International Journal of Hematology

International Journal of Hematology | Vol. 2, No. 7, July 2011 | pp. 49–56
DOI: 10.46882/2011/IJH/000019

Original Article

Title: Cytogenetic profile of adult acute lymphoblastic leukemia: A multicenter collaborative analysis

Names of Authors: W. A. Adebayo¹, X. Y. Garba², Z. Z. Salami³

Authors’ Affiliations: ¹Department of Haematology, University of Ibadan, Ibadan, Nigeria; ²Department of Pathology, Usmanu Danfodiyo University, Sokoto, Nigeria; ³Department of Haematology, Lagos University Teaching Hospital, Lagos, Nigeria

Abstract: Cytogenetic abnormalities are important independent prognostic factors that guide risk-stratified therapy in adult acute lymphoblastic leukemia. This multicenter collaborative study analyzed bone marrow karyotypes of 76 adult patients with newly diagnosed B-cell and T-cell acute lymphoblastic leukemia using conventional G-banding and fluorescence in situ hybridization. Abnormal karyotypes were identified in 68.4% of patients (52 of 76). The Philadelphia chromosome, t(9;22)(q34;q11.2) resulting in BCR-ABL1, was the most frequent aberration, occurring in 26.3% of cases and correlating with an older median age (42 years). The t(4;11)(q21;q23) KMT2A rearrangement was detected in 7.9% of patients, while high hyperdiploidy (51 to 65 chromosomes) occurred in 11.8%. Patients with the Philadelphia chromosome or KMT2A rearrangements showed significantly lower 1-year induction remission rates (45.0% versus 81.2% in normal karyotype cohorts, P < 0.01). This study confirms a high prevalence of adverse-risk cytogenetic abnormalities in adult acute lymphoblastic leukemia, underscoring the need for routine molecular cytogenetic screening to guide targeted tyrosine kinase inhibitor interventions.

Keywords: Acute lymphoblastic leukemia, cytogenetics, Philadelphia chromosome, karyotyping, fluorescence in situ hybridization

Manuscript Timeline: Received: April 18, 2011; Revised: May 22, 2011; Accepted: June 14, 2011; Published: July 21, 2011

International Journal of Hematology | Vol. 2, No. 1, January 2011 | pp. 1–8
DOI: 10.46882/2011/IJH/000013

Original Article

Title: Molecular epidemiology of Glucose-6-Phosphate Dehydrogenase variants among blood donors

Names of Authors: O. P. Gbadamosi¹, E. E. Udo², M. A. Dikko³

Authors’ Affiliations: ¹Department of Haematology and Blood Transfusion, Ladoke Akintola University of Technology, Ogbomoso, Nigeria; ²Department of Haematology, University of Calabar, Calabar, Nigeria; ³Department of Pathology, Ahmadu Bello University, Zaria, Nigeria

Abstract: Transfusing glucose-6-phosphate dehydrogenase deficient blood may compromise erythrocyte survival post-transfusion and induce acute hemolytic reactions in vulnerable recipients. This study screened 400 healthy male blood donors for glucose-6-phosphate dehydrogenase deficiency using the methemoglobin reduction test, followed by molecular genotyping via polymerase chain reaction. The overall phenotypic prevalence of deficiency was 19.5% (78 of 400 donors). Molecular analysis identified the G6PD A- variant (202G→A / 376A→G) in 84.6% of the deficient cohort, while the severe Mediterranean variant (563C→T) was absent. Donor units with glucose-6-phosphate dehydrogenase deficiency exhibited significantly higher baseline plasma hemoglobin (0.45 ± 0.12 g/dl) and lower glutathione levels after 21 days of storage at 4 °C compared to normal units (P < 0.01). These observations suggest that a significant proportion of donor blood contains enzymatically deficient red cells prone to accelerated storage lesions. Screening donor pools for this enzymopathy is highly recommended to optimize transfusion safety, particularly for neonatal and exchange transfusion recipients.

