Serial Changes in Coagulation and Viscosity during Sickle‐Cell Crisis

Richardson, S. G. N.; Matthews, Kerryn; Stuart, J.; Geddes, A. M.; Wilcox, R. M.

doi:10.1111/j.1365-2141.1979.tb03685.x

Cited by 92 publications

(48 citation statements)

References 24 publications

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“…For example, fibrinogen enhances the adhesion of pathological RBC to EC (12, 13), which is consistent with the observation that the onset of vaso-occlusive crisis in sickle cell disease is always accompanied by a temporally elevated level of this acute phase protein (12,14). However, the underlying mechanisms behind the increased adhesion efficiency in the presence of this acute phase protein remain obscure.…”

Section: The Adhesion Of Red Blood Cells (Rbc)supporting

confidence: 64%

Specific Binding of Red Blood Cells to Endothelial Cells Is Regulated by Nonadsorbing Macromolecules

Yang

Koo

Lin

et al. 2010

Journal of Biological Chemistry

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Abnormal adhesion of red blood cells to the endothelium has been linked to the pathophysiology of several diseases associated with vascular disorders. Various biochemical changes, including phosphatidylserine exposure on the outer membrane of red blood cells as well as plasma protein levels, have been identified as being likely to play a key role, but the detailed interplay between plasma factors and cellular factors remains unknown. It has been proposed that the adhesionpromoting effect of plasma proteins originates from ligand interaction, but evidence substantiating this assumption is often missing. In this work, we identified an alternative pathway by demonstrating that nonadsorbing macromolecules can also have a marked impact on the adhesion efficiency of red blood cells with enhanced phosphatidylserine exposure to endothelial cells. It is concluded that this adhesion-promoting effect originates from macromolecular depletion interaction and thereby presents an alternative mechanism by which plasma proteins could regulate cell-cell interactions. These findings should thus be of potential value for a detailed understanding of the pathophysiology of diseases associated with vascular complications and might be applicable to a wide range of cellcell interactions in plasma or plasma-like media. The adhesion of red blood cells (RBC)2 to endothelial cells (EC) is usually insignificant. However, increased RBC adhesion to endothelial cells has been observed in various clinical states such as sickle cell disease, ␤-thalassemia, and diabetes mellitus, and the degree of RBC-EC adhesiveness has been linked to the vascular complications associated with these diseases (1-5). There is now general agreement that various cell surface alterations control the increased RBC adhesiveness in such disease states. For example, an enhanced phosphatidylserine (PS) exposure on the outer leaflet of the RBC membrane has been linked to abnormal RBC-EC adhesion in sickle cell disease, hereditary hydrocytosis, and chronic uremia (6 -8). Usually this anionic phospholipid is located exclusively on the inner leaflet of the RBC membrane but is translocated to the outer leaflet in hemoglobinopathies and oxidative stress states (9). The role of PS in adhesion has not been fully understood, but RBC with enhanced PS exposure have been identified to establish specific interactions with EC or the endothelial matrix via several receptors including thrombospondin, ␣ V ␤ 3 , CD36, and PS receptor (6, 10, 11).Moreover, several plasma factors have been identified to be involved in abnormal RBC adhesion to EC. For example, fibrinogen enhances the adhesion of pathological RBC to EC (12, 13), which is consistent with the observation that the onset of vaso-occlusive crisis in sickle cell disease is always accompanied by a temporally elevated level of this acute phase protein (12,14). However, the underlying mechanisms behind the increased adhesion efficiency in the presence of this acute phase protein remain obscure. It has been suggested that fibrinogen acts...

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Section: The Adhesion Of Red Blood Cells (Rbc)supporting

confidence: 64%

Specific Binding of Red Blood Cells to Endothelial Cells Is Regulated by Nonadsorbing Macromolecules

Yang

Koo

Lin

et al. 2010

Journal of Biological Chemistry

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“…The small sample size in the study by Richardson may also contribute to the discrepancy observed. 22 A number of studies have confirmed the activation of the coagulation system in SCA patients in steady state. The mechanisms include a decrease in levels of physiological anticoagulants (ATIII, Protein C and Protein S) and/or increased levels of pro-coagulant factors.…”

Section: Resultsmentioning

confidence: 98%

“…21,22 However, subjects enrolled into aforementioned studies were of different age group compared to the population being reported in this study. The small sample size in the study by Richardson may also contribute to the discrepancy observed.…”

Section: Resultsmentioning

confidence: 99%

“…27 A decline in levels of ATIII, reaching its nadir on the third day was reported by Richardson among HbS patients having vaso-occlusive crisis. 22 However, this could be a secondary response to the stasis created by sickled erythrocytes, leading to further activation of coagulation and thrombin generation, resulting in increased consumption of ATIII. The progressive decline in ATIII reaching its lowest level on the third day suggests that rather than playing an aetiologic role in the pathogenesis of vaso-occlusive crisis, ATIII deficiency occurred as a secondary phenomenon.…”

