International Blood Research & Reviews

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.

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.