Thrombosis Risk Factors Assessment In Children Treated For Acute Lymphoblastic Leukemia

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4791-4791
Author(s):  
Katarzyna Smalisz-Skrzypczyk ◽  
Anna Klukowska ◽  
Katarzyna Pawelec ◽  
Michal Matysiak
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Central Venous Catheter ◽  
Lymphoblastic Leukemia ◽  
Age At Onset ◽  
Factor V Leiden ◽  
Venous Catheter ◽  
Factor V ◽  
Central Venous ◽  
Protein C Deficiency ◽  
Factor V Leiden Mutation

The aim of the study was to evaluate factors predisposing to thrombosis in children treated for acute lymphoblastic leukemia according to ALL IC BFM 2002. An analysis of 30 cases of thrombosis in 210 children (14%) treated due to ALL in the Department in years 2007-2011 was carried out. Age at onset, location, cause and treatment methods were taken into consideration. All analyzed patients underwent screening for congenital thrombophilia. The age of patients ranged from 1.5 to 16 years with the median of 7.5 years. Arterial thrombosis occurred in 1 person (3%), venous thrombosis in 29 (97%) patients. Thromboembolism was usually related to the central venous catheter (n = 27, 90%). Massive thrombosis occurred in 6 patients (20%). Relapses occurred in 2 children. The most common causes of thrombosis were: the presence of the central catheter (n = 27, 90%) and L-asparaginase treatment (n = 16, 53%). The factor V Leiden mutation was diagnosed in 1 patient, protein C deficiency in 1 patient as well, and elevated levels of factor VIII were detected in 3 cases. Five children (16%) underwent systemic thrombolysis with recombinant tissue plasminogen activator and 17 patients (52%) had local thrombolysis. Anticoagulation with warfarin following low-molecular-weight heparin discontinuation was used in 6 patients (20%). The complete resolution of the thrombus was observed in the whole group of patients. Conclusions 1. A risk factor for thrombosis in children with ALL is the treatment of L-asparaginase and the presence of central venous catheter. 2. Screening for congenital thrombophilia in children treated for ALL should not be done routinely since the coexistence of this two conditions is rare. Thrombosis in children with ALL responds well to treatment. Disclosures: Klukowska: Octapharma AG: Investigator Other.

The Prevalence of Congenital Trombophilia in Children Treated for Acute Lymphoblastic Leukemia with Thrombosis As a Complication

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 5251-5251
Author(s):  
Katarzyna Smalisz-Skrzypczyk ◽  
Anna Klukowska ◽  
Katarzyna Pawelec ◽  
Michal Matysiak
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Central Venous Catheter ◽  
Factor Viii ◽  
Conflicts Of Interest ◽  
Lymphoblastic Leukemia ◽  
Age At Onset ◽  
Factor V Leiden ◽  
Venous Catheter ◽  
Central Venous ◽  
Factor V Leiden Mutation

Abstract The aim of the study was to evaluate factors predisposing to thrombosis, especially congenital trombophilia, in children treated for acute lymphoblastic leukemia according to ALL IC BFM 2002 and 2009. An analysis of 36 cases of thrombosis in 242 children (15%) treated due to ALL in the Department in years 2007-2013 was carried out. Age at onset, location, cause and treatment methods were taken into consideration. All analyzed patients underwent screening for congenital thrombophilia. The age of patients ranged from 1.5 to 17 years with the median of 8.5 years. Arterial thrombosis occurred in 2 persons (1%), venous thrombosis in 34 (99%) patients. Thromboembolism was usually related to the central venous catheter (n = 31, 91%). Massive thrombosis occurred in 7 patients (20%). Relapses occurred in 3 children. The most common causes of thrombosis were: the presence of the central catheter (n = 31, 91%) and L-asparaginase treatment (n = 19, 55%). The factor V Leiden mutation was diagnosed in 1 patient, protein C deficiency in 1 patient as well, and elevated levels of factor VIII were detected in 4 cases. The mean concentrations of factor VIII, von Willebrand factor and antithrombin were not different in the groups with and without thrombosis (table 1 ). The concentration of fibrinogen measured after finishing the chemotherapy was similar in both groups. Conclusions 1. A risk factor for thrombosis in children with ALL is the treatment of L-asparaginase and the presence of central venous catheter. 2. Screening for congenital thrombophilia in children treated for ALL should not be done routinely because the coexistence of this two conditions is rare. Table 1FVIII (%)Fibrinogen ( g/l)AT (%)Patients with thrombosis1012,776Patients without thrombosis892,4382p0,45 ( ns)0,2 (ns)0,34 (ns) Disclosures No relevant conflicts of interest to declare.

