BackgroundMicronutrient deficiencies occur commonly in people infected with the human immunodeficiency virus. Since aflatoxin exposure also results in reduced levels of several micronutrients, HIV and aflatoxin may work synergistically to increase micronutrient deficiencies. However, there has been no report on the association between aflatoxin exposure and micronutrient deficiencies in HIV-infected people. We measured aflatoxin B1 albumin (AF-ALB) adduct levels and vitamins A and E concentrations in the plasma of HIV-positive and HIV-negative Ghanaians and examined the association of vitamins A and E with HIV status, aflatoxin levels and hepatitis B virus (HBV) infection.MethodsA cross-sectional study was conducted in which participants completed a demographic survey and gave a 20 mL blood sample for analysis of AF-ALB levels, vitamins A and E concentrations, CD4 counts, HIV viral load and HBV infection.ResultsHIV-infected participants had significantly higher AF-ALB levels (median for HIV-positive and HIV-negative participants was 0.93 and 0.80 pmol/mg albumin, respectively; p <0.01) and significantly lower levels of vitamin A (-16.94 μg/dL; p <0.0001) and vitamin E (-0.22 mg/dL; p <0.001). For the total study group, higher AF-ALB was associated with significantly lower vitamin A (-4.83 μg/dL for every 0.1 pmol/mg increase in AF-ALB). HBV-infected people had significantly lower vitamin A (-5.66 μg/dL; p = 0.01). Vitamins A and E levels were inversely associated with HIV viral load (p = 0.02 for each), and low vitamin E was associated with lower CD4 counts (p = 0.004).ConclusionsOur finding of the significant decrease in vitamin A associated with AF-ALB suggests that aflatoxin exposure significantly compromises the micronutrient status of people who are already facing overwhelming health problems, including HIV infection.

Background Although aflatoxin exposure has been shown to be associated with micronutrient deficiency in animals, there are few investigations on the effects of aflatoxin exposure on micronutrient metabolism in humans. Objective To examine the relationship between aflatoxin B1 (AFB1) albumin adducts (AF-ALB) in plasma and the aflatoxin M1 (AFM1) metabolite in urine and plasma concentrations of retinol (vitamin A) and α-tocopherol (vitamin E) in Ghanaians. Methods A cross-sectional study of 147 adult participants was conducted. Blood and urine samples were tested for aflatoxin and vitamins A and E levels. Results Multivariable analysis showed that participants with high AF-ALB (≥ 0.80 pmol/mg albumin) had increased odds of having vitamin A deficiency compared to those with lower AF-ALB [Odds Ratio (OR) = 2.61; CI = 1.03 – 6.58; p=0.04]. Participants with high AF-ALB also showed increased odds of having vitamin E deficiency but this was not statistically significant (OR = 2.4; CI = 0.96–6.05; p = 0.06). Conversely, those with higher AFM1 values had a statistically nonsignificant reduced odds of having vitamin A deficiency (OR = 0.31; CI = 1.15–0.09; p=0.05) and statistically significant reduced odds of having vitamin E deficiency (OR = 0.31; CI = 0.10 – 0.97; p = 0.04). Participants with high AF-ALB or high AFM1 (≥ 437.95 pg/dL creatinine) were almost 6 times more likely to be hepatitis B virus surface antigen (HBsAg)- positive (OR = 5.88; CI = 1.71–20.14; p = 0.005) and (OR = 5.84; CI = 1.15–29.54; p = 0.03) respectively. Conclusions These data indicate that aflatoxin may modify plasma micronutrient status. Thus, preventing aflatoxin exposure may greatly reduce vitamins A and E deficiencies.

The natural history of omphalocele and gastroschisis co-varies with race. Black infants with gastroschisis have worse survival outcomes while those with omphalocele have better chances of survival than their White or Hispanic counterparts.

Although low plasma vitamin A concentrations are associated with increased incidence or severity of infections such as respiratory tract infection and measles in children, there is a paucity of data on the effect of vitamin A deficiency on the distribution of, and cytokine production by, the different cellular immune subsets in humans. We conducted a cross-sectional study in a district in Ghana to characterize cellular subsets and functional capacity of peripheral blood mononuclear cells from vitamin A deficient and vitamin A sufficient (normal) individuals, and evaluated the relationships between vitamin A concentration in plasma and cellular immune status. We measured the percentages of selected cellular phenotypes and intracellular cytokine expression and describe the differential cellular subset distributions and alterations in cytokine expression in participants with normal and deficient vitamin A concentrations. The major change observed in the constitution of cellular subsets was a decrease in TNF-α expressing CD3-CD56+ NK cells in those with vitamin A deficiency compared with normal individuals. CD4+ T cell proliferation and production of IFN-γ and IL-4 were not statistically different between the two groups. These results support previous studies that demonstrated decreased NK cell activity in vitamin A deficient animals. The decrease in TNF-α expressing NK cells observed in vitamin A deficient individuals in this study could help to explain the decreased resistance to infections observed in those with vitamin A deficiency.

The stigma of SCHIP may be less than that often associated with Medicaid; however, this investigation should be considered with others that have identified barriers for provider's participation. This study indicates that provider satisfaction is related to their perceptions of SCHIP policies and families, though it does not tell us what factors might contribute to this perception, such as, previous experience with public insurance (Medicaid) and publicly insured patients. Increasing reimbursement rates may not address perceptions that affect provider views of publicly-supported health plans and the participating families.