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Article ; Online: Hydroxyurea for the treatment of sickle cell anemia.

Platt, Orah S

2008 Volume 358, Issue 13, Page(s) 1362–1369

MeSH term(s)	Adolescent ; Anemia, Sickle Cell/drug therapy ; Anemia, Sickle Cell/physiopathology ; Antisickling Agents/adverse effects ; Antisickling Agents/pharmacology ; Antisickling Agents/therapeutic use ; Female ; Humans ; Hydroxyurea/adverse effects ; Hydroxyurea/pharmacology ; Hydroxyurea/therapeutic use ; Practice Guidelines as Topic
Chemical Substances	Antisickling Agents ; Hydroxyurea (X6Q56QN5QC)
Language	English
Publishing date	2008-03-27
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMct0708272
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Article ; Online: Preventing stroke in sickle cell anemia.

Platt, Orah S

The New England journal of medicine

2005 Volume 353, Issue 26, Page(s) 2743–2745

MeSH term(s)	Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/physiopathology ; Anemia, Sickle Cell/therapy ; Blood Flow Velocity ; Blood Transfusion ; Brain/blood supply ; Cerebral Arteries/diagnostic imaging ; Cerebral Arteries/pathology ; Cerebral Arteries/physiopathology ; Child ; Humans ; Oxygen/blood ; Stroke/prevention & control ; Ultrasonography, Doppler, Transcranial
Chemical Substances	Oxygen (S88TT14065)
Language	English
Publishing date	2005-12-29
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMp058274
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Article: Prevention and management of stroke in sickle cell anemia.

Platt, Orah S

Hematology. American Society of Hematology. Education Program

2006 , Page(s) 54–57

Abstract: As the overall health of patients with sickle cell anemia (SS) improves and diagnostic techniques become more sensitive, physicians are seeing patients with an increasingly wide range of subtle and not-so-subtle brain injury. The major breakthrough in ... ...

Abstract	As the overall health of patients with sickle cell anemia (SS) improves and diagnostic techniques become more sensitive, physicians are seeing patients with an increasingly wide range of subtle and not-so-subtle brain injury. The major breakthrough in the field of sickle-related brain injury has been the unprecedented success of transcranial Doppler ultrasonography (TCD) to identify asymptomatic patients at high risk of stroke, coupled with chronic transfusion therapy to prevent it. The evidence for TCD screening and preventive treatment is strong and compelling, but there are still important unanswered questions regarding the implications of "silent infarcts" found in the magnetic resonance images (MRIs) of asymptomatic individuals, and the growing awareness of the burden of neuropsychiatric dysfunction in otherwise apparently healthy individuals.
MeSH term(s)	Anemia, Sickle Cell/complications ; Disease Management ; Humans ; Magnetic Resonance Imaging ; Stroke/diagnostic imaging ; Stroke/prevention & control ; Stroke/therapy ; Ultrasonography, Doppler, Transcranial
Language	English
Publishing date	2006
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1520-4391
ISSN	1520-4391
DOI	10.1182/asheducation-2006.1.54
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Article ; Online: Heritability of fetal hemoglobin, white cell count, and other clinical traits from a sickle cell disease family cohort.

Bao, Erik L / Lareau, Caleb A / Brugnara, Carlo / Fulcher, Isabel R / Barau, Caroline / Moutereau, Stephane / Habibi, Anoosha / Badaoui, Bouchra / Berkenou, Jugurtha / Bartolucci, Pablo / Galactéros, Frédéric / Platt, Orah S / Mahaney, Michael / Sankaran, Vijay G

American journal of hematology

2019 Volume 94, Issue 5, Page(s) 522–527

Abstract: Sickle cell disease (SCD) is the most common monogenic disorder in the world. Notably, there is extensive clinical heterogeneity in SCD that cannot be fully accounted for by known factors, and in particular, the extent to which the phenotypic diversity ... ...

