Publications by authors named "Marcos André Cavalcanti Bezerra"

16 Publications

  • Page 1 of 1

Alpha thalassemia, but not β-globin haplotypes, influence sickle cell anemia clinical outcome in a large, single-center Brazilian cohort.

Ann Hematol 2021 Apr 13;100(4):921-931. Epub 2021 Feb 13.

Genetics Postgraduate Program, Centre of Biosciences, Federal University of Pernambuco, Recife, Brazil.

Alpha thalassemia and beta-globin haplotype are considered classical genetic disease modifiers in sickle cell anemia (SCA) causing clinical heterogeneity. Nevertheless, their functional impact on SCA disease emergence and progression remains elusive. To better understand the role of alpha thalassemia and beta-globin haplotype in SCA, we performed a retrospective study evaluating the clinical manifestations of 614 patients. The univariate analysis showed that the presence of alpha-thalassemia -3.7-kb mutation (αα/-α and -α/-α) decreased the risk of stroke development (p = 0.046), priapism (p = 0.033), and cholelithiasis (p = 0.021). Furthermore, the cumulative incidence of stroke (p = 0.023) and cholelithiasis (p = 0.006) was also significantly lower for patients carrying the alpha thalassemia -3.7-kb mutation. No clinical effects were associated with the beta-globin haplotype analysis, which could be explained by the relatively homogeneous haplotype composition in our cohort. Our results reinforce that alpha thalassemia can provide protective functions against hemolysis-related symptoms in SCA. Although, several genetic modifiers can impact the inflammatory state of SCA patients, the alpha thalassemia mutation remains one of the most recurrent genetic aberration and should therefore always be considered first.
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http://dx.doi.org/10.1007/s00277-021-04450-xDOI Listing
April 2021

Polymorphisms in the heme oxygenase-1 and bone morphogenetic protein receptor type 1b genes and estimated glomerular filtration rate in Brazilian sickle cell anemia patients.

Hematol Transfus Cell Ther 2021 Apr-Jun;43(2):165-170. Epub 2020 May 16.

Faculdade de Ciências Médicas, Universidade Estadual de Campinas (FCM/UNICAMP), Campinas, SP, Brazil. Electronic address:

Introduction: Mutations affecting genes involved in oxidative and signaling pathways may be associated with kidney disease in sickle cell anemia. We determined the allele and genotype frequencies of some polymorphisms in the promoter regions of the Heme Oxygenase-1 (HMOX1) [rs2071746 (A>T) and (GT)n repeats, short (S) and long (L) alleles] and Bone Morphogenetic Protein Receptor type-1B (BMPR1B) [rs17022863 (A>G), rs4331783 (A>G) and rs1470409 (A>G)] genes in 75 adult patients with sickle cell anemia and 160 healthy controls and investigated whether these polymorphisms may influence the estimated glomerular filtration rate for the patients.

Methods: The single nucleotide polymorphisms were genotyped using the TaqMan assays, the HMOX1(GT)n repeats were determined by polymerase chain reaction fragment size analysis and the estimated glomerular filtration rate was calculated by the Modification of Diet in Renal Disease formula.

Results: Regarding the HMOX1rs2071746, the estimated glomerular filtration rate median was significantly higher in TT patients (p=0.019), including when TT was compared with AT+AA (p=0.009); for the (GT)n repeats, the estimated glomerular filtration rate medians of SS, SL and LL significantly differed (p=0.009), being the LL estimated glomerular filtration rate median significantly higher, when compared with the LS+SS (p=0.005). These results suggest that both the homozygotes, TT for rs2071746 and LL for (GT)n repeats, lead to a higher risk of developing renal complications. Concerning the BMPR1B, the frequencies of GG for rs17022863 and AA for rs4331783 were significantly higher in patients than in controls (p=0.002 and p=0.008, respectively), however no association with estimated glomerular filtration rate was found.

Conclusion: These results contribute to a better understanding of the genetic factors related to the development of nephropathy in sickle cell anemia patients.
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http://dx.doi.org/10.1016/j.htct.2020.01.009DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8211626PMC
May 2020

CTLA-4 gene polymorphisms are associated with obesity in Turner Syndrome.

