None.

Compared with FS for AVR, MS did not result in shorter hospital stay, faster recovery, or improved survival and was not cost-effective. The MS approach is not superior to FS for performing AVR.

Background: Despite the high burden of Sickle Cell Disease (SCD) in Nigeria, the underlying haemoglobinopathy profile remains uncertain. Although a number of urbanised areas have pilot hospital-based newborn screening programmes, the impact of the disease in rural areas is unknown.Methods: From January 2010 to December 2011 this community-based study screened children aged 0-60 months in 29 randomly selected local communities of three adjoining northern Nigerian states -Abuja, Kaduna and Katsina. For infants 0-6 months, blood spots were used and for infants 7-60 months EDTA blood samples were analysed using high performance liquid chromatography (HPLC). 31 selected sample with high Hb A2 (3.5-7.4%) were further analysed using molecular diagnosis to ascertain the presence of the Beta Thalassemia gene.Findings of 10,001 infants and children screened, 269 (2.69%) had a SCD diagnosis; 90% of which were HbSS (n=243), 5% HbSC (n=13), 3% with high A2 > 6% (possible S with existence β thalassaemia (n=9) and 1% HbSD (n=2). 74% of infants screened were HbAA (n=7,391). 2,341 (23%) were carriers; 96% HbAS (n=2,236), 2% HbAC (n=51), 1% HbAD (n=25) and 1% HbABeta-thal (n=22). HbSβo was confirmed by molecular analysis from the 31 selected samples. Conclusion:Early infant diagnosis of SCD in Northern reports an incidence of 1.72%, Homozygous SS accounts for over 90% of cases; double heterozygous SC is very low (4%). The presence of beta (β) thalassemia coinheritance is now confirmed using molecular analysis. Community and family counselling and educational material in Northern Nigeria must include the risk of beta thalasemia inheritance.

The pathogenesis of autoimmune diseases includes a combination of genetic factors and environmental exposures including infectious agents. Infectious triggers are commonly indicated as being involved in the induction of autoimmune disease, with Epstein-Barr virus (EBV) being implicated in several autoimmune disorders. EBV is appealing in the pathogenesis of autoimmune disease, due to its high prevalence worldwide, its persistency throughout life in the host's B lymphocytes, and its ability to alter the host's immune response and to inhibit apoptosis. However, the evidence in support of EBV in the pathogenesis varies among diseases. Autoimmune liver diseases (AiLDs), including autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), and primary sclerosing cholangitis (PSC), have a potential causative link with EBV. The data surrounding EBV and AiLD are scarce. The lack of evidence surrounding EBV in AiLD may also be reflective of the rarity of these conditions. EBV infection has also been linked to other autoimmune conditions, which are often found to be concomitant with AiLD. This paper will critically examine the literature surrounding the link between EBV infection and AiLD development. The current evidence is far from being conclusive of the theory of a link between EBV and AiLD.