Cerebrovascular Complications of Anemia

Fonseca, Ana Catarina; Silva, Daniela P.; Infante, Joana; Ferro, José M.

doi:10.1007/s11910-021-01141-y

Cited by 9 publications

(7 citation statements)

References 92 publications

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“…The youth population can experience both hypoproliferative anemia and hyperproliferative anemia, which are linked to cerebrovascular diseases. These diseases range from transient ischemic attacks to ischemic stroke and hemorrhagic stroke ( 26 ). In adults, low hemoglobin levels have been associated with an increased risk of stroke in both men and women, irrespective of their gender.…”

Section: Discussionmentioning

confidence: 99%

Investigation on the relationship between hemoglobin concentration and stroke risk: a bidirectional Mendelian randomization study

Wu,

Fan,

Que

et al. 2024

Front. Neurol.

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BackgroundThe relationship between hemoglobin concentration and stroke has garnered significant interest in the research community. However, findings from published observational epidemiological studies on this relationship have been inconclusive. By using publicly available genome-wide association study (GWAS) aggregated statistics, a two-sample Mendelian randomization analysis is conducted to explore the causal relationship between hemoglobin concentration and stroke.MethodsSummary statistics data from UK Biobank for hemoglobin concentration and from the FinnGen R9 and MEGASTROKE consortium for stroke are used. A series of quality control steps are taken to select eligible instrumental SNPs closely related to exposure. In order to make the conclusion more robust and reliable, several robust analysis methods are employed including inverse variance weighted, weighted median, MR-Egger regression, which are based on different assumptions of two-sample MR Analysis. Meanwhile, sensitivity analyses such as pleiotropy test and MR-Egg regression, are performed to mitigate horizontal pleiotropy and heterogeneity.ResultsThe two-sample Mendelian randomized study indicates a negative association between hemoglobin concentration and stroke, suggesting that hemoglobin concentration acts as a protective factor against stroke. From the FinnGen database, there is a negative association between hemoglobin concentration and stroke, with an odds ratio (OR) of 0.82 and a 95% confidence interval (CI) of 0.73–0.92, p = 0.0006. Similarly, the MEGASTROKE database findings reinforce this observation. The negative association between hemoglobin concentration and stroke (OR: 0.91, 95%CI: 0.83–1.00, p = 0.040), ischemic stroke (OR: 0.87, 95%CI: 0.79–0.96, p = 0.004), and cardiogenic stroke (OR: 0.82, 95% CI: 0.69–0.99, p = 0.039) further suggests that higher hemoglobin levels might confer a protective effect against these conditions.ConclusionHemoglobin concentration serves as a protective factor against stroke, and managing abnormal hemoglobin levels can effectively reduce the incidence of stroke.

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Section: Discussionmentioning

confidence: 99%

Investigation on the relationship between hemoglobin concentration and stroke risk: a bidirectional Mendelian randomization study

Wu,

Fan,

Que

et al. 2024

Front. Neurol.

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“…The known causes include anemia, stress-induced erythrocyte sickling, faster thrombus formation, chronic vasculopathy, and sensitivity to transient hypoxia-ischemia ( 17 , 26–28 ). While anemia is a common risk factor for cerebrovascular complications, the presence of inflammatory or proliferative-occlusive vasculopathy in SCA is unique among hemoglobinopathy and contributes greatly to the high incidence of stroke in this population ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

Impaired post-stroke collateral circulation in sickle cell anemia mice

Bian,

Chen,

Cheng

et al. 2023

Front. Neurol.

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Patients with sickle cell anemia (SCA) have a high incidence of ischemic stroke, but are usually excluded from thrombolytic therapy due to concerns for cerebral hemorrhage. Maladaptation to cerebral ischemia may also contribute to the stroke propensity in SCA. Here we compared post-stroke cortical collateral circulation in transgenic sickle (SS) mice, bone marrow grafting-derived SS-chimera, and wildtype (AA) controls, because collateral circulation is a critical factor for cell survival within the ischemic penumbra. Further, it has been shown that SS mice develop poorer neo-collateral perfusion after limb ischemia. We used the middle cerebral artery (MCA)-targeted photothrombosis model in this study, since it is better tolerated by SS mice and creates a clear infarct core versus peri-infarct area. Compared to AA mice, SS mice showed enlarged infarction and lesser endothelial proliferation after photothrombosis. SS-chimera showed anemia, hypoxia-induced erythrocyte sickling, and attenuated recovery of blood flow in the ipsilateral cortex after photothrombosis. In AA chimera, cerebral blood flow in the border area between MCA and the anterior cerebral artery (ACA) and posterior cerebral artery (PCA) trees improved from 44% of contralateral level after stroke to 78% at 7 d recovery. In contrast, blood flow in the MCA-ACA and MCA-PCA border areas only increased from 35 to 43% at 7 d post-stroke in SS chimera. These findings suggest deficits of post-stroke collateral circulation in SCA. Better understanding of the underpinnings may suggest novel stroke therapies for SCA patients.

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“…The major anemia classes comprise hyperproliferative (RI ≥ 2.5) and hypoproliferative (RI < 2.5) anemia. Hypoproliferative anemias divide into microcytic (MCV < 80 femtoliters (fL)), normocytic (MCV 80–100 fL), and macrocytic (MCV > 100 fL) anemia types [ 5 ]. Anemia is not a disease, but a presentation of an underlying condition [ 6 ].…”

Section: Anemia: Classifications and Global Significancementioning

confidence: 99%

“…The decrease in the total content of iron in the body leads to iron deficiency. Severe iron deficiency can reduce Hb levels, decrease erythropoiesis, and result in hypoproliferative microcytic anemia, which is defined as iron deficiency anemia (IDA) [ 5 , 11 ]. Iron deficiency [ 12 , 13 ] underlies the majority of anemia cases, affecting 1.6 billion people, which comprise 24.8% of the world population [ 8 ].…”

Section: Anemia: Classifications and Global Significancementioning

confidence: 99%

Iron Deficiency Anemia: Efficacy and Limitations of Nutritional and Comprehensive Mitigation Strategies

et al. 2022

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Iron deficiency anemia (IDA) has reached epidemic proportions in developing countries and has become a major global public health problem, affecting mainly 0–5-year-old children and young women of childbearing age, especially during pregnancy. Iron deficiency can lead to life-threatening loss of red blood cells, muscle function, and energy production. Therefore, the pathogenic features associated with IDA are weakness and impaired growth, motor, and cognitive performance. IDA affects the well-being of the young generation and the economic advancement of developing countries, such as India. The imbalance between iron intake/absorption/storage and iron utilization/loss culminates into IDA. However, numerous strategic programs aimed to increase iron intake have shown that improvement of iron intake alone has not been sufficient to mitigate IDA. Emerging critical risk factors for IDA include a composition of cultural diets, infections, genetics, inflammatory conditions, metabolic diseases, dysbiosis, and socioeconomic parameters. In this review, we discuss numerous IDA mitigation programs in India and their limitations. The new multifactorial mechanism of IDA pathogenesis opens perspectives for the improvement of mitigation programs and relief of IDA in India and worldwide.

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Cerebrovascular Complications of Anemia

Cited by 9 publications

References 92 publications

Investigation on the relationship between hemoglobin concentration and stroke risk: a bidirectional Mendelian randomization study

Investigation on the relationship between hemoglobin concentration and stroke risk: a bidirectional Mendelian randomization study

Impaired post-stroke collateral circulation in sickle cell anemia mice

Iron Deficiency Anemia: Efficacy and Limitations of Nutritional and Comprehensive Mitigation Strategies

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