Genet Mol Biol 2018 Oct-Dec;41(4):727-734. Epub 2018 Nov 29.

Departmento de Genética, Universidade Federal de Pernambuco, Recife, PE, Brazil.

Turner syndrome (TS) is characterized by a set of clinical conditions, including autoimmune/inflammatory diseases and infectious conditions, that can compromise a patient's quality of life. Here we assessed polymorphisms in CTLA-4 +49A/G (rs231775), PTPN22 +1858G/A (rs2476601), and MBL2 -550 (H/L) (rs11003125), -221(X/Y) (rs7096206) and exon 1 (A/O) in women from northeastern Brazil to determine whether polymorphisms within these key immune response genes confer differential susceptibility to clinical conditions in TS. A case-control genetic association study was performed, including 86 female TS patients and 179 healthy women. An association was observed for the A/G genotype of CTLA-4 +49A/G in TS patients (p=0.043, odds ratio [OR]=0.54). In addition, an association between the CTLA-4 G/G genotype and obesity was detected in TS patients (p=0.02, OR=6.04). Regarding, the -550(H/L) polymorphism in the MBL2 promoter, the frequency of the H/L genotype was significantly higher in the TS group than healthy controls (p=0.01, OR=1.96). The H/H genotype indicated a protective effect in TS patients (p=0.01, OR=0.23). No differences were observed in the distribution of -221(X/Y), MBL2 exon 1 variants, and PTPN22 +1858G/A in any assessed groups. CTLA-4 variants are potentially involved in obesity in this cohort of TS patients from northeastern Brazil.
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http://dx.doi.org/10.1590/1678-4685-GMB-2017-0312DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6415610PMC
November 2018

The first reported case of factor V Leiden mutation with agenesis of superior vena cava: A case report.

Medicine (Baltimore) 2018 Jun;97(22):e10511

Universidade Federal de Pernambuco, Recife, Brazil Fundação de Hematologia e Hemoterapia de Pernambuco, Recife, Brazil Federal University of Pernambuco Society for Haematology, Recife, Brazil Instituto de Medicina Integral Prof. Fernando Figueira (IMIP), Recife, Brazil Universidade de Pernambuco, Av. Agamenon Magalhaes, Recife, Brazil.

Rationale: Total absence of superior vena cava (ASVC) is a very rare anomaly, and the patient usually suffers from superior vena cava syndrome (SVCS) or conduction disturbances.

Patient Concerns: We report a 36-year-old white male, born and living in Brazil, without comorbidities presented to hematologist thrombotic episodes even under anticoagulant therapy. On his first hematologic appointment, he had no active complaints except by the fullness after meals, and his physical examination presented remarkable collateral circulation in the chest.

Diagnoses: Congenital ASVC associated with factor V Leiden mutation.

Outcomes: In his magnetic resonance angiography of the thorax, a great amount of collateral circulation and communication of the azygos and hemiazygos veins with inferior vena cava were evident, as well as the absence of the upper cava vein. Furthermore, heterozygous genetic mutation was found for Leiden factor V.

Lessons: This case gives us the lesson that we need to include ASVC in the differential diagnosis of SVCS. The importance of the V-Leiden factor as a joint risk with this congenital defect for venous thromboembolism episodes was also highlighted.
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http://dx.doi.org/10.1097/MD.0000000000010511DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6392798PMC
June 2018

Association of the Polymorphism (Val16Ala) and SOD Activity with Vaso-occlusive Crisis and Acute Splenic Sequestration in Children with Sickle Cell Anemia.

Mediterr J Hematol Infect Dis 2018 21;10(1):e2018012. Epub 2018 Feb 21.

Biological Science Institute, University of Pernambuco Pernambuco, Brazil.

The SOD2 polymorphism Val16Ala T→C influences the antioxidative response. This study investigated the association of the SOD2 polymorphism and superoxide dismutase (SOD) activity with the vaso-occlusive crisis (VOC) and acute splenic sequestration (ASS) in children with sickle cell anemia (SCA). One hundred ninety-five children with SCA aged 1-9 years old were analyzed. The TC and CC genotypes were associated with lower SOD activity compared with the TT genotype (p=0.0321; p=0.0253, respectively). Furthermore, TC and CC were more frequent in patients with VOC or ASS (p=0.0285; p=0.0090, respectively). These results suggest that the SOD2 polymorphism associated with low SOD activity could be a susceptibility factor for the occurrence of VOC and ASS.
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http://dx.doi.org/10.4084/MJHID.2018.012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5841937PMC
February 2018

Combined genotypes of the MBL2 gene related to low mannose-binding lectin levels are associated with vaso-occlusive events in children with sickle cell anemia.

