scholarly journals Impact of Blood Groups on Clinical Outcomes in Patients with Von Willebrand Disease

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 3519-3519
Author(s):  
Shahzaib Nabi ◽  
Arshad Adeel ◽  
Daryl Sudasena ◽  
Absia Jabbar ◽  
Farshid Bozorgnia ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Cerebrovascular Disease ◽  
Vascular Disease ◽  
Peripheral Vascular Disease ◽  
Blood Group ◽  
Blood Groups ◽  
Von Willebrand Disease ◽  
Abo Blood Groups ◽  
Peripheral Vascular ◽  
Von Willebrand

Abstract INTRODUCTION Von Willebrand Disease (vWD) is the most common hereditary hemorrhagic disorder with diverse clinical and genetic characteristics. Transmitted as an autosomal dominant trait (except Type III), it is caused primarily by the quantitative or qualitative deficiency of von Willebrand factor (vWF). ABO blood group types can affect the pathology, severity and hence the presentation of this clinically heterogeneous entity as the genes responsible for ABO blood groups also affects vWF levels in the plasma. We conducted a study to analyze and compare different clinico-demographic aspects among O and non-O blood group patients with Von Willebrand Disease. Our primary aim was to determine the relationship of different blood groups with venous thromboembolism (VTE) in patient with vWD. Our secondary aim was to determine the association of blood groups with different comorbid conditions such as coronary artery disease, cerebrovascular disease, peripheral vascular disease, chronic liver disease, chronic kidney disease etc. in patients with vWD. METHODS A retrospective review was carried out to include all patients diagnosed with Von Willebrand Disease from year 2002 to 2012. Patient population was obtained by using International Classification of Diseases, 9th revision (ICD9) codes. Data was collected with the help of electronic medical records. Multiple clinical variables and demographic characteristics of Von Willebrand Disease patients (n=381) were analyzed and compared between those with type O blood group (205 patients; 54%) and those with type non-O blood groups (176 patients; 46%). Univariate logistic regression was used to obtain crude odds ratios. Predictors with statistically significant p-values were included in a multivariable logistic regression model in order to yield adjusted odds ratio. Statistical significance was set at p<0.05 RESULTS Patients with O blood groups were less likely to develop VTE (OR 0.29, 95% CI 0.16-0.52, p < 0.001) as compared to Non-O blood groups in which the prevalence of VTE was much higher (25% vs. 9%). Additionally, patients with O blood groups had relatively lower factor 8 activity (125.9±90.8%; OR 0.99, 95% CI 0.99-1.00, p = 0.018) when compared with Non-O blood groups (168.5±120.6%). Patients with O-blood group had significant, life threatening bleeds at an early age (40.4±20.8 years; OR 0.99, 95% CI 0.97-1.00, p = 0.008) when compared with patients with type non-O blood group (Age 47.1±21.9 years). Additionally, O-Blood groups were related to a lesser prevalence of cerebrovascular disease (OR 0.48, 95% CI 0.29-0.79, p = 0.004) and peripheral vascular disease (OR 0.47, 95% CI 0.25-0.87, p = 0.015) as compared to Non-O blood groups. DISCUSSION Our study consolidates the fact that vWD patients with O blood group have a lesser risk of developing VTE as compared to non-O blood group patients. Additionally, strokes and peripheral vascular disease is also seen less frequently in O blood groups in patients with Von Willebrand disease. These results suggest that the genes responsible for ABO blood groups also have a significant effect on clinical outcomes in patients with vWD. There are multiple proposed mechanisms to explain this association including presence of ABO antigens on several platelet glycoproteins and glycosphingolipids as well as on the surface of vascular endothelium. More sophisticated, large-scale studies are needed to strengthen the associations we observed in our retrospective study. Disclosures Kuriakose: Kedrion: Speakers Bureau.

