International Journal of Hematology

International Journal of Hematology | Vol. 4, No. 12, December 2013 | pp. 89–96
DOI: 10.46882/2013/IJH/000048

Original Article

Title: Evaluation of automated reticulocyte hemoglobin content in the early detection of iron deficiency in blood donors

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: Regular blood donation depletes iron stores, often causing subclinical iron deficiency before it manifests as an absolute drop in total hemoglobin. This study evaluated the diagnostic performance of reticulocyte hemoglobin content (Ret-He) compared to traditional biochemical parameters for identifying latent iron deficiency in 200 regular male blood donors. Full blood counts and reticulocyte indices were measured on an automated hematology analyzer, with serum ferritin serving as the reference standard. Latent iron deficiency, defined by a serum ferritin below 30 ng/ml despite a normal total hemoglobin (≥ 12.5 g/dl), was identified in 24.5% (49 of 200) of the donors. The mean reticulocyte hemoglobin content was significantly lower in the iron-deficient donor cohort (26.4 ± 1.8 pg) compared to iron-replete donors (33.2 ± 2.1 pg, P < 0.001). Receiver operating characteristic analysis established a reticulocyte hemoglobin content threshold below 29.5 pg as optimal for predicting latent iron deficiency, achieving a sensitivity of 87.8% and a specificity of 84.1%. Measuring reticulocyte hemoglobin provides a real-time, cost-effective assessment of iron-restricted erythropoiesis that can be performed directly during routine pre-donation screening.

Keywords: Blood donors, reticulocyte hemoglobin content, latent iron deficiency, ferritin, blood donor selection

Manuscript Timeline: Received: September 10, 2013; Revised: October 20, 2013; Accepted: November 05, 2013; Published: December 11, 2013.

International Journal of Hematology | Vol. 4, No. 7, July 2013 | pp. 49–56
DOI: 10.46882/2013/IJH/000043

Review Article

Title: Transfusion-associated circulatory overload: Evolving physiological mechanisms and preventive strategy guidelines

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: Transfusion-associated circulatory overload is a leading cause of transfusion-related morbidity and mortality in acute hospital settings. This review synthesizes current insights into its pathophysiology, distinguishing it from transfusion-related acute lung injury by examining volume expansion kinetics, hydrostatic pressure elevations, and underlying cardiopulmonary vulnerability. High-risk patient characteristics include advanced age, chronic kidney disease, severe baseline anemia, and positive fluid balance states. Clinical identification relies on respiratory distress emerging within 6 hours of transfusion, accompanied by elevated brain natriuretic peptide levels (> 1.5 times baseline) and acute hypertension. Prevention strategies emphasize risk stratification prior to blood administration. Utilizing a slow infusion rate (1.0 to 1.5 ml/kg/hour) and implementing proactive prophylactic diuretic regimens (e.g., 20 mg to 40 mg intravenous furosemide) significantly reduce pulmonary hydrostatic pressure. Splitting multi-unit blood requests into single units with mandatory reassessments further minimizes volume overload. This review outlines an operational nursing and medical workflow checklist designed to optimize bedside surveillance and reduce preventable circulatory distress in high-risk transfusion recipients.

Keywords: Transfusion-associated circulatory overload, hydrostatic pressure, brain natriuretic peptide, fluid balance, blood safety

Manuscript Timeline: Received: April 11, 2013; Revised: May 20, 2013; Accepted: June 12, 2013; Published: July 16, 2013

International Journal of Hematology | Vol. 4, No. 8, August 2013 | pp. 57–64
DOI: 10.46882/2013/IJH/000044

Original Article

Title: Prevalence and molecular characteristics of Alpha-Thalassemia deletions among infants with microcytic indices

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: Alpha-thalassemia deletions frequently cause microcytosis in infants, often mimicking or complicating nutritional iron deficiency definitions. This study investigated the prevalence and molecular characteristics of single and two-gene alpha-thalassemia deletions in 160 infants aged 6 to 24 months who presented with microcytic indices (MCV < 70 fl) and normal iron stores. Genomic DNA was extracted from peripheral blood leucocytes, followed by multiplex polymerase chain reaction analysis to detect common deletional variants (-alpha³.⁷, -alpha⁴.², --MED, and --alpha²⁰.⁵). Alpha-thalassemia variants were identified in 38.1% (61 of 160) of the microcytic infant cohort. The single-gene deletion homozygous state (-alpha³.⁷/-alpha³.⁷) was the most frequent molecular finding, occurring in 68.8% of positive cases, while the heterozygous state (-alpha³.⁷/alpha alpha) was found in 26.2%. The two-gene deletion variants (--MED) were rare, identified in only 2 infants. Infants with homozygous -alpha³.⁷ deletions showed a mean hemoglobin value of 9.4 ± 1.1 g/dl and significantly lower mean corpuscular volume values compared to heterozygous infants (58.4 fl versus 66.2 fl, P < 0.01). Multiplex polymerase chain reaction profiling is highly useful for identifying inherited hemoglobin gene deletions, helping prevent unnecessary iron supplementation in microcytic pediatric cohorts.