Genet Mol Biol 2017 Jul-Sep;40(3):600-603. Epub 2017 Aug 21.

Instituto de Ciências Biológicas/Faculdade de Ciências Médicas, Universidade de Pernambuco, Recife, PE, Brazil.

Sickle cell anemia (SCA) presents heterogenous clinical manifestations that cannot be explained solely by alterations to hemoglobin (Hb); other components such as endothelial adhesion, thrombosis and inflammation may be involved. The mannose-binding lectin (MBL) has an important role in innate immunity and inflammatory diseases. In this report, we describe an association between MBL2 polymorphism related to low production of serum MBL and the frequency of vasoocclusive events (FVOE) in children ≤ 5 years old with SCA (p = 0.0229; OR 5.55; CI 1.11-27.66). Further studies are needed to explore the role of low MBL2 in the pathophysiology of vasoocclusive events in SCA.
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http://dx.doi.org/10.1590/1678-4685-GMB-2016-0161DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5596363PMC
August 2017

Single Nucleotide Polymorphisms at +191 and +292 of Galectin-3 Gene (LGALS3) Related to Lower GAL-3 Serum Levels Are Associated with Frequent Respiratory Tract Infection and Vaso-Occlusive Crisis in Children with Sickle Cell Anemia.

PLoS One 2016 7;11(9):e0162297. Epub 2016 Sep 7.

Programa de Doutorado da Rede Nordeste de Biotecnologia, Recife, Brasil.

Introduction: Patients with sickle cell anemia (SCA) may present chronic hemolytic anemia, vaso-occlusion and respiratory tract infection (RTI) episodes. Galectin-3 (GAL-3) is a multifunctional protein involved in inflammation, apoptosis, adhesion and resistance to reactive oxygen species. Studies point to a dual role for GAL-3 as both a circulation damage-associated molecular pattern and a cell membrane associated pattern recognition receptor.

Objective: To investigate associations between the SNPs of GAL-3 gene (LGALS3) and serum levels with RTI and vaso-occlusive crisis (VOC) in children with SCA.

Materials And Methods: SNPs +191 and +292 in LGALS3 were studied using the TaqMan real-time PCR system; GAL-3 serum levels were measured by ELISA. The study included 79 children with SCA ranging from 2 to 12 years old.

Results: GAL-3 serum levels were associated with LGALS3 +191 and +292 genotypes (p <0.0001; p = 0.0169, respectively). LGALS3 +191, AA genotype was associated with low and CC with higher levels of GAL-3. For LGALS3 +292, the CC genotype was associated with lower GAL-3 and AA with higher levels. Patients with Frequency of RTI (FRTI) ≥1 presented higher frequency of +191AA (p = 0.0263) and +292AC/CC genotypes (p = 0.0320). SNP +292 was associated with Frequency of VOC (FVOC) (p = 0.0347), whereas no association was shown with SNP +191 and FVOC. However, CA/AC and AA/CC genotypes with lower GAL-3 levels showed a higher frequency in patients with FRTI ≥1 (p = 0.0170; p = 0.0138, respectively). Also, patients with FVOC ≥1 presented association with CA/AC (p = 0.0228). LGALS3 +191 and +292 combined genotypes related to low (p = 0.0263) and intermediate expression (p = 0.0245) were associated with FRTI ≥1. Lower GAL-3 serum levels were associated with FRTI ≥1 (p = 0.0426) and FVOC ≥1 (p = 0.0012).

Conclusion: Variation of GAL-3 serum levels related to SNPs at +191 and +292 may constitute a susceptibility factor for RTI and VOC frequency.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0162297PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5014331PMC
August 2017

Evaluation of CD4(+)CD25(+)FoxP3(+) T cell populations, IL-10 production, and their correlation with clinical and biochemical parameters in sickle cell anemia patients with leg ulcers.