Factor V Leiden Mutation in Patients with Breast Cancer with a Central Venous Catheter: Risk of Deep Vein Thrombosis

2006 ◽  
Vol 3 (2) ◽  
pp. 98-102 ◽  
Author(s):  
Giuseppe Curigliano ◽  
Mario Mandalà ◽  
Alberto Sbanotto ◽  
Marco Colleoni ◽  
Gianluigi Ferretti ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Deep Vein Thrombosis ◽  
Central Venous Catheter ◽  
Factor V Leiden ◽  
Venous Catheter ◽  
Factor V ◽  
Central Venous ◽  
Factor V Leiden Mutation ◽  
Vein Thrombosis ◽  
Deep Vein

Thromboelastography to Detect Hypercoagulability in Patients with Newly Diagnosed Acute Lymphoblastic Leukemia

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 1118-1118 ◽  
Author(s):  
Richard Har Ko ◽  
Richard Sposto ◽  
Fariba Goodarzian ◽  
Roxana Carmona ◽  
Siobhan Vasquez ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Central Venous Catheter ◽  
Prospective Study ◽  
Thrombin Generation ◽  
Lymphoblastic Leukemia ◽  
Venous Catheter ◽  
Newly Diagnosed ◽  
Older Children ◽  
Central Venous ◽  
Patient Demographics

Abstract Background: Patients with newly diagnosed acute lymphoblastic leukemia (ALL) are known to be hypercoagulable due to their disease and from side effects of chemotherapy. Studies have shown rates of venous thromboembolism (VTE) between 5-70% in patients with ALL (depending on various definitions and modalities of investigation) (Caruso et al, 2006, Mitchell et al, 2003). Established methods to monitor hypercoagulability or predict VTE do not exist. We have previously described methods using thromboelastography (TEG) to detect hypercoagulability (Ko et al., 2013). We believe that a global assay of hemostasis such as TEG holds promise to monitor hypercoagulability in patients with newly diagnosed ALL. Methods: This was a prospective study of newly diagnosed ALL patients between 1-21 years in whom a central venous catheter (either a peripherally inserted central catheter [PICC] or a subcutaneously implanted port) was placed at diagnosis. Patients were enrolled at Children's Hospital Los Angeles from September 2012 until July 2015. None of the patients had a known past medical or family history of thrombosis or bleeding or clotting disorders and none were taking any medications (other than induction chemotherapy) that could affect coagulation (e.g. NSAIDs). Patients had complete blood counts (CBC), TEG, and markers of thrombin generation (quantitative D-dimers, thrombin:antithrombin complexes, and prothrombin fragment 1.2) performed before initiation of treatment and then once weekly during induction until they either presented with a symptomatic VTE or completed Induction therapy. All patients had a Doppler ultrasound of the extremity in which their central venous catheter was placed at the end of induction or at presentation with symptoms suggesting thrombosis. Results: Eighty patients have been enrolled (see Table 1 for demographics) with 72 being fully evaluable currently. Three (4.3%) patients developed symptomatic VTE and 7 (15%) patients had an asymptomatic VTE for an overall incidence of VTE of 21.7%. We demonstrate that R time gradually increases over time from baseline during induction therapy. Additionally, maximum amplitude (MA) is initially diminished, but then increases with time. There were no statistically significant differences in VTE incidence between males and females, different age groups (though there was a trend towards increased incidence for older children), or CVC type (none of the patients with an implanted port had a VTE). Interestingly, MA did not seem to be associated with platelet count. Conclusion: Patients in this prospective study of patients with newly diagnosed ALL during induction at a single institution show rates of thrombosis in patients with ALL similar to that in the literature. Furthermore, TEG results demonstrated a shortening of the clotting time (R) and an increase in the clot rigidity (MA) during induction. Though not statistically significant, older children and patients with HR-ALL were more likely to have a VTE. Additional analyses will be performed to investigate the ability of the TEG, as well as the CBC and markers of thrombin generation, in predicting the development of VTE in these patients. Table 1. Patient Demographics Patient Demographics Gender Female 33 (46%) Male 38 (54%) Age < 5 years 28 (39%) 9-12 years 26 (37%) 10+ years 17 (24%) Patient VTE classification Symptomatic VTE 3 (4%) Asymptomatic VTE 12 (17%) No VTE 56 (79%) Demographics by CVC Type Type of CVC PICC Port-a-Cath Total Gender Female 35 (45%) 3 (100%) 38 (48%) Male 42 (55%) 0 (0%) 42 (53%) Age < 5 years 29 (38%) 2 (67%) 31 (39%) 9-12 years 30 (39%) 0 (0%) 30 (38%) 10+ years 18 (23%) 1 (33%) 19 (24%) Type of ALL SR-ALL 54 (70%) 0 (0%) 54 (68%) HR-ALL 23 (30%) 2 (67%) 25 (31%) T-ALL 0 (0%) 1 (33%) 1 (1%) Patient VTE classification Symptomatic VTE 3 (4%) 0 (0%) 3 (4%) Asymptomatic VTE 12 (17%) 0 (0%) 12 (17%) No VTE 54 (78%) 2 (100%) 56 (79%) Patient VTE classification Demographics by VTE Symptomatic VTE Asymptomatic VTE No VTE Total Gender Female 1 (33%) 7 (58%) 25 (45%) 33 (46%) Male 2 (67%) 5 (42%) 31 (55%) 38 (54%) Age categories < 5 years 1 (33%) 4 (33%) 23 (41%) 28 (39%) 9-12 years 0 (0%) 3 (25%) 23 (41%) 26 (37%) 10+ years 2 (67%) 5 (42%) 10 (18%) 17 (24%) Type of ALL SR-ALL 1 (33%) 7 (58%) 39 (70%) 47 (66%) HR-ALL 2 (67%) 5 (42%) 16 (29%) 23 (32%) T-ALL 0 (0%) 0 (0%) 1 (2%) 1 (1%) Figure 1. Figure 1. Figure 2. Figure 2. Disclosures Ko: Alexion: Honoraria; NovoNordisk: Consultancy. Young:Bayer: Consultancy; Kedrion: Consultancy; Novo Nordisk: Consultancy, Honoraria; Baxter: Consultancy; Biogen Idec: Consultancy, Honoraria.