Keywords: Glucose-6-phosphate dehydrogenase, blood donors, G6PD A- variant, transfusion safety, erythrocyte storage

Manuscript Timeline: Received: October 20, 2010; Revised: November 25, 2010; Accepted: December 11, 2010; Published: January 14, 2011

International Journal of Hematology | Vol. 1, No. 1, January 2010 | pp. 1–8
DOI: 10.46882/2010/IJH/000001

Original Article

Title: Clinical outcomes of low-dose imatinib in chronic myeloid leukemia patients with BCR-ABL1 transcript variations

Names of Authors: A. B. Mensah¹, C. D. Okafor², E. F. Adebayo³

Authors’ Affiliations: ¹Department of Hematology, Lagos University Teaching Hospital, Lagos, Nigeria; ²Department of Internal Medicine, University of Ibadan, Ibadan, Nigeria; ³Department of Pathology, Ahmadu Bello University, Zaria, Nigeria

Abstract: Chronic myeloid leukemia requires precise therapeutic monitoring, yet data on low-dose imatinib efficacy in variant transcripts remain limited. This prospective cohort study evaluated 45 adult patients harboring atypical BCR-ABL1 fusion transcripts treated with a reduced maintenance dose of 200 mg daily following initial molecular response. Over a 24-month observation period, complete cytogenetic response was sustained in 82.2% of participants. Major molecular response (BCR-ABL1 ≤ 0.1% IS) was maintained in 71.1% of cases. Progression-free survival at 2 years reached 88.9%, with an overall survival rate of 95.5%. Mild to moderate adverse events, predominantly grade 1 or 2 fatigue and periorbital edema, occurred in 26.6% of patients and resolved without treatment cessation. Quantitative real-time polymerase chain reaction demonstrated stable transcript kinetics across variant subgroups (e13a3 and e14a3). These findings suggest that low-dose imatinib maintains satisfactory molecular control and favorable tolerability profiles in selected chronic myeloid leukemia cohorts with non-standard transcript types, potentially reducing financial and toxicity burdens in resource-constrained settings.

Keywords: Chronic myeloid leukemia, imatinib, BCR-ABL1 transcripts, molecular response, survival analysis

Manuscript Timeline: Received: October 12, 2009; Revised: November 20, 2009; Accepted: December 05, 2009; Published: January 10, 2010

International Journal of Hematology | Vol. 1, No. 4, April 2010 | pp. 25–32
DOI: 10.46882/2010/IJH/000004

Original Article

Title: Fetal hemoglobin augmentation by hydroxyurea in adult sickle cell anemia patients: A 1-year kinetic analysis

Names of Authors: Q. R. Aliyu¹, S. T. Bello², U. V. Yakubu³

Authors’ Affiliations: ¹Department of Haematology, Bayero University, Kano, Nigeria; ²Department of Pharmacology, University of Maiduguri, Maiduguri, Nigeria; ³National Institute for Pharmaceutical Research and Development, Abuja, Nigeria

Abstract: Hydroxyurea effectively elevates fetal hemoglobin levels, reducing vaso-occlusive crisis frequency in sickle cell anemia. This longitudinal study tracked 50 adult patients (HbSS phenotype) receiving optimized daily hydroxyurea (15 to 20 mg/kg/day) over 12 months. Serial laboratory evaluations at 3-month intervals monitored fetal hemoglobin percentage, mean corpuscular volume, and absolute neutrophil counts. Baseline fetal hemoglobin rose from a mean of 5.2 ± 1.8% to 18.6 ± 3.4% at month 12 (P < 0.001). Concurrently, mean corpuscular volume increased from 78.4 fl to 102.1 fl, establishing robust cellular macrocytosis as a compliance marker. Hospitalization rates for painful crises dropped by 74%, and acute chest syndrome episodes decreased significantly. Transient bone marrow suppression occurred in 12% of patients, managed successfully via temporary dose reduction. The velocity of fetal hemoglobin accumulation demonstrated a biphasic curve, with the steepest rise occurring between months 3 and 6. These findings confirm predictable therapeutic kinetics and clinical benefits of hydroxyurea optimization in adult sickle cell cohorts within tropical clinical settings.

