A preliminary study of the frequency of focal neurological deficits in HIV/AIDS patients seropositive for Toxoplasma gondii IgG in Lagos, Nigeria

Background: Cerebral toxoplasmosis is a common cause of focal neurologic deficits in HIV/AIDS. Financial constraints and access to neuroradiological facilities limit definitive  diagnosis  and  first-line  treatments  are  largely expensive and cumbersome.ObjectiveThis study examined the frequency of focal neurological signs in HIV/AIDS patients with positive Toxoplasma gondii IgG antibodies (and thus at high risk of reactivation), and the relationship to CD4 count.Methods: Using a case-control design, T. gondii IgG serology was determined in 83 HIV/AIDS patients on HAART and 42 HIV seronegative controls. Neurological evaluation and CD4 count (mm3) was conducted in all subjects.Results: A total of 71 (85.5%) HIV/AIDS patients were seropositive for T. gondii IgG. The IgG seroprevalence was 84.8% for cases with CD4 count <200 and 86.0% with CD4>200 (P=0.46). Of the cases with positive Toxoplasma antibodies, the frequency of neurological lateralizing signs was higher in those with CD4 count <200 (32.6%) compared to persons with CD4 count >200 (7.1%) (X2 = 4.90, Fisher exact P < 0.01). The mean CD4 count of cases with lateralizing signs was 113.7±113.9 in contrast to 254.0±218.9 in those without lateralizing signs (P < 0.01).Conclusion: In our study, a higher frequency of focal neurological signs was found in the T. gondii seropositive HIV/AIDS patients with a higher degree of immune compromise (CD4 count <200). We suggest the adoption of routine prophylactic anti-toxoplasma therapy in this subgroup given that cerebral toxoplasmosis is a leading cause of intracranial space occupying lesions in HIV/AIDS.Keyword: Cerebral toxoplasmosis, IgG antibodies, focal neurological signs, HIV/AIDS, Nigeri

Seroprevalence of Hepatitis C infection in HIV patients using a rapid one-step test strip kit

Background: Hepatitis C virus (HCV) and HIV are transmitted via similar routes making co-infection with these viruses a common event. In addition, HIV infection and related immunosupression in patients with hepatitis C may be associated with more rapid progression of liver disease to cirrhosis, end-stage liver disease and death.Objective: The study is to determine the seroprevalence of HIV/HCV co-infection rate.Methods: A cross -sectional study was carried out from January to March 2010 at the HIV clinic of the Lagos State University Teaching Hospital. About 5 mls of blood sample was collected from each consenting participant. Sera were subjected to HCV rapid kit as recommended by the manufacturer (Dia Spot HCV one step test strip). The descriptive data was given as means ± standard deviation (SD). The chi-squared test was used for analytical assessment. The differences were considered statistically significant when P value obtained < 0.05.Results: The overall seroprevalence rate of HIV/HCV co- infection was 3.3%.Only 6 of 194 female HIV subjects screened tested positive for HCV (3.1%), while 3 of 73 male subjects tested positive for HCV (4.1%) (P value 0.001). None of the 9 co-infected HIV/HCV participants (both male and female) had CD4 count of 350 and above, 3 had a count of 1-100 cells/ ìl., 4 had 100-200, while 2 had 201-350 .Conclusion: There  is  the  need  to  include  hepatitis  C  screening routinely in all HIV-infected patients undergoing  pre-HAART evaluation in HIV clinics in order to lower liver-related morbidity and mortality associated with them.Keywords: Seroprevalence, HIV/HCV co-infection, one step rapid ki

