ABO Group as a Thrombotic Risk Factor in Children With Acute Lymphoblastic Leukemia

2015 ◽  
Vol 37 (5) ◽  
pp. e328-e332 ◽  
Author(s):  
Terry Mizrahi ◽  
Jean-Marie Leclerc ◽  
Michèle David ◽  
Thierry Ducruet ◽  
Nancy Robitaille
Keyword(s):  
Risk Factor ◽  
Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia ◽  
Thrombotic Risk ◽  
Thrombotic Risk Factor

Isolated Familial Plasminogen Deficiency May not Be a Risk Factor for Thrombosis

1996 ◽  
Vol 76 (06) ◽  
pp. 1004-1008 ◽  
Author(s):  
R C Tait ◽  
Isobel D Walker ◽  
J A Conkie ◽  
S I A M Islam ◽  
Frances McCall
Keyword(s):  
Risk Factor ◽  
Prevalence Rate ◽  
Blood Donors ◽  
Compound Heterozygous ◽  
Thrombotic Risk ◽  
Deficiency State ◽  
Thrombotic Risk Factor ◽  
Plasminogen Deficiency ◽  
Old Donor ◽  
Heterozygous Deficiency

SummaryDespite many reports of individuals with congenital plasminogen deficiency and thrombosis, there is still uncertainty whether heterozygous deficiency represents a real thrombophilic risk factor or simply a coincidental finding. We have addressed this issue by testing for plasminogen deficiency in a cohort of 9611 blood donors. Out of 66 donors with reduced plasminogen activity on two occasions 28 were shown to have a familial deficiency state (including 3 with dysplasminogen-aemia). Our observed prevalence rate for familial plasminogen deficiency, calculated at 2.9/1000 (95% Cl = 1.9-4.2 per 1000), was not significantly different from that calculated from published reports of congenital plasminogen deficiency in thrombotic cohorts (5.4/1000). Furthermore, with only two exceptions, all 80 donors and relatives with familial deficiency were asymptomatic with regard to thrombosis -including a 29 year old donor with suspected compound heterozygous hypoplasminogenaemia. These findings add further weight to the argument that familial heterozygous plasminogen deficiency, at least in isolation, does not constitute a significant thrombotic risk factor. However, it remains uncertain whether plasminogen deficiency, when combined with other thrombophilic conditions, may become more clinically important.

Nijmegen breakage syndrome (NBS) as a risk factor for CNS involvement in childhood acute lymphoblastic leukemia

2011 ◽  
Vol 57 (1) ◽  
pp. 160-162 ◽  
Author(s):  
Agata Pastorczak ◽  
Malgorzata Stolarska ◽  
Joanna Trelińska ◽  
Joanna Zawitkowska ◽  
Jerzy Kowalczyk ◽  
...  
Keyword(s):  
Risk Factor ◽  
Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia ◽  
Nijmegen Breakage Syndrome ◽  
Childhood Acute Lymphoblastic Leukemia ◽  
Cns Involvement

Thrombocytopenia as a thrombotic risk factor in patients with antiphospholipid antibodies without disease criteria

2017 ◽  
Vol 148 (9) ◽  
pp. 394-400
Author(s):  
Rosalia Demetrio Pablo ◽  
Pedro Muñoz ◽  
Marcos López-Hoyos ◽  
Vanesa Calvo ◽  
Leyre Riancho ◽  
...  
Keyword(s):  
Risk Factor ◽  
Antiphospholipid Antibodies ◽  
Thrombotic Risk ◽  
Thrombotic Risk Factor

scholarly journals Cytokine Release Syndrome Is an Independent Risk Factor Associated With Platelet Transfusion Refractoriness After CAR-T Therapy for Relapsed/Refractory Acute Lymphoblastic Leukemia

2021 ◽  
Vol 12 ◽  
Author(s):  
Yadan Liu ◽  
Bin Liang ◽  
Yan Liu ◽  
Guoqing Wei ◽  
Wenjun Wu ◽  
...  
Keyword(s):  
Risk Factor ◽  
Acute Lymphoblastic Leukemia ◽  
Platelet Transfusion ◽  
Independent Risk Factor ◽  
Lymphoblastic Leukemia ◽  
Cytokine Release ◽  
Cytokine Release Syndrome ◽  
Car T ◽  
Grade 3 ◽  
Platelet Transfusions