Naftidrofuryl (praxilene)

1988 ◽  
Vol 26 (7) ◽  
pp. 25-27
Keyword(s):  
Cerebrovascular Disease ◽  
Vascular Disease ◽  
Peripheral Vascular Disease ◽  
Clinical Benefit ◽  
Senile Dementia ◽  
Peripheral Vascular ◽  
The Past ◽  
New Information

We have discussed the use of naftidrofuryl oxalate (Praxilene - Lipha) in peripheral vascular disease, senile dementia and acute cerebrovascular disease several times over the past 16 years. On each occasion we concluded that the evidence that naftidrofuryl gave clinical benefit was at best equivocal, and further trials were needed. We now review recent trials and other new information about the drug.

Anti-Von Willebrand Factor Antibody Is Responsible for Lower Levels of Plasma vWF in Blood Group O Individuals.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 254-254 ◽  
Author(s):  
Letian Dai ◽  
Shawn Cotton ◽  
Alistair Macartney ◽  
Geoffrey Savidge ◽  
Anwar Alhaq
Keyword(s):  
Blood Group ◽  
Blood Groups ◽  
Bleeding Tendency ◽  
Plasma Samples ◽  
Abo Blood Groups ◽  
Acquired Von Willebrand Syndrome ◽  
Significant Difference ◽  
Group A ◽  
Group B ◽  
Von Willebrand

Abstract Plasma levels of vWF are known to be influenced by ABO blood groups, although the mechanism remains unresolved. Group O individuals have a significantly lower level of plasma vWF than those with group A, B or AB. This relative lower level of plasma vWF may result in a bleeding tendency and a shorter half-life of infused factor VIII in group O individuals. The formation of immune complexes between vWF and autoantibodies has been shown to accelerate vWF clearance from plasma in acquired von Willebrand syndrome. However, so far no evidence has been presented that the presence of autoantibodies against vWF is involved in lowering plasma level of vWF in group O individuals. In the present study, plasma samples were obtained from 199 healthy blood donors of blood group O (50), group A (50), group B (49), and group AB (50). A time-resolved fluorescence immunoassay (TRFIA) was developed to detect anti-vWF IgG in plasma samples. Briefly, 100 μl of diluted plasma was loaded on to duplicated vWF-coated and untreated control wells of a microplate. After incubation and washing, 100 μl of Europium-labeled anti-human IgG conjugate (1:500 dilution) was added to the plate to detect vWF IgG. The time-delayed fluorescence was then measured with a Victor microplate reader (PerkinElmer, Turku, Finland). The fluorescence counts of the control wells were subtracted from those of the vWF-coated wells. The results show that anti-vWF IgG was present in all four blood groups (Table 1). Of these blood groups, group O had the highest anti-vWF IgG level with 9.8 x 105 fluorescence counts, which was 2.7- to 3.5-fold higher than that of group A, B or AB. There was a significant difference in the anti-vWF IgG levels between group O and the rest of group A, B or AB. Quantitative analysis of plasma vWF by ELISA showed that the concentration of plasma vWF of group O was 29 to 35% lower than that of group A, B or AB (Table 1). These results suggest that TRFIA is a sensitive assay for detection of anti-vWF IgG in plasma samples, and the presence of the high level of anti-vWF Ig G in group O individuals may be responsible for lowing plasma vWF by acceleration of vWF clearance. Anti-VWF IgG levels and vWF concentrations in diffeent ABO blood groups Group O (n=50) Group A (n=50) Group B (n=49) Group AB (n=50) Data are presented as a mean ± SD. *P<0.01 compared with group A, B or AB. +P<0.01 compared with group A,B or AB. Anti-vWF IgG (x 105 Fluorescence counts) 9.8 ± 6.9* 2.8 ± 2.8 3.1 ± 3.0 3.6 ± 3.5 Concentration of vWF (% of normal controls) 116 ± 42+ 165 ± 46 165 ± 42 179 ± 49

scholarly journals Elucidating the Thrombogenic Risk of Non-O Blood Groups in Children with Acute Lymphoblastic Leukemia (ALL): Is Von Willebrand Factor a Culprit ?

