International Journal of Hematology

International Journal of Hematology | Vol. 8, No. 11, November 2017 | pp. 81–88
DOI: 10.46882/2017/IJH/000095

Original Article

Title: Screening for lupus anticoagulant using a simplified textrin time and ecarin clotting time ratio protocol in patients with unprovoked venous thromboembolism

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: Diagnosing antiphospholipid syndrome requires specialized testing protocols that minimize false-positive results caused by concurrent therapeutic anticoagulants. This prospective study evaluated the diagnostic accuracy of a combined snake venom clotting protocol using the textrin time (TT) and the ecarin clotting time (ECT) to detect lupus anticoagulant in 62 adult patients presenting with unprovoked deep vein thrombosis. Both test systems utilized baseline screening steps followed by high-phospholipid confirmation loops to generate diagnostic ratios, with results cross-validated against reference diluted Russell’s viper venom time guidelines. Lupus anticoagulant presence was confirmed in 20.9% (13 of 62) of the thrombotic patients. The textrin-ecarin dual ratio protocol achieved a diagnostic sensitivity of 92.3% and a specificity of 91.8%. Notably, the ecarin-based confirmation step resisted interference from therapeutic low-molecular-weight heparin or therapeutic warfarin due to direct prothrombin activation pathways. Utilizing this dual snake venom protocol offers an accurate, cost-effective screening alternative for specialized thrombosis laboratories handling patients on active anticoagulant regimens.

Keywords: Lupus anticoagulant, textrin time, ecarin clotting time, venous thromboembolism, snake venoms

Manuscript Timeline: Received: August 15, 2017; Revised: September 22, 2017; Accepted: October 10, 2017; Published: November 18, 2017

International Journal of Hematology | Vol. 8, No. 4, April 2017 | pp. 25–32
DOI: 10.46882/2017/IJH/000088

Original Article

Title: Evaluation of automated immature platelet fraction parameters in distinguishing immune thrombocytopenia from gestational thrombocytopenia

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: Differentiating immune thrombocytopenia from benign gestational thrombocytopenia in pregnant women is vital for avoiding unnecessary immunosuppressive or obstetric interventions. This prospective study evaluated the diagnostic accuracy of the automated immature platelet fraction (IPF) in 65 pregnant women presenting with unexplained isolated thrombocytopenia (platelets 50 to 120 × 10⁹/L) in their third trimester. Immature platelet fractions were quantified on an automated fluorescent flow cytometry hematology analyzer, and diagnoses were validated via clinical tracking, bleeding score instruments, and postpartum platelet recovery. Gestational thrombocytopenia was confirmed in 45 cases, while 20 were diagnosed with maternal immune thrombocytopenia. The mean immature platelet fraction was significantly higher in the immune thrombocytopenia cohort compared to gestational thrombocytopenia cases (16.4 ± 3.8% versus 5.2 ± 1.1%, P < 0.001), reflecting accelerated peripheral destruction and a compensatory megakaryocytic response. Receiver operating characteristic analysis established an immature platelet fraction threshold above 8.5% as optimal for identifying immune-mediated clearance, achieving a sensitivity of 90.0% and a specificity of 86.6%. Measuring the immature platelet fraction provides a rapid, non-invasive indicator that differentiates consumer thrombocytopenias from benign gestational variations.

Keywords: Immature platelet fraction, gestational thrombocytopenia, immune thrombocytopenia, megakaryopoiesis, flow cytometry

Manuscript Timeline: Received: January 15, 2017; Revised: February 22, 2017; Accepted: March 14, 2017; Published: April 19, 2017

International Journal of Hematology | Vol. 7, No. 6, June 2016 | pp. 41–48
DOI: 10.46882/2016/IJH/000078

Original Article

Title: Evaluation of cell-free hemoglobin and haptoglobin consumption dynamics as hemolytic severity indices in glucose-6-phosphate dehydrogenase deficiency

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: Acute hemolytic crises in glucose-6-phosphate dehydrogenase (G6PD) deficiency can be triggered by oxidative stress from infections or drugs, requiring quantitative monitoring metrics. This prospective study evaluated plasma cell-free hemoglobin, serum haptoglobin concentrations, and total bilirubin variations in 45 male children presenting with acute hemolytic anemia secondary to confirmed glucose-6-phosphate dehydrogenase deficiency. Parameters were monitored during the acute phase (days 1 to 3) and following clinical recovery at day 14. Mean baseline cell-free hemoglobin was markedly elevated during the acute phase (142.5 ± 24.5 mg/dl) compared to post-recovery values (8.4 ± 2.1 mg/dl, P < 0.001). Concurrently, serum haptoglobin levels were completely suppressed (< 10 mg/dl) in 88.8% of the children, indicating massive intravascular hemolysis and haptoglobin saturation. Cell-free hemoglobin levels correlated positively with the absolute drop in total hemoglobin (r = 0.62, P < 0.01) and served as a superior index for identifying children at high risk for acute kidney injury. Quantifying plasma cell-free hemoglobin levels helps clinicians monitor hemolytic severity and manage fluid balancing during oxidative crises.

