BackgroundDiabetic ketoacidosis (DKA) is a potentially life-threatening acute complication of type 1 diabetes mellitus (T1DM). Although the frequency of DKA as first manifestation of T1DM is higher in developing compared developed countries, there is paucity of information on its characteristics in developing countries.MethodsThis retrospective study determined the frequency of ketoacidosis at diagnosis of new-onset type 1 diabetes and described the clinical characteristics of the patients seen between 1996 and 2011 by auditing the hospital records of all cases. The diagnosis of diabetic ketoacidosis (DKA) was based on the presence of hyperglycaemia (blood glucose > 11 mmol/L), acidosis (serum bicarbonate < 15 mmol/L) and ketonuria (urine ketone ≥1+).ResultsAt diagnosis of new-onset type 1 diabetes mellitus, three-quarter (77.1%) of the children and adolescents presented with DKA. Comparing the frequency of DKA during the initial 8 years (1996–2003) with the later 8 years (2004–2011), it was 81.8% vs 73.1%; p > 005. The frequency has not shown any significant declined over a 16-year period. The frequency of re-admission in ketoacidosis was 24.3%.ConclusionThree-quarter of children and adolescents present with DKA as first manifestation of T1DM with no significant decline in frequency over a 16-year period in our hospital.

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Introduction Malaria is a blood vector-borne disease with high morbidity and mortality in children in sub-Saharan Africa [1]. The 2017 malaria report of the World Health Organization (WHO) stated there were 216 million malaria cases worldwide in 2016, which was 5 million cases more than the 211 million observed in 2015 [1]. Malaria infection rate rises rapidly from 0% to 2% during the first three months of life, reaches 50% by the age of one1 year and then remains persistently high through the period of childhood in malaria stable endemic regions [1, 2]. Malaria disease is commonly associated with alterations in haematologic cells of the peripheral blood of infected individuals in both the acute uncomplicated and severe phases [3, 4]. The haematologic picture, however, varies from person to person and largely depends on nutritional status (parameters are severely depleted in malnourished than well-nourished children) [4], intensity of malaria transmission [4, 5], age [3, 6, 7], and co-morbidities, such as helminthiasis [3]. Anaemia is a complication contributing significantly to mortality from malaria disease [3-8]. This usually results from excessive removal of non-parasitized erythrocytes, immune destruction of parasitized red cells, and impaired erythropoiesis by the bone marrow dysfunction [9]. Leukocytosis/monocytosis [4, 10] or leucopaenia [4, 5] and thrombocytopenia [4, 5, 9] have been documented in most severe acute disease [4, 6]. The hypersplenism observed during acute malaria episodes is associated with splenomegaly and might also contribute to reduction in all the three blood cells causing anaemia, thrombocytopaenia, and leucopaenia [8]. The hypersplenism and malaria inflammatory response and endothelial activation have also been implicated as a cause of leukocytosis (monocytosis) [8, 9]. The spleen is the vital organ for both malaria parasite clearance from the peripheral circulation and the observed immunological response to parasite clearance during the acute malaria episodes [8,