International Journal of Hematology

International Journal of Hematology | Vol. 9, No. 12, December 2018 | pp. 89–96
DOI: 10.46882/2018/IJH/000108

Original Article

Title: Evaluation of automated reticulocyte maturation parameters and zinc protoporphyrin variants in separating iron deficiency from beta-thalassemia trait profiles

Names of Authors: Q. S. Abubakar¹, U. T. Maina²

Authors’ Affiliations: ¹Department of Haematology, National Hospital, Abuja, Nigeria; ²Department of Pathology, Bayero University, Kano, Nigeria

Abstract: Ineffective iron utilization and hemoglobin production variations generate overlapping microcytic red blood cell indices, requiring rapid laboratory differentiation models. This prospective diagnostic study evaluated the performance of automated immature reticulocyte fractions (IRF) and zinc protoporphyrin (ZPP) variants for separating absolute iron deficiency anemia from beta-thalassemia trait carriers. Evaluations were conducted on 135 adult patients presenting with persistent microcytosis (MCV < 76 fl). Diagnoses were validated using serum ferritin and high-performance liquid chromatography (HPLC) to measure hemoglobin A2 levels. Absolute iron deficiency was confirmed in 85 patients, while 50 were diagnosed with beta-thalassemia trait (HbA2 > 3.5%). The mean immature reticulocyte fraction was significantly higher in beta-thalassemia trait carriers compared to the iron-deficient cohort (0.28 ± 0.06 versus 0.12 ± 0.03, P < 0.001), reflecting an accelerated erythroid drive. Conversely, zinc protoporphyrin ratios were markedly elevated in absolute iron deficiency. Receiver operating characteristic analysis established a combined IRF and ZPP model that achieved a diagnostic sensitivity of 91.2% and a specificity of 88.4% for identifying thalassemia traits. Utilizing automated reticulocyte maturity indices provides an efficient, low-cost asset for screening inherited hemoglobin anomalies before completing advanced chromatography.

Keywords: Immature reticulocyte fraction, zinc protoporphyrin, iron deficiency anemia, beta-thalassemia trait, cell counter indices

Manuscript Timeline: Received: September 15, 2018; Revised: October 22, 2018; Accepted: November 11, 2018; Published: December 14, 2018

International Journal of Hematology | Vol. 9, No. 4, April 2018 | pp. 25–32
DOI: 10.46882/2018/IJH/000100

Short Communication

Title: Evaluation of automated white blood cell precursor flagging efficiency on a five-part differential cell counter in acute sepsis

Names of Authors: B. C. Akpan¹, D. E. Usman²

Authors’ Affiliations: ¹Department of Haematology, University of Calabar, Calabar, Nigeria; ²Department of Clinical Pharmacology, Ahmadu Bello University, Zaria, Nigeria

Abstract: Severe systemic bacterial infections trigger acute bone marrow left shifts, resulting in the release of immature granulocytic precursors that can generate automated cell counter flags. This operational study evaluated the flagging efficiency and positive predictive value of an automated immature granulocyte (IG) flag parameter on a five-part differential cell counter in 120 intensive care patients suspected of having acute sepsis. Automated results were cross-validated against manual visual peripheral blood smear differential counts. True immature granulocytic lines (metamyelocytes, myelocytes) were microscopically confirmed in 75.8% (91 of 120) of the flagged samples. The automated cell counter achieved a sensitivity of 91.2% and a false-positive rate of 14.2%, with misclassifications occurring primarily in specimens containing highly reactive atypical lymphocytes. An absolute immature granulocyte count exceeding 0.45 × 10⁹/L correlated strongly with positive blood culture matrices. Utilizing automated precursor flags offers a fast, low-cost screening tool that alerts clinicians to prominent marrow left shifts during acute infective stress.