Background: Chimeric antigen receptor T cell (CAR-T) therapy is successful in improving treatment outcomes for relapsed/refractory acute lymphoblastic leukemia (R/R ALL). However, toxicities associated with CAR-T therapy are being increasingly identified. Pancytopenia is one of the most common complications after CAR-T therapy, and platelet transfusions are an essential part of its supportive care.Study Design and Methods: This study aimed to assess the effectiveness of platelet transfusions for R/R ALL patients at our single center and identify associated risk factors. Overall, 44 R/R ALL patients were enrolled in this study, of whom 26 received CAR-T therapy and 18 received salvage chemotherapy.Result: Patients in the CAR-T group had a higher incidence of platelet transfusion refractoriness (PTR) (15/26, 57.7%) than those in the chemotherapy group (3/18, 16.7%) (p = 0.007). For patients receiving CAR-T therapy, multivariate analysis showed that the grade of cytokine release syndrome (CRS) was the only independent risk factor associated with PTR (p = 0.007). Moreover, higher peak serum IL-6 and IFN-γ levels suggested a higher risk of PTR (p = 0.024 and 0.009, respectively). Patients with PTR received more platelet infusion doses than those without PTR (p = 0.0426). Patients with PTR had more grade 3–4 bleeding events than those without PTR (21.4 vs. 0%, p = 0.230), and the cumulative incidence of grade 3–4 bleeding event was different (p = 0.023).Conclusion: We found for the first time that PTR is associated with the CRS grade. Improved knowledge on the mechanisms of PTR after CAR-T therapy is needed to design a rational therapeutic strategy that aims to improve the efficiency of transfusions.

The C282Y Mutation of HFE Is Another Male-Specific Risk Factor for Childhood Acute Lymphoblastic Leukemia

Blood ◽  
1999 ◽  
Vol 94 (11) ◽  
pp. 3957-3958 ◽  
Author(s):  
M. Tevfik Dorak ◽  
Alan K. Burnett ◽  
Mark Worwood ◽  
Anne M. Sproul ◽  
Brenda E.S. Gibson
Keyword(s):  
Risk Factor ◽  
Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia ◽  
Childhood Acute Lymphoblastic Leukemia ◽  
C282y Mutation ◽  
Specific Risk Factor ◽  
Specific Risk ◽  
Male Specific

A Retrospective Multicenter Study from the Nordic Society of Pediatric Hematology and Oncology (NOPHO) on Cerebral Sinus Venous Thromboses in Children with Acute Lymphoblastic Leukemia

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 584-584
Author(s):  
Susanna Ranta ◽  
Nadine Gretenkort Andersson ◽  
Ulf R. Tedgard ◽  
Tony Frisk ◽  
Maria Winther Gunnes ◽  
...  
Keyword(s):  
Risk Factors ◽  
Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia ◽  
Clinical Risk Factors ◽  
Bleeding Complications ◽  
Cerebral Veins ◽  
Thrombotic Risk ◽  
Clinical Risk ◽  
Cerebral Sinus ◽  
D Dimer

Abstract Introduction Cerebral sinus venous thrombosis (CSVT) is potentially life-threatening thrombosis with mortality around 10%. Venous thromboembolism (VTE) is a common complication in children with cancer. These children have several thrombotic risk factors such as the malignancy itself, severe infections, prothrombotic medication and immobilization. The treatment of acute lymphoblastic leukemia (ALL) includes steroids and asparaginase (ASP), raising the VTE risk. In children with ALL the central nervous system (CNS) is a common localization for VTE. However, retrospective studies on small numbers of patients, larger studies and population-based data in children are scarce. The five Nordic countries, Estonia and Lithuania have a common treatment protocol for children with ALL between 1 and 18 years of age with prospective registration of toxicities, including CSVT offering a unique opportunity to study CSVT in this patient group. This is to our knowledge the largest report of children with ALL and CSVT describing the incidence, symptoms, treatment and the effect of CSVT on ALL treatment. Methods We assessed the symptoms, treatment, clinical risk factors and outcome of all children between ages 1 and 17 years at diagnosis of B-cell precursor or T-cell ALL between June 2008 and July 2013 and with CSVT. Data were collected from the patients’ medical records and the NOPHO leukemia registry. Results In total, 20 (1.9%) of the 1038 children with ALL treated according to the NOPHO ALL 2008 protocol developed CSVT. The cumulative incidence of CSVT was 2.0%. All the thromboses occurred within the first 5 months of treatment. The most common symptoms at the diagnosis of CSVT were headache, convulsions, weakness/fatigue and cerebral nerve palsy/hemiparesis/hemiplegia. The most frequent localizations for CSVT were sinus sagittalis (n=16) and sinus transversus (n=10). However, in most cases multiple cerebral veins were involved ( 70%). Median D-dimer at time of the CSVT diagnosis was 0.85 mg/L (range 0.19-4.7 mg/L) with 5 patients having normal D-dimer. We could not identify any clinical risk factors for CSVTs. CSVT was associated with steroids (treatment within 2 weeks before the diagnosis of CSVT) in 16/20 and with Pegylated asparaginase in 16/20. Fifteen patients were later screened for the inherited thrombophilic factors; one child had heterozygous prothrombin G20110A mutation and another heterozygous factor V (R506Q) Leiden mutation. Most patients (19/20) were treated with anticoagulants: mostly low molecular weight heparin (LMWH). The median treatment with LMWH was 26 weeks (range 14-119 weeks). No bleeding complications were observed in connection with LMWH. Two deaths were directly related to CSVT. Asparaginase was omitted from the treatment in 7 and delayed or reduced in 5 of the cases raising the risk for subsequent suboptimal leukaemia treatment. Of the surviving 18 patients, follow-up imaging revealed complete recanalization in 7 and partial recanalization in 7 cases. No imaging was available for the remaining 4 patients. Conclusions The incidence of CSVT in children with ALL was approximately 2%. No statistically significant clinical predictors for CSVT were identified. The mortality related to CSVT was 10%. Anticoagulation with LMWH was the treatment of choice in most cased and was well tolerated. Disclosures No relevant conflicts of interest to declare.