Serum ferritin levels in adults with sickle cell disease in Lagos, Nigeria

Background: Serum ferritin is considered to be one of the most important tools in the measurement of iron balance in steady-state sickle cell disease. Increased gastrointestinal absorption of iron has been reported in sickle cell disease because of the associated chronic hemolysis, and it is also thought that repeated red cell transfusion consequent to chronic hemolysis and anemia causes excessive iron levels. The aim of this study was to determine overall and gender-specific mean ferritin levels in patients with steady-state sickle cell disease in order to establish the prevalence of iron deficiency and overload. Methods: This was a cross-sectional study in homozygous patients with sickle cell disease attending the sickle cell clinic at Lagos State University Teaching Hospital, Ikeja. A 5 mL blood sample was collected in plain bottles from consenting participants during steady-state periods. The serum was separated and analyzed for ferritin by enzyme-linked immunosorbent assay. Another 5 mL sample was collected for a full blood count, done on the same day of collection, to determine red blood cell indices, ie, mean cell volume, mean cell hemoglobin concentration, and mean corpuscular hemoglobin concentration. The Pearson Chi-square test was used for statistical analysis. The differences were considered to be statistically significant when P was <0.05. Results: In total, 103 patients were recruited for this study and comprised 58 women (56.40%) and 45 men (43.70%). The overall mean ferritin concentration was 93.72 ± 92.24 ng/mL. The mean ferritin concentration in the women was 92.00 ± 88.07 ng/mL and in men was 96.41 ± 99.80 ng/mL. Only eight (7.76%) of the 103 patients had a serum ferritin level 300 ng/mL. Ninety-three subjects (90.29%) had serum ferritin within the normal reference range of 15–300 ng/mL. Conclusion: In this study, 90% of subjects with sickle cell disease had normal iron stores; serum ferritin was higher in men than in women, and iron deficiency was more common than overload in the disease

AMPA receptor GluA2 subunit defects are a cause of neurodevelopmental disorders

AMPA receptors (AMPARs) are tetrameric ligand-gated channels made up of combinations of GluA1-4 subunits encoded by GRIA1-4 genes. GluA2 has an especially important role because, following post-transcriptional editing at the Q607 site, it renders heteromultimeric AMPARs Ca2+-impermeable, with a linear relationship between current and trans-membrane voltage. Here, we report heterozygous de novo GRIA2 mutations in 28 unrelated patients with intellectual disability (ID) and neurodevelopmental abnormalities including autism spectrum disorder (ASD), Rett syndrome-like features, and seizures or developmental epileptic encephalopathy (DEE). In functional expression studies, mutations lead to a decrease in agonist-evoked current mediated by mutant subunits compared to wild-type channels. When GluA2 subunits are co-expressed with GluA1, most GRIA2 mutations cause a decreased current amplitude and some also affect voltage rectification. Our results show that de-novo variants in GRIA2 can cause neurodevelopmental disorders, complementing evidence that other genetic causes of ID, ASD and DEE also disrupt glutamatergic synaptic transmission. © 2019, The Author(s)

AMPA receptor GluA2 subunit defects are a cause of neurodevelopmental disorders

AMPA receptors (AMPARs) are tetrameric ligand-gated channels made up of combinations of GluA1-4 subunits encoded by GRIA1-4 genes. GluA2 has an especially important role because, following post-transcriptional editing at the Q607 site, it renders heteromultimeric AMPARs Ca2+-impermeable, with a linear relationship between current and trans-membrane voltage. Here, we report heterozygous de novo GRIA2 mutations in 28 unrelated patients with intellectual disability (ID) and neurodevelopmental abnormalities including autism spectrum disorder (ASD), Rett syndrome-like features, and seizures or developmental epileptic encephalopathy (DEE). In functional expression studies, mutations lead to a decrease in agonist-evoked current mediated by mutant subunits compared to wild-type channels. When GluA2 subunits are co-expressed with GluA1, most GRIA2 mutations cause a decreased current amplitude and some also affect voltage rectification. Our results show that de-novo variants in GRIA2 can cause neurodevelopmental disorders, complementing evidence that other genetic causes of ID, ASD and DEE also disrupt glutamatergic synaptic transmission. © 2019, The Author(s)