Keywords: Immature granulocytes, automated cell counter, left shift, sepsis screening, peripheral blood film

Manuscript Timeline: Received: January 15, 2018; Revised: February 20, 2018; Accepted: March 11, 2018; Published: April 14, 2018

International Journal of Hematology | Vol. 9, No. 2, February 2018 | pp. 9–16
DOI: 10.46882/2018/IJH/000098

Original Article

Title: Evaluation of automated reticulocyte cellular volume and mean reticulocyte hemoglobin parameters in separating iron deficiency from alpha-thalassemia traits

Names of Authors: Q. S. Abubakar¹, U. T. Maina²

Authors’ Affiliations: ¹Department of Haematology, National Hospital, Abuja, Nigeria; ²Department of Pathology, Bayero University, Kano, Nigeria

Abstract: Microcytic hypochromic anemias require fast, automated differentiation protocols to prevent inappropriate therapeutic decisions. This prospective diagnostic study evaluated the performance of automated reticulocyte cell parameters, specifically mean reticulocyte volume (MRV) and mean reticulocyte hemoglobin content (CHr), in separating absolute iron deficiency anemia from alpha-thalassemia trait variants. Evaluations were conducted on 125 adult patients presenting with microcytosis (MCV < 75 fl), and diagnoses were validated via serum ferritin and molecular multiplex polymerase chain reaction assays. Absolute iron deficiency was confirmed in 75 cases, while 50 carried the single-gene alpha-deletion (-alpha³.⁷/alpha alpha). The mean reticulocyte volume was significantly lower in alpha-thalassemia trait carriers compared to iron deficiency cohorts (54.2 ± 3.8 fl versus 68.5 ± 4.2 fl, P < 0.001). Conversely, the mean reticulocyte hemoglobin content was severely reduced in iron deficiency. Receiver operating characteristic analysis established an MRV threshold below 58.0 fl as optimal for predicting alpha-thalassemia gene deletions, achieving a sensitivity of 88.0% and a specificity of 85.3%. Utilizing automated reticulocyte volume parameters provides a highly efficient screening asset for differentiating inherited hemoglobin traits from nutritional deficiencies.

Keywords: Reticulocyte volume, reticulocyte hemoglobin, iron deficiency anemia, alpha-thalassemia trait, cell counter indices

Manuscript Timeline: Received: November 15, 2017; Revised: December 22, 2017; Accepted: January 11, 2018; Published: February 14, 2018

International Journal of Hematology | Vol. 9, No. 8, August 2018 | pp. 57–64
DOI: 10.46882/2018/IJH/000104

Original Article

Title: Impact of systemic hydroxyurea on nitric oxide metabolite concentrations and endothelial activation indices in adult sickle cell anemia

Names of Authors: S. T. Adeyemi¹, U. V. Okoye², W. X. Salami³

Authors’ Affiliations: ¹Department of Haematology and Blood Transfusion, Obafemi Awolowo University, Ile-Ife, Nigeria; ²Department of Medicine, University of Nigeria Teaching Hospital, Enugu, Nigeria; ³Department of Paediatrics, Ahmadu Bello University, Zaria, Nigeria

Abstract: Severe reduction in nitric oxide availability driven by cell-free hemoglobin consumption causes widespread vasoconstriction and endothelial stress in sickle cell anemia. This prospective cohort study evaluated the long-term impact of optimized hydroxyurea therapy on plasma nitric oxide metabolites (NOx) and soluble vascular cell adhesion molecule-1 (sVCAM-1) concentrations in 50 adult patients with stable sickle cell anemia (HbSS). Hydroxyurea was administered at 15 to 20 mg/kg/day and monitored over 12 months. Plasma markers were quantified via colorimetric and enzyme-linked immunosorbent assays at baseline, 6 months, and 12 months. Baseline mean nitric oxide metabolite concentration rose significantly from 14.2 ± 3.8 μmol/L to 38.6 ± 6.2 μmol/L at month 12 (P < 0.001). Concurrently, plasma sVCAM-1 levels decreased by 42.1%, falling from a mean baseline of 1,240 ng/ml to 718 ng/ml. This endothelial improvement correlated positively with an increase in fetal hemoglobin from 5.2% to 15.6% and a drop in serum lactate dehydrogenase. These chemical kinetics demonstrate that hydroxyurea acts as a direct nitric oxide donor alongside its fetal hemoglobin-inducing properties, successfully reducing endothelial activation and microvascular stress indices in adult sickle cell cohorts.

