International Blood Research & Reviews

Spontaneous Non-traumatic Epidural Hematoma in Sickle Cell Disease: A Case Report

Fri, 03 Jul 2026 00:00:00 +0000

Spontaneous non-traumatic epidural haematoma is an uncommon but potentially fatal neurological complication of sickle cell disease. This case report describes a 13-year-old girl with homozygous sickle cell disease who was admitted with a non-febrile vaso-occlusive crisis after inadequate hydration during a period of extreme heat. On admission, she was conscious and had no sensory or motor deficit, but she presented with diffuse osteoarticular pain. Laboratory testing showed severe anaemia, with haemoglobin at 6.6 g/dL, elevated C-reactive protein at 97 mg/L, hyperbilirubinaemia and elevated D-dimer, while malaria testing was negative. Initial treatment included intravenous rehydration and step-2 analgesia, with an early reduction in pain intensity. Two hours later, she developed a sudden severe diffuse headache in a non-traumatic context, followed by altered consciousness, a Glasgow Coma Scale score of 12/15 and left hemibody motor deficit. Emergency cranio-cerebral computed tomography demonstrated three extra-axial hyperdense biconvex lesions consistent with epidural haematomas in the right parieto-occipital, left parietal and left frontal regions, with mass effect and a 9 mm midline shift. A multidisciplinary team recommended urgent craniotomy with haematoma evacuation. During the surgical procedure, the patient developed cardiorespiratory arrest, and resuscitation was unsuccessful. Review of reported cases suggests that spontaneous epidural haematoma in homozygous sickle cell disease is rare, is often associated with headache or vaso-occlusive crisis, and may be linked to cranial bone infarction, marrow expansion or venous congestion. This case emphasises the need for urgent neuroimaging when acute non-traumatic headache, altered consciousness or focal neurological deterioration occurs in patients with sickle cell disease. Early recognition may support faster therapeutic decision-making in this high-risk context.

Assessment of Autoimmune and Inflammatory Biomarkers in Rheumatoid Arthritis Subjects in Port Harcourt, Nigeria

Fri, 17 Jul 2026 00:00:00 +0000

Background: Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disorder characterised by persistent synovial inflammation and progressive joint damage.

Aim: This study assessed selected autoimmune and inflammatory biomarkers among individuals with RA in Port Harcourt, Nigeria.

Methods: A cross-sectional study included 78 participants aged 35–75 years, comprising 31 participants with RA and 47 apparently healthy controls. Serum anti-cyclic citrullinated peptide (anti-CCP) and anti-β2-glycoprotein I (anti-β2GPI) IgG antibodies were measured by indirect enzyme-linked immunosorbent assay, while erythrocyte sedimentation rate (ESR) was determined using the Westergren method. Data were analysed using GraphPad Prism version 10.6.1, with significance set at p ≤ 0.05.

Results: Participants with RA had higher anti-CCP concentrations than controls (0.56 ± 0.47 versus 0.35 ± 0.21 U/mL; p = 0.0222) and higher ESR values (11.7 ± 5.6 versus 6.6 ± 3.5 mm/hr; p < 0.0001). Anti-β2GPI concentrations did not differ significantly between groups (p = 0.4602). In sex-stratified comparisons, ESR was significantly elevated among both male and female participants with RA. Anti-CCP was significantly elevated among female participants but not among males, whereas anti-β2GPI showed no significant difference in either subgroup.

Conclusion: Anti-CCP and ESR demonstrated potential utility in the assessment of RA in this population, while the clinical relevance of anti-β2GPI remains uncertain. Larger studies incorporating disease-activity and treatment data are required.

Geographic Disparities in Haematological and Biochemical Profiles among HIV-Positive Adults on Antiretroviral Therapy across Three Senatorial Districts of Rivers State, Nigeria

P. H. Chukwu — Tue, 11 Aug 2026 00:00:00 +0000

Background: Routine haematological and biochemical indices support monitoring of adults with HIV, but geographical variation in Rivers State is insufficiently described.