Abstract	Sickle cell disease (SCD) is the most common monogenic disorder in the world. Notably, there is extensive clinical heterogeneity in SCD that cannot be fully accounted for by known factors, and in particular, the extent to which the phenotypic diversity of SCD can be explained by genetic variation has not been reliably quantified. Here, in a family-based cohort of 449 patients with SCD and 755 relatives, we first show that 5 known modifiers affect 11 adverse outcomes in SCD to varying degrees. We then utilize a restricted maximum likelihood procedure to estimate the heritability of 20 hematologic traits, including fetal hemoglobin (HbF) and white blood cell count (WBC), in the clinically relevant context of inheritance from healthy carriers to SCD patients. We report novel estimations of heritability for HbF at 31.6% (±5.4%) and WBC at 41.2% (±6.8%) in our cohort. Finally, we demonstrate shared genetic bases between HbF, WBC, and other hematologic traits, but surprisingly little overlap between HbF and WBC themselves. In total, our analyses show that HbF and WBC have significant heritable components among individuals with SCD and their relatives, demonstrating the value of using family-based studies to better understand modifiers of SCD.
MeSH term(s)	Adult ; Anemia, Sickle Cell/blood ; Anemia, Sickle Cell/genetics ; Cohort Studies ; Family ; Female ; Fetal Hemoglobin/genetics ; Fetal Hemoglobin/metabolism ; Humans ; Leukocyte Count ; Male ; Quantitative Trait, Heritable
Chemical Substances	Fetal Hemoglobin (9034-63-3)
Language	English
Publishing date	2019-02-06
Publishing country	United States
Document type	Clinical Trial ; Journal Article ; Multicenter Study ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	196767-8
ISSN	1096-8652 ; 0361-8609
ISSN (online)	1096-8652
ISSN	0361-8609
DOI	10.1002/ajh.25421
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Article: Age- and gender-dependent obesity in individuals with 16p11.2 deletion.

Yu, Yongguo / Zhu, Haitao / Miller, David T / Gusella, James F / Platt, Orah S / Wu, Bai-Lin / Shen, Yiping

Journal of genetics and genomics = Yi chuan xue bao

2011 Volume 38, Issue 9, Page(s) 403–409

Abstract: Recurrent genomic imbalances at 16p11.2 are genetic risk factors of variable penetrance for developmental delay and autism. Recently, 16p11.2 (chr16:29.5 Mb-30.1 Mb) deletion has also been detected in individuals with early-onset severe obesity. The ... ...

Abstract	Recurrent genomic imbalances at 16p11.2 are genetic risk factors of variable penetrance for developmental delay and autism. Recently, 16p11.2 (chr16:29.5 Mb-30.1 Mb) deletion has also been detected in individuals with early-onset severe obesity. The penetrance of 16p11.2 deletion as a genetic risk factor for obesity is unknown. We evaluated the growth and body mass characteristics of 28 individuals with 16p11.2 (chr16:29.5 Mb-30.1 Mb) deletion originally ascertained for their developmental disorders by reviewing their medical records. We found that nine individuals could be classified as obese and six as overweight. These individuals generally had early feeding and growth difficulties, and started to gain excessive weight around 5-6 years of age. Thirteen out of the 18 deletion carriers aged 5 years and older (72%) were overweight or obese, whereas only two of 10 deletion carriers (20%) younger than five were overweight or obese. Males exhibited more severe obesity than females. Thus, the obesity phenotype of 16p11.2 deletion carriers is of juvenile onset, exhibited an age- and gender-dependent penetrance. 16p11.2 deletion appears to predispose individuals to juvenile onset obesity and in this case are similar to the well-described Prader-Willi syndrome (PWS). Early detection of this deletion will provide opportunity to prevent obesity.
MeSH term(s)	Aging/genetics ; Child ; Child, Preschool ; Chromosome Deletion ; Chromosomes, Human, Pair 16/genetics ; Female ; Genotype ; Growth and Development/genetics ; Humans ; Infant ; Male ; Obesity/diagnosis ; Obesity/genetics ; Obesity/physiopathology ; Oligonucleotide Array Sequence Analysis ; Pregnancy ; Sex Characteristics
Language	English
Publishing date	2011-09-20
Publishing country	China
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2374568-X
ISSN	1873-5533 ; 1673-8527
ISSN (online)	1873-5533
ISSN	1673-8527
DOI	10.1016/j.jgg.2011.08.003
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Article: Genetic influences on peripheral blood cell counts: a study in baboons.

