International Journal of Hematology

International Journal of Hematology | Vol. 7, No. 8, August 2016 | pp. 57–64
DOI: 10.46882/2016/IJH/000080

Short Communication

Title: Validation of an automated delta check protocol for detecting mislabeled blood transfusion cross-match matrices

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: Pre-analytical specimen labeling errors carry an exceptionally high risk of inducing fatal ABO hemolytic transfusion reactions in blood bank practice. This operational study evaluated the sensitivity and positive predictive value of an automated laboratory information system delta check protocol, utilizing mean corpuscular volume (MCV) and hemoglobin variations, for detecting mislabeled blood transfusion cross-match tubes. Over a 12-month audit window, the delta check flag was triggered in 145 out of 12,400 blood grouping and cross-matching requests. Manual review confirmed a true mislabeling error (wrong blood in tube) in 48.2% (70 of 145) of the flagged samples. The remaining flags were caused by severe acute hemorrhage or massive intra-operative fluid resuscitation. The MCV delta check (variation > 4.5 fl from historical baseline) demonstrated an isolated sensitivity of 92.8% for detecting wrong-patient specimens. Implementing automated multi-parameter delta check systems provides a vital electronic safety filter that alerts laboratory staff to potential specimen mismatches before cross-matching is completed.

Keywords: Blood transfusion safety, delta check, pre-analytical error, mislabeled specimen, laboratory automation

Manuscript Timeline: Received: May 15, 2016; Revised: June 22, 2016; Accepted: July 11, 2016; Published: August 19, 2016

International Journal of Hematology | Vol. 7, No. 5, May 2016 | pp. 33–40
DOI: 10.46882/2016/IJH/000077

Case Report

Title: Spontaneous retroperitoneal hemorrhage secondary to acquired Factor IX inhibitor development in an elderly patient

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

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

Abstract: Acquired hemophilia B is an exceptionally rare autoantibody-mediated bleeding disorder characterized by the development of inhibitors against coagulation Factor IX. We report a 72-year-old male who presented with sudden, severe left flank pain, lower abdominal distension, and hypovolemic shock. Abdominal computed tomography revealed a massive retroperitoneal hematoma measuring 12.4 × 8.5 cm without a history of trauma or anticoagulant exposure. Coagulation screens demonstrated an isolated, markedly prolonged activated partial thromboplastin time of 92.4 seconds that did not correct following a 1:1 mixture with normal pooled plasma, pointing to a circulating inhibitor. Factor IX activity was severely reduced to 2.0%, and a Bethesda assay quantified a Factor IX inhibitor titer of 18.0 Bethesda Units. Immediate hemostasis was achieved using recombinant activated Factor VII bypassing agents (90 μg/kg every 3 hours), combined with packed cell support. Epigenetic immunosuppressive therapy utilizing oral prednisone (1 mg/kg) paired with low-dose cyclophosphamide cleared the inhibitor by week 8. This case demonstrates that acquired Factor IX autoantibodies can cause life-threatening retroperitoneal bleeding in elderly individuals, requiring prompt deployment of bypassing therapeutics.

Keywords: Acquired hemophilia B, Factor IX inhibitor, retroperitoneal hemorrhage, Bethesda assay, bypassing agents

Manuscript Timeline: Received: February 15, 2016; Revised: March 24, 2016; Accepted: April 11, 2016; Published: May 19, 2016

International Journal of Hematology | Vol. 7, No. 7, July 2016 | pp. 49–56
DOI: 10.46882/2016/IJH/000079

Original Article

Title: Characterization of aberrant lymphoid marker expressions in adult acute myeloid leukemia variants

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: Aberrant expression of lymphoid-associated antigens on acute myeloid leukemia blasts is a well-recognized phenomenon that can complicate lineage determination but may serve as a useful tumor marker for monitoring minimal residual disease. This prospective study evaluated the immunophenotypic profiles of 58 adult patients with newly diagnosed acute myeloid leukemia utilizing multiparameter flow cytometry panels. Myeloid lineage was established via CD13, CD33, and cytoplasmic myeloperoxidase positivity. Lymphoid marker expression was identified in 29.3% (17 of 58) of the leukemia cases. The T-cell marker CD7 was the most frequent aberrant finding, occurring in 15.5% of patients, followed by the B-cell marker CD19 in 8.6%, and CD2 in 5.1%. Aberrant CD7 expression correlated significantly with the presence of monocytic differentiation (FAB M4/M5 subtypes) and a higher baseline white blood cell count (P < 0.05). Patients demonstrating aberrant lymphoid markers showed a lower rate of complete remission following initial cytarabine-daunorubicin induction. Multi-color flow cytometry profiling is highly useful for identifying these unique immunophenotypic shifts, helping pathologists build customized tracking vectors for residual blast monitoring.

