International Journal of Hematology

International Journal of Hematology | Vol. 6, No. 1, January 2015 | pp. 1–8
DOI: 10.46882/2015/IJH/000061

Original Article

Title: Impact of pre-analytical storage duration and temperature variables on routine plasma coagulation screening assays

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: Delays in sample processing can alter coagulation test results, leading to erroneous clinical decisions. This prospective study evaluated the stability of prothrombin time and activated partial thromboplastin time in 100 healthy adult plasma samples stored under varying temperature conditions (4 °C and 25 °C) for up to 24 hours. Baseline assays were performed within 1 hour of venipuncture, and repeat testing was conducted at 2, 4, 8, 12, and 24 hours. Prothrombin time values remained stable for up to 24 hours across both storage temperatures, with a mean variation below 5.0% (P > 0.05). In contrast, activated partial thromboplastin time demonstrated significant prolongation when stored at 25 °C starting at 8 hours, increasing from a baseline mean of 32.4 ± 2.8 seconds to 38.6 ± 3.4 seconds at 12 hours (P < 0.01), primarily due to the rapid degradation of labile factor VIII. Storage at 4 °C preserved activated partial thromboplastin time stability for up to 12 hours. These findings demonstrate that while prothrombin time is relatively stable, plasma samples for activated partial thromboplastin time screening should be analyzed within 4 to 6 hours if kept at room temperature, or refrigerated to ensure diagnostic accuracy.

Keywords: Prothrombin time, activated partial thromboplastin time, sample stability, pre-analytical variables, coagulation assays

Manuscript Timeline: Received: October 10, 2014; Revised: November 18, 2014; Accepted: December 05, 2014; Published: January 14, 2015

International Journal of Hematology | Vol. 6, No. 11, November 2015 | pp. 81–88
DOI: 10.46882/2015/IJH/000071

Original Article

Title: Clinical features and therapeutic response to low-dose cyclophosphamide in warm autoimmune hemolytic anemia

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: Corticosteroids serve as the standard primary intervention for warm autoimmune hemolytic anemia, but long-term maintenance can induce significant toxicity or treatment dependency. This prospective study evaluated the clinical efficacy and safety profiles of low-dose oral cyclophosphamide (50 mg to 100 mg daily) as a steroid-sparing agent in 24 adult patients with relapsed or steroid-dependent warm autoimmune hemolytic anemia. Clinical responses were determined by tracking stabilization of hemoglobin values above 10.5 g/dl without packed red cell support. Complete remission was achieved in 58.3% (14 of 24) of patients within a median window of 8 weeks, while 25.0% (6 of 24) attained a partial remission. The mean baseline hemoglobin rose from 6.4 ± 1.2 g/dl to 11.2 ± 1.4 g/dl by month 6 of therapy (P < 0.001). Concurrently, the maintenance prednisone dose was tapered by over 75.0% in responsive individuals. Mild, transient leukopenia occurred in 12.5% of the cases, but resolved without necessitating drug discontinuation. Oral cyclophosphamide represents a highly cost-effective and well-tolerated second-line protocol for sustaining remission in low-resource environments.

Keywords: Autoimmune hemolytic anemia, cyclophosphamide, prednisone, steroid-sparing agent, remission

Manuscript Timeline: Received: August 14, 2015; Revised: September 20, 2015; Accepted: October 12, 2015; Published: November 15, 2015

International Journal of Hematology | Vol. 5, No. 1, January 2014 | pp. 1–8
DOI: 10.46882/2014/IJH/000049

Original Article

Title: Cytogenetic aberrations and IGHV mutation status profiles in newly diagnosed chronic lymphocytic leukemia patients

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: Chromosomal aberrations and immunoglobulin heavy chain variable region (IGHV) mutational status are critical prognostic markers in chronic lymphocytic leukemia. This prospective study analyzed bone marrow and peripheral blood samples from 45 newly diagnosed chronic lymphocytic leukemia patients using fluorescence in situ hybridization panels and Sanger sequencing. Chromosomal deletions were detected in 71.1% (32 of 45) of the patients. Deletion 13q14 was the most frequent isolated finding, occurring in 44.4% of cases and correlating with a lower Binet clinical stage. Adverse risk aberrations, including deletion 17p13 (TP53 locus) and deletion 11q22, were identified in 11.1% and 13.3% of the cohort, respectively. An unmutated IGHV status (identity ≥ 98% to germline) was identified in 53.3% (24 of 45) of patients, correlating strongly with advanced clinical stages and the presence of 17p deletions (r = 0.52, P < 0.01). Patients with unmutated IGHV profiles demonstrated a significantly shorter median time to first treatment compared to those with mutated profiles (14 months versus 48 months, P < 0.001). Combining cytogenetic evaluations with molecular IGHV sequencing provides essential prognostic data that can help guide personalized treatment pathways.