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 4990-4990
Author(s):  
Terry Mizrahi ◽  
Caroline Laverdière ◽  
Michele David ◽  
Jean-Marie Leclerc ◽  
Lehana Thabane ◽  
...  
Keyword(s):  
Risk Factors ◽  
Blood Group ◽  
Lymphoblastic Leukemia ◽  
Blood Groups ◽  
Older Age ◽  
Abo Blood Group ◽  
Abo Blood Groups ◽  
Increased Risk ◽  
Von Willebrand ◽  
The Relationship

Abstract Background: Individuals with non-O blood group are shown to have increased risk of thromboembolism (TE). The exact pathogenesis of the prothrombotic effect of non-O blood group, is however not known. Because individuals with O-blood group have low levels of von Willebrand factor (vWF) compared to those with non-O blood group, vWF has been contemplated as a pathogenetic mechanism in ABO blood group-related prothrombotic risk. However, the available data regarding the role of vWF in the thrombotic risk of non-O blood group are inconclusive. Children with acute lymphoblastic leukemia (ALL) are at increased risk of TE. Several factors such as older age, leukemia phenotype and asparaginase have been shown to impact the risk of TE in children with ALL. We have recently shown that non-O blood group and circulating blasts were significant risk factors for TE in children with ALL. We have also shown that at diagnosis of ALL patients with circulating blasts have significantly higher levels of vWF compared to those without circulating blasts.  Within the context of a larger study aimed to define risk factors for symptomatic TE (sTE) in children with de novo ALL, we undertook a sub-study to evaluate the relationship of ABO blood groups and vWF level at diagnosis of ALL, and to evaluate the impact of circulating blasts on the vWF levels in children with O and non-O blood groups. We hypothesized that compared to patients with O-blood group, those with non-O blood group will have significantly higher levels of vWF and that circulating blasts will have additive effect on the vWF levels in patients with non-O blood group.  Methods : The multicenter, prospective, analytical cohort study included consenting patients (1-≤18 yrs. of age) with de novo ALL enrolled on the Dana-Farber Cancer Institute 05-001 therapeutic trial. Details of patient demography including ABO blood group, ALL diagnosis, therapy and symptomatic TE (sTE) were collected. Samples collected prior to starting ALL-therapy were analyzed centrally for prothrombotic defects (PD) including [protein C, S, antithrombin, Factor VIII:C, vWF, anticardiolipin antibodies and gene polymorphisms of methylene tetrahydrofolate reductase C677T, prothrombin G20210A, Factor V Leiden]. Age-adjusted standardized laboratory data defined PD. Regression analyses evaluated relationship between risk factors and sTE. Thrombosis-free survival was estimated using Kaplan-Meier method.  Results : Of 131 enrolled patients [mean age (range) 6.4 (1-17) yrs.; 70 boys], 21 (16%) developed sTE. ABO blood group information was available for 127 patients; 51 patients had blood group O and 76 non-O (57 with blood group A, 15 with B, and 4 with AB). There was no impact of PD including vWF on the risk of sTE. Older age compared to age ≤ 5 yr. [Odds Ratio (OR) 1.9, p=0.029] and non-O blood-group (OR 4.27, p=0.028) compared to O group were identified as independent predictors for development of sTE. Patients with peripheral blasts had higher odds of developing sTE (OR 7.79; p=0.059).The sTE-free survival was affected by older age (Hazard ratio (HR) 1.1, p 0.03), ALL risk type (HR 3.0, p 0.025) and blood group (O blood group vs non-O blood group, HR 0.23, p 0.03). Table 1 compares the vWF levels in patients with O and non-O blood group and those with and without circulating blasts. Overall, there was no difference in the vWF level at ALL diagnosis between patients with O vs. Non-O blood group. Patients with circulating blasts had higher levels of vWF at ALL diagnosis compared to those without circulating blasts; this comparison was statistically significant for non-O blood group. However, there was no interaction between ABO blood group and circulating blasts on vWF levels (p=0.723)  Conclusion : There was no effect of blood group type on the vWF level at diagnosis of ALL. Patients with circulating blasts had significantly higher levels of vWF at ALL diagnosis and the vWF levels were significantly higher in patients with non-O blood group and circulating blasts. Although it is likely that the relationship between blood group and vWF may be affected by effect of circulating blasts on vWF, we showed no interaction between ABO blood groups and circulating blasts on the vWF levels at diagnosis of ALL in children. Small sample size is a limitation of current study. Further studies with larger sample size are needed to elaborate the relationship between vWF, ABO blood groups, and circulating blasts. Disclosures No relevant conflicts of interest to declare.

