophylaxis is unknown. Such data are required for estimating the potential costs and benefits of prophylaxis in reducing VTE incidence. Objective To estimate the number of Y2002 US acute-care hospital inpatients who are potentially eligible for VTE prophylaxis. Methods We applied the 7th (2004) American College of Chest Physician (ACCP) Consensus Conference VTE prophylaxis guidelines (Geerts et al. Chest2004;126:338S–400S) to inpatients with hospital discharge International Classification of Disease (ICD-9) codes for major surgery or medical illness identified from the Healthcare Utilization and Cost Database (HCUP), a national acute-care hospital database supported by the US Agency for Health Care Quality Research. Results Of a total of 37.8 million inpatients discharged from US acute-care hospitals in Y2002, 13.4 million (35%) met ACCP guideline criteria for VTE prophylaxis (Table). Table. Inpatients Discharged from US Acute-Care Hospitals with ACCP Guideline Defined Risk of VTE in Y2002 Surgical VTE Risk N Highest risk surgery 744,465 High risk surgery 3,031,318 Moderate risk surgery 2,019,696 Surgical subtotal 5,795,479 Medical VTE Risk N Heart failure 1,867,576 Cancer 1,017,356 Stroke 515,370 Other medical conditions 4,196,343 Medical subtotal 7,596,645 Grand Total 13,392,124 Among the 37.8 million Y2002 discharged inpatinets, 7.7 million were defined by HCUP criteria as having had a major operative procedure. When ACCP surgical risk criteria were applied to this population, 1.9 (25%) were at low VTE risk, while 5.8 million (75%) were at moderate (26%), high (39%) or highest (10%) VTE risk. Among the patients without a major operative procedure, 7.6 million met the ACCP criteria for VTE prophylaxis based on medical illness risk factors. Conclusions In total, 13.4 million US residents meet ACCP criteria for VTE prophylaxis annually due to hospitalization for either major surgery or medical illness. Given that almost 60% of all VTE events occurring in the community are related to recent acute-care hospitalization, providing universal, safe and effective VTE prophylaxis to this population affords an important opportunity to significantly reduce the incidence of VTE. These data provide support for developing and monitoring compliance with hospital-wide guidelines for VTE prevention.

Abstract Background: While several uncommon disorders (e.g., myeloproliferative diseases, connective tissue disease, etc.) have been suggested as potential risk factors for VTE, the independence and magnitude of any risk is uncertain. Objective: To test uncommon characteristics as potential independent risk factors for VTE, and estimate the magnitude of risk for each. Methods: Using the resources of the Rochester Epidemiology Project, we identified all incident cases of deep vein thrombosis and pulmonary embolism over the 6-year period, 1992–1997. For each objectively confirmed case (n=562), we identified up to two Olmsted County residents without VTE who most closely matched a case on age, gender, and medical record number (n=755). Because medical record numbers are assigned sequentially, such matching assures a similar duration of medical follow-up. For all cases and controls, we reviewed the complete medical records in the community for over 125 baseline characteristics which were tested for an association with VTE using conditional logistic regression. Results: The mean ± SD (range) ages for cases and controls were 65.71 ± 18.85 (0–102) and 64.90 ± 18.66 (0–102) years, respectively, and 55.5% were female. Novel univariate risk factors for incident VTE included former tobacco smoker, ischemic heart disease, valvular heart disease, chronic lung disease, all-cause pulmonary hypertension, chronic renal disease, myeloproliferative disorders, any infection, femoral artery catheterization (angiography or percutaneous intervention), ICU admission and angiotensin converting enzyme (ACE) inhibitor therapy. Among infections, septicemia, pneumonia, and ENT, cardiovascular, GI, urinary tract and skin/soft tissue infections were univariately associated with VTE; reproductive tract infection was not. Diabetes mellitus, hyperlipidemia, lipid-lowering drugs (including statins), inflammatory bowel disease, asthma, connective tissue disease, and influenza were not univariately associated with VTE, and beta-blocker therapy was not protective. A multivariate analysis will test these characteristics as potential independent VTE risk factors. Conclusions: Several novel characteristics are univariately associated with VTE. Such novel characteristics may provide new insights into VTE mechanisms if, upon further analysis, these characteristics are independent VTE risk factors.

