International Journal of Hematology

International Journal of Hematology | Vol. 8, No. 6, June 2017 | pp. 41–48
DOI: 10.46882/2017/IJH/000090

Short Communication

Title: Evaluation of automated microcytic hypochromic cell flag accuracy in detecting latent iron deficiency in volunteer blood donors

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: Frequent blood donations deplete donor iron reserves, often inducing latent iron deficiency before manifesting as a drop in total hemoglobin screening tests. This diagnostic study evaluated the accuracy and predictive value of an automated microcytic hypochromic cell flag, derived from an automated five-part differential cell counter, for detecting pre-anemic iron depletion in 120 regular blood donors with qualifying hemoglobin counts (≥ 12.5 g/dl). Automated flag metrics were validated against biochemical serum ferritin panels. Latent iron deficiency, defined by a serum ferritin below 20 ng/ml, was confirmed in 20.8% (25 of 120) of the donors. The automated microcytic hypochromic flag achieved a sensitivity of 84.0% and a positive predictive value of 72.4% for identifying donors with depleted iron reserves. Incorporating these cell counter algorithmic flags into routine pre-donation assessments offers an efficient and low-cost tool to monitor iron-restricted erythropoiesis and preserve blood donor safety.

Keywords: Blood donors, latent iron deficiency, automated cell counter, flagging efficiency, serum ferritin

Manuscript Timeline: Received: March 20, 2017; Revised: April 26, 2017; Accepted: May 15, 2017; Published: June 18, 2017

International Journal of Hematology | Vol. 8, No. 8, August 2017 | pp. 57–64
DOI: 10.46882/2017/IJH/000092

Original Article

Title: Clinical profile and molecular characterization of CALR exon 9 insertion and deletion variants in essential thrombocythemia

Names of Authors: G. M. Babalola¹, I. N. Nwosu², K. S. Abubakar³

Authors’ Affiliations: ¹Department of Haematology and Blood Transfusion, Lagos University Teaching Hospital, Lagos, Nigeria; ²Department of Medicine, University of Nigeria, Nsukka, Nigeria; ³Department of Pathology, Bayero University, Kano, Nigeria

Abstract: Calreticulin (CALR) exon 9 mutations represent the second most frequent driver alteration in BCR-ABL1-negative myeloproliferative neoplasms, but the distinct hematological variations between Type 1 and Type 2 variants remain unresolved in sub-Saharan cohorts. This cross-sectional study investigated the molecular profiles of 48 adult patients presenting with JAK2-negative essential thrombocythemia. Genomic DNA was isolated from peripheral blood leucocytes, followed by polymerase chain reaction amplification and direct Sanger sequencing to determine mutation architecture. CALR mutations were detected in 37.5% (18 of 48) of the patients. Molecular characterization identified Type 1 mutations (a 52-base pair deletion) in 61.1% (11 of 18) of positive cases, while Type 2 mutations (a 5-base pair insertion) accounted for 38.9% (7 of 18). Patients harboring Type 1 deletion variants exhibited significantly higher mean baseline platelet counts (892.4 ± 114.0 × 10⁹/L versus 612.5 ± 84.0 × 10⁹/L, P < 0.05) and lower total white blood cell counts compared to Type 2 cohorts. No thromboembolic events were recorded during a 12-month follow-up window among CALR-positive individuals. Screening for specific calreticulin mutation subclasses provides valuable prognostic utility, refining risk-stratified management protocols in essential thrombocythemia.

Keywords: Essential thrombocythemia, Calreticulin mutation, deletion variants, insertion variants, molecular genetics

Manuscript Timeline: Received: May 12, 2017; Revised: June 22, 2017; Accepted: July 10, 2017; Published: August 16, 2017

International Journal of Hematology | Vol. 8, No. 1, January 2017 | pp. 1–8
DOI: 10.46882/2017/IJH/000085

Original Article

Title: Screening for lupus anticoagulant utilizing a simplified dilute prothrombin time assay protocol in patients with unexplained recurrent fetal loss

Names of Authors: Y. Z. Ibrahim¹, A. B. Okafor², C. D. Danjuma³

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

Abstract: Lupus anticoagulant is an important acquired thrombophilic indicator linked to recurrent pregnancy complications and early fetal death. This prospective diagnostic study evaluated the performance of a simplified dilute prothrombin time (dPT) assay protocol, utilizing a 1:100 dilution of standard thromboplastin reagent, for identifying lupus anticoagulant in 80 women with a history of unexplained recurrent fetal loss. Test samples underwent automated screening and subsequent high-phospholipid confirmation steps to establish diagnostic correction ratios, with results compared to reference diluted Russell’s viper venom time guidelines. Lupus anticoagulant presence was confirmed in 17.5% (14 of 80) of the patient cohort. The simplified dilute prothrombin time protocol demonstrated a sensitivity of 85.7% and a specificity of 89.3% when evaluated against the reference method. Dilute prothrombin time confirmation ratios correlated with a history of mid-trimester pregnancy loss (r = 0.45, P < 0.05). Utilizing this simplified, low-phospholipid clot protocol provides an accessible and cost-effective screening alternative for maternal health facilities lacking advanced specialized thrombophilia diagnostic profiles.