Aims: To compare blood count indices, inflammatory cell ratios, biochemical parameters and physical indicators between HIV-positive adults receiving antiretroviral therapy (ART) and healthy controls across three senatorial districts of Rivers State, Nigeria.

Study Design: Cross-sectional comparative study.

Place and Duration of Study: Nine HIV clinics across Rivers East, Rivers South-East and Rivers West.

Methodology: One hundred and twenty-six adults aged 20–45 years were recruited by stratified random sampling: 63 HIV-positive participants receiving ART and 63 controls, with 21 pairs per district. Full blood counts were measured with a Mindray BC-5000 analyser. PLR, NLR, MLR, PMR, NMR, LMR, ENR, SII and SIRI were derived. Serum IFN-γ and IL-10 were quantified by sandwich ELISA. Biochemical and physical indicators were assessed using standard methods. Data were analysed by independent-samples t-tests and one-way ANOVA; p < 0.05 indicated significance.

Results: In Rivers East, no haematological parameter differed significantly, although AST was higher (7.70 ± 3.33 vs 4.65 ± 2.88 U/L; p = 0.003) and creatinine lower (0.91 ± 0.24 vs 1.17 ± 0.18 μmol/L; p < 0.001) among HIV-positive participants. In Rivers South-East, white cell, lymphocyte and monocyte counts were lower (p = 0.017, 0.030 and 0.046), while total and conjugated bilirubin were higher (p = 0.048 and 0.027). In Rivers West, these counts were lower (p = 0.044, 0.030 and 0.040), while alkaline phosphatase was higher (p = 0.010). Inter-district variation occurred in eosinophils, mean cell volume, mean cell haemoglobin concentration, PMR, SIRI, alkaline phosphatase, AST, ALT and bicarbonate (p = 0.010–0.034).

Conclusion: The findings demonstrate geographical heterogeneity and support evaluation of district-sensitive laboratory monitoring rather than a state-wide approach.

Haemostatic Dysfunction in Lassa Fever: Implications for Disease Severity and Outcome

Sat, 22 Aug 2026 00:00:00 +0000

Background: Lassa fever is a viral haemorrhagic illness endemic to Nigeria and other West African countries. Severe cases are often associated with abnormal coagulation and impaired platelet function.

Objective: This study primarily assessed coagulation parameters and examined their correlation with clinical outcomes in patients with acute Lassa fever.

Patients and Methods: This hospital-based case-control study included 324 participants: 108 Lassa virus-positive patients, 108 febrile Lassa-negative patients (Control 1), and 108 afebrile Lassa-negative individuals (Control 2). Prothrombin time (PT) and activated partial thromboplastin time (APTT) were measured using standard methods. Fibrinogen and D-dimer levels were determined via a sandwich enzyme-linked immunosorbent assay technique.

Results: Mean PT and APTT were significantly higher in the Lassa-positive group compared with both control groups (PT: p < 0.001; APTT: p = 0.048). Prolonged coagulation times were observed in 23 of 108 (21.3%) patients with Lassa fever (p < 0.001). Median fibrinogen levels (mg/dL) were lower in patients with Lassa fever [272.65 (interquartile range (IQR): 204.8–366.8)] than in Control 1 [335.55 (258.5–398.6)] and Control 2 [306.90 (245.6–355.2)], with statistically significant differences (p < 0.001). Median D-dimer levels (ng/mL) were elevated in patients with Lassa fever [1054.00 (593–1588)] compared with Control 1 [325.50 (173–715)] and Control 2 [188.00 (145–273)] (p < 0.001).

Conclusions: Lassa fever is associated with significant alterations in coagulation parameters. Patients with acute Lassa infection showed elevated PT, APTT, and D-dimer levels, along with decreased fibrinogen levels, compared with controls. These findings underscore the role of coagulopathy in the pathogenesis and severity of Lassa fever.