Mahaney, Michael C / Brugnara, Carlo / Lease, Loren R / Platt, Orah S

Blood

2005 Volume 106, Issue 4, Page(s) 1210–1214

Abstract: Interperson differences in peripheral blood cell counts in healthy individuals result from genetic and environmental influences. We used multivariate genetic analyses to assess the relative impact of genes and environment on baseline blood cell counts ... ...

Abstract	Interperson differences in peripheral blood cell counts in healthy individuals result from genetic and environmental influences. We used multivariate genetic analyses to assess the relative impact of genes and environment on baseline blood cell counts and indices using a pedigreed colony of baboons, an animal with well-documented analogies to human blood physiology. After accounting for age, sex, and weight, we found that genetic influences explain a significant proportion of the remaining variability, ranging from a low of 13.7% for mean corpuscular hemoglobin concentration (MCHC) to a high of 72.4% for red blood cell (RBC) number. Genes influence 38.5% of the variation in baseline white blood cell (WBC) count, a characteristic that correlates with mortality in both the general human population and clinically defined subgroups such as individuals with sickle-cell disease. We examined the interaction between pairs of traits and identified those that share common genetic influences (pleiotropy). We unexpectedly observed that the same gene or group of genes influences both WBC count and mean platelet volume (MPV). We anticipate that this approach will ultimately lead to discovery of novel insights into the biology of related traits, and ultimately identify important genes that affect hematopoiesis.
MeSH term(s)	Animals ; Blood Cell Count ; Blood Cells/cytology ; Erythrocyte Indices ; Genetic Variation ; Hematologic Tests ; Inheritance Patterns ; Multivariate Analysis ; Papio
Language	English
Publishing date	2005-05-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2004-12-4863
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Article: Acquisition of mutans streptococci and caries prevalence in pediatric sickle cell anemia patients receiving long-term antibiotic therapy.

Fukuda, James T / Sonis, Andrew L / Platt, Orah S / Kurth, Susan

Pediatric dentistry

2005 Volume 27, Issue 3, Page(s) 186–190

Abstract: Purpose: The purpose of this study was to: (1) evaluate the prevalence of mutans streptococci (MS) and dental caries in sickle cell anemia (SCA) patients receiving long-term prophylactic penicillin therapy; and (2) determine changes in MS colonization ... ...

Abstract	Purpose: The purpose of this study was to: (1) evaluate the prevalence of mutans streptococci (MS) and dental caries in sickle cell anemia (SCA) patients receiving long-term prophylactic penicillin therapy; and (2) determine changes in MS colonization and dental caries upon discontinuing the antibiotic. Methods: Sixty subjects with SCA and 60 age- and race-matched control subjects participated in this study. The SCA subjects were divided into 2 separate age groups: (1) group 1 subjects were under 6 years of age and received penicillin twice a day; and (2) group 2 subjects were 6 to 12 years old and received no daily prophylactic antibiotics, although up to age 6 they had received daily penicillin before it was discontinued. DMFS/dmfs scores for all subjects were obtained through a comprehensive dental examination including bitewing radiographs. Stimulated salivary samples to assess MS levels were obtained on all subjects. Data on medical, dental, fluoride, and dietary history were obtained on all patients through a written parental questionnaire. Results: No group 1 patients had positive cultures for MS. In contrast, 70% of marched controls cultured positively for MS (P<.01). The DMFS/dmfs score for group 1 was 0.21 vs 5.1 for the control group (P<.01). Differences in surfaces affected were also noted, with no group 1 patients having interproximal lesions compared to 47% of control subjects having these lesions (P<.01). Group 2 also had significantly lower levels of MS than matched controls (47% vs 97%, P<.01), although there was no statistically significant difference in caries prevalence or surfaces involved. Conclusions: These findings demonstrate that long-term penicillin prophylaxis in SCA patients likely prevents the acquisition of MS, resulting in significantly lower caries rates in these patients. This benefit occurs only during active administration of the drug, however, and only delays the acquisition of MS.
MeSH term(s)	Anemia, Sickle Cell/complications ; Anti-Bacterial Agents/administration & dosage ; Antibiotic Prophylaxis ; Case-Control Studies ; Child ; Child, Preschool ; DMF Index ; Dental Caries/complications ; Dental Caries/prevention & control ; Female ; Humans ; Male ; Penicillins/administration & dosage ; Saliva/microbiology ; Streptococcus mutans/drug effects ; Streptococcus mutans/pathogenicity ; Surveys and Questionnaires ; Time Factors
Chemical Substances	Anti-Bacterial Agents ; Penicillins
Language	English
Publishing date	2005-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	604709-9
ISSN	1942-5473 ; 0164-1263
ISSN (online)	1942-5473
ISSN	0164-1263
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Article: Age- and gender-dependent obesity in individuals with 16p11.2 deletion

