All Relations between Stroke and scd

Publication Sentence Publish Date Extraction Date Species
R E Ware, S A Zimmerman, W H Schult. Hydroxyurea as an alternative to blood transfusions for the prevention of recurrent stroke in children with sickle cell disease. Blood. vol 94. issue 9. 1999-11-30. PMID:10556185. these preliminary data suggest some children with scd and stroke may discontinue chronic transfusions and use hu therapy to prevent stroke recurrence. 1999-11-30 2023-08-12 Not clear
V V Balasa, R A Gruppo, P S Gartside, K A Kalinya. Correlation of the C677T MTHFR genotype with homocysteine levels in children with sickle cell disease. Journal of pediatric hematology/oncology. vol 21. issue 5. 1999-11-01. PMID:10524453. to determine the role of hyperhomocysteinemia in the pathogenesis of stroke in children with sickle cell disease (scd), hcy levels and c677t mthfr genotype were determined in 40 patients homozygous for hemoglobin ss and compared with 197 healthy children. 1999-11-01 2023-08-12 Not clear
V V Balasa, R A Gruppo, P S Gartside, K A Kalinya. Correlation of the C677T MTHFR genotype with homocysteine levels in children with sickle cell disease. Journal of pediatric hematology/oncology. vol 21. issue 5. 1999-11-01. PMID:10524453. eleven of 40 patients with scd had a history of stroke. 1999-11-01 2023-08-12 Not clear
V V Balasa, R A Gruppo, P S Gartside, K A Kalinya. Correlation of the C677T MTHFR genotype with homocysteine levels in children with sickle cell disease. Journal of pediatric hematology/oncology. vol 21. issue 5. 1999-11-01. PMID:10524453. in patients with scd and stroke, the median hcy level was 4.8 micromol/l versus 6.0 micromol/l in those without stroke (p = 0.44, mann-whitney rank sum test). 1999-11-01 2023-08-12 Not clear
V V Balasa, R A Gruppo, P S Gartside, K A Kalinya. Correlation of the C677T MTHFR genotype with homocysteine levels in children with sickle cell disease. Journal of pediatric hematology/oncology. vol 21. issue 5. 1999-11-01. PMID:10524453. there was no difference in the proportion of patients with scd with or without stroke who were homozygous for the c677t mthfr mutation (0/11 versus 2/29; fisher's, p = 1.000). 1999-11-01 2023-08-12 Not clear
V V Balasa, R A Gruppo, P S Gartside, K A Kalinya. Correlation of the C677T MTHFR genotype with homocysteine levels in children with sickle cell disease. Journal of pediatric hematology/oncology. vol 21. issue 5. 1999-11-01. PMID:10524453. furthermore, hyperhomocysteinemia did not seem to be a significant factor in the pathogenesis of stroke in children with scd. 1999-11-01 2023-08-12 Not clear
R G Steen, X Xiong, R K Mulhern, J W Langston, W C Wan. Subtle brain abnormalities in children with sickle cell disease: relationship to blood hematocrit. Annals of neurology. vol 45. issue 3. 1999-03-29. PMID:10072041. our objective was to test a hypothesis that subtle brain abnormality can be present in pediatric sickle cell disease (scd) patients who are clinically free of stroke. 1999-03-29 2023-08-12 Not clear
R G Steen, X Xiong, R K Mulhern, J W Langston, W C Wan. Subtle brain abnormalities in children with sickle cell disease: relationship to blood hematocrit. Annals of neurology. vol 45. issue 3. 1999-03-29. PMID:10072041. our findings suggest that chronic hypoxia of brain tissue can occur in scd patients free of clinical stroke. 1999-03-29 2023-08-12 Not clear
S A Zimmerman, R E War. Inherited DNA mutations contributing to thrombotic complications in patients with sickle cell disease. American journal of hematology. vol 59. issue 4. 1998-12-14. PMID:9840906. thrombosis may play an important role in the pathophysiology of certain complications of sickle cell disease (scd), including stroke and avascular necrosis (avn). 1998-12-14 2023-08-12 Not clear
S A Zimmerman, R E War. Inherited DNA mutations contributing to thrombotic complications in patients with sickle cell disease. American journal of hematology. vol 59. issue 4. 1998-12-14. PMID:9840906. we hypothesized that some patients with scd have an inherited hypercoagulable state that results in an increased risk of developing stroke or avn. 1998-12-14 2023-08-12 Not clear