Keywords: Alpha-thalassemia, microcytosis, infants, polymerase chain reaction, hemoglobin deletions

Manuscript Timeline: Received: May 12, 2013; Revised: June 22, 2013; Accepted: July 10, 2013; Published: August 14, 2013

International Journal of Hematology | Vol. 4, No. 1, January 2013 | pp. 1–8
DOI: 10.46882/2013/IJH/000037

Case Report

Title: Delayed hemolytic transfusion reaction mimicking a vaso-occlusive crisis in a patient with sickle cell anemia

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

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

Abstract: Delayed hemolytic transfusion reactions are underdiagnosed complications in sickle cell anemia that can mimic acute vaso-occlusive crises and lead to severe hyperhemolysis. We report a 26-year-old female with sickle cell anemia (HbSS) who received 2 units of packed red blood cells for severe symptomatic anemia. Ten days post-transfusion, she presented with generalized bone pain, dark urine, and a rapid drop in hemoglobin from 9.5 g/dl to 4.1 g/dl. This drop fell below her baseline value of 6.8 g/dl, confirming a hyperhemolytic state. Total serum bilirubin rose to 6.2 mg/dl, and lactate dehydrogenase reached 1450 U/L. A repeat direct antiglobulin test was strongly positive (IgG and C3d), and an antibody eluate assay identified anti-Fya alloantibodies that were undetectable during pre-transfusion testing. Intravenous methylprednisolone (1 g daily for 3 days) and high-dose intravenous immunoglobulin (1 g/kg for 2 days) were initiated immediately. Hemolysis stabilized, reticulocytosis returned, and hemoglobin rose to 7.0 g/dl without further transfusions. This case highlights the need to consider delayed hemolytic reactions in patients presenting with severe pain and an unexplained drop in hemoglobin within two weeks of a transfusion.

Keywords: Sickle cell anemia, delayed hemolytic transfusion reaction, hyperhemolysis, alloantibodies, intravenous immunoglobulin

Manuscript Timeline: Received: October 18, 2012; Revised: November 24, 2012; Accepted: December 15, 2012; Published: January 18, 2013

International Journal of Hematology | Vol. 4, No. 10, October 2013 | pp. 73–80
DOI: 10.46882/2013/IJH/000046

Original Article

Title: Serum hepcidin levels and erythropoiesis indices in pregnant women with varying iron status profiles

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

Abstract: Hepcidin regulates systemic iron homeostasis by controlling iron absorption and macrophage recycling, yet its expression patterns shift during pregnancy. This study cross-sectionally evaluated serum hepcidin concentrations, soluble transferrin receptor levels, and hemoglobin values in 120 pregnant women in their third trimester and 60 non-pregnant female controls. Serum hepcidin was quantified using a competitive enzyme-linked immunosorbent assay. Pregnant women demonstrated significantly lower mean serum hepcidin levels (4.2 ± 1.8 ng/ml) compared to non-pregnant controls (18.6 ± 4.5 ng/ml, P < 0.001), reflecting a physiological adaptation to enhance dietary iron absorption. Among the pregnant cohort, women with established iron deficiency anemia (hemoglobin < 11.0 g/dl, ferritin < 15 ng/ml) exhibited near-complete suppression of hepcidin (< 1.5 ng/ml). Serum hepcidin levels correlated positively with ferritin (r = 0.58, P < 0.01) and inversely with soluble transferrin receptor values (r = -0.42, P < 0.05). This physiological suppression of hepcidin during late gestation facilitates maximal maternal-fetal iron transport. Measuring hepcidin provides deep insight into iron utilization, helping guide targeted oral versus intravenous iron replacement in gestational anemias.

Keywords: Hepcidin, pregnancy, iron deficiency anemia, ferritin, soluble transferrin receptor

Manuscript Timeline: Received: July 02, 2013; Revised: August 14, 2013; Accepted: September 04, 2013; Published: October 12, 2013

International Journal of Hematology | Vol. 4, No. 4, April 2013 | pp. 25–32
DOI: 10.46882/2013/IJH/000040

Short Communication

Title: Prevalence of prolonged activated partial thromboplastin time due to intrinsic pathway factor deficiencies in elective pre-operative screening

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: Unsuspected coagulation abnormalities detected during pre-operative screening can cause cancellations or delays in elective surgical procedures. This study evaluated the causes of an isolated prolonged activated partial thromboplastin time discovered during routine pre-operative assessments in 75 asymptomatic adult patients. A 1:1 mixing study with normal pooled plasma was performed to differentiate factor deficiencies from circulating inhibitors, followed by specific factor assays. Corrected mixing study profiles confirmed an intrinsic pathway factor deficiency in 68.0% (51 of 75) of the cases. Factor XII deficiency was the most common cause, identified in 28.0% of the cohort, followed by Factor XI deficiency in 14.6% and Factor IX deficiency in 12.0%. A circulating lupus anticoagulant was confirmed in 18.6% of patients with non-corrected mixing studies. Asymptomatic Factor XII deficiency does not require therapeutic intervention or surgical delay because it does not cause clinical bleeding. Routine pre-operative screening panels should include immediate plasma mixing steps to prevent unnecessary surgical cancellations for benign coagulation abnormalities.

Keywords: Activated partial thromboplastin time, pre-operative screening, mixing study, Factor XII deficiency, intrinsic pathway

Manuscript Timeline: Received: January 15, 2013; Revised: February 22, 2013; Accepted: March 11, 2013; Published: April 18, 2013