Keywords: Acute myeloid leukemia, flow cytometry, aberrant expression, CD7, minimal residual disease

Manuscript Timeline: Received: April 14, 2016; Revised: May 20, 2016; Accepted: June 08, 2016; Published: July 20, 2016

International Journal of Hematology | Vol. 7, No. 12, December 2016 | pp. 89–96
DOI: 10.46882/2016/IJH/000084

Original Article

Title: Evaluation of automated microcytic red blood cell sub-populations in the early identification of latent iron deficiency

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: Latent iron deficiency involves the depletion of tissue iron stores before an absolute drop in total hemoglobin concentration occurs. This prospective study evaluated the screening performance of automated red blood cell sub-populations, specifically the percentage of hypochromic red cells (%Hypo) and microcytic red cells (%Micro), for identifying latent iron depletion in 150 non-anemic adult women. Erythrocyte parameters were determined on an advanced multi-angle scatter hematology analyzer, with a serum ferritin value below 15 ng/ml serving as the reference standard for depleted stores. Latent iron deficiency was identified biochemically in 22.6% (34 of 150) of the participants. The mean percentage of hypochromic red blood cells was significantly higher in the iron-deficient group (4.8 ± 1.2% versus 1.1 ± 0.3% in iron-replete cohorts, P < 0.001). Receiver operating characteristic curve analysis established a %Hypo threshold above 2.5% combined with a %Micro above 3.2% as optimal for predicting iron depletion, yielding a diagnostic sensitivity of 88.2% and a specificity of 84.4%. Measuring automated red blood cell sub-populations provides a real-time, low-cost screening tool that can identify iron-restricted erythropoiesis during routine health evaluations.

Keywords: Latent iron deficiency, hypochromic red cells, serum ferritin, cell counter indices, iron-restricted erythropoiesis

Manuscript Timeline: Received: September 14, 2016; Revised: October 22, 2016; Accepted: November 10, 2016; Published: December 15, 2016

International Journal of Hematology | Vol. 7, No. 10, October 2016 | pp. 73–80
DOI: 10.46882/2016/IJH/000082

Original Article

Title: Prevalence and clinicopathological characteristics of B-cell prolymphocytic leukemia variations

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: B-cell prolymphocytic leukemia is an aggressive mature B-cell malignancy requiring precise differentiation from chronic lymphocytic leukemia with increased prolymphocytes. This 5-year retrospective audit investigated the prevalence, morphological features, and immunophenotypic panels of 18 cases of confirmed B-cell prolymphocytic leukemia. Diagnosis was established based on World Health Organization criteria, where circulating prolymphocytes exceeded 55.0% of total lymphocytes. Morphological analysis revealed a classic large blastic outline with a prominent, single, centrally located nucleolus in a mean of 72.4% of lymphoid cells. Multiparameter flow cytometry demonstrated strong surface IgM expression, bright CD20, and bright CD22 co-expression in all 18 cases, while CD5 expression was detected in only 22.2% of the cohort. Deletion 17p13 (TP53 locus) was identified via fluorescence in situ hybridization in 61.1% (11 of 18) of the patients, correlating strongly with primary chemoresistance to initial purine analog-based regimens. The median overall survival was 18.5 months, with advanced clinical stage and TP53 abnormalities predicting poorer outcomes. Comprehensive immunophenotypic and cytogenetic screening is essential to identify this rare, aggressive leukemic variant and guide early targeted therapeutic strategies.

Keywords: B-cell prolymphocytic leukemia, prolymphocytes, flow cytometry, TP53 deletion, immunophenotyping

Manuscript Timeline: Received: July 12, 2016; Revised: August 22, 2016; Accepted: September 10, 2016; Published: October 18, 2016

International Journal of Hematology | Vol. 7, No. 1, January 2016 | pp. 1–8
DOI: 10.46882/2016/IJH/000073

Review Article

Title: Structural mechanisms and targeted chemical inhibition of the BCL-2 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: Evading apoptosis is a foundational hallmark of hematological malignancies, heavily driven by the upregulation of anti-apoptotic B-cell lymphoma 2 (BCL-2) family proteins. This comprehensive review examines the molecular structural mechanisms of BCL-2 mediated survival in acute myeloid leukemia blasts, focusing on the competitive interaction dynamics between pro-apoptotic BH3-only proteins and downstream mitochondrial outer membrane permeabilization cascades. Traditional cytotoxic chemotherapy often fails to clear leukemia stem cells that overexpress BCL-2. Evolving therapeutic paradigms emphasize the selective deployment of small-molecule BH3 mimetics, such as venetoclax, which competitively binds the hydrophobic groove of BCL-2 to displace pro-apoptotic factors. Combining venetoclax with low-dose cytarabine or hypomethylating backbones has demonstrated high complete remission rates in elderly or treatment-naive acute myeloid leukemia populations unsuitable for intensive induction. However, secondary drug resistance mechanisms, such as upregulation of MCL-1 or BAX mutations, present ongoing clinical challenges. This review details practical biomarker-driven strategies and clinical combination pathways designed to bypass intrinsic resistance and maximize clonal eradication in myeloid leukemias.

Keywords: Acute myeloid leukemia, BCL-2 pathway, venetoclax, apoptosis, BH3 mimetics

Manuscript Timeline: Received: October 12, 2015; Revised: November 22, 2015; Accepted: December 10, 2015; Published: January 16, 2016