Schistocytic Hemolytic Anemia Owing to Central Venous Catheter in a Child With Acute Lymphoblastic Leukemia

2010 ◽  
Vol 32 (6) ◽  
pp. e233-e235 ◽  
Author(s):  
Seda Öztürkmen ◽  
Ayşenur Paç ◽  
Atilla Şenayl ◽  
Tuğçin Bora Polat ◽  
İbrahim İlker Çetin ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Central Venous Catheter ◽  
Hemolytic Anemia ◽  
Lymphoblastic Leukemia ◽  
Venous Catheter ◽  
Central Venous

Is Thrombophilia a Risk Factor for Peripheral Vein Infusion Thrombophlebitis?.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4047-4047
Author(s):  
Vicky Tagalakis ◽  
Susan R. Kahn ◽  
Michael Libman ◽  
Mark Blostein ◽  
Susan Solymoss ◽  
...  
Keyword(s):  
Risk Factors ◽  
Central Venous Catheter ◽  
Factor V Leiden ◽  
Venous Catheter ◽  
Hospitalized Patients ◽  
Patient Specific ◽  
Prothrombin G20210a ◽  
Factor V ◽  
Peripheral Vein ◽  
Central Venous

Abstract Background and Objectives. Peripheral vein infusion thrombophlebitis (PVIT) is a common complication in hospitalized patients receiving peripheral intravenous (IV) therapy. Although catheter-related risk factors such as catheter material have been well elucidated, patient-related factors have received little attention, despite evidence that (1) individuals vary in biologic vulnerability to developing PVIT; (2) there is biological evidence that thrombus formation may play a role in the pathogenesis of PVIT; and (3) thrombophilic disorders have been linked to central venous catheter thrombosis. We conducted a nested case-control study to determine whether patients who developed PVIT were more likely to have thrombophilia than patients without PVIT. Methods. A cohort of consecutive, hospitalized patients with peripheral IV catheters was prospectively assembled from 8 wards in 2 large tertiary care hospitals and followed until PVIT developed, the catheter was removed for reasons other than PVIT, or the patient was transferred with catheter in place to a non-study ward. Recruitment to the cohort continued until 100 patients, who developed PVIT, were eligible for case enrolment. For each case, 2 control patients who had not developed PVIT and who were matched to cases on catheter duration (days) were identified. PVIT was defined as the presence of two or more of the following at the catheter site: pain, tenderness, erythema, swelling, purulence, or a palpable cord. Factor V Leiden and prothrombin G20210A mutations and homocysteine levels were measured. Homocysteine levels ≥ 15μmol/L were considered elevated. The association between PVIT and thrombophilia was tested using multivariate conditional logistic regression analysis to account for the matched design. Results. From the cohort of 6426 patients with catheters, there were 113 PVIT episodes (PVIT incidence of 4.4 per 1000 catheter-days) of which 100 cases were eligible and matched to 200 randomly chosen controls. There were no differences between cases and controls with regard to age, sex distribution, history of previous venous thromboembolism (VTE) or presence of active cancer. Cases were less likely than controls to be taking anticoagulant medication(s) (9% vs. 16%, respectively, OR=0.46; 95% confidence interval (CI) [0.19, 1.12]). One or more prior episodes of PVIT was reported by 18% of cases vs. 6% of controls (OR=3.0; 95% CI [1.4, 6.2]). Prothrombin G20210A or Factor V Leiden was detected in 6% of cases and 6% of controls. Hyperhomocysteinemia was present in 24% of cases vs. 22% of controls (OR=1.23; 95% CI [0.69, 2.19]). Multivariable conditional regression analyses adjusted for age, sex and anticoagulant use showed that prior PVIT was an independent predictor of PVIT (OR=2.8; 95% CI [1.3, 6.0]), but thrombophilia did not predict PVIT (OR=1.02; 95% CI [0.57, 1.84]). Conclusions. We did not find an association between PVIT and Factor V Leiden, prothrombin gene mutation, or hyperhomocysteinemia, although our results suggest an unidentified patient-specific predisposition to PVIT. The pathogenesis of PVIT appears to be different than that of central venous catheter thrombosis, since thrombophilia, cancer and prior VTE, which are known risk factors for central venous catheter thrombosis, were not significantly associated with PVIT in our study.

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