Abstract Background The total annual number of VTE events and related deaths in the US is unknown, largely because the complete spectrum of disease (including asymptomatic events and sudden deaths) occurring in the community is under-recognized. Objective To estimate the total annual number of non-fatal and fatal deep vein thrombosis (DVT) and pulmonary embolism (PE) events (incident and recurrent) in the US. Methods We developed an incidence-based model that included both hospital- and community-acquired VTE events as well as death from recognized and unrecognized VTE. We estimated the annual number of community-acquired events using the average age-, sex-, and event-specific incidence rates in Olmsted County, MN (1966–1990) and Y2000 US census data. We estimated the annual number of hospital-acquired events using patient age and Y2002 International Classification of Disease (ICD-9) discharge diagnosis codes for major surgery types or acute medical illnesses within the Healthcare Utilization and Cost Database, which includes major discharge diagnoses from all US acute-care hospitals. Patients were included in the hospital model if they were deemed at risk of VTE according to current American College of Chest Physicians definitions. The hospital at-risk population was divided into categories according to type of surgery or medical diagnosis on admission. We estimated the annual number of VTE events based on the published probability of VTE with and without prophylaxis, and US prophylaxis rates, by risk group. Fatal and recurrent events were estimated based on published data. The effects of VTE and prophylaxis rate uncertainty on our estimates were tested using sensitivity analyses. Results The estimated total annual number of symptomatic VTE events in the US exceeded 600,000, (DVT, n=376,365; PE, n=237,058. Table). Table. Annual Number of Non-Fatal and Fatal, Community- and Hospital-Acquired Symptomatic VTE Events in the US Event Type Community Hospital Total Non-Fatal ---------n---------- DVT 108,240 268,125 376,365 PE 85,358 151,700 237,058 Total 193,598 419,825 613,423 Fatal DVT 649 1,609 2,258 PE 105,902 188,210 294,112 Total 106,550 189,819 296,370 VTE-related deaths were estimated at 296,370 annually. Of these deaths, 21,223 (7%) patients were diagnosed with VTE and treated, 101,032 (34%) were sudden fatal PE and 174,115 (59%) followed undetected PE. Approximately two-thirds of symptomatic VTE events were hospital-acquired and one-third were community-acquired. Conclusions Our study confirms that VTE is a major US health problem. Given that effective VTE prophylaxis and expert consensus prophylaxis guidelines are widely available, these data suggest that universal, safe and effective prophylaxis could significantly reduce US VTE incidence and related deaths. Future studies should address the impact of universal VTE prophylaxis on VTE incidence and survival.

Abstract Background AL amyloidosis can be associated with coagulopathy due to acquired factor X (FX) deficiency. Published experience, limited to case reports, suggests that infusion of fresh frozen plasma (FFP), platelets, plasma exchange, and vitamin K are of limited hemostatic efficacy for periprocedural management of coagulopathy. Therefore, we reviewed our cumulative experience of managing patients (pt) with FX deficiency due to AL amyloidosis who underwent an invasive procedure. Methods Pt with AL amyloidosis and isolated FX deficiency (≤ 50%), who underwent an invasive procedure between January 1975 and May 2007, were retrospectively identified from institutional databases. We excluded bone marrow biopsies as well as procedures >3 months prior to the diagnosis of FX deficiency. Endpoints of the study were bleeding, thrombosis, and death. Results Sixty-one pt fit the study criteria. They were arbitrarily classified as having severe (<10%; n=6), moderate (10–25%; n=16), or mild (26–50%; n=39) FX deficiency. The pt underwent a total of 115 procedures, 13 (11.3%) of which were considered major procedures and 102 (88.7%) were minor procedures. Major Procedures 13 pt underwent a major procedure; 4 had severe FX deficiency, 2 moderate, and 7 mild. Procedures included splenectomy, colon resection, renal transplant, and others. All 4 of the pt with severe deficiency were treated with hemostatic agents (FFP, plasma exchange, tranexamic