Background: The two major comrbidities (anemia and poor nutrition) are common manifestations of HIV-infected children, which threaten their lives. In Ethiopia, there is limited information on the magnitude and factors associated with anemia among HIV-infected children. Thus, this study was aimed to determine the magnitude and factors associated with anemia among HIV-infected children receiving antiretroviral therapy in the Afar region, Ethiopia.
Methods: A cross-sectional retrospective record review was conducted on a sample size of 102 HIV-infected children aged 6 months to < 15 years in selected ART sites of the Afar region from May 1 to 25, 2018. Patient cards from 2009 to 2017 with the required information were considered. A paired sample t-test was used to assess whether there is a significant difference in the hemoglobin level before and after the HAART regimen. Multivariable logistic regression was used to determine predictors of anemia. Statistical significance was determined atp value < 0.05.
Result: At baseline, 53.9% of study participants were anemic, from which 8.7%, 36.3%, and 9.8% were mild, moderate, and severe, respectively. There was a statistically significant improvement of hemoglobin level following the one-year course of ART treatment from 10.67 ± 1.82 to 11.5 ± 1.5 (p value ≤ 0.001): an improvement of 0.83 ± 1.74. Children who were moderately and severely stunted were more than five (AOR = 5.16, 95% CI (1.71, 15.56)) and more than twelve (AOR = 12.45, 95% CI (2.62, 59.21)) times more likely to be anemic than children who were not stunted, respectively. Children whose mothers had not attended ANC follow-up were more than three (AOR = 3.68, 95% CI (1.38, 9.81)) times more likely to be anemic than children whose mothers attended ANC. Children who were in clinical stages 3 and 4 were more than five (AOR = 5.07, 95% CI (1.79, 14.37)) times more likely to be anemic than children who were in clinical stage 1 and 2.
Conclusion: The magnitude of anemia among HIV-infected children was found to be high, which is 53.9%. Nutritional status (stunting), WHO clinical stage, and history of ANC follow-up were the predictors significantly associated with childhood anemia. Thus, interventions for HIV-infected children should consider those factors.
Background: The one-stage assay is the most common method to measure factor VIII activity (FVIII : C) in hemophilia A patients. The chromogenic assay is another two-stage test involving purified coagulation factors followed by factor Xa-specific chromogenic substrate.
Aim: This study aimed to assess the discrepancy and correlation between the chromogenic and one-stage assays in measuring FVIII : C levels in hemophilia patients receiving Extended Half-Life Elocta® as a recombinant extended half-life coagulation factor.
Methods: We performed a study comparing the measurements of FVIII : C levels by the chromogenic versus the one-stage assays at different drug levels. Data of FVIII : C levels, dosage, and the time interval from administration to measurement were retrieved from the hospital records. The correlation, mean differences, and discrepancy between the two assays were calculated. The linear regression analysis was used to predict the time interval till reaching 1% FVIII : C.
Results: Fourteen patients with 56 samples were included in the study. Of them, 13 patients were receiving Elocta® as a prophylactic, while one was receiving Elocta® on demand. One-third of these samples showed a discrepancy between the chromogenic and one-stage assays. The two assays were well correlated. Mean differences were significant at the individual and the time interval level. The time since the last Elocta® injection could significantly predict FVIII : C levels (β = 0.366, P < 0.001).
Conclusion: Our findings suggested a significant difference between both methods; the FVIII : C levels measured by the one-stage assay were less than those estimated by the chromogenic assay. However, the measurements of FVIII levels by the two assays were well correlated but discrepant in one-third of the samples. The levels of FVIII : C reach 1% after 5.4 days since the last Elocta® administration.
Background: Rhesus antigens have been documented to cause haemolytic disease of the newborn as well as acute and delayed transfusion reactions. This study was performed to evaluate the frequency of rhesus antigens (C, c, D, E, and e) in the studied population.
Method: This study was a cross-sectional study involving 130 prospective blood donors attending University of Calabar Teaching Hospital (UCTH) donor clinic. Donors were grouped for Rh antisera (anti-E, anti-e, anti-C, anti-c, and anti-D) using the standard serologic technique.
Result: The most prevalent Rh antigen was "c" (98.5%), followed by "D" (97.7%), while the least was "C" (30.7%). The most prevalent phenotype was cDe/cDe (R0R0).
Conclusion: This work therefore concludes that the most prevalent rhesus antigen and rhesus phenotype was c and cDe/cDe among blood donors in University of Calabar Teaching Hospital.
Close to half of all patients with sickle cell disease (SCD) will have at least one episode of acute chest syndrome (ACS) during their lifetime. Multiple cells and molecules involved with the inflammatory cascade play a role in the development of ACS. We found that patients with SCD who developed ACS as a complication of a vaso-occlusive crisis (VOC) had a significant increase in leukocytes and decrease in platelets from their steady state when compared with a separate admission for VOC without ACS development. No significant change from steady state hemoglobin or reticulocyte count was noted between the two admissions. These results indicate that trending laboratory markers may be useful to predict patients at risk for ACS development.