Keywords: Chronic lymphocytic leukemia, fluorescence in situ hybridization, IGHV mutation, deletion 17p, prognosis

Manuscript Timeline: Received: October 14, 2013; Revised: November 25, 2013; Accepted: December 10, 2013; Published: January 15, 2014

International Journal of Hematology | Vol. 5, No. 9, September 2014 | pp. 65–72
DOI: 10.46882/2014/IJH/000057

Case Report

Title: Acquired Factor VIII inhibitor development in a patient with chronic lymphocytic leukemia: Successful eradication with rituximab

Names of Authors: K. L. Musa¹, M. N. Lawal², O. P. Dikko³

Authors’ Affiliations: ¹Department of Haematology, Federal Medical Centre, Katsina, Nigeria; ²Department of Internal Medicine, Bayero University, Kano, Nigeria; ³Department of Pathology, Ahmadu Bello University Teaching Hospital, Zaria, Nigeria

Abstract: Acquired hemophilia A is a rare, severe bleeding disorder caused by autoantibodies directed against coagulation Factor VIII, occasionally presenting as a paraneoplastic manifestation of B-cell malignancies. We report a 62-year-old male with stable Binet stage A chronic lymphocytic leukemia who presented with spontaneous, extensive soft tissue ecchymoses on his right thigh. Coagulation screens revealed an isolated, prolonged activated partial thromboplastin time of 84.5 seconds that failed to correct during a 1:1 mixing study with normal pooled plasma, confirming the presence of an inhibitor. Factor VIII activity was profoundly reduced (< 1.0%), and a Bethesda assay quantified a Factor VIII inhibitor titer of 24.5 Bethesda Units. Immunosuppressive therapy with high-dose prednisone failed to clear the inhibitor after 3 weeks. Subsequently, a targeted rituximab protocol (375 mg/m² weekly for 4 weeks) was initiated. Complete clinical resolution of bleeding and clearance of the inhibitor (0 BU) was achieved by week 6, alongside a normalization of Factor VIII activity (94.2%). This case highlights that acquired autoantibodies should be considered in lymphocytic leukemia patients with unprovoked bleeding, and demonstrates that rituximab provides rapid eradication of pathogenic clones.

Keywords: Acquired hemophilia A, Factor VIII inhibitor, chronic lymphocytic leukemia, rituximab, Bethesda assay

Manuscript Timeline: Received: June 18, 2014; Revised: July 28, 2014; Accepted: August 15, 2014; Published: September 17, 2014

International Journal of Hematology | Vol. 5, No. 12, December 2014 | pp. 89–96
DOI: 10.46882/2014/IJH/000060

Short Communication

Title: Evaluation of automated platelet clumps flagging efficiency on a five-part differential cell counter

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: Ethylenediaminetetraacetic acid (EDTA)-induced platelet clamping is a well-known cause of pseudothrombocytopenia, leading to unnecessary clinical consultations and diagnostics. This study evaluated the flagging efficiency and diagnostic accuracy of an automated five-part differential cell counter for detecting platelet clumps in 120 blood samples that triggered a platelet clump flag. Automated results were verified using manual peripheral blood smear evaluation as the reference standard. True platelet clumps were confirmed microscopically in 72.5% (87 of 120) of the flagged samples. In the remaining 33 samples, flags were triggered by micro-clots, giant platelets, or cold agglutinins. The automated counter achieved a positive predictive value of 72.5% for platelet clump detection. Re-collecting samples using sodium citrate tubes in confirmed cases resolved the clamping and corrected the platelet counts, increasing values from a flagged mean of 42.6 × 10⁹/L to a true mean of 214.5 × 10⁹/L. While automated cell counter flags are useful indicators, visual examination of a peripheral blood film remains mandatory to rule out pseudothrombocytopenia before executing clinical management.

Keywords: Pseudothrombocytopenia, platelet clumps, automated cell counter, flagging efficiency, peripheral blood film

Manuscript Timeline: Received: September 15, 2014; Revised: October 22, 2014; Accepted: November 10, 2014; Published: December 12, 2014

International Journal of Hematology | Vol. 5, No. 7, July 2014 | pp. 49–56
DOI: 10.46882/2014/IJH/000055

Original Article

Title: Association of plasma lupus anticoagulant with structural target organ damage in primary antiphospholipid syndrome

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: Primary antiphospholipid syndrome causes thrombosis and pregnancy complications without an underlying connective tissue disease. This study evaluated the specific association between persistent plasma lupus anticoagulant positivity and structural target organ damage, including ischemic stroke, renal microangiopathy, and valvular heart defects, in 44 patients with primary antiphospholipid syndrome. Lupus anticoagulant was identified using the diluted Russell’s viper venom time confirmation index, while target organ damage was assessed via magnetic resonance imaging, renal function panels, and transthoracic echocardiography. Persistent lupus anticoagulant positivity was documented in 54.5% (24 of 44) of the patients. Patients with persistent lupus anticoagulant demonstrated a significantly higher prevalence of multi-focal ischemic white matter lesions on brain imaging compared to those with isolated anticardiolipin antibodies (41.6% versus 10.0%, P < 0.05). Furthermore, a significant positive correlation was found between lupus anticoagulant confirmation ratios and the severity of chronic renal insufficiency (r = 0.48, P < 0.01). Persistent lupus anticoagulant is a high-risk indicator for microvascular tissue injury and progressive target organ damage in primary antiphospholipid variants, requiring aggressive, long-term therapeutic anticoagulation.

Keywords: Antiphospholipid syndrome, lupus anticoagulant, thrombophilia, ischemic stroke, microangiopathy

Manuscript Timeline: Received: April 14, 2014; Revised: May 20, 2014; Accepted: June 08, 2014; Published: July 15, 2014