ArticleClinical hemorheology and microcirculation2018
Vascular complications of sickle cell disease.
Article in Clinical hemorheology and microcirculation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.
- Relevance of Plasma Homocysteine and Methylenetetrahydrofolate Reductase 677TT Genotype in Sickle Cell Disease: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2022Pooled it
- Antiphospholipid Antibodies in Sickle Cell Disease: A Systematic Review and Exploratory Meta-Analysis.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisPooled it
- Antibody-Dependent and Antibody-Independent Hemolysis in Sickle Cell Disease.Antibodies (Basel, Switzerland) · 2026Review
- More than a ring: the emerging role of heme in angiogenesis.Cell communication and signaling : CCS · 2026Review
- Astrocytic frataxin deficiency drives neurocognitive impairment in sickle cell mice.PNAS nexus · 2026Article
- Elevated tricuspid regurgitation velocity in adults with sickle cell disease and HbAA controls in Kinshasa, Democratic Republic of the Congo: a comparative cross-sectional study.Annals of hematology · 2026Article
- Ciliary protein ARL13b detected on RBCs as a potential indicative biomarker of vaso-occlusive crisis and disease severity in SCD: a retrospective pilot study.Journal of sickle cell disease · 2026Article
- The Breakdown of Neurovascular Barriers: Molecular Mechanisms of Tight Junction Dysfunction.Molecular neurobiology · 2025Review
- Femoral neck fracture in sickle cell anemia: A comprehensive case study.Clinical case reports · 2024Article
- Genetic Modifiers of Stroke in Patients with Sickle Cell Disease-A Scoping Review.International journal of molecular sciences · 2024Article
- Cystatin C-derived estimated glomerular filtration rate in children with sickle cell anaemia.BMC nephrology · 2023Article
- Thrombo-Inflammation in COVID-19 and Sickle Cell Disease: Two Faces of the Same Coin.Biomedicines · 2023Review
- Vascular Aging and Damage in Patients with Iron Metabolism Disorders.Diagnostics (Basel, Switzerland) · 2022Review
- Microfluidic methods to advance mechanistic understanding and translational research in sickle cell disease.Translational research : the journal of laboratory and clinical medicine · 2022Review
- Chronic anemia: The effects on the connectivity of white matter.Frontiers in neurology · 2022Article
- cGMP modulation therapeutics for sickle cell disease.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Article
- The Association of Sickle-Cell Disorders With Diabetic Retinopathy: A Large Database Study.Ophthalmology scienceArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Sickle cell disease (SCD) is a monogenetic disorder caused by a mutation in the β-globin gene HBB leading to polymerization of red blood cells causing damage to cell membranes, increasing its rigidity and intravascular hemolysis. Multiple lines of evidence suggest that SCD can be viewed as pan-vasculopathy associated with multiple mechanisms but driven by hemoglobin S polymerization. Here we review the pathophysiology, clinical manifestations and management strategies for cerebrovascular disease, pulmonary hypertension and renal disease associated with SCD. These "vascular phenotypes" reflect the systemic nature of the complications of SCD and are a major threat to the well-being of patients with the disorder.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.