acid, danazol, aminocaproic acid, and rFVIIa) in the perioperative period. Two (50%) of these patients had complications: intraabdominal hematoma and death. The death occurred in a patient with splenic rupture and uncontrolled hemorrhage refractory to rFVIIa and FFP. None of the pt with moderate deficiency experienced complications, despite not receiving hemostatic agents. Similarly, 0/7 patients with mild deficiency developed complications (2 received hemostatic agents FFP, platelets, vitamin K, and DDAVP). Minor Procedures All 61 pt underwent a minor procedure; central venous catheter placement was the most common (n=26), followed by EGD with biopsy (n=16) and renal biopsy (n=10). Six pt with severe deficiency underwent 7 minor procedures, 2 (29%) of which were associated with excess bleeding, despite rFVIIa treatment in both cases. An additional 3 procedures were performed with hemostatic agents and were uncomplicated. 2/16 (13%) pt with moderate deficiency had excess bleeding, 1 of whom was treated with rFVIIa and the other was not treated. Two others received perioperative treatment and did not have a complication. There were 7 complications in the 39 patients with mild deficiency (18%), including 1 AV fistula thrombosis after rFVIIa. Five of the patients with a bleeding complication did not receive treatment. One patient with mild deficiency received procoagulants and did not have excess bleeding. Conclusions -This is the largest series examining the perioperative management of pt with FX deficiency due to AL amyloidosis -Complications occurred in 11.3% of procedures, including one death -In this series, there were no clear predictors of bleeding -FX deficiency did not contribute to mortality, with the exception of 1 case -Bleeding risk is relatively infrequent in pt with mild or moderate FX deficiency, particularly with non-vascular procedures -Although optimal management of pt with severe FX deficiency is unclear, options include rhFVIIa +/− FFP and aminocaproic acid in those requiring procoagulant therapy.

Abstract Background: While currently-diagnosable hematological cancer is a potent VTE risk factor (RR range =12–32), whether undiagnosable hematological cancer is a risk factor is uncertain. Objective: To estimate the hazard of subsequent hematological cancer among incident VTE patients with no apparent active hematological cancer within ± 3 months of the VTE event. Methods: In a population-based cohort study, we followed Olmsted County, MN residents with incident VTE over the 27-year period, 1973–1999, and previously matched Olmsted County residents without VTE, who survived with no apparent active hematological cancer within ± 3 months of the VTE event or a routine medical visit date, respectively, forward in time through their complete medical records in the community for hematological cancer. Data were abstracted on baseline demographic and clinical characteristics, type and stage of hematological cancer, and any prior solid tumor treatments. For cases and controls, hematological cancer-free survival from the event date was estimated by the Kaplan Meier method, and the homogeneity of survival curves was examined by the log-rank test. Cox proportional hazards regression was used to adjust for covariates. Results: 1860 VTE cases (56% females) and 1890 controls (53% females) were followed for 16,497 and 15,320 person-years, respectively, conditional on surviving 3-months free of hematological cancer. 43 VTE cases and 24 controls developed hematological cancer at a median of 63.5 months (range 0.7 – 334 months). The median age for cases was 63.2 years compared to 67.8 years for the controls (p<0.001). Hematological cancer types included non-Hodgkin’s lymphoma (n=19), chronic lymphocytic leukemia (n=11), acute myeloid leukemia (n=1), multiple myeloma (n=9), myeloproliferative disorders (n=10), and myelodysplastic syndromes (n=14). Case status was not univariately associated with subsequent hematologic cancer (HR=1.42; 95% CI: 0.85, 2.39; p=0.18). After adjusting for age, also associated with cancer, case status was significantly associated with hematological cancer (HR=1.90; 95% CI: 1.13, 3.20; p=0.015). Conclusions: Incident VTE patients have nearly a two-fold increased risk of subsequent hematological cancer. We hypothesize that VTE can be the initial manifestation of an occult hematological cancer clone.