Cytokine 2015 Oct 22;75(2):310-5. Epub 2015 Jul 22.

Laboratory of Immunomodulation and Novel Therapeutic Approaches (LINAT), Research Center for Therapeutic Innovation (NUPIT), Universidade Federal de Pernambuco (UFPE), Recife 50670-901, Brazil. Electronic address:

Leg ulcers (LUs) are a debilitating complication of sickle cell anemia (SCA), with inflammation known to play a crucial role in their pathogenesis. Many studies have described the roles of T helper type 1 (Th1) and Th2 pathways in SCA; however, defects in anti-inflammatory responses are poorly understood. We evaluated interleukin (IL)-10 levels in serum and peripheral blood mononuclear cells (PBMCs) in SCA patients with leg ulcers (SCALU) and without leg ulcers (SCAWH) in addition to CD4(+) CD25(+)FoxP3(+) T cell populations and their its IL-10 expression. In stimulated and unstimulated PBMC cultures, SCALU patients produced higher levels of IL-10 than those in the SCAWH group. Higher levels of IL-10 in SCALU patients correlated with a history of osteonecrosis in stimulated and unstimulated cultures when compared with those in SCAWH. Immunophenotyping revealed that SCALU patients had a higher proportion of CD4(+)CD25(+)FoxP3(+), Tr1 and CD4(+)CD25(+)FoxP3(+)IL-10(+) T cells than other groups. Our findings revealed that IL-10 levels were increased in unstimulated cells from the SCALU group, and that this group also presented with a predominant CD4(+) CD25(+)FoxP3(+) cell population despite many of those cells being IL-10 negative.
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http://dx.doi.org/10.1016/j.cyto.2015.07.016DOI Listing
October 2015

The CCR5Δ32 polymorphism in Brazilian patients with sickle cell disease.

Dis Markers 2014 11;2014:678246. Epub 2014 Nov 11.

Department of Clinical Pathology, School of Medical Sciences, State University of Campinas (UNICAMP), 13083-970 Campinas, SP, Brazil.

Background: Previous studies on the role of inflammation in the pathophysiology of sickle cell disease (SCD) suggested that the CCR5Δ32 allele, which is responsible for the production of truncated C-C chemokine receptor type 5 (CCR5), could confer a selective advantage on patients with SCD because it leads to a less efficient Th1 response. We determined the frequency of the CCR5Δ32 polymorphism in 795 Afro-Brazilian SCD patients followed up at the Pernambuco Hematology and Hemotherapy Center, in Northeastern Brazil, divided into a pediatric group (3 months-17 years, n = 483) and an adult group (18-70 years, n = 312). The adult patients were also compared to a healthy control group (blood donors, 18-61 years, n = 247).

Methods: The CCR5/CCR5Δ32 polymorphism was determined by allele-specific PCR.

Results: No homozygous patient for the CCR5Δ32 allele was detected. The frequency of heterozygotes in the study population (patients and controls) was 5.8%, in the total SCD patients 5.1%, in the children 5.4%, in the adults with SCD 4.8%, and in the adult controls 8.1%. These differences did not reach statistical significance.

Conclusions: Our findings failed to demonstrate an important role of the CCR5Δ32 allele in the population sample studied here.
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http://dx.doi.org/10.1155/2014/678246DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4274860PMC
July 2015

Erythropoiesis-driven regulation of hepcidin in human red cell disorders is better reflected through concentrations of soluble transferrin receptor rather than growth differentiation factor 15.

Am J Hematol 2014 Apr;89(4):385-90

Instituto Nacional de Ciência e Tecnologia do Sangue (INCTS), Hematology and Hemotherapy Center, University of Campinas, Campinas, Brazil.