Yu, Yongguo / Zhu, Haitao / Miller, David T / Gusella, James F / Platt, Orah S / Wu, Bai-Lin / Shen, Yiping

Journal of genetics and genomics. 2011 Sept. 20, v. 38, no. 9

2011

Abstract: Recurrent genomic imbalances at 16p11.2 are genetic risk factors of variable penetrance for developmental delay and autism. Recently, 16p11.2 (chr16:29.5 Mb–30.1 Mb) deletion has also been detected in individuals with early-onset severe obesity. The ... ...

Abstract	Recurrent genomic imbalances at 16p11.2 are genetic risk factors of variable penetrance for developmental delay and autism. Recently, 16p11.2 (chr16:29.5 Mb–30.1 Mb) deletion has also been detected in individuals with early-onset severe obesity. The penetrance of 16p11.2 deletion as a genetic risk factor for obesity is unknown. We evaluated the growth and body mass characteristics of 28 individuals with 16p11.2 (chr16:29.5 Mb–30.1 Mb) deletion originally ascertained for their developmental disorders by reviewing their medical records. We found that nine individuals could be classified as obese and six as overweight. These individuals generally had early feeding and growth difficulties, and started to gain excessive weight around 5–6 years of age. Thirteen out of the 18 deletion carriers aged 5 years and older (72%) were overweight or obese, whereas only two of 10 deletion carriers (20%) younger than five were overweight or obese. Males exhibited more severe obesity than females. Thus, the obesity phenotype of 16p11.2 deletion carriers is of juvenile onset, exhibited an age- and gender-dependent penetrance. 16p11.2 deletion appears to predispose individuals to juvenile onset obesity and in this case are similar to the well-described Prader–Willi syndrome (PWS). Early detection of this deletion will provide opportunity to prevent obesity.
Keywords	females ; males ; obesity ; penetrance ; phenotype ; risk factors
Language	English
Dates of publication	2011-0920
Size	p. 403-409.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	2374568-X
ISSN	1873-5533 ; 1673-8527
ISSN (online)	1873-5533
ISSN	1673-8527
DOI	10.1016/j.jgg.2011.08.003
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Article ; Online: Pulmonary hypertension and nitric oxide depletion in sickle cell disease.

Bunn, H Franklin / Nathan, David G / Dover, George J / Hebbel, Robert P / Platt, Orah S / Rosse, Wendell F / Ware, Russell E

Blood

2010 Volume 116, Issue 5, Page(s) 687–692

Abstract: During the past decade a large body of experimental and clinical studies has focused on the hypothesis that nitric oxide (NO) depletion by plasma hemoglobin in the microcirculation plays a central role in the pathogenesis of many manifestations of sickle ...

