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Objectives To provide lay information about genetics and sickle cell disease (SCD) and to identify and address ethical issues concerning the Sickle Cell Disease Genomics of Africa Network covering autonomy and research decision-making, risk of SCD complications and organ damage, returning of genomic findings, biorepository, data sharing, and healthcare provision for patients with SCD.Design Focus groups using qualitative methods.Setting Six cities in Ghana, Nigeria and Tanzania within communities and secondary care.Participants Patients, parents/caregivers, healthcare professionals, community leaders and government healthcare representatives.Results Results from 112 participants revealed similar sensitivities and aspirations around genomic research, an inclination towards autonomous decision-making for research, concerns about biobanking, anonymity in data sharing, and a preference for receiving individual genomic results. Furthermore, inadequate healthcare for patients with SCD was emphasised.Conclusions Our findings revealed the eagerness of patients and parents/caregivers to participate in genomics research in Africa, with advice from community leaders and reassurance from health professionals and policy-makers, despite their apprehensions regarding healthcare systems.

Introduction Pre‐treatment HIV drug resistance (PDR) is an increasing problem in sub‐Saharan Africa. Children are an especially vulnerable population to develop PDR given that paediatric second‐line treatment options are limited. Although monitoring of PDR is important, data on the paediatric prevalence in sub‐Saharan Africa and its consequences for treatment outcomes are scarce. We designed a prospective paediatric cohort study to document the prevalence of PDR and its effect on subsequent treatment failure in Nigeria, the country with the second highest number of HIV‐infected children in the world. Methods HIV‐1‐infected children ≤12 years, who had not been exposed to drugs for the prevention of mother‐to‐child transmission (PMTCT), were enrolled between 2012 and 2013, and followed up for 24 months in Lagos, Nigeria. Pre‐antiretroviral treatment (ART) population‐based pol genotypic testing and six‐monthly viral load (VL) testing were performed. Logistic regression analysis was used to assess the effect of PDR (World Health Organization (WHO) list for transmitted drug resistance) on subsequent treatment failure (two consecutive VL measurements >1000 cps/ml or death). Results Of the total 82 PMTCT‐naïve children, 13 (15.9%) had PDR. All 13 children harboured non‐nucleoside reverse transcriptase inhibitor (NNRTI) mutations, of whom seven also had nucleoside reverse transcriptase inhibitor resistance. After 24 months, 33% had experienced treatment failure. Treatment failure was associated with PDR and a higher log VL before treatment initiation (adjusted odds ratio (aOR) 7.53 (95%CI 1.61–35.15) and 2.85 (95%CI 1.04–7.78), respectively). Discussion PDR was present in one out of six Nigerian children. These high numbers corroborate with recent findings in other African countries. The presence of PDR was relevant as it was the strongest predictor of first‐line treatment failure. Conclusions Our findings stress the importance of implementing fully active regimens in children living with HIV. This includes the implementation of protease inhibitor (PI)‐based first‐line ART, as is recommended by the WHO for all HIV‐infected children

Background. Despite the increased incidence of Kaposi sarcoma (KS) resulting from the Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome (HIV/AIDS) pandemic, there is still significant underreporting of KS in this environment. Objectives. This study was aimed at determining the incidence and clinicopathologic patterns of KS among HIV infected patients in Lagos University Teaching Hospital (LUTH), Nigeria, over a 14-year period: January 2000 to December 2013. Methodology. The materials for this study included patients’ hospital clinical files, duplicate copies of histopathologic reports, and tissue blocks and corresponding archival slides in the Anatomic and Molecular Pathology Department and the HIV/AIDS unit of the Department of Haematology. Results. Within the study period, 182 cases of KS were diagnosed, accounting for 1.2% of all patients managed for HIV/AIDS and 2.99% of solid malignant tumours. The male-to-female ratio and modal age group were 1 : 1.3 and 5th decade, respectively. Most cases (90%) had purely mucocutaneous involvement with the lower limb being the commonest site (65.8%). The majority of lesions were plaques (65.8%). Vascular formation was the predominant histologic type seen (43.5%). Conclusion. KS in Lagos followed the same epidemiologic trend as other centers in Nigeria, with an increasing incidence in this era of HIV/AIDS.