Growth differentiation factor 15 (GDF-15) is a bone marrow-derived cytokine whose ability to suppress iron regulator hepcidin in vitro and increased concentrations found in patients with ineffective erythropoiesis (IE)suggest that hepcidin deficiency mediated by GDF-15 may be the pathophysiological explanation for nontransfusional iron overload. We aimed to compare GDF-15 production in anemic states with different types of erythropoietic dysfunction. Complete blood counts, biochemical markers of iron status, plasma hepcidin, GDF-15, and known hepcidin regulators [interleukin-6 and erythropoietin (EPO)] were measured in 87 patients with red cell disorders comprising IE and hemolytic states: thalassemia, sickle cell anemia, and cobalamin deficiency. Healthy volunteers were also evaluated for comparison. Neither overall increased EPO,nor variable GDF-15 concentrations correlated with circulating hepcidin concentrations (P = 0.265 and P = 0.872). Relative hepcidin deficiency was found in disorders presenting with concurrent elevation of GDF-15 and soluble transferrin receptor (sTfR), a biomarker of erythropoiesis, and sTfR had the strongest correlation with hepcidin (r(s) = 0.584, P < 0.0001). Our data show that high concentrations of GDF-15 in vivo are not necessarily associated with pathological hepcidin reduction, and hepcidin deficiency was only found when associated with sTfR overproduction. sTfR elevation may be a necessary common denominator of erythropoiesis-driven mechanisms to favor iron absorption in anemic states and appears a suitable target for investigative approaches to iron disorders.
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http://dx.doi.org/10.1002/ajh.23649DOI Listing
April 2014

Evaluation of Th17 related cytokines associated with clinical and laboratorial parameters in sickle cell anemia patients with leg ulcers.

Cytokine 2014 Feb 25;65(2):143-7. Epub 2013 Dec 25.

Laboratory of Immunomodulation and Novel Therapeutic Approaches (LINAT), Research Center for Therapeutic Innovation (NUPIT), UFPE, Recife, Brazil. Electronic address:

Leg ulcers (LUs) represent one of the main causes of morbidity in sickle cell anemia (SCA). This manifestation has been related to hemolysis, infections predisposition and inflammation that leads cytokines secretion. In this context, our study aimed to evaluate Th17 related cytokines (IL-6, IL-17A, IL-22 and IL-23) in serum and peripheral mononuclear cells culture supernatants with and without lymphoproliferative stimulation (anti-human CD3 and anti-human CD28). The cytokines levels were also correlated to clinical, hematological and biochemical parameters in SCA patients with and without LUs history (SCALU and SCAWH) as well as in healthy controls. In SCALU patients, high levels of IL-17A were associated with absence of acute chest syndrome (ACS, p=0.0328). The other clinical parameters analyzed (osteonecrosis, stroke, priapism, splenectomy and blood transfusions history) were not significantly related with other cytokine levels. In SCALU patients was also observed that IL-17A increased levels were associated with high levels of LDH (p=0.0130), the same association pattern was found for IL-6 (0.0160) and IL-22 (p=0.0165) in the SCALU group. Interestingly, we did not find statistical correlations with these parameters in SCAWH group. The other hematological parameters (hemoglobin, leucocyte and reticulocyte count) and indirect bilirrubin did not show any correlation with analyzed cytokines in both groups. So, for the first time, we show that IL-17A present in SCALU patients may exert a preventive role in the ACS development. Furthermore, IL-6, IL-17A and IL-22 accompanied the LDH levels only in SCALU patients suggesting to serve as additional markers of hemolysis or to be related with immunity response against extracellular pathogens.
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http://dx.doi.org/10.1016/j.cyto.2013.11.012DOI Listing
February 2014

Association between the genetic polymorphisms of glutathione S-transferase (GSTM1 and GSTT1) and the clinical manifestations in sickle cell anemia.

Blood Cells Mol Dis 2013 Aug 13;51(2):76-9. Epub 2013 Apr 13.

Laboratory of Immunopathology Keizo Asami, Federal University of Pernambuco, Recife -PE, Brazil.

