Acute myeloid leukaemia (AML) is a group of haematological diseases, characterized by abnormal accumulation of blast cells in the bone marrow and peripheral blood. The disease has a mutable prognosis and a high mortality rate: 5-year overall survival is lesser than 50%, and in elderly patients, only 20% will survive for 2 years after diagnosis. Two systems currently exist to diagnose and classify AML: the French American British (FAB) and the World Health Organization (WHO) classifications. The FAB classification system dates to 1976 and specifies a diagnosis of AML when there is greater than 30% blast population in the peripheral blood and bone marrow. 2008 WHO revision classifies neoplasms based on morphologic cytogenetic, clinical, and phenotypic criteria. They define AML as a myeloid neoplasm with a greater than 20% blast population in the peripheral blood and bone marrow. Hematology facilities in sub-Saharan Africa are still insufficient; few centres in the region can provide specialist care and training. There is a lack of skilled personnel. Few haematological specialists are overwhelmed, in this region, they fall below WHO’s target of one haematologist per 100 000 people, while the laboratory technologists are unskilled in reading and reporting Peripheral blood film (PBF). Most of these technologists cannot identify a real blast cell in a PBF. There is a lack of advanced diagnostic tools like digital microscopes and flow cytometers for analysis to identify acute myeloid leukemia in the facilities within this region. In this presentation, I intend to discuss how to best implement screening programs, how to improve early detection rates and guarantee access to treatment, and how to deliver effective, locally appropriate care. The discussion will also cover blood transfusion, cost-effective treatment for many AMLs, and a key component to providing acute hematological care that is still not explicitly covered in any healthcare programs in the region. The presentation advocates for the need to invest in research and clinical care in Hematology, analyze key challenges in this region and programs that succeeded in improving care in the past years, and provide recommendations to help specialists working in sub-Saharan Africa to provide tailored, evidence-based care in the region. To improve the diagnosis of AML, innovative intervention strategies must be developed and implemented. Investing in training healthcare workers for better diagnostics and developing Hematology services in sub-county, county, and county referral hospitals in this region will be key to realizing my vision of longer and healthier lives for all Africans in the western Kenya region. We also hope that the Series' recommendations will serve as a guide and inspire young Kenyan researchers and healthcare professionals in this, the youngest region in the world, to lead the change and improve hematological care for future generations.

Blast crisis and the associated hyperleukocytosis/leukostasis syndromes denote a medical emergency and require both rapid assessment and initiation of specific therapies. Any delays to the commencement of therapy are directly related to increased mortality in an already highly fatal condition. The mainstay of therapy is rapid initiation of supportive care and commencement of induction antineoplastic therapy. Leukapheresis and treatment with hydroxyurea, despite being quite common in clinical practice, are not the standard of care and do not carry with them any meaningful improvements in long-term mortality [1]. Leukostasis is an important aspect of the syndrome defined by hyperleukocytosis, occurring mainly in the sensitive tissue comprising lung parenchyma and cerebral vascular architecture. Two major theories exist to explain the mortality caused by said phenomenon: stasis in the microvasculature and massive cytokine release [2]. It has been noted that endothelial cells release massive cytokine cascades and signaling markers to attract even more blasts to a specific site, causing a systemic inflammatory reaction that seems to persist even after leukapheresis, with most cases of mortality being documented in the days to weeks following initiation of therapy and hospital admission [3]. This suggests there exists myriad other factors, many of them possibly unknown, which predispose individuals afflicted with this unfortunate illness to high mortality with little in the way of effective treatment.   

Statement of the Problem: Human Platelet Alloantigens (HPA) expresses Polymorphisms that arise from single base pair substitutions in alleles (their alleles are designated as ‘a’ or ‘b’ which usually occurs in pairs of homozygous or heterozygous forms) and lead to changes in amino acids of glycoproteins expressed on platelets. In a previous study, alloantibodies to human platelet antigens (HPA) were carried out using the GTI PakPlus solid phase enzyme-linked immunosorbent assay (ELISA) method. This present study was a follow-up to the serological study aimed at the molecular determination of gene frequencies of human platelet alloantigens among major ethnic groups in the Niger Delta region of Nigeria.

Materials and methods: This was a cross-sectional, randomized research. Five major ethnic groups were considered which include Etche, Ikwerre, Ijaw, Ogba, and Ogoni. A total of 104 participants between the ages of 16 – 42 years were recruited for the study of which 59 of the subjects were males and 45 were females. They were undergraduate and post-graduate students of Rivers State University, Port Harcourt, recruited during their pre-admission medical examination into the University. They were apparently healthy individuals who were serologically screened, and negative for HIV 1 &11, HBsAg, HCV, and VDRL (syphilis). In the study 25 of the subjects were of Ikwerre origin, 22 from Ogoni, 24 from Ijaw, 6 from Etche, and 22 from the Ogba region. Ten milliliters (10 ml) of blood was collected from each of the participants using standard venipuncture while maintaining good laboratory practice and quality control. HPA genes (genotype) were determined using the state-of-the-art Magnetic induction Cycler MiC-PCR Real-Time PCR System Australia. Data generated were analyzed using melt curve analysis in the micPCR software while the frequency distribution was done using Number Cruncher Statistical Software (NCSS) Version 13.0.  P values less than 0.05 was considered statistically significant.

Findings: Frequency distribution of HPA gene typing in the overall population shows that HPA 1a/a (32.70%) HPA 1 a/b (40.40%) HPA 1b/b (26. 93%), HPA 2 a/a (1.9%) HPA 2a/b (40,42%) HPA 2b/b (57.7%), HPA 3a/a (2.9%) HPA 3a/b (25.0%), HPA 3b/b (72.1%). HPA 4a/a (81.7%), HPA 4a/b (8.7%), HPA 4 b/b (9.6%), HPA 5a/a was absent, HPA 5a/b (1.9%) and HPA 5b/b (98.1%) For the various ethnic groups; in Etche and Ijaw HPA 4a/a and HPA 5b/b were the most predominant, interestingly this was also the case in Ogba, Ikwerre and Ogoni.

 Conclusion and Clinical Significance: Homozygous ‘b’ was more prevalent among all the populations, followed by homozygous ‘a and heterozygous a/b. HPA-5 b/b is most prevalent in the general population while the HPA-5a/a was completely absent. Since Human platelet antibodies are often implicated in conditions such as alloimmune thrombocytopenia(NAIT), Idiopathic thrombocytopenic purpura(ITP) and platelet refractoriness, a molecular study to determine the human platelet genes in this part of this world became necessary hence this study.