S A Zimmerman, R E War. Inherited DNA mutations contributing to thrombotic complications in patients with sickle cell disease. American journal of hematology. vol 59. issue 4. 1998-12-14. PMID:9840906. we analyzed genomic dna from 86 children and adults with scd, including 16 patients with a history of a clinical stroke and 14 patients with avn, for the presence of these mutations. 1998-12-14 2023-08-12 Not clear
S A Zimmerman, R E War. Inherited DNA mutations contributing to thrombotic complications in patients with sickle cell disease. American journal of hematology. vol 59. issue 4. 1998-12-14. PMID:9840906. although each of these mutations is relatively common in patients with scd, neither is independently associated with an increased risk of developing stroke or avn. 1998-12-14 2023-08-12 Not clear
R G Steen, W E Reddick, R K Mulhern, J W Langston, R J Ogg, A A Bieberich, P B Kingsley, W C Wan. Quantitative MRI of the brain in children with sickle cell disease reveals abnormalities unseen by conventional MRI. Journal of magnetic resonance imaging : JMRI. vol 8. issue 3. 1998-08-27. PMID:9626865. conventional mri (cmri) has shown that brain abnormalities without clinical stroke can manifest in patients with sickle cell disease (scd). 1998-08-27 2023-08-12 Not clear
P E Houston, S Rana, S Sekhsaria, E Perlin, K S Kim, O L Castr. Homocysteine in sickle cell disease: relationship to stroke. The American journal of medicine. vol 103. issue 3. 1997-10-23. PMID:9316551. the risk factors and pathophysiology of stroke and other serious complications of sickle cell disease (scd) are poorly defined. 1997-10-23 2023-08-12 Not clear
P E Houston, S Rana, S Sekhsaria, E Perlin, K S Kim, O L Castr. Homocysteine in sickle cell disease: relationship to stroke. The American journal of medicine. vol 103. issue 3. 1997-10-23. PMID:9316551. hyperhomocysteinemia has recently been identified as a risk factor for stroke and other vascular diseases in the general population, however its role in scd has not been investigated. 1997-10-23 2023-08-12 Not clear
R G Steen, J W Langston, W E Reddick, R Ogg, G Chen, W C Wan. Quantitative MR imaging of children with sickle cell disease: striking T1 elevation in the thalamus. Journal of magnetic resonance imaging : JMRI. vol 6. issue 1. 1996-12-06. PMID:8851433. nonparametric kruskal-wallis analysis of variance of control subjects, of scd patients without stroke, and of scd patients with stroke showed that t1 increased with disease severity in the thalamus, frontal white matter, genu, and occipital white matter. 1996-12-06 2023-08-12 human
R G Steen, J W Langston, W E Reddick, R Ogg, G Chen, W C Wan. Quantitative MR imaging of children with sickle cell disease: striking T1 elevation in the thalamus. Journal of magnetic resonance imaging : JMRI. vol 6. issue 1. 1996-12-06. PMID:8851433. t1 was significantly longer in scd patients without stroke (n = 13) than in control subjects (n = 21) in the thalamus and frontal white matter. 1996-12-06 2023-08-12 human
R G Steen, J W Langston, W E Reddick, R Ogg, G Chen, W C Wan. Quantitative MR imaging of children with sickle cell disease: striking T1 elevation in the thalamus. Journal of magnetic resonance imaging : JMRI. vol 6. issue 1. 1996-12-06. PMID:8851433. in addition, t1 values were significantly longer in scd patients with stroke than in patients without stroke in the genu and frontal white matter. 1996-12-06 2023-08-12 human
R G Steen, J W Langston, W E Reddick, R Ogg, G Chen, W C Wan. Quantitative MR imaging of children with sickle cell disease: striking T1 elevation in the thalamus. Journal of magnetic resonance imaging : JMRI. vol 6. issue 1. 1996-12-06. PMID:8851433. abnormality of the thalamus was identified by qmri in a substantial fraction of patients read as normal by both cmri and mra, suggesting that it may be possible to use t1 elevation to identify a subset of patients with scd who are at elevated risk for stroke. 1996-12-06 2023-08-12 human
S Hayashi, H Toyoshima, N Tanabe, K Miyanish. Daily peaks in the incidence of sudden cardiac death and fatal stroke in Niigata Prefecture. Japanese circulation journal. vol 60. issue 4. 1996-11-21. PMID:8726167. we concluded that 1) a circadian variation with two peak incidences, one between 6 and 8 am, and one between 6 and 8 pm, was characteristic of scd in general, 2) there was a primary peak between 4 and 6 am for scd due to ami in males, and 3) there was a peak between 6 and 8 pm in the incidence of fatal stroke for both men and women. 1996-11-21 2023-08-12 Not clear