From Antigens to Alleles: Evolving Strategies in Blood Group Typing

I. Abdel Wadoud, V. Zammit, B. Baron — Wed, 08 Jul 2026 00:00:00 +0000

Blood group typing has changed more in the past three decades than in the preceding hundred years. What began as an exercise in observing agglutination reactions has become, increasingly, an exercise in reading DNA: a shift from describing antigens as they appear on the red cell surface to interpreting the alleles that put them there. Serological methods remain fast, cheap, and well understood, but they falter in predictable ways — when a patient has been recently transfused, when an antigen is weakly expressed, when a needed antiserum is no longer manufactured, or when a therapeutic monoclonal antibody swamps the test with false reactivity. Molecular genotyping has closed these gaps gradually rather than all at once, moving from single-locus PCR assays to dense microarrays, then to targeted next-generation sequencing, and now to long-read whole-genome approaches capable of resolving structurally complex loci such as Rh and ABO at the level of individual alleles. This review traces that progression and weighs the comparative strengths and limitations of each generation of technology, with particular attention to transfusion support in sickle cell disease and thalassaemia, the classification of weak and partial D phenotypes, noninvasive fetal blood group prediction from maternal plasma, large-scale donor genotyping, and the recent entry of machine learning into antigen prediction from genome-wide data. It also considers the problems that remain unresolved: incomplete genotype-to-phenotype concordance for structurally variable genes, the cost and infrastructure required to run sequencing-based assays routinely, and the continuing under-representation of non-European ancestries in the reference panels on which much of this technology was built. The overall picture is one in which genotyping has become indispensable alongside serology rather than a replacement for it, and in which the technology's remaining promise depends as much on equitable access and standardisation as on further refinement of the assays themselves.

Gonadotropin–Testosterone Axis and Semen Response after Correction of Chronic Anaemia in β-Thalassaemia, Sickle Cell Disease, and Iron-Deficiency Anaemia: A Structured Review

Mon, 13 Jul 2026 00:00:00 +0000

Background: Male reproductive dysfunction is increasingly relevant in chronic anaemias as survival into adulthood has improved in β-thalassaemia and sickle cell disease, while iron-deficiency anaemia remains globally common. Impaired fertility arises through hypoxia, oxidative stress, gonadal axis dysfunction, iron overload, and treatment-related gonadotoxicity. The key clinical question is whether correcting anaemia improves semen quality and gonadal function.

Objectives: To review PubMed-indexed human studies on the effect of correcting β-thalassaemia, sickle cell disease, and iron-deficiency anaemia on semen parameters, gonadal-axis markers, and fertility outcomes; to distinguish reversible from persistent reproductive injury; and to derive a practical diagnostic framework.

Methods: A structured PubMed-only review (search date: 2026-04-26) combined disease terms with fertility-related keywords. Only human male studies reporting fertility-relevant outcomes were included. No meta-analysis was performed. Quality was assessed using NIH and Joanna Briggs Institute checklists.

Results: Fifteen original studies met inclusion criteria; four directly evaluated anaemia correction. Transfusion in β-thalassaemia and sickle cell disease increased haemoglobin, testosterone, gonadotropins, and sperm count within 7 days. Intravenous iron in iron-deficiency anaemia similarly improved hormonal and semen variables. Persistent injury — sperm DNA fragmentation, pituitary iron deposition, compensated hypogonadism, and transplant-related gonadotoxicity — coexisted with reversible changes. No study demonstrated conception or live-birth benefit.

Conclusions: Anaemia correction improves male reproductive physiology, but evidence is limited by small uncontrolled studies. Correction should precede infertility labelling and prompt repeat endocrine and semen assessment. Durable fertility in β-thalassaemia and sickle cell disease requires managing iron toxicity, vaso-occlusive damage, and treatment-related gonadotoxicity.

