Hemoglobin (Hemoglobin)

Publisher: Informa Healthcare

Journal description

Hemoglobin emphasizes several topic areas: normal, modified, and abnormal human hemoglobins including new variants, structure-function relationships, physicochemical characteristics, physiological properties, biosynthetic analyses, the thalassemias, and new therapeutic approaches; the genetic aspects of the hemoglobinopathies, including family and population studies; International Hemoglobins Information Center reports of all published hemoglobin variants; and reviews of hemoglobin abnormalities in selected countries and continents.

Current impact factor: 0.79

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 0.787
2013 Impact Factor 0.955
2012 Impact Factor 0.894
2011 Impact Factor 1.304
2010 Impact Factor 1.414
2009 Impact Factor 1.274
2008 Impact Factor 1
2007 Impact Factor 0.843
2006 Impact Factor 0.516
2005 Impact Factor 0.363
2004 Impact Factor 0.36
2003 Impact Factor 0.505
2002 Impact Factor 0.57
2001 Impact Factor 0.398
2000 Impact Factor 0.631
1999 Impact Factor 0.577
1998 Impact Factor 0.897
1997 Impact Factor 1.26
1996 Impact Factor 0.906
1995 Impact Factor 1.129
1994 Impact Factor 1.102
1993 Impact Factor 1
1992 Impact Factor 1.204

Impact factor over time

Impact factor

Additional details

5-year impact 1.06
Cited half-life 6.10
Immediacy index 0.18
Eigenfactor 0.00
Article influence 0.27
Website Hemoglobin website
Other titles Hemoglobin (Online), Hemoglobin
ISSN 1532-432X
OCLC 48882271
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Informa Healthcare