Keywords: Glucose-6-phosphate dehydrogenase, acute hemolysis, cell-free hemoglobin, haptoglobin, oxidative stress

Manuscript Timeline: Received: March 20, 2016; Revised: April 28, 2016; Accepted: May 15, 2016; Published: June 18, 2016

International Journal of Hematology | Vol. 7, No. 9, September 2016 | pp. 65–72
DOI: 10.46882/2016/IJH/000081

Original Article

Title: Serum ferritin kinetics and subclinical organ dysfunction in non-transfused adult sickle cell anemia patients

Names of Authors: A. I. Ibrahim¹, C. D. Balogun², E. O. Ojo³

Authors’ Affiliations: ¹Department of Haematology, Ahmadu Bello University, Zaria, Nigeria; ²Department of Medicine, University of Ilorin, Ilorin, Nigeria; ³Department of Chemical Pathology, Ladoke Akintola University of Technology, Ogbomoso, Nigeria

Abstract: Iron overload is widely studied in transfusion-dependent hemoglobinopathies, but hyperferritinemia and tissue iron deposit kinetics in non-transfused or minimally transfused sickle cell anemia cohorts remain poorly characterized. This cross-sectional study evaluated steady-state serum ferritin levels, transferrin saturation, and biochemical markers of hepatic and renal function in 94 adult sickle cell anemia (HbSS) patients who had received fewer than three lifetime blood transfusions. Steady-state serum ferritin was measured via an enzyme-linked immunosorbent assay. Hyperferritinemia (ferritin > 300 ng/ml in males, > 200 ng/ml in females) was detected in 31.9% (30 of 94) of the non-transfused patients, despite normal or low transferrin saturation profiles (< 30.0%). Elevated serum ferritin levels correlated positively with serum lactate dehydrogenase (r = 0.58, P < 0.001) and alanine aminotransferase activity, reflecting a state of chronic intravascular hemolysis and ongoing chronic inflammation rather than true parenchymal iron accumulation. Patients within the highest ferritin quartile demonstrated significantly higher microalbuminuria rates. These findings indicate that elevated ferritin in non-transfused sickle cell cohorts serves as an acute-phase reactant driven by chronic hemolytic endothelial stress, functioning as an adjunctive biomarker for subclinical microvascular target-organ damage.

Keywords: Sickle cell anemia, serum ferritin, chronic hemolysis, microalbuminuria, hyperferritinemia

Manuscript Timeline: Received: June 15, 2016; Revised: July 28, 2016; Accepted: August 14, 2016; Published: September 15, 2016

International Journal of Hematology | Vol. 7, No. 3, March 2016 | pp. 17–24
DOI: 10.46882/2016/IJH/000075

Original Article

Title: Screening for lupus anticoagulant utilizing an integrated dRVVT and Silica Clot Time ratio algorithm in unprovoked venous thrombosis

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: Guidelines for diagnosing antiphospholipid antibodies recommend utilizing at least two separate phospholipid-dependent clotting assays to minimize false-negative results. This prospective study evaluated the diagnostic efficiency of combining the diluted Russell’s viper venom time (dRVVT) with the Silica Clot Time (SCT) in an integrated screening algorithm for 76 adult patients presenting with unprovoked lower limb venous thrombosis. Both test methodologies included initial screening steps followed by high-phospholipid confirmation steps to establish diagnostic ratios. Lupus anticoagulant presence was confirmed in 23.6% (18 of 76) of the thromboembolic cohort. The diluted Russell's venom assay demonstrated an isolated sensitivity of 77.7%, missing 4 positive patients who were subsequently captured by the Silica Clot Time protocol. The combined dual-assay testing algorithm achieved an overall diagnostic sensitivity of 94.4% and a specificity of 91.3%. Utilizing both mechanisms reduces test gaps caused by varying autoantibody specificities, improving the accuracy of long-term thrombophilia risk profiling.

Keywords: Lupus anticoagulant, diluted Russell’s viper venom time, Silica Clot Time, venous thrombosis, thrombophilia screening

Manuscript Timeline: Received: December 04, 2015; Revised: January 15, 2016; Accepted: February 10, 2016; Published: March 17, 2016

International Journal of Hematology | Vol. 7, No. 11, November 2016 | pp. 81–88
DOI: 10.46882/2016/IJH/000083

Review Article

Title: Evolving mechanisms of immune escape and therapeutic checkpoint blockade targets in classical Hodgkin lymphoma

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: Classical Hodgkin lymphoma is characterized by a unique tumor microenvironment where neoplastic Hodgkin and Reed-Sternberg cells are outnumbered by an abundant background of non-neoplastic inflammatory cells. This review examines the complex molecular structural mechanisms of microenvironmental immune escape, focusing on the genetic amplification of the 9p24.1 locus, which drives over-expression of programmed death ligands 1 and 2 (PD-L1 and PD-L2) on Reed-Sternberg cells. This ligand upregulation leads to direct binding with PD-1 receptors on tumor-infiltrating T lymphocytes, downregulating cytotoxic immune responses and inducing immune exhaustion. Evolving therapeutic models focus on restoring immune recognition via monoclonal antibodies targeting the PD-1 axis, such as nivolumab and pembrolizumab. Clinical trials evaluating checkpoint inhibitors in relapsed or refractory settings demonstrate remarkable efficacy, achieving objective response rates of 65% to 70% even after autologous stem cell transplantation failures. However, immune-related adverse events, including pneumonitis and thyroiditis, require proactive management algorithms. This review outlines structural biomarkers, tissue PD-L1 expression metrics, and clinical combination pathways designed to optimize checkpoint therapy and maximize long-term survival in refractory Hodgkin lymphoma cohorts.

Keywords: Classical Hodgkin lymphoma, Reed-Sternberg cells, immune escape, PD-1 checkpoint, microenvironment

Manuscript Timeline: Received: August 20, 2016; Revised: September 25, 2016; Accepted: October 14, 2016; Published: November 19, 2016