Abstract Menorrhagia is a common clinical problem among reproductive age women and annually 5% of reproductive age women seek medical attention, usually with gynecologists and other primary care physicians, for this symptom. Since underlying bleeding disorders are common in women presenting with menorrhagia, and referral for comprehensive hemostatic testing of substantial numbers of women with otherwise unexplained menorrhagia is problematic from the public health and cost perspective, a short, easy-to-administer screening tool comprised of 8 questions for identifying women with menorrhagia for hemostatic evaluation was previously developed (Am J Ob Gyn2008;198:e1–163e8). In the present study, the validity of the screening tool was evaluated in a multi-site, prospectively recruited cohort of women with menorrhagia. 232 women with menorrhagia age 18 and older with a pictorial blood assessment chart (PBAC) score > 100 were recruited from 5 US centers as potential subjects for a prospective cross-over study for evaluation of intranasal DDAVP versus tranexamic acid. All subjects underwent comprehensive laboratory testing for bleeding disorders, including VWF, platelet aggregation/ATP release, and factor assays. Study participants were administered a questionnaire which included the 8 screening tool questions in 4 categories, including history of duration and severity of menorrhagia, anemia treatment, excessive bleeding with hemostatic challenges, and family diagnosis of bleeding disorder. A screening tool was considered positive if there was a positive response for any of the questions in the four categories. Sensitivity of the screening tool with 95% confidence interval was calculated for bleeding disorders and also separately for low VWF (ristocetin cofactor < 50%), and platelet function defects.217 women with menorrhagia including 78% white and 16% black women with complete data were evaluated. In this population, a positive screening tool had a sensitivity of 89% (95% CI, 83–93) for bleeding disorders, 89% for platelet function defects (95% CI, 82–94), and 73% for low VWF (95% CI, 39–94). The sensitivity for bleeding disorders was 87% (95% CI, 79–92) among white women and 94% (95% CI, 79–99) among black women. Adding a PBAC score > 185 increased the sensitivity of the screening tool for bleeding disorders to 95% (95% CI, 90–98). Using a multi-site US population of adult women with menorrhagia, this study confirms the benefit of a short screening tool to assist primary care physicians in the selection of women with menorrhagia to refer for comprehensive hemostatic testing and evaluation. population of adult women with menorrhagia, this study confirms the benefit of a short screening tool to assist primary care physicians in the selection of women with menorrhagia to refer for comprehensive hemostatic testing and evaluation.

Abstract Background & Objectives: Diagnosis and classification of VWD are currently based on integration of personal and family bleeding histories and results of protein-based diagnostic tests (VWF:Ag, VWF:RCo, FVIII:C, VWF:CB and VWF multimers) which have performance limitations. Genetic testing is emerging as a complementary diagnostic tool. We have identified mutations and correlated VWF multimer patterns in our patients (pt) with types 2 & 3 VWD, and report novel candidate mutations. Patients & Methods: Unrelated pt with type 3 (n=6) and subtypes 2 (n=22) VWD, from Mayo Comprehensive Hemophilia Center, consented to this IRB approved study. PCR amplification, from genomic DNA, of VWF gene (splice junctions, coding and promoter regions), avoiding pseudogene amplification, followed by ABI® sequencing and analysis (Mutation Surveyor: SoftGenetic®) were performed. Mutations were compared to VWD (ISTH), NCBI NR nucleotide and DV SNP databases. Comparison with available VWF sequences from other vertebrate species was performed. Selected regions not known to contain mutations remain to be sequenced. VWF multimer analysis was performed using a novel in-gel immunostaining and infrared imaging system. Results: Type 2A VWD (n=10), a novel mutation in exon 28 (E28) (V1524G: 2 pt) with characteristic VWF multimer abnormalities (decreased HMWM, increased satellite banding, suggesting enhanced VWF proteolysis). Type 2B VWD (n=6), 2 pt were compound heterozygous for 2 previously reported mutations, the first in E28 (R1306W)/E48 (T2647M) and the second in E28 (V1316M)/E20 (R854Q). Type 2M VWD (n=4): an 84 yr female with personal (spontaneous and post-surgical) and family bleeding histories, VWF:RCo 72%, VWF:Ag 118% (RCo:Ag ratio 0.61), normal FVIII and platelets, and aberrant VWF multimer banding pattern without substantive reduction of HMWM, had a novel mutation in E52 (S2775C; conserved in mouse, rat, chicken and dog); a 14 yr female with a history of bleeding, VWF:RCo 34%, VWF:Ag 68% (RCo:Ag ratio 0.5) and normal FVIII and platelets, was compound heterozygous for a known mutation (R1399C subtype not classified in VWD database) and two novel mutations: E30 (P1725S) (conserved in mouse, rat, dog, cow and chimp) & E49 (T2666M) (conserved in mouse, dog, rat not in chicken). VWF multimers demonstrated abnormal banding pattern without substantive reduction of HMWM; 2 unrelated pt and families with ultra-large and smeary multimers, previously classified as Vicenza variant, had R1374C mutations and were reclassified as Type 2M VWD. Type 2N VWD (n=1) previously reported mutation E20 (R854Q) was confirmed. Type 3 VWD, 2 pt had novel mutations, the first in E22 (E950X) and the second was a compound heterozygote for E43 (R2478Q)/E40 (E2322V) mutations. In general, patients with similar mutations had similar multimer patterns. Conclusions: We report novel candidate mutations in types 2 & 3 VWD and demonstrate novel VWF multimer patterns with our in-gel staining system. Multimer patterns correlated well with the underlying genotype. The novel mutations are likely causative, given their occurrence at highly conserved residues, but this needs to be confirmed with expression studies. Integration of genetic testing into the diagnostic workup of VWD will potentially lead to more accurate diagnosis and subtyping of VWD, and may further refine protein based testing and provide additional biological insight into VWD.

Abstract Background: Hematological cancer patients are at an increased risk for VTE (RR range = 12–32). However, whether VTE risk among such patients can be further stratified is uncertain. Objective: To test hematological cancer type, stage, stage progression and chemotherapy as potential risk factors for VTE among active hematological cancer patients after controlling for other previously-identified VTE risk factors. Methods: Using the resources of the Rochester Epidemiology Project, Mayo Clinic Master Diagnostic Index and Mayo Clinic Tumor Registry, we identified all Olmsted County, MN residents with active hematological cancer over the 28-year period, 1973–2000. From this prevalence cohort, we identified 86 patients with no prior VTE (controls) who were matched on age and date of hematological cancer diagnosis to 86 hematological cancer patients with incident VTE over the same time frame (cases). For all cases and controls, we reviewed the complete medical records in the community for baseline and hematological cancer-related characteristics. Hematological cancers were re-staged at the dates of the cancer and VTE diagnosis. We tested these characteristics as potential risk factors for VTE in active hematological cancer using conditional logistic regression. Results: In an initial multivariate analysis that included body mass index (BMI), hospitalization, and any infection or central venous catheter placement within 90 days prior to the VTE event, VTE was significantly associated with hospitalization (OR=6.70; p<0.001), and marginally associated with any infection (OR=2.18; p=0.09). After adjusting for the above variables, chemotherapy administered within the preceding 90 days was significantly associated with VTE (OR=4.25; p=0.02), while stage progression was marginally associated (OR=4.79; p=0.10). Compared to all other hematological cancer types, acute leukemia (OR=5.95; p=0.01) and non-Hodgkin’s lymphoma (OR=2.61; p=0.01) were associated with VTE. However, after adjusting for BMI, hospitalization, any infection and central venous catheter, only non-Hodgkin’s lymphoma was independently associated with VTE (OR=3.79, p=0.009), while acute leukemia was not (OR=2.66, p=0.35). Conclusions: Hematological cancer type (in particular, non-Hodgkin’s lymphoma and possibly acute leukemia), recent hospitalization, recent chemotherapy, and possibly stage progression and recent infection, are risk factors for VTE among patients with active hematological cancer.