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • On author's personal website or institution website
    • Publisher copyright and source must be acknowledged
    • Non-commercial
    • Must link to publisher version
    • Publisher's version/PDF cannot be used
    • NIH funded authors may post articles to PubMed Central for release 12 months after publication
    • Wellcome Trust authors may deposit in Europe PMC after 6 months
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Hb Constant Spring (Hb CS, HBA2: c.427T > C) is a common nondeletional α-thalassemia (α-thal) that results from a nucleotide substitution at the termination codon of the α2-globin gene. Homozygosity for Hb CS (α(CS)α/α(CS)α) is relatively rare, and generally characterized with mild hemolytic anemia, jaundice, and splenomegaly. In this report we present a fetus with cardiomegaly, pericardial effusion, enlarged placenta and increased middle cerebral artery-peak systolic velocity (MCA-PSV) at 24 weeks' gestation. Fetal blood sampling revealed the severe anemia [hemoglobin (Hb) level being 4.8 g/dL] and Hb H (β4) disease-like hematological findings with Hb Bart's (γ4) level of 17.9%. DNA sequencing of the α-globin genes found that both partners were Hb CS carriers and the fetus was an Hb CS homozygote. Therefore, this was a rare case of homozygous Hb CS which demonstrated an unusual and serious anemia and hydrops fetalis in utero.
    No preview · Article · Jan 2016 · Hemoglobin
  • [Show abstract] [Hide abstract]
    ABSTRACT: The purpose of this meta-study was to investigate β-thalassemia (β-thal) mutations and their chromosomal background in order to highlight the origin and spread of thalassemia alleles in the European and Mediterranean areas. Screening of more than 100 new Romanian β-thal alleles was also conducted. The results suggest an ancient introduction of mutations at codon 39 (C > T) (HBB: c.118C > T) and IVS-I-6 (T > C) (HBB: c.92 + 6T > C) in Romania. A comparative study was performed based on restriction fragment length polymorphism (RFLP) haplotypes associated with β-thal mutations in Romania and in Mediterranean countries. Each common β-thal allele from different populations exhibits a high degree of haplotype similarity, a sign of a clear unicentric origin for the IVS-I-110 (G > A) (HBB: c.93-21G > A), IVS-I-6, IVS-II-745 (C > G) (HBB: c.316-106C > G) and codon 39 mutations (the 17a [+ - - - - + +], 13c [ - + + - - - +], 17c [ + - - - - - +] and 14a [- + + - + + + ] ancestral RFLP background, respectively), followed by recurrent recombination events. This study also showed that geographic distances played a major role in shaping the spread of the predominant β-thal alleles, whereas no genetic boundaries were detected between broad groups of populations living in the Middle East, Europe and North Africa. The analyses revealed some discrepancies concerning Morocco and Serbia, which suggest some peculiar genetic flows. Marked variations in β(A) were observed between Southeast Asia and the Mediterranean, whereas a relative genetic homogeneity was found around the Mediterranean Basin. This homogeneity is undoubtedly the result of the high level of specific historic human migrations that occurred in this area.
    No preview · Article · Dec 2015 · Hemoglobin
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    ABSTRACT: Hemoglobin (Hb) variants may be associated with low oxygen saturation and exacerbated episodes of anemia from common stressors such as viral infections. These attributes frequently cause increased clinical concern and unnecessary and expensive testing if not considered early in the evaluation of the patient. Some clinically significant Hb variants result in a normal Hb electrophoresis result, which can be method-dependent. Herein we describe a patient with low oxygen saturation and a history of hemolytic anemia who was subsequently found to carry a novel, unstable β-globin variant that we have named Hb Allentown [β137(H15)Val→Trp (GTG>TGG) HBB: c.412_413delinsTG, p.Val138Trp] for the place of identification of the variant. Hb Allentown is formed by a rare double nucleotide substitution within the same codon. Additionally, positive identification of rare Hb variants characterized by a single method is discouraged, as the Hb variant was misclassified as Hb S-South End or β6(A3)Glu→Val;β132(H10)Lys→Asn (HBB: c.[20A > T;399A > C]) by the initial laboratory.
    No preview · Article · Dec 2015 · Hemoglobin
  • [Show abstract] [Hide abstract]