Section: Resultsmentioning

confidence: 99%

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A study of antithrombin 111 in sickle cell anaemia patients in steady state and during vaso-0cclusive crisis in North-Eastern Nigeria

Ladu¹,

Abjah²

2013

AJSIR

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Sickle cell anaemia (SCA) is a genetic disorder which can be complicated by haemolytic, vasoocclusive and thrombotic processes. Antithrombin III (ATIII) is a naturally occurring anticoagulant with anti inflammatory properties. The objective of this study was to determine the level of ATIII in individuals with SCA and to assess its role in vaso-occlusive crisis. This was an observational cross sectional study in which 60 adult HbSS (34 in steady state and 26 in vaso-occlusive crisis) subjects and 60 apparently healthy adults matched for sex and age served as controls. Haemoglobin (Hb) electrophoresis of subjects and controls was determined using Hb electrophoresis. Nine and a half (9.5) milliliters of blood, divided into two aliquots of 4.5mls (in 0.5mls of tri sodium citrate for coagulation studies) and 5mls (in EDTA containing bottle for full blood count) was obtained. Quantitative assessment of antithrombin III by chromogenic assay with Factor Xa was carried out using Diachrom ATIII test kit. Prothrombin time(PT), activated partial thromboplastin time(APTT), haematocrit, total white blood cells (WBC) and platelets count were assessed using standard protocol. SPSS (version 13 for windows) was used for data analysis. A p value of <0.05 was considered significant. The subjects were made up of 33(55%) males and 27(45%) females, with a mean age of 22.52(5.21) years whilst the controls consisted of 34(56.7%) males and 26(43.3%) females with a mean age of 22.85 (4.20). HbS subjects had a significantly lower ATIII levels compared with controls (p=0.009). Levels of ATIII that was found in SCA patients in steady state and in vaso-occlusive crisis did not differ significantly (p=0.468). Haematocrit was significantly lower in HbS than controls (p=0.000), whereas total WBC count (p=0.000), absolute platelet count (p=0.003), and Prothrombin time (0.008) were significantly higher in the HbS subjects. ATIII levels did not differ significantly between steady state and vasoocclusive crisis, suggesting that ATIII does not play an active role in pathogenesis of vasoocclusive crisis.

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“…Ischemic stroke (IS) results from the abrupt interruption of focal cerebral blood flow (2). The causes of IS include an embolic or thrombotic occlusion or a decrease in cerebral blood flow resulting from the abrupt occlusion of arteries and arterioles, poor blood circulation, arteritis, venous occlusion, anemia or hyperviscosity (2)(3)(4)(5). Potent independent risk factors for IS include abdominal obesity and body mass index (BMI) (6,7).…”

Section: Introductionmentioning

confidence: 99%

Association between cytochrome P450 promoter polymorphisms and ischemic stroke

Kim

Yim

Lee

2011

Experimental and Therapeutic Medicine

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Abstract. The human cytochrome P450 (CYP) superfamily includes at least 57 genes that encode enzymes with diverse metabolic and biosynthetic functions. This study was conducted in order to investigate the associations between polymorphisms in CYP superfamily genes (CYP11B2, CYP17A1, CYP2B6, CYP2C9, CYP2E1 and CYP7A1) and ischemic stroke (IS). Six single nucleotide polymorphisms (SNPs) of CYP superfamily genes were selected and genotyped by direct sequencing in 121 patients with IS and 321 control subjects. The genetic data were analyzed using SNPStats and SPSS 18.0. Multiple logistic regression models (codominant 1, codominant 2, dominant, recessive and log-additive) were used to evaluate odds ratios (ORs), 95% confidence intervals (CIs) and p-values. The rs179998 SNP of CYP11B2 was significantly associated with IS (p=0.0336 in a log-additive model). The rs3813867 SNP of CYP2E1 was significantly associated with smoking in IS (p=0.0336 in a log-additive model). The rs1799998 SNP of CYP11B2 and rs3808607 of CYP7A1 were related to diabetes mellitus in IS (p<0.05). CYP11B2, CYP2E1 and CYP7A1 SNPs were associated with IS in the population studied. Further study is required to confirm these associations and to determine their biological significance.

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Serial Changes in Coagulation and Viscosity during Sickle‐Cell Crisis

Cited by 92 publications

References 24 publications

Specific Binding of Red Blood Cells to Endothelial Cells Is Regulated by Nonadsorbing Macromolecules

Specific Binding of Red Blood Cells to Endothelial Cells Is Regulated by Nonadsorbing Macromolecules

A study of antithrombin 111 in sickle cell anaemia patients in steady state and during vaso-0cclusive crisis in North-Eastern Nigeria

Association between cytochrome P450 promoter polymorphisms and ischemic stroke

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