International Journal of Hematology

International Journal of Hematology | Vol. 3, No. 3, March 2012 | pp. 17–24
DOI: 10.46882/2012/IJH/000027

Case Report

Title: Deep vein thrombosis associated with congenital antithrombin III deficiency in a young pregnant female

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

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

Abstract: Pregnancy induces a physiological hypercoagulable state that increases the risk of thromboembolic events in women with underlying inherited thrombophilias. We report a 23-year-old primigravida at 14 weeks of gestation who presented with painful, progressive swelling of the left lower limb lasting 4 days. Doppler ultrasonography confirmed an extensive deep vein thrombosis involving the left common femoral and popliteal veins. Functional coagulation assays revealed a severe reduction in antithrombin III activity (42.0%), while protein C, protein S, and lupus anticoagulant screens were normal. Family history revealed recurrent thromboembolism in her maternal uncle. Anticoagulant therapy was initiated with therapeutic low-molecular-weight heparin (enoxaparin, 1 mg/kg subcutaneously every 12 hours), achieving complete resolution of symptoms and preserving fetal viability. Enoxaparin was adjusted based on anti-Factor Xa levels and continued throughout pregnancy, followed by a transition to oral warfarin postpartum. This case demonstrates the importance of considering congenital anticoagulant deficiencies in young pregnant patients presenting with unprovoked venous thrombosis.

Keywords: Antithrombin III deficiency, pregnancy, deep vein thrombosis, low-molecular-weight heparin, thrombophilia

Manuscript Timeline: Received: December 01, 2011; Revised: January 12, 2012; Accepted: February 02, 2012; Published: March 16, 2012

International Journal of Hematology | Vol. 3, No. 5, May 2012 | pp. 33–40
DOI: 10.46882/2012/IJH/000029

Original Article

Title: Immunophenotypic profile of chronic lymphocytic leukemia using a concise five-marker flow cytometry panel

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: Flow cytometry is the gold standard for differentiating chronic lymphocytic leukemia from other mature B-cell lymphoproliferative disorders. This study evaluated the diagnostic utility of a concise five-marker flow cytometry immunophenotyping panel (CD5, CD19, CD20, CD23, and Kappa/Lambda light chains) in 42 patients presenting with persistent absolute lymphocytosis (> 5.0 × 10⁹/L). Co-expression of CD5 and CD19 on clonal B-cells was identified in 78.6% (33 of 42) of the suspected cases. Chronic lymphocytic leukemia was confirmed in 28 patients based on strong CD23 expression, weak CD20 expression, and monotypic surface immunoglobulin light chain restriction (Matutes score ≥ 4). Five patients demonstrated strong CD20 expression without CD23, consistent with mantle cell lymphoma profiles. The concise immunophenotypic panel demonstrated a diagnostic sensitivity of 93.3% and a specificity of 90.0% for chronic lymphocytic leukemia confirmation. This focused flow cytometry panel offers a highly accurate and cost-effective diagnostic protocol for low-resource hematopathology laboratories.

Keywords: Chronic lymphocytic leukemia, flow cytometry, immunophenotyping, Matutes score, lymphocytosis

Manuscript Timeline: Received: February 12, 2012; Revised: March 22, 2012; Accepted: April 08, 2012; Published: May 19, 2012

International Journal of Hematology | Vol. 3, No. 12, December 2012 | pp. 89–96
DOI: 10.46882/2012/IJH/000036

Original Article

Title: Prevalence and clinical correlates of lupus anticoagulant positivity in adult patients with systemic lupus erythematosus

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 and Rheumatology, Lagos State University Teaching Hospital, Ikeja, Nigeria; ³Department of Chemical Pathology, University of Ilorin, Ilorin, Nigeria

Abstract: Lupus anticoagulant is an important acquired thrombophilic factor that increases the risk of arterial and venous thrombosis. This study cross-sectionally evaluated the prevalence and clinical correlates of lupus anticoagulant in 60 adult patients diagnosed with systemic lupus erythematosus. Lupus anticoagulant screening was conducted using the diluted Russell’s viper venom time assay, followed by phospholipid confirmation steps. Lupus anticoagulant positivity was detected in 23.3% (14 of 60) of the systemic lupus erythematosus cohort. A history of objective thromboembolic events was significantly higher in lupus anticoagulant-positive patients compared to negative individuals (28.5% versus 4.3%, P < 0.01). Furthermore, obstetric complications, including recurrent early pregnancy loss or unexplained fetal death, were documented in 42.8% of positive females. Activated partial thromboplastin time prolongation did not reliably predict lupus anticoagulant presence due to variable reagent sensitivities. Routine screening utilizing specialized phospholipid-dependent assays is highly recommended in systemic lupus erythematosus patients to identify high-risk thrombotic phenotypes requiring long-term antiplatelet or anticoagulant interventions.