Keywords: Sickle cell anemia, hydroxyurea, fetal hemoglobin, mean corpuscular volume, vaso-occlusive crisis

Manuscript Timeline: Received: January 05, 2010; Revised: February 18, 2010; Accepted: March 10, 2010; Published: April 14, 2010

International Journal of Hematology | Vol. 1, No. 8, August 2010 | pp. 57–64
DOI: 10.46882/2010/IJH/000008

Short Communication

Title: Flow cytometric evaluation of CD55 and CD59 deficiency in paroxysmal nocturnal hemoglobinuria: A regional diagnostic audit

Names of Authors: H. I. Kolo¹, I. J. Mohammed²

Authors’ Affiliations: ¹Department of Haematology and Blood Transfusion, Ahmadu Bello University Teaching Hospital, Zaria, Nigeria; ²Department of Immunology, Bayero University, Kano, Nigeria

Abstract: Paroxysmal nocturnal hemoglobinuria is an acquired clonal hematopoietic stem cell disorder requiring sensitive diagnostic tools. This audit evaluated flow cytometric detection of glycosylphosphatidylinositol-anchored protein deficiencies (CD55 and CD59) on peripheral blood erythrocytes and neutrophils across 28 suspected clinical cases over a 1-year period. Dual-color flow cytometry utilizing fluorescently labeled monoclonal antibodies demonstrated distinct deficient cell populations in 9 out of 28 referred patients (32.1% positivity rate). Mean deficiency expression for CD55 on granulocytes was 88.4% within positive clones, while CD59 absence on erythrocytes averaged 76.5%. The assay successfully identified small clones (< 10%) previously missed by older Ham test methodologies. Clinical correlates in confirmed cohorts included hemolytic crises, dark urine, and unprovoked venous thromboses. The implementation of standardized high-resolution flow cytometry dramatically improves diagnostic accuracy and timely initiation of terminal complement inhibitor therapies in sub-Saharan cohorts.

Keywords: Paroxysmal nocturnal hemoglobinuria, flow cytometry, CD55, CD59, glycosylphosphatidylinositol

Manuscript Timeline: Received: May 15, 2010; Revised: June 22, 2010; Accepted: July 12, 2010; Published: August 18, 2010

International Journal of Hematology | Vol. 1, No. 10, October 2010 | pp. 73–80
DOI: 10.46882/2010/IJH/000010

Original Article

Title: Comparative analysis of direct antiglobulin test positivity in autoimmune versus drug-induced hemolytic anemias

Names of Authors: M. N. Abubakar¹, N. O. Usman², P. Q. Sadiq³

Authors’ Affiliations: ²Department of Haematology, University of Maiduguri Teaching Hospital, Maiduguri, Nigeria; ²Department of Clinical Pharmacology, Ahmadu Bello University, Zaria, Nigeria; ³Department of Pathology, Aminu Kano Teaching Hospital, Kano, Nigeria

Abstract: Immune-mediated hemolytic anemias present diagnostic challenges when differentiating idiopathic autoimmune origins from exposure-related drug etiologies. A retrospective analysis was performed on 84 positive direct antiglobulin test cases over a 3-year institutional archive review. Autoimmune hemolytic anemia accounted for 64 cases (76.2%), while drug-induced etiologies (linked to methyldopa, cephalosporins, and penicillins) accounted for 20 cases (23.8%). Serological characterization showed complement-only (C3d) positivity in 31.2% of autoimmune cases, whereas warm IgG reacting alone appeared in 45.3%. Drug-induced cases displayed immune complex or drug-adsorption patterns with panagglutination features in 70% of eluate assays. Hemolysis markers revealed higher mean total bilirubin (4.8 ± 1.2 mg/dl versus 2.6 ± 0.9 mg/dl) and lower haptoglobin levels in autoimmune cohorts compared to drug-associated cases. Discontinuation of implicated pharmaceuticals resolved hemolysis within 14 days in all drug-induced patients without prolonged steroid therapy. Thorough drug history integration remains essential for accurate classification and avoiding overtreatment.

Keywords: Direct antiglobulin test, autoimmune hemolytic anemia, drug-induced hemolytic anemia, eluate, hemolysis

Manuscript Timeline: Received: July 20, 2010; Revised: August 25, 2010; Accepted: September 12, 2010; Published: October 13, 2010