RESUMEN
Background: The number of antiretroviral drugs (ARVs) available to HIV/AIDS patients in Tanzania is increasing due to a number of intervention programs such as PEPFAR and the Clinton Foundation. These ARVs are imported from a number of countries. However; currently there are no reports on the quality of these medicines imported into Tanzania.The sale of substandard and counterfeit drugs has been well documented particularly in developing countries. The marketing of counterfeit and substandard antiretroviral drugs has also been widely reported in Africa. It is therefore important to closely monitor the quality of ARVs marketed in Tanzania to ensure that substandard or fake products are uncovered before great harm is done to public health.Objective: To assess the quality of ARVs marketed in Tanzania.Methodology: A total of five samples of two generic drugs (stavudine and indinavir) from different manufacturers were randomly collected from various retail pharmacies.Assessment of package inserts and labels was carried out using the Tanzania Food and Drugs Authority (TFDA) specifications. The capsules were analyzed for the content of the active components using validated in-house methodsResults: All samples of Indinavir and Stavudine investigated conformed to the packaging and labeling specifications. However; all Indinavir samples were found to contain excess amount of active ingredient (112.6- 118) compared to the official limit of 95 - 105. One sample of stavudine capsules failed the dissolution test; releasing only 56instead of the specified 80of the active ingredient. Conclusion: The results of this study emphasize the need for careful monitoring of the quality of drugs to ensure their safety and efficacy
Asunto(s)
Antirretrovirales/provisión & distribución , Indinavir , Estavudina , TanzaníaRESUMEN
A number of biological risk factors have been implicated for Alzheimer's disease (AD). The investigation of prevalence rates of AD in crosscultural populations has much potential in validating these factors. We previously assessed brain amyloid beta (A beta) protein deposition and other lesions associated with AD as possible markers for preclinical AD in elderly nondemented East Africans. In further analysis, we demonstrate that 17-19% of elderly East African subjects without clinical neurological disease exhibited neocortical A beta deposits and minimal neurofibrillary changes at necropsy that was qualitatively and quantitatively similar to that in an age-matched elderly control sample from Cleveland, OH. A beta deposits varied from numerous diffuse to highly localized neuritic plaques and were predominantly reactive for the longer A beta 42 species. In parallel studies, we evaluated another recently implicated factor in AD, the apolipoprotein E genotype. We found relatively high frequencies of the apolipoprotein E-epsilon 4 allele in elderly nondemented East Africans. The frequencies were comparable to those in other African populations but higher than in subjects from developed countries. Our limited study suggests that elderly East Africans acquire cerebral lesions found in AD subjects but the apolipoprotein E-epsilon 4 allele may not be a highly specific factor for the disease among East Africans.
Asunto(s)
Enfermedad de Alzheimer/epidemiología , Péptidos beta-Amiloides/análisis , Encéfalo/patología , África Oriental/epidemiología , Anciano , Enfermedad de Alzheimer/genética , Enfermedad de Alzheimer/patología , Apolipoproteínas E/genética , Cromosomas Humanos Par 19 , Femenino , Humanos , Masculino , Persona de Mediana Edad , Factores de RiesgoRESUMEN
Current advances have shown the apolipoprotein E (APOE)-epsilon 4 allele to be highly associated with late-onset familial and sporadic Alzheimer's disease (AD) in Western populations. The association of APOE allele frequencies and dementia remain unknown in populations from developing countries. We recently initiated a project to examine APOE frequencies in non-demented and demented elderly East Africans. Blood DNA collected from two hospital-based populations showed that the APOE allele frequencies in a group of non-demented 67 Tanzanians over the age of 65 years were found to be 14% for epsilon 2, 61% for epsilon 3 and 25% for epsilon 4. By comparison, the frequency of APOE-epsilon 4 in an age-matched demented group was also 25%. Assessment of APOE genotypes in the group of elderly Kenyan subjects from Nairobi also revealed high frequencies of the epsilon 4 allele with no clear difference in frequency between demented and non-demented subjects. Our preliminary observations suggest that elderly East Africans with no apparent clinical AD possess relatively high APOE-epsilon 4 allele frequencies compared to normal ageing subjects from Western countries including African-Americans. These results appear similar to those reported in a recent study in Nigerian Africans where a lack of correlation between APOE-epsilon 4 allele frequency and Alzheimer type of dementia was noted, and imply that APOE-epsilon 4 allele may not necessarily be a risk factor in some populations of Africa.
Asunto(s)
Anciano , Enfermedad de Alzheimer/genética , Apolipoproteínas E/genética , Frecuencia de los Genes , Polimorfismo Genético/genética , Anciano de 80 o más Años , Enfermedad de Alzheimer/sangre , Estudios de Casos y Controles , Genotipo , Humanos , Kenia , Escala del Estado Mental , Persona de Mediana Edad , TanzaníaRESUMEN
There is little knowledge of the existence of Alzheimer disease (AD) or Alzheimer type of dementia in indigenous populations of developing countries. In an effort to evaluate this, we assessed the deposition of amyloid beta (A beta) protein and other lesions associated with AD in brains of elderly East Africans. Brain tissues were examined from 32 subjects, aged 45 to 83 years with no apparent neurological disease, who came to autopsy at two medical Institutions in Nairobi and Dar es Salaam. An age-matched sample from subjects who had died from similar causes in Cleveland was assessed in parallel. Of the 20 samples from Nairobi, 3 (15%) brains exhibited neocortical A beta deposits that varied from numerous diffuse to highly localized compact or neuritic plaques, many of which were also thioflavin S positive. Two of the cases had profound A beta deposition in the prefrontal and temporal cortices and one of these also exhibited moderate to severe cerebral amyloid angiopathy. Similarly, 2 of the 12 samples from Dar es Salaam exhibited diffuse and compact A beta deposits that were also predominantly reactive for the longer A beta 42 species compared to A beta 40. We also noted that A beta plaques were variably immunoreactive for amyloid associated proteins, apolipoprotein E, serum amyloid P and complement C3. Tau protein reactive neurofibrillary tangles (NFT) were also evident in the hippocampus of 4 subjects. By comparison, 4 (20%) of the 20 samples from randomly selected autopsies performed in Cleveland showed A beta deposits within diffuse and compact parenchymal plaques and the vasculature. These observations suggest A beta deposition and some NFT in brains of non-demented East Africans are qualitatively and quantitatively similar to that in age-matched elderly controls from Cleveland. While our small scale study does not document similar prevalence rates of preclinical AD, it suggests that elderly East Africans are unlikely to escape AD as it is known in developed countries.