    ABSTRACT: The aim of the present study was to report the use of analysis of fetal blood in prenatal diagnosis (PND) of β- and α-thalassemia (β- and α-thal), at a Chinese tertiary, maternity center. All cases undergoing invasive testing for PND of thalassemias from 1 January 2010 to 31 December 2014 were included. The main clinical characteristics of these invasive procedures were retrieved from the database software used for analysis. One thousand, nine hundred and six invasive PNDs were carried out for thalassemia, including 904 cases for β-thal and 1002 for α-thal. In the 904 PNDs for β-thal, chorionic villus sampling (CVS) was done in 321 cases and amniocentesis in 583 cases. No fetal blood analysis was used for cases at-risk for β-thal. In the 1002 PNDs for α-thal, CVS was done in 724 cases, amniocentesis in 137 cases and fetal blood analysis in 141 cases. All the 278 cases sampled by amniocentesis or fetal blood analysis were found to be affected by Hb Bart's (γ4) disease. Currently, fetal blood analysis is considered only in relatively late gestation when Hb Bart's disease has already been identified by ultrasound in a fetus at-risk for α-thal.
    No preview · Article · Nov 2015 · Hemoglobin
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    ABSTRACT: Hemoglobin (Hb) variants are abnormalities resulting from point mutations in either of the two α-globin genes (HBA2 or HBA1) or the β-globin gene (HBB). Various reports of Hb variants have been described in Iran and other countries around the world. Hb Setif (or HBA2: c.283G>T) is one of these variants with a mutation at codon 94 of of the α2-globin gene that is characterized in clinically normal heterozygous individuals. We here report clinical and hematological findings in two homozygous cases of Iranian origin for this unstable Hb variant.
    No preview · Article · Nov 2015 · Hemoglobin
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    ABSTRACT: Most people with Hb H disease live normal lives; however, a minority of cases requires lifelong regular transfusions. An atypical form of nondeletional Hb H disease was reported in a Thai boy, characterized by severe persistent hemolytic anemia since the age of 2 months. Molecular diagnosis revealed the apparent compound heterozygosity for the Southeast Asian (- -(SEA)) and α2 polyadenylation (polyA) signal (AATAAA>AATA- -) deletions. The proband was successfully treated with allogeneic hematopoietic stem cell transplantation (HSCT). Accurate phenotypic and genotypic diagnosis in atypically severe Hb H disease is helpful for the understanding of its pathophysiology, the institution of appropriate management, and provision of genetic counseling and prenatal diagnosis. Hematopoietic stem cell transplantation is a potentially curative treatment option for this severe α-thalassemia (α-thal) syndrome.
    No preview · Article · Nov 2015 · Hemoglobin
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    ABSTRACT: We here report an unusual case of Hb Bart's (γ4) disease. Thalassemia screening of a couple showed that the wife was an α(0)-thalassemia (α(0)-thal) carrier and her husband's mean corpuscular volume (MCV) was normal. Chorionic villus sampling (CVS) was performed at 13 weeks' gestation for positive Down syndrome screening and chromosomal study of the cultured CVS showed a normal karyotype. Ultrasound examination at 22 weeks' gestation showed fetal cardiomegaly and raised middle cerebral artery peak systolic velocity. Cordocentesis confirmed fetal anemia and showed Hb Bart's disease. Multiplex gap-polymerase chain reaction (gap-PCR) for α-thal deletions on DNA extracted from the CVS showed the presence of a homozygous α(0)-thal - -(SEA) (Southeast Asian) deletion. The husband was found to be a carrier of the α(+)-thal -α(3.7) (rightward) deletion. Non paternity was excluded by fluorescent PCR using short tandem repeat (STR) markers on chromosomes 13, 18 and 21. A de novo terminal deletion of chromosome 16 was excluded by array comparative genomic hybridization (aCGH). Detection of uniparental disomy (UPD), using STR markers on chromosome 16 showed maternal uniparental isodisomy from 16pter to 16p13.2, and uniparental heterodisomy from 16p13.13 to 16qter.
    No preview · Article · Nov 2015 · Hemoglobin
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    ABSTRACT: We present the first description of a novel β-thalassemia (β-thal) mutation in a Chinese family. This mutation is located at -27 of the TATA box in the promoter of the β-globin gene (HBB: c.-77A > G) and is likely associated with a phenotype of β(+)-thalassemia (β(+)-thal).
    No preview · Article · Nov 2015 · Hemoglobin
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    ABSTRACT: Homozygous Hb E [β26(B8)Glu→Lys; HBB: c.79G > A] is a clinically mild disease with no significant symptoms. Very few studies are available on clinical variability in Hb E disorders. We report the profile of a series of homozygous Hb E patients in the Indian population. We analyzed various genetic factors that contribute to the heterogeneity in the phenotype of homozygous Hb E patients. Analysis of these parameters further enhances our understanding of the Hb E syndrome.
    No preview · Article · Nov 2015 · Hemoglobin