Keywords: Systemic lupus erythematosus, lupus anticoagulant, diluted Russell’s viper venom time, thrombosis, pregnancy loss

Manuscript Timeline: Received: September 02, 2012; Revised: October 12, 2012; Accepted: November 04, 2012; Published: December 10, 2012

International Journal of Hematology | Vol. 3, No. 9, September 2012 | pp. 65–72
DOI: 10.46882/2012/IJH/000033

Review Article

Title: Molecular landscape and targeted therapeutic inhibitors in myelofibrosis

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: Myelofibrosis is a clonal hematopoietic stem cell disorder characterized by bone marrow fibrosis, extramedullary hematopoiesis, and splenomegaly. This review synthesizes the molecular landscape of myelofibrosis, focusing on driver mutations in JAK2 (V617F), CALR, and MPL genes that induce constitutive activation of the JAK-STAT signaling pathway. The prognostic impact of high molecular risk mutations, including ASXL1, EZH2, and IDH1/2, is explored in relation to accelerated leukemic transformation. Therapeutic paradigms have shifted from supportive care toward targeted tyrosine kinase inhibitors. Small-molecule JAK1/JAK2 inhibitors like ruxolitinib demonstrate substantial efficacy in reducing spleen volume, suppressing inflammatory cytokine cascades, and improving constitutional symptoms. However, these agents often induce dose-dependent myelosuppression, requiring careful dose titration. Allogeneic hematopoietic stem cell transplantation remains the only curative strategy, but it is limited by high treatment-related mortality. Emerging combination protocols incorporating JAK inhibitors with bromodomain inhibitors or BCL-2 inhibitors represent the next frontier in reversing marrow fibrosis and eliminating neoplastic clones.

Keywords: Myelofibrosis, JAK2 mutation, ruxolitinib, JAK-STAT pathway, splenomegaly

Manuscript Timeline: Received: June 11, 2012; Revised: July 20, 2012; Accepted: August 10, 2012; Published: September 15, 2012

International Journal of Hematology | Vol. 3, No. 10, October 2012 | pp. 73–80
DOI: 10.46882/2012/IJH/000034

Original Article

Title: Transfusion transmissible infections among multi-transfused 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 transfusion therapy exposes patients with sickle cell anemia to the risk of transfusion-transmissible infections, particularly in areas with a high prevalence of endemic pathogens. This cross-sectional study evaluated the seroprevalence of Human Immunodeficiency Virus, Hepatitis B Virus, Hepatitis C Virus, and Syphilis among 130 multi-transfused patients with sickle cell anemia who had received over 10 packed red blood cell units. Screening was performed using third-generation enzyme-linked immunosorbent assays. The overall seroprevalence of any transfusion-transmissible infection was 16.9% (22 of 130). Specifically, Hepatitis B surface antigen positivity was 8.5%, Hepatitis C Virus antibodies were detected in 5.4%, Human Immunodeficiency Virus was present in 2.3%, and Syphilis serology was positive in 0.8% of cases. The infection rate correlated significantly with the total number of transfusions received (P < 0.05) and transfusions administered prior to the implementation of automated screening methods. These findings highlight a substantial burden of viral hepatitis among chronically transfused patients, emphasizing the need for more sensitive nucleic acid testing in blood donor centers and universal hepatitis B vaccination for sickle cell cohorts.

Keywords: Sickle cell anemia, transfusion-transmissible infections, Hepatitis B, Hepatitis C, blood safety

Manuscript Timeline: Received: July 12, 2012; Revised: August 22, 2012; Accepted: September 05, 2012; Published: October 11, 2012

International Journal of Hematology | Vol. 3, No. 7, July 2012 | pp. 49–56
DOI: 10.46882/2012/IJH/000031

Original Article

Title: Serum erythropoietin kinetics and iron status parameters in patients with chronic kidney disease 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 and Nephrology, University of Ilorin, Ilorin, Nigeria; ³Department of Chemical Pathology, Ladoke Akintola University of Technology, Ogbomoso, Nigeria

Abstract: Anemia in chronic kidney disease is primarily attributed to impaired erythropoietin production, but functional iron deficiency often complicates management. This cross-sectional study evaluated serum erythropoietin levels, ferritin, and soluble transferrin receptor concentrations in 85 non-dialysis chronic kidney disease patients (stages 3 to 5). Serum erythropoietin was quantified using an enzyme-linked immunosorbent assay. Despite severe anemia (mean hemoglobin 7.8 ± 1.2 g/dl), the median serum erythropoietin level was 12.4 mIU/ml, reflecting an inappropriately blunted response relative to the degree of hypoxia. Functional iron deficiency, defined by a transferrin saturation below 20% and serum ferritin above 100 ng/ml, was identified in 41.2% (35 of 85) of the patients. Soluble transferrin receptor levels correlated inversely with hemoglobin (r = -0.45, P < 0.01) and served as a superior index of marrow iron demand compared to ferritin alone. These results indicate that blunted endogenous erythropoietin production and restricted iron utilization are co-dominant factors in renal anemia. Integrating soluble transferrin receptor assays into routine diagnostic panels allows for more accurate identification of functional iron deficits prior to initiating recombinant erythropoietin therapy.

Keywords: Chronic kidney disease, renal anemia, erythropoietin, ferritin, soluble transferrin receptor

Manuscript Timeline: Received: April 10, 2012; Revised: May 18, 2012; Accepted: June 05, 2012; Published: July 12, 2012