Background: Sickle cell patients produce more reactive oxygen species (ROS) than healthy individuals, leading to increased cell membrane damage. Theoretically, reducing ROS formation would preserve red cell membranes of sickle cell patients. Vitamin C is a powerful anti-oxidant capable of inhibiting ROS formation in a variety of situations, by functioning as an electron donor to reduce molecular oxygen. This study aimed to determine whether Vitamin C reduced ROS formation in sickle red cells. Methods: 27 homozygous (HbSS) patients were recruited from the outpatient clinics of Lagos University Teaching Hospital, Nigeria, and annex at the Sickle Cell Foundation, Lagos, Nigeria. Demographic information and EDTA patient blood samples were collected. The test group were red cells preincubated in 80uM and 100uM Vitamin C concentrations before stressing with tertbutylhydroperoxide. These were compared to stressed matched controls preincubated in phosphate buffered saline. Cell staining was done with CellRox Orange followed by flow cytometry to quantify ROS. Results: ROS count for Vitamin C pre-treated red cells was significantly lower than matched controls (p Conclusion: Vitamin C reduced ROS formation in HbSS cells. Future studies should focus on a role for Vitamin C as a safe, cheap addition to maintenance therapy of sickle cell patients.

Background: Cobalamin deficiency and peripheral neuropathy (PN) are commonly seen in HIV-infected adults. The level of urine methylmalonic acid (UMMA), a reliable indicator of tissue cobalamin status, was determined in HIV infected subjects with and without PN to establish this association., Methods: One hundred and ninety-eight (198) consenting HIV infected subjects with and without PN were recruited for the study. UMMA level was determined by Cation Exchange High Performance Liquid Chromatography (HPLC) with Ultraviolet detector in 165 subjects. Simple proportions of patients with raised UMMA (defined as value> 3.4 mg in 24hr) were determined for each arm., Results: Among the 198 subjects studied, 146 had PN and 52 had no PN. From the 165 subjects whose UMMA was studied, raised UMMA was found in 76.6% (36 of 47) of subjects with no PN as compared with 53.4% (63 of 118) of those with PN (p=0.018)., Conclusion: Cobalamin deficiency (measured by UMMA level) even though common in HIV infected subjects, may not be the cause of peripheral neuropathy in these subjects.

OBJECTIVES: To determine the rate and pattern of disclosure and non disclosure of HIV serostatus among people living with HIV and the psychosocial impact of disclosure. METHODS: Participants were drawn from the adult HIV clinic at the Lagos University Teaching Hospital, Lagos, Nigeria. An interviewer-administered questionnaire was used to collect data from consenting participants that included socio-demographic information, pattern and reason for non-disclosure and the possible consequences of disclosure of HIV serostatus to their sexual partners. RESULTS: Four hundred and ninety nine respondents with a mean age of 37.3 ± 9.6 years were recruited into the study. There were 157 males and 342 females. Majority of the participants were married (62%) and belonged to the low socio-economic class. Overall 61.5% (307 of 499) had disclosed their status to sex partner(s). Gender, social class and length of year of diagnosis were not associated with disclosure but number of sexual partners was strongly associated with non disclosure. P=0.0063. The most common reason for non-disclosure was fear of rejection (65%). Majority (96.7%) of those who disclosed their status had no regret and majority (81.1%) of those who had not disclosed had protected sex. After counseling, only18.8% (36 of 192) of those that had not disclosed thought that the counseling had helped them overcome the fear of disclosure and were willing to disclose. CONCLUSION: Many people would disclose their HIV serostatus to sex partner(s). Protected sex (through the use of condom) is widely accepted in our setting.

Introduction: In various studies globally, the prevalence of anemia in persons with HIV infection range from 10 to 20% at initial presentation, and anemia is diagnosed in 70 to 80% of these patients over the course of HIV disease. The etiology of anemia in this group of patients has not been fully established, thus a need to evaluate the role of plasma folate as a possible etiological factor., Objective: This study was set to determine plasma folate levels in newly diagnosed, treatment naïve, HIV-positive patients, and relate this to other hematological changes., Materials and Methods: A total of 200 participants were recruited for this study, of which 100 were HIV positive, treatment naive patients who were recruited at the point of registration and 100 were HIV-negative subjects (controls). 5 ml of venous blood was collected and plasma extracted for folic acid estimation by HPLC. A full blood count, CD4 and Viral load were estimated., Results: Mean ages for control and study group were 38 ± 2.3 and 32 ± 1.7 years, respectively. Mean plasma folate concentration among the study group (5.04 μg/l) was significantly lower than that for the control group (15.89 μg/l; P = 0.0002). Prevalence of anemia among the study group was 72% (144 of 200), with a mean hemoglobin (Hb) concentration of 9.5 g/dl compared with mean Hb of 13.0 g/dl among the control group (P = 0.002). Plasma folate correlated positively with CD4 cell count (r = 0.304, P<0.05) and inversely with the viral load (r = -0.566; P<0.05)., Conclusion: Plasma folate level is a predictor of anemia in early HIV infections.