Cyclospasmol and other vasodilators in cerebrovascular disease

1964 ◽  
Vol 2 (11) ◽  
pp. 42-43
Keyword(s):  
Cerebrovascular Disease ◽  
Vascular Disease ◽  
Peripheral Vascular Disease ◽  
Blood Supply ◽  
Peripheral Vascular ◽  
Arterial Spasm

Cyclandelate (Cyclospasmol - Camden) is offered for use in peripheral vascular disease1 and in cerebrovascular disease. It is claimed to improve blood supply by relieving arterial spasm. Similar claims are made for isoxsuprine and other vasodilators in other countries.

Variation of Both Blood Group H and ABO Glycans Is Associated with VWF Levels

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 3314-3314
Author(s):  
Jill M. Johnsen ◽  
Kerry W Lannert ◽  
Ermias Yohannes ◽  
Xiomara Castillo ◽  
Karl C. Desch
Keyword(s):  
Blood Group ◽  
Blood Groups ◽  
Buffy Coat ◽  
Abo Blood Group ◽  
Abo Blood Groups ◽  
Significant Difference ◽  
Post Hoc ◽  
Von Willebrand ◽  
The Impact ◽  
One Way Anova

Abstract Abstract 3314 ABO(H) is a carbohydrate blood group system primarily expressed on red cells, blood vessels, and mucosal surfaces. ABO blood group is known to influence von Willebrand Factor (VWF) levels, with low VWF associated with blood group O and increased diagnosis of von Willebrand Disease. Conversely, non-O blood group is associated with high VWF levels, and both non-O blood group and high VWF are associated with thrombotic vascular disease. We sought to characterize VWF levels relative to ABH glycan phenotypes in 1129 individuals from a healthy sibling cohort, the Genes and Blood Clotting Cohort (GABC). VWF:Ag levels were determined by AlphaLISA (Perkin Elmer) in platelet poor plasma. ABH forensic techniques were adapted to samples of RBC-rich, frozen buffy coat in the study repository. In brief, buffy coat fractions were diluted in TBS, applied to nitrocellulose, and A and B glycans detected using murine monoclonal anti-A (Immucor) or murine monoclonal anti-B (Immucor) followed by and streptavidin-conjugated donkey anti-mouse IgG HRP (Jackson ImmunoResearch). A biotinylated Ulex europaeus agglutinin (UEA lectin, Vector Labs) was used to detect H, followed by streptavidin-HRP. Blots were imaged using ImageQuant (GE) and scored semi-quantitatively for glycan density by two blinded independent observers using reference buffy coats from normal blood donors. ABO blood group frequencies were similar to that of the U.S. population (O=40%, A=42%, B=12%, AB=6%). Also consistent with previous reports, VWF:Ag levels varied significantly between ABO blood groups (O<A<B=AB, see Table 1). Within blood group A, we observed variation in A glycan density (scored 1+ to 3+). Lower A glycan density (similar to the A2 reference) correlated significantly (p<0.01) with lower VWF:Ag levels (see Table 1), and also appeared to have higher detectable H antigen. We also observed wide variation in H glycan density (scored 1+ to 5+). Overall, detection of A and B glycan density patterns were inversely related to H glycan, consistent with glycosylation of H by the ABO enzyme. Interestingly, higher H density correlated significantly (p<0.01) with lower VWF:Ag levels, even within