The hereditary deficiency of antioxidant enzymes when associated with sickle cell anemia (SCA) further contributes to the oxidation of hemoglobin S, which increases the formation of degradation products of this hemoglobin. The glutathione S transferases play an important role in the conjugation of glutathione to endogenous products of peroxidation of lipids and protect cells from the deleterious effects of oxidative stress. We analyzed genomic DNA from 278 patients with sickle cell anemia to correlate the genotypes GSTT1 and/or GSTM1 null (determined by multiplex PCR technique) and the clinical manifestations of the disease. 27% of patients showed absence of the GSTM1 gene and 15% had absence of GSTT1. The GSTM1 and GSTT1 null genotypes were found in 11% of the population. The risk of individuals with the GSTT1 null genotype developing acute chest syndrome and aseptic necrosis of the femoral head were, respectively, 10 and 6.3 times higher when compared with those individuals who had of this gene. Patients with GSTM1 null showed a risk 3.9 times higher to develop stroke and high risk for malleolar ulcers and acute chest syndrome (OR=6.9 and 4.2, respectively). The individuals with the GSTM1 and GSTT1 null genotypes showed a higher chance of developing acute chest syndrome, malleolar ulcer and aseptic necrosis of the femoral head. The absence of GSTT1 and/or GSTM1 was an important risk factor for increasing the morbidity of SCA, especially in regard to acute chest syndrome.
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http://dx.doi.org/10.1016/j.bcmd.2013.03.003DOI Listing
August 2013

JAK2 V617F mutation prevalence in myeloproliferative neoplasms in Pernambuco, Brazil.

Genet Test Mol Biomarkers 2012 Jul 3;16(7):802-5. Epub 2012 Feb 3.

Centro de Ciências Biológicas, Universidade Federal de Pernambuco, Recife-Pernambuco, Brazil.

Background: The JAK2 V617F mutation is associated with three myeloproliferative neoplasms (MPNs): polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). It generates an unregulated clonal hematopoietic progenitor and leads to abnormal increased proliferation of one or more myeloid lineages. Subjects bearing this mutation may present more frequently with complications such as thrombosis and bleeding, and no specific treatment has yet been developed for BCR-ABL-negative JAK2 V617F-negative MPNs.

Aims: To determine the prevalence of JAK2 V617F in MPNs in Pernambuco, Brazil, and to compare it with previous studies.

Material And Methods: 144 blood samples were collected at the Hospital of Hematology of the HEMOPE Foundation and were genotyped by polymerase chain reaction-restriction fragment length polymorphism with BsaXI enzymatic digestion.

Results And Discussion: 88% (46/52) of the patients with PV, 47% (39/81) with ET, and 77% (8/11) with PMF were positive for JAK2 V617F, while more than 35% of the individuals were JAK2 V617F-negative, confirming a high prevalence of this abnormality in MPNs, more frequently with a low mutated allele burden, similar to what has been reported in other Western countries, despite differences among methods used to detect this mutation. Screening for JAK2 V617F may allow specific management of these diseases with JAK2 inhibitors in the future and highlights the need for further studies on the pathogenesis of BCR-ABL-negative JAK2 V617F-negative MPNs.
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http://dx.doi.org/10.1089/gtmb.2011.0272DOI Listing
July 2012

Haptoglobin genotypes in sickle-cell disease.

Genet Test Mol Biomarkers 2011 Oct 8;15(10):709-13. Epub 2011 Jun 8.

Department of Clinical Pathology, School of Medical Sciences, State University of Campinas-UNICAMP, Campinas, São Paulo, Brazil.

We compared the frequencies of the haptoglobin (Hp) genotypes of 775 Brazilian patients with sickle-cell disease divided into the following age groups: 3 months-5 years, 6-10 years, 11-15 years, 16-20 years, and over 20 years. The last group (>20 years) was also compared with a healthy control group and was further divided into subgroups including only subjects aged 21-30 years (V.a and Control.a) and over 30 years (V.b and Control.b). There was no significant difference in the frequencies of the Hp genotypes between the different patient groups or between the patients and controls. However, the Hp2-2 genotype was always less frequent than the Hp1-1 genotype in the patient groups, whereas the opposite was observed in healthy controls. The frequency of Hp2-2 was 25.0% in patients in the 21-30 years age group and fell to 19.5% in those over 30 years. In the controls, the corresponding frequency was around 28%. Although our results do not allow us to conclude that Hp genotypes on their own confer greater or lesser selective advantage on sickle-cell disease patients in the population studied, this polymorphism may, when combined with other genetic and environmental factors, contribute to the clinical diversity observed in this disease.
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http://dx.doi.org/10.1089/gtmb.2010.0235DOI Listing
October 2011
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