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    ABSTRACT: The Qinzhou α-thalassemia (α-thal) or -α(21.9) deletion was first described at the Qinzhou Maternal and Child Health Care Hospital, Qinzhou, Guangxi, People's Republic of China (PRC) in 2013. The molecular biological mechanism by which this allele leads to α-thal involves the deletion of a 21.9 kb DNA fragment of the α-globin gene cluster (NG_000006.1), designated as -α(21.9). During routine screening, a new family with -α(21.9) was found by the research group. This is the first time that an adult patient with the -α(21.9)/αα genotype and a 6-month-old baby with the -α(21.9)/- -(SEA) (Southeast Asian) genotype were detected in one family. The discovery of this family demonstrates that there is a certain risk for the Qinzhou α-thal deletion in the southern regions of Guangxi Province, PRC. The detection of the adult patient with the -α(21.9)/αα genotype and the analysis of hematological data are important supplements for -α(21.9) research. Additionally, Hb Bart's (γ4) and Hb H (β4) were detected in the 6-month-old, confirming that the baby with the -α(21.9)/- -(SEA) genotype also carries Hb H disease. The analysis of this family verifies that the -α(21.9) deletion is an α(+)-thal allele.
    No preview · Article · Oct 2015 · Hemoglobin
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    ABSTRACT: Thalassemia is one of the most common autosomal recessive blood disorders in the world. It shows a variety of clinical expression, starting from asymptomatic to severe blood transfusion dependence. More than 500 alleles have been characterized in or around the β-globin region. Moreover, most geographical regions have their own characteristics, frequency and availability of these alleles, predominantly circulating within the communities present in that particular region. In this study, we explored the spectrum of β-thalassemia (β-thal) alleles present in Chittagong, Southeast Bangladesh. This study comprises β-thal and Hb E (HBB: c.79 G > A) patients from in and around the area of Chittagong. Not only exploring the complete β-globin mutation spectrum of the area, but we also tried to look at the origin of the mutated alleles. The β-thal mutations of Bangladesh show a relatively wide spectrum of alleles, which further demonstrates the heterogeneity of the disease in this country. Although our study showed that the majority of the mutations have their origin in neighboring countries such as India, countries of Southeast Asia, Pakistan, etc., some unusual alleles do not originate in neighboring countries and put a little more diversity in the overall spectrum of β-thal-specific alleles. Overall, this study demonstrates the mutation spectrum related to β-thal in Chittagong, Southeast Bangladesh.
    No preview · Article · Sep 2015 · Hemoglobin
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    ABSTRACT: The St. Jude Children's Research Hospital (St. Jude) comprehensive sickle cell center serves a 150 mile catchment radius around Memphis, TN, USA. Full travel expenses are provided for routine and acute care visits for sickle cell disease patients living ≥35 miles from St. Jude. We compared hospitalization rates to national estimates and assessed if driving distance was a barrier to sickle cell healthcare despite the travel reimbursement policy. We evaluated the associations between hospitalizations and routine clinic visits and distance from St. Jude using negative binomial models and we conducted bias analyses by Monte Carlo simulation. We followed 545 patients (2550 patient-years) aged ≤18 years with sickle cell disease (Hb SS only) from 2007 to 2012. The hospitalization rate per patient-year was 0.65 [95% CI (confidence interval): 0.62, 0.68), significantly lower than the national rate of 1.16 (95% CI: 1.14, 1.18). Children living <35 miles from St. Jude had 1.75 (95% CI: 1.41, 2.17) times the rate of hospitalization and 1.22 (95% CI: 1.07, 1.39) times the rate of clinic visits compared to those ≥35 miles. Bias analysis suggested that under-reporting could explain the observed difference in hospitalization rates if 30.0% of patients who lived ≥35 miles from the hospital under-reported six hospitalizations over 6 years. The hospitalization rate at St. Jude in children with sickle cell disease was lower than expected from national rates. Greater distance from the sickle cell center (>35 miles) was associated with decreased hospitalization rates, despite the travel allowances that are provided for those who live ≥35 miles from the hospital.
    No preview · Article · Sep 2015 · Hemoglobin
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    ABSTRACT: Hereditary persistence of fetal hemoglobin (HPFH) can be caused by point mutations in the γ-globin gene promoters. We report three rare cases: a child compound heterozygous for Hb S (HBB: c.20A > T) and HPFH with a novel point mutation in the (A)γ-globin gene promoter who had 42.0% Hb S, 17.0% Hb A and 38.0% Hb F; a man with Hb SC (HBB: c.19G > A) disease and a point mutation in the (G)γ-globin gene promoter who had 54.0% Hb S, 18.0% Hb C and 25.0% Hb F; a child heterozygous for Hb S and HPFH due to mutations in both the (A)γ- and (G)γ-globin gene promoters in cis [(G)γ(A)γ(β(+)) HPFH], with 67.0% Hb A, 6.5% Hb S and 25.0% Hb F.
    No preview · Article · Sep 2015 · Hemoglobin