blood group O (see Table 2). In summary, ABH glycan variation may impact VWF in a more complex fashion than previously suspected. Although these data are limited to semi-quantitative analyses by the heterogeneous nature of RBC-rich buffy coat, our findings are consistent with expectations for major ABO blood group frequencies and show that variation of RBC rich-buffy coat ABH glycan density within and between ABO blood groups correlates with VWF:Ag level. This work also suggests a previously unsuspected association between VWF and variation in H antigen, which we hypothesize may be due to variation in the FUT genes or other loci affecting H glcosylation patterns. Further work to characterize the complexity of the ABH carbohydrate system and its genetic determinants is warranted to better understand the impact of ABH subtypes on VWF and vascular phenotypes. Table 1. ABO Blood Groups, Buffy Coat A Glycan Density, and VWF:Ag Level Number of Subjects ABO Blood Group VWF:Ag (+/−1SD) VWF Difference (Ovs.Avs.Bvs.AB)* Difference from Group O* 454 O 90+/−35 473 A 119+/−45 p<0.01 p<0.01 138 B 130+/−50 p<0.01 p<0.01 64 AB 128+/−52 NS p<0.01 Number of Subjects A Glycan Density Avg H Glycan Density VWF:Ag (+/−1SD) VWF Difference (A1+vs.2+vs.3+)* Difference from A 1+* 68 1+ 3.5 98+/−40 195 2+ 2.4 123+/−44 p<0.01 p<0.01 210 3+ 2.0 123+/−45 NS p<0.01 * Each section above: One-way ANOVA; post-hoc Tukey's Least Significant Difference. Table 2. Buffy Coat H Glycan Density and VWF:Ag Level H Glycan Density in All Subjects Number of Subjects H Glycan Density VWF:Ag (+/−1SD) VWF Difference (H1vs.2vs.3vs.4vs.5)* Difference from H 1+* 52 1+ 135+/−46 257 2+ 130+/−53 NS NS 260 3+ 117+/−44 p<0.01 p<0.01 307 4+ 99+/−37 p<0.01 p<0.01 252 5+ 88+/−32 p<0.05 p<0.01 H Glycan Density in Blood Group O Subjects Number of Subjects H Glycan Density** VWF:Ag (+/−1SD) VWF Difference (H3+vs.4+vs.5+)* Difference from H 3+* 29 3+ 115+/−57 207 4+ 92+/−33 p<0.01 p<0.01 214 5+ 85+/−30 NS p<0.01 * One-way ANOVA; post-hoc: Tukey's Least Significant Difference. ** No blood group O individuals scored <3+ H glycan density. Disclosures: No relevant conflicts of interest to declare.

scholarly journals New Medications in the Treatment of Acute Migraine

2019 ◽  
Vol 54 (4) ◽  
pp. 229-231
Author(s):  
Scot Walker
Keyword(s):  
Cardiovascular Disease ◽  
Pain Relief ◽  
Cerebrovascular Disease ◽  
Vascular Disease ◽  
Peripheral Vascular Disease ◽  
Uncontrolled Hypertension ◽  
Acute Migraine ◽  
Peripheral Vascular ◽  
Migraine Pain ◽  
The Us

Migraine is a common disorder affecting 12% of the US population. Use of triptans results in migraine pain relief within 2 hours in 16% to 51% of patients. However, due to their vasoconstrictive properties, triptans are contraindicated in patients with cardiovascular disease, peripheral vascular disease, cerebrovascular disease, and uncontrolled hypertension because of the potential for ischemia. This article will review 2 new classes of drugs being developed for the treatment of acute migraine without vasoconstrictive effects.

scholarly journals ABO blood group, glycosyltransferase activity and risk of Venous Thrombosis