Peripheral Blood Mononuclear Cells (PBMCs) Biobanking for HIV Vaccine Trials in Nigeria: A Narrative Review of Challenges, Governance, and Strategies for Sustainable Biorepository Development

Helen Ogochukwu Nwandu, Chizaram Onyeaghala, Stephen Oluwasegun Adetunji — Mon, 10 Aug 2026 00:00:00 +0000

Background: Nigeria is home to more than two million people living with HIV, yet it remains underrepresented in HIV vaccine trials. Peripheral blood mononuclear cells (PBMCs) are vital for assessing vaccine-induced immunity; however, biobanking in resource-limited settings presents challenges that can compromise sample integrity and research validity.

Objective: This narrative review aims to summarise the evidence on PBMC biobanking for HIV vaccine trials in Nigeria, focusing on infrastructure, regulation, quality assurance, capacity building and sustainability.

Methods: We searched PubMed, Scopus, Web of Science, African Journals Online and institutional websites for studies published from January 2000 to December 2024. Of 321 records identified, 42 studies were selected and thematically analysed.

Results: Infrastructure gaps, including an inadequate electricity supply, limited access to liquid nitrogen and cold-chain vulnerabilities, compromise PBMC quality and stability. Incoherent regulatory and governance frameworks contribute to critical gaps because Nigeria lacks a dedicated national human tissue authority and specific biobanking standards. Capacity is constrained by the absence of formal training curricula and high staff turnover, while quality assurance is limited by the lack of national biobank registries and external quality assessment schemes.

Conclusion: Developing robust PBMC biobanking capacity in Nigeria requires comprehensive strategies to improve infrastructure reliability, institutionalise training, harmonise regulatory frameworks and establish quality-improvement networks that can support HIV vaccine development and promote global health equity.

Haematological Consequences of Systemic Inflammation: A Critical Narrative Review of Pathophysiology, Clinical Manifestations, Biomarkers and Therapeutic Implications

Zaccheaus Awortu Jeremiah, Joyce Ezekiel Etura — Thu, 20 Aug 2026 00:00:00 +0000

Inflammation is inseparable from blood-cell biology: circulating cells detect inflammatory cues, bone-marrow progenitors alter lineage output, erythroid iron supply is actively restricted, and haemostatic pathways can be recruited as components of host defence. Yet the expression “haematological inflammation” is used inconsistently and can obscure the distinction between adaptive haematopoietic responses, secondary cytopenias or cytoses, thrombo-inflammation, and primary haematological disease. This critical narrative review integrates mechanistic, translational and clinical evidence on the major ways systemic inflammation remodels haematopoiesis and peripheral blood phenotypes. Literature indexed from 1 January 2000 to 11 June 2026 was considered, with earlier work retained only when conceptually indispensable. The evidence indicates that acute inflammatory signalling can beneficially accelerate myeloid production and mobilise innate effector functions, whereas persistent interferon, interleukin-1, tumour necrosis factor and related signals can impose lineage bias, impaired stem-cell fitness and a marrow environment permissive to clonal selection. In erythropoiesis, the interleukin-6–hepcidin–ferroportin axis provides the strongest mechanistic link between inflammation and functional iron restriction, although shortened erythrocyte survival and direct cytokine-mediated suppression of erythropoiesis remain important. Platelets and neutrophil extracellular traps connect inflammation to coagulation, providing a biological continuum from protective immunothrombosis to sepsis-induced coagulopathy and disseminated intravascular coagulation. Common biomarkers, including C-reactive protein, erythrocyte sedimentation rate, ferritin, procalcitonin and cell-count ratios, are clinically useful only when interpreted as context-dependent signals rather than disease-specific tests. Therapeutic implications therefore differ by mechanism: control of the initiating disease remains primary, while cytokine blockade, manipulation of the hepcidin–ferroportin axis, and selective anti-thrombo-inflammatory strategies may be useful in defined phenotypes. The most important unresolved challenge is to distinguish adaptive, reversible inflammatory haematopoiesis from maladaptive programmes that become self-sustaining, clonal or organ-damaging.