Abstract	During the past decade a large body of experimental and clinical studies has focused on the hypothesis that nitric oxide (NO) depletion by plasma hemoglobin in the microcirculation plays a central role in the pathogenesis of many manifestations of sickle cell disease (SCD), particularly pulmonary hypertension. We have carefully examined those studies and believe that the conclusions drawn from them are not adequately supported by the data. We agree that NO depletion may well play a role in the pathophysiology of other hemolytic states such as paroxysmal nocturnal hemoglobinuria, in which plasma hemoglobin concentrations are often at least an order of magnitude greater than in SCD. Accordingly, we conclude that clinical trials in SCD designed to increase the bioavailability of NO or association studies in which SCD clinical manifestations are related to plasma hemoglobin via its surrogates should be viewed with caution.
MeSH term(s)	Adult ; Anemia, Sickle Cell/blood ; Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/drug therapy ; Anemia, Sickle Cell/physiopathology ; Animals ; Child ; Clinical Trials as Topic ; Disease Models, Animal ; Echocardiography, Doppler ; Endothelium, Vascular/physiopathology ; False Positive Reactions ; Female ; Hemoglobins/analysis ; Hemoglobins/chemistry ; Hemoglobinuria, Paroxysmal/complications ; Hemolysis ; Humans ; Hydroxyurea/pharmacology ; Hydroxyurea/therapeutic use ; Hypertension, Pulmonary/blood ; Hypertension, Pulmonary/diagnostic imaging ; Hypertension, Pulmonary/etiology ; Hypertension, Pulmonary/physiopathology ; L-Lactate Dehydrogenase/blood ; Leg Ulcer/etiology ; Leg Ulcer/physiopathology ; Male ; Microcirculation ; Models, Biological ; Multicenter Studies as Topic ; Nitric Oxide/administration & dosage ; Nitric Oxide/blood ; Nitric Oxide/deficiency ; Nitric Oxide/physiology ; Nitric Oxide/therapeutic use ; Priapism/etiology ; Priapism/physiopathology ; Thromboembolism/etiology ; Thromboembolism/physiopathology ; Tricuspid Valve Insufficiency/diagnostic imaging ; Tricuspid Valve Insufficiency/etiology ; Tricuspid Valve Insufficiency/physiopathology
Chemical Substances	Hemoglobins ; Nitric Oxide (31C4KY9ESH) ; L-Lactate Dehydrogenase (EC 1.1.1.27) ; Hydroxyurea (X6Q56QN5QC)
Language	English
Publishing date	2010-04-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2010-02-268193
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Article: Quantitative trait loci for baseline erythroid traits.

Peters, Luanne L / Lambert, Amy J / Zhang, Weidong / Churchill, Gary A / Brugnara, Carlo / Platt, Orah S

Mammalian genome : official journal of the International Mammalian Genome Society

2006 Volume 17, Issue 4, Page(s) 298–309

Abstract: A substantial genetic contribution underlies variation in baseline peripheral blood counts. We performed quantitative trait locus/loci (QTL) analyses to identify chromosome (Chr) regions harboring genes influencing the baseline erythroid parameters in F2 ...

Abstract	A substantial genetic contribution underlies variation in baseline peripheral blood counts. We performed quantitative trait locus/loci (QTL) analyses to identify chromosome (Chr) regions harboring genes influencing the baseline erythroid parameters in F2 intercrosses between NZW/LacJ, SM/J, and C57BLKS/J inbred mice. We identified multiple significant QTL for red blood cell (RBC) count, hemoglobin (Hgb) and hematocrit (Hct) levels, mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and mean cell hemoglobin concentration (CHCM). We identified four RBC count QTL: Rbcq1 (Chr 1, peak LOD score at 62 cM,), Rbcq2 (Chr 4, 60 cM), Rbcq3 (Chr 11, 34 cM), and Rbcq4 (Chr 10, 60 cM). Three MCV QTL were identified: Mcvq1 (Chr 7, 30 cM), Mvcq2 (Chr 11, 6 cM), and Mcvq3 (Chr 10, 60 cM). Single significant loci for Hgb (Hgbq1, Chr 16, 32 cM), Hct (Hctq1, Chr 3, 42 cM), and MCH (Mchq1, Chr 10, 60 cM) were identified. The data support the existence of a common RBC/MCH/MCV locus on Chr 10. Two QTL for CHCM (Chcmq1, Chr 2, 48 cM; Chcmq2, Chr 9, 44 cM) and an interaction between Chcmq2 with a locus on Chr 19 were identified. These analyses emphasize the genetic complexity underlying the regulation of erythroid peripheral blood traits in normal populations and suggest that genes not previously recognized as significantly impacting normal erythropoiesis exist.
MeSH term(s)	Animals ; Chromosomes/genetics ; Crosses, Genetic ; Erythrocyte Count ; Erythropoiesis/genetics ; Female ; Hematocrit ; Hemoglobins/analysis ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NZB ; Quantitative Trait Loci/genetics ; Quantitative Trait, Heritable
Chemical Substances	Hemoglobins
Language	English
Publishing date	2006-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1058547-3
ISSN	1432-1777 ; 0938-8990
ISSN (online)	1432-1777
ISSN	0938-8990
DOI	10.1007/s00335-005-0147-3
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