scholarly journals The methylenetetrahydrofolate reductase 677T-1298C haplotype is a risk factor for acute lymphoblastic leukemia in children

Medicine ◽  
2017 ◽  
Vol 96 (51) ◽  
pp. e9290 ◽  
Author(s):  
Ewelina Maria Kałużna ◽  
Ewa Strauss ◽  
Bogna Świątek-Kościelna ◽  
Olga Zając-Spychała ◽  
Ewelina Gowin ◽  
...  
Keyword(s):  
Risk Factor ◽  
Acute Lymphoblastic Leukemia ◽  
Methylenetetrahydrofolate Reductase ◽  
Lymphoblastic Leukemia ◽  
Leukemia In Children

Intermediate and Severe Hyperhomocysteinemia with Thrombosis: A Study of Genetic Determinants

2000 ◽  
Vol 83 (04) ◽  
pp. 554-558 ◽  
Author(s):  
Mette Gaustadnes ◽  
Niels Rüdiger ◽  
Karsten Rasmussen ◽  
Jørgen Ingerslev
Keyword(s):  
Risk Factor ◽  
Methylenetetrahydrofolate Reductase ◽  
Missense Mutations ◽  
Strongly Correlated ◽  
Genetic Determinants ◽  
Thrombotic Risk ◽  
Genotype Combination ◽  
Thrombotic Risk Factor ◽  
Plasma Thcy ◽  
Total Homocysteine

SummaryHyperhomocysteinemia is an independent risk factor for cardiovascular disease. In search of genetic factors causing elevated levels of total homocysteine in plasma (tHcy), we investigated a cohort of consecutively identified, unrelated thrombosis patients (n = 28) having intermediate or severe hyperhomocysteinemia (30 µmol/l<tHcy ≤100 µmol/l, and tHcy >100 µmol/l, respectively). The methylenetetrahydrofolate reductase (MTHFR) 677C→T genotype, and the complete cystathionine β-synthase (CBS) genotype was determined in all patients. We found that the MTHFR T/T genotype was strongly correlated with intermediate hyperhomocysteinemia, being present in 73.9 % of those cases (17 of 23). In three of five patients with severe hyperhomocysteinemia, compound heterozygosity for CBS mutations was detected. Among the mutations, two novel missense mutations: 1265C→T (S422L) and 1397C→T (S466L) were detected. The phenotype in those patients was quite mild, thromboembolism apart. This indicates that a search for CBS mutations in patients with severe hyperhomocysteinemia is important to ensure the detection of a possible CBS deficiency, thus enabling treatment. Co-existence of the MTHFR T/T genotype and the common CBS 844ins68 variant was significantly higher among patients (10.7%) as compared to controls (1.2%), indicating that this genotype combination is a thrombotic risk factor (P <0.05). In a few patients, hyperhomocysteinemia could not be explained by this genetic approach, suggesting that other genetic risk factors were implicated.Abbreviations: MTHFR, methylenetetrahydrofolate reductase; CBS, cystathionine β-synthase; tHcy, total homocysteine in plasma.

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