Keywords: Sickle cell anemia, hydroxyurea, nitric oxide, cell adhesion molecules, endothelial activation

Manuscript Timeline: Received: May 05, 2018; Revised: June 15, 2018; Accepted: July 09, 2018; Published: August 14, 2018

International Journal of Hematology | Vol. 9, No. 3, March 2018 | pp. 17–24
DOI: 10.46882/2018/IJH/000099

Original Article

Title: Immunophenotypic profile and clinical stage stratification of B-cell chronic lymphoproliferative disorders using CD200 and CD43 expression markers

Names of Authors: W. A. Adebayo¹, X. Y. Emeka², Z. Z. Salami³

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

Abstract: Multiparameter flow cytometry immunophenotyping plays a critical role in distinguishing chronic lymphocytic leukemia from other mature B-cell lymphoproliferative variants. This prospective study evaluated the diagnostic performance of incorporating CD200 and CD43 markers into a standard screening protocol for 65 adult patients presenting with persistent absolute lymphocytosis (> 5.0 × 10⁹/L). Lineage restriction was verified via monoclonal light chain patterns. Chronic lymphocytic leukemia was confirmed in 48 patients based on clinical features and Matutes scores, while 17 cases were diagnosed with non-CLL lymphoproliferative disorders. Strong, uniform surface co-expression of CD200 and CD43 was detected in 95.8% (46 of 48) of the chronic lymphocytic leukemia cases. In contrast, all 17 non-CLL variants (including mantle cell lymphoma and marginal zone lymphoma) demonstrated complete absence or dim expression of these markers (P < 0.001). High CD200 density expressions correlated with early Binet clinical stages (Stage A). Incorporating CD200 and CD43 into routine flow screening provides excellent diagnostic accuracy, reducing ambiguous scores and optimizing lineage separation.

Keywords: Chronic lymphocytic leukemia, CD200, CD43, flow cytometry, lymphoproliferative disorders, immunophenotyping

Manuscript Timeline: Received: December 05, 2017; Revised: January 14, 2018; Accepted: February 04, 2018; Published: March 19, 2018

International Journal of Hematology | Vol. 9, No. 7, July 2018 | pp. 49–56
DOI: 10.46882/2018/IJH/000103

Review Article

Title: Structural architecture and chemical inhibition mechanisms of the FLT3 receptor tyrosine kinase pathways in acute myeloid leukemia cells

Names of Authors: M. A. Bello¹, O. R. Eze²

Authors’ Affiliations: ¹Department of Haematology, Aminu Kano Teaching Hospital, Kano, Nigeria; ²Department of Pathology, University of Benin, Benin City, Nigeria

Abstract: Activating mutations in the Fms-like tyrosine kinase 3 (FLT3) receptor occur frequently in acute myeloid leukemia, translating to a high relapse rate and short survival duration. This review synthesizes current knowledge on the molecular structural architecture of FLT3 mutations, contrasting internal tandem duplications (FLT3-ITD) within the juxtamembrane domain with point mutations in the tyrosine kinase domain (FLT3-TKD). These structural alterations disrupt auto-inhibitory loops, leading to continuous ligand-independent autophosphorylation and the activation of downstream STAT5, MAPK, and PI3K/Akt signaling networks. Traditional intensive chemotherapy regimens fail to achieve durable remission in patients with high FLT3-ITD mutant allele fractions. Evolving clinical models highlight the therapeutic integration of small-molecule FLT3 inhibitors. First-generation multi-kinase inhibitors like midostaurin and selective second-generation agents like gilteritinib act by blocking ATP-binding pockets within the mutated kinase domains. However, secondary drug resistance often emerges via novel point mutations or microenvironmental cytokine overrides. This review provides a clinical decision-making algorithm incorporating early molecular testing, mutant allele ratio calculation, and maintenance inhibitor pathways to maximize survival outcomes in FLT3-mutated acute myeloid leukemia.

Keywords: Acute myeloid leukemia, FLT3-ITD mutation, juxtamembrane domain, gilteritinib, tyrosine kinase inhibitor

Manuscript Timeline: Received: April 15, 2018; Revised: May 22, 2018; Accepted: June 12, 2018; Published: July 18, 2018