Keywords: Lupus anticoagulant, dilute prothrombin time, thrombophilia, recurrent fetal loss, antiphospholipid syndrome

Manuscript Timeline: Received: October 18, 2016; Revised: November 24, 2016; Accepted: December 12, 2016; Published: January 14, 2017

International Journal of Hematology | Vol. 8, No. 12, December 2017 | pp. 89–96
DOI: 10.46882/2017/IJH/000096

Original Article

Title: Evaluation of baseline plasma antithrombin III activity as an independent predictor of induction mortality in acute promyelocytic leukemia

Names of Authors: E. F. Chinedu¹, G. H. Haruna², I. J. Balogun³

Authors’ Affiliations: ¹Department of Haematology, University of Nigeria Teaching Hospital, Enugu, Nigeria; ²Department of Medicine, Lagos State University Teaching Hospital, Ikeja, Nigeria; ³Department of Chemical Pathology, University of Ilorin, Ilorin, Nigeria

Abstract: Acute promyelocytic leukemia drives a catastrophic consumptive coagulopathy resulting in severe intracranial hemorrhage during initial induction therapy. This prospective study evaluated baseline plasma antithrombin III activity levels in 32 adult patients with newly diagnosed acute promyelocytic leukemia harboring the t(15;17) PML-RARA translocation to assess its value for predicting early induction survival. Antithrombin III activity was quantified via chromogenic substrate assays prior to starting all-trans retinoic acid and arsenic trioxide induction. Severe antithrombin III depletion (< 60.0%) was identified in 28.1% (9 of 32) of the patients. Multivariable logistic regression revealed that baseline antithrombin III activity below 60.0% was an independent predictor of early fatal hemorrhagic complications within the first 14 days of therapy (odds ratio = 4.82, P < 0.01). Furthermore, depressed antithrombin III levels correlated strongly with high D-dimer values and low fibrinogen concentrations. Profiling baseline functional antithrombin III provides high clinical utility, helping identify promyelocytic leukemia patients requiring aggressive supportive fresh frozen plasma or antithrombin concentrate interventions.

Keywords: Acute promyelocytic leukemia, antithrombin III, consumptive coagulopathy, early mortality, prognosis

Manuscript Timeline: Received: September 05, 2017; Revised: October 14, 2017; Accepted: November 05, 2017; Published: December 14, 2017

International Journal of Hematology | Vol. 8, No. 10, October 2017 | pp. 73–80
DOI: 10.46882/2017/IJH/000094

Original Article

Title: Association between steady-state plasma endothelin-1 levels and pulmonary hypertension index indices in adult sickle cell anemia patients

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: Chronic vascular endothelial damage in sickle cell anemia shifts the homeostatic balance toward continuous vasoconstriction, predisposing individuals to severe cardiopulmonary complications. This prospective study evaluated the relationship between steady-state plasma endothelin-1 levels, an endothelial-derived vasoconstrictor peptide, and pulmonary hypertension risk indices in 84 adult patients with stable sickle cell anemia (HbSS). Plasma endothelin-1 concentrations were quantified via an enzyme-linked immunosorbent assay, while pulmonary hypertension risk was estimated using tricuspid regurgitant jet velocity (TRJV) on transthoracic Doppler echocardiography. Elevated endothelin-1 levels (≥ 5.2 pg/ml) were identified in 35.7% (30 of 84) of the patients. The high endothelin-1 subgroup demonstrated a significantly higher mean tricuspid regurgitant jet velocity (2.92 ± 0.38 m/s versus 2.18 ± 0.22 m/s in lower endothelin cohorts, P < 0.001) and lower total hemoglobin values. Plasma endothelin-1 concentrations correlated positively with serum lactate dehydrogenase activity (r = 0.54, P < 0.01), linking peptide release to chronic intravascular hemolytic intensity. Elevated plasma endothelin-1 serves as a reliable marker of severe endothelial dysfunction, identifying adult sickle cell patients at high risk for progressive pulmonary vascular remodeling.

Keywords: Sickle cell anemia, endothelin-1, endothelial dysfunction, tricuspid regurgitant jet velocity, hemolysis

Manuscript Timeline: Received: July 10, 2017; Revised: August 20, 2017; Accepted: September 12, 2017; Published: October 14, 2017

International Journal of Hematology | Vol. 8, No. 9, September 2017 | pp. 65–72
DOI: 10.46882/2017/IJH/000093

Review Article

Title: Epigenetic alterations and cellular signaling mechanisms in the pathogenesis of myelodysplastic syndromes

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: Myelodysplastic syndromes are complex clonal hematopoietic stem cell disorders characterized by ineffective hematopoiesis, cytopenias, and a high propensity for transformation into acute myeloid leukemia. This comprehensive review synthesizes contemporary evidence regarding the epigenetic landscape driving this marrow failure, focusing on somatic mutations within DNA methylation controllers (TET2, DNMT3A, IDH1/2) and histone modification structures (ASXL1). These epigenetic alterations interrupt gene expression patterns, driving hypermethylation within tumor suppressor promoters and inducing proliferative advantages in neoplastic clones. Furthermore, the role of altered RNA splicing machinery (SF3B1, SRSF2) is evaluated relative to megakaryocytic and erythroid dysplasia phenotypes. Concurrently, microenvironmental immune stress cascades within the bone marrow niche, involving elevated tumor necrosis factor-alpha and interleukin-6 signaling, promote accelerated apoptosis of healthy hematopoietic precursors. Understanding these interconnected molecular pathways has led to the successful development of hypomethylating therapies and emerging small-molecule spliceosome inhibitors. This review details structural biomarkers and molecular targets designed to guide risk-stratified therapy and minimize leukemic evolution in high-risk patients.

Keywords: Myelodysplastic syndromes, DNA methylation, epigenetic regulation, spliceosome mutations, marrow niche

Manuscript Timeline: Received: June 18, 2017; Revised: July 24, 2017; Accepted: August 11, 2017; Published: September 15, 2017