Endothelial Function in Patients with Sickle Cell Anemia During and After Sickle Cell Crises

Blum, Arnon; Yeganeh, Shay; Peleg, Aviva; Vigder, Fina; Kryuger, Konstantin; Khatib, Ahmed; Khazim, Khalid; Dauerman, Harold L.

doi:10.1007/s11239-005-1377-7

Cited by 44 publications

(29 citation statements)

References 13 publications

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“…In addition to other medical complications, anemia dominates for the accumulation damage course of cerebral autoregulation. With the progress of the disease, patients with anemia will suffer from many complications, such as heart failure31, chronic kidney disease32 and vascular endothelial cells3334, which play a more important role than anemia in the development of stroke. This effect may partly explain why Sico and colleagues found a positive relationship in patients with less severe stroke but not in severe stroke17.…”

Section: Discussionmentioning

confidence: 99%

Anemia increases the mortality risk in patients with stroke: A meta-analysis of cohort studies

Zhou

et al. 2016

Sci Rep

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The impact of anemia on the outcome of patients with stroke remains inconsistent. We performed a meta-analysis of cohort studies to assess the mortality risk in stroke patients with and without anemia. Systematic searches were conducted in the PubMed, China National Knowledge Infrastructure, Web of Science and Wanfang databases to identify relevant studies from inception to November 2015. The estimated odds ratio with a 95% confidence interval was pooled. subgroup analyses and sensitivity analyses were also conducted. We used Begg’s funnel plot and Egger’s test to detect the potential publication bias. Thirteen cohort studies with a total of 19239 patients with stroke were included in this meta-analysis. The heterogeneity among studies was slight (I2 = 59.0%, P = 0.031). The results from a random-effect model suggest that anemia is associated with an increased mortality risk in patients with stroke (adjusted odds ratio = 1.39, 95% confidence interval: 1.22–1.58, P < 0.001). The subgroup analyses are consistent with the total results. This meta-analysis of 13 cohort studies finds that anemia increases the mortality risk in patients with stroke. Future studies should perform longer follow-up to confirm this finding and explore its possible mechanism.

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Section: Discussionmentioning

confidence: 99%

Anemia increases the mortality risk in patients with stroke: A meta-analysis of cohort studies

Zhou

et al. 2016

Sci Rep

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“…15,16 Thrombocytosis and platelet activation are also well-recognized features of SCD. 4,13,14,[16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35] Thrombotic events including pulmonary embolism, deep vein thrombosis, and SCD-related stroke are common. 17,[36][37][38][39][40] SCD-associated pulmonary hypertension (PHT) is associated with endothelial cell activation (as measured by soluble vascular cell adhesion molecule-1 [sVCAM-1]), which would also support procoagulant activity.…”

Section: Introductionmentioning

confidence: 99%

“…17,[36][37][38][39][40] SCD-associated pulmonary hypertension (PHT) is associated with endothelial cell activation (as measured by soluble vascular cell adhesion molecule-1 [sVCAM-1]), which would also support procoagulant activity. 14,20,23,41 However, the precise contribution of hemostatic factors to SCD-induced pathobiologies and particularly progressive end-organ damage has not been thoroughly explored.…”

Section: Introductionmentioning

confidence: 99%

Genetic diminution of circulating prothrombin ameliorates multiorgan pathologies in sickle cell disease mice

Arumugam

Mullins²,

Shanmukhappa

et al. 2015

Blood

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• Reduced prothrombin improves survival and ameliorates inflammation and end-organ damage without spontaneous bleeding in sickle cell mice.• An individual procoagulant, prothrombin, represents a novel therapeutic target that can improve sickle cell disease outcome.Sickle cell disease (SCD) results in vascular occlusions, chronic hemolytic anemia, and cumulative organ damage. A conspicuous feature of SCD is chronic inflammation and coagulation system activation. Thrombin (factor IIa [FIIa]) is both a central protease in hemostasis and a key modifier of inflammatory processes. To explore the hypothesis that reduced prothrombin (factor II [FII]) levels in SCD will limit vaso-occlusion, vasculopathy, and inflammation, we used 2 strategies to suppress FII in SCD mice. Weekly administration of FII antisense oligonucleotide "gapmer" to Berkeley SCD mice to selectively reduce circulating FII levels to ∼10% of normal for 15 weeks significantly diminished early mortality. More comprehensive, long-term comparative studies were done using mice with genetic diminution of circulating FII. Here, cohorts of FII lox/2 mice (constitutively carrying ∼10% normal FII) and FII WT mice were tracked in parallel for a year following the imposition of SCD via hematopoietic stem cell transplantation. This genetically imposed suppression of FII levels resulted in an impressive reduction in inflammation (reduction in leukocytosis, thrombocytosis, and circulating interleukin-6 levels), reduced endothelial cell dysfunction (reduced endothelial activation and circulating soluble vascular cell adhesion molecule), and a significant improvement in SCD-associated end-organ damage (nephropathy, pulmonary hypertension, pulmonary inflammation, liver function, inflammatory infiltration, and microinfarctions). Notably, all of these benefits were achieved with a relatively modest 1.25-fold increase in prothrombin times, and in the absence of hemorrhagic complications. Taken together, these data establish that prothrombin is a powerful modifier of SCD-induced end-organ damage, and present a novel therapeutic target to ameliorate SCD pathologies. (Blood. 2015;126(15):1844-1855

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“…Decline in endothelial function was observed with increasing duration of symptoms and vaso-occlusive crisis/year in SCD cases. While others had mentioned that FMD was decreased or impaired in SCD patients in steady states (18)(19)(20) . One possible explanation for the insignificant difference in FMD could be due to fact that the control subjects enrolled in this study had have higher BMI than patients.…”

Section: Discussionmentioning

confidence: 99%

Brachial Artery Diameter as a Predictor of Endothelial Dysfunction in Sickle Cell Disease

Al-Janabi¹,

Al-Saadi²,

Hamdani³

et al. 2016

IJMS

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Endothelial Function in Patients with Sickle Cell Anemia During and After Sickle Cell Crises

Cited by 44 publications

References 13 publications

Anemia increases the mortality risk in patients with stroke: A meta-analysis of cohort studies

Anemia increases the mortality risk in patients with stroke: A meta-analysis of cohort studies

Genetic diminution of circulating prothrombin ameliorates multiorgan pathologies in sickle cell disease mice

Brachial Artery Diameter as a Predictor of Endothelial Dysfunction in Sickle Cell Disease

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