2020 ◽  
Author(s):  
Manal Ibrahim Kosta ◽  
Pascal Bailly ◽  
Monique Silvy ◽  
Noemie Saut ◽  
Pierre Suchon ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Blood Group ◽  
Plasma Levels ◽  
Blood Groups ◽  
Abo Blood Group ◽  
Abo Blood Groups ◽  
Factor Assay ◽  
Von Willebrand ◽  
First Time ◽  
Willebrand Factor

AbstractIntroductionABO blood group influence the risk of venous thrombosis (VT) by modifying A and B glycosyltransferases (AGT and BGT) activities that further modulates Factor VIII (FVIII) and von Willebrand Factor (VWF) plasma levels. The aim of this work was to evaluate the association of plasma GTs activities with VWF/FVIII plasma levels and VT risk in a case-control study.Materials and Methods420 cases were matched with 420 controls for age and ABO blood group. GT activities in plasma were measured using the quantitative transfer of tritiated N-acetylgalactosamine or galactose to the 2’-fucosyl-lactose and expressed in disintegration per minute/30µL of plasma and 2 hours of reaction (dpm/30µL/2H). FVIII and VWF plasma levels were respectively measured using human FVIII-deficient plasma in a 1-stage factor assay and STA LIATEST VWF (Diagnostica Stago).ResultsA and B GT activities were significantly lower in cases than in controls (8119±4027 vs 9682±4177 dpm/30µL/2H, p=2.03 × 10−5, and 4931±2305 vs 5524±2096 dpm/30µL/2H, p=0.043 respectively). This association was observed whatever the ABO blood groups. The ABO A1 blood group was found to explain∼80% of AGT activity. After adjusting for ABO blood groups, AGT activity was not correlated to VWF/FVIII plasma levels. Conversely, there was a moderate correlation (ρ∼0.30) between BGT activity and VWF/ FVIII plasma levels in B blood group carriers.ConclusionThis work showed, for the first time, that GT activities were decreased in VT patients in comparison to controls with the same ABO blood group. The biological mechanisms responsible for this association remained to be determined.

scholarly journals ABO Blood Groups and Risk of Glioma

2021 ◽  
Author(s):  
Ana Azanjac Arsic
Keyword(s):  
Blood Group ◽  
Blood Groups ◽  
Abo Blood Groups ◽  
Increased Risk ◽  
Hereditary Factors ◽  
The One ◽  
Von Willebrand ◽  
Relationship Of ◽  
The Relationship

Gliomas are one of the most common primary brain tumors and the etiology of gliomas remains unknown in most cases. The aim of this case–control study was to investigate possible association between incidence in relation to glioma and certain blood groups. This study included 100 histopathologically verified cases of glioma and 200 age and sex-matched controls without malignant diseases that were admitted to the same hospital. The results revealed that the patients with group AB were at 3.5-fold increased risk of developing glioma compared to the patients with other ABO blood groups. In this particular study, there was more male patients with glioma with the blood group AB. However, mechanisms that explain the relationship between the blood groups ABO and a cancer risk are unclear. Several hypotheses have been proposed, including the one with a modulatory role of blood group ABO antigens. In addition, the blood group ABO system regulates the level of circulating proinflammatory and adhesion molecules which play a significant role in the tumorigenesis process. Additionally, the recent discovery that includes the von Willebrand factor (vWF) as an important modulator of angiogenesis and apoptosis provides one plausible explanation as regards the role of the blood group ABO in the tumorigenesis process. To our knowledge, this is the first study that examined the relationship of blood group in patients diagnosed with glioma among the Serbian population. Moreover, for the first time our study results suggested that blood group AB increased the risk of glioma. The results of this study suggested that the blood group AB could be one of hereditary factors which had an influence on the occurrence of glioma. The further research is needed on a larger sample, to confirm these findings and the possible mechanisms by which the ABO system contributes to the pathology of glioma.

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