Background: Due to the sustained morbidity and mortality that malaria-associated anaemia imposes on patients, malaria is still a global threat, most especially, to residents in sub-Saharan Africa. Merozoite invasion and destruction of erythrocytes, a target for this study, have been necessary due to its unique nature and also since the erythrocytes suffer the most brunt of malarial infection leading to anaemia. The issue of malaria anaemia has to do with why uninfected RBCs get destroyed and even more so than infected ones. Studies have proposed that cytophilic anti-RSP2 (ring surface protein 2-merozoite rhoptry protein 2) antibodies present in sera enhance phagocytosis of RSP2-tagged RBCs by macrophages either directly or via complement, while others have proposed transfer of RSP2 to both infected and uninfected RBCs which may render them susceptible to phagocytosis. What is missing is the agent involved in the transfer of these parasite-induced surface proteins onto the uninfected RBCs, i.e., the mediator molecules. Considering the intracellular location of the parasite in the parasitophorous vacuolar membrane and the absence of a transport mechanism such as the Golgi apparatus within the mature RBC, since the latter has no nucleus, we propose that erythrocyte-derived microparticles (EMPs) may be the possible mediators.
Aim: This study aimed at examining the immunological interactions between EMPs released during malarial infections and host erythrocytes that may lead to their lysis possibly through complement mediation.
Methods: This was an experimental study during which malarial EMPs were isolated by differential centrifugation of malaria-positive plasma. This was followed by cell-based in vitro assays where malaria-positive EMPs were added to uninfected blood group "O" negative erythrocytes in the presence of complement and haemolysis checked for. Results and Conclusion. At a fixed volume of 50 μL complement, there were statistically significant (p < 0.01) increases in mean percentage haemolysis as the volume of EMPs increased. Similarly, at a fixed volume of 50 μL EMPs, there were statistically significant (p < 0.01) increases in mean percentage haemolysis with increasing volumes of complement. This was an indication that both complement and EMPs contribute significantly to uninfected erythrocyte haemolysis during malaria infection.
Rituximab hypersensitivity reactions are rare but are one of the main causes of rituximab elimination from antilymphoma immunochemotherapy treatments. While the clinical picture may be indistinguishable from other infusion-related reactions, hypersensitivity reactions (HSR) do not disappear and instead become more intense with subsequent administrations. Objective. To describe the use of the 12-step protocol for desensitization to intravenous rituximab in clinical practice and the complementary study of a possible IgE-mediated HSR in the context of B-cell lymphoma treatment. Methods. A 12-step rituximab desensitization protocol was performed prospectively within clinical practice in 10 patients with a history of severe infusion reactions or in patients who had a repeated reaction at subsequent doses despite taking more intense preventive measures. Skin prick tests were performed at the time of reaction and at a later time to eliminate false negatives due to possible drug interference. Results. Overall, with the desensitization protocol, 70% of patients were able to complete the scheduled immunochemotherapy. Two patients had to discontinue the therapy due to clinical persistence and the third due to lymphoma progression. Intradermal tests with 0.1% rituximab were positive in only 20% of cases, demonstrating a mechanism of hypersensitivity. Conclusions. The 12-step desensitization protocol is very effective and assumable within healthcare practice. There is a need to determine the mechanism underlying the infusion reaction in a large proportion of cases due to the risk of future drug exposure.
Background: The high prevalence of haemoglobin variants and glucose 6-phosphate dehydrogenase disorder (G6PDd) in sub-Saharan Africa means that substantial proportions of donor blood units carry these red cell abnormalities.
Aim: This study investigated the impact that inherited haemoglobin variants and/or G6PD status have on whole blood banked at 4-6°C for 35 days.
Method: This repeated-measure cohort study was undertaken on 103 donor blood units collected into blood bag containing CPDA-1 anticoagulant. On days 0, 7, 14, 21, and 35, full blood count, osmotic-induced haemolysis, and plasma K+ levels were estimated. Also, on day 0, G6PD status, haemoglobin variants, % foetal haemoglobin, and blood group of donor units were determined using methaemoglobin reductase, cellulose acetate electrophoresis, modified Bekte alkali denaturation assay, and slide haemagglutination test, respectively.
Result: Overall, although plasma K+ levels increased during storage, donor units from individuals ≥20 years, G6PD normal, Hb AC, or blood group B had comparatively higher percentage change in plasma K+ during storage. Osmotically induced haemolysis of donor units was significantly decreased in Hb AC (compared with Hb A or AS) donor units on days 7, 14, 21, and 35 (p < 0.0001 in each case). G6PDd donor units had comparatively reduced osmotic-induced lysis compared with G6PD normal units, reaching a statistical significance on day 35 (p = 0.043). Also, Hb AC units had comparatively nonstatistically higher plasma K+ at all time points (compared with Hb A or AS). Furthermore, whereas donor units from individuals ≥20 years showed significantly higher median free haemoglobin on day 21 (compared to donor <20 years), when donor units were stratified per Hb variants, only Hb AS units had median free haemoglobin below the 0.8% threshold after 35 days' storage.
Conclusion: Age of donor, blood group, Hb AC variant, and G6PD status may be important considerations in the storability of whole blood.