BackgroundThe insecticide dichlorodiphenyltrichloroethane (DDT) has been used for malaria vector control in the northern and eastern parts of the Vhembe District of Limpopo Province, South Africa, since 1945. Bioaccumulation of DDT raises concern because it reportedly affects thyroid function.ObjectiveOur objective was to investigate the association between DDT uptake (as reflected in plasma concentrations) and thyroid homeostasis while considering related factors.MethodsWe compared dietary intake, serum retinol-binding protein (RBP), transthyretin (TTR) and albumin concentrations, and liver and thyroid function between cases with evidence of a body burden of DDT in the circulation (concentration of any DDT isomer ≥ 0.02 μg/g lipid; n = 278) and controls (concentration of all DDT isomers < 0.02 μg/g lipid; n = 40) in a cross-sectional study. Further analyses were performed to assess the relevance of changes in RBP status associated with DDT uptake.ResultsRBP concentrations below the reference range were more prevalent in cases (54% vs. 10% in controls; χ2 = 27.4; p < 0.001), which could not be explained by nutrient intake. We observed significantly lower thyroid hormone concentrations among cases (p ≤ 0.01). We also observed a significant linear trend for serum concentrations of free thyroxine and free triiodothyronine (p < 0.001) and a significant quadratic trend for serum thyroid-stimulating hormone (p = 0.025) and TTR (p < 0.001) across the control group and case groups with normal and relatively low RBP concentrations. Relatively low RBP concentrations were associated with significantly higher DDT and 1,1-dichloro-2,2-bis(p-chlorophenyl) ethylene (DDE) isomer concentrations and with a higher DDE/DDT ratio (p ≤ 0.01), which signifies long-term exposure. Inadequate intake of vitamin A and zinc were observed in 84% and 58%, respectively, of the total study population.ConclusionRBP concentrations appear to decrease in the presence of long-term DDT uptake, which may have deleterious effects on thyroid function and vitamin A nutritional status. This is of major concern in a population with poor vitamin A and zinc intake.

Folic acid or folate is a water-soluble vitamin from the B group and is involved in one-carbon metabolism. Folate deficiency or inadequate folate intake is associated with anaemia, neural tube defects and neuropsychiatric disorders. Furthermore, insufficient dietary intake of folate results in elevated plasma homocysteine, which is a risk factor for cardiovascular disease.As with most other vitamins, the assessment of biological stores and intake is based on the concentration in body fluids. Studies of folate status have traditionally used serum/plasma or red blood cell folate. Both assays are widely available in laboratories. Red cell folate, favoured by many clinicians, is the more labour intensive test and therefore more costly than serum folate. Turnaround time is also longer because of the need to determine the haematocrit using a haematology cell counter followed by preparation of a haemolysate from the whole blood prior to running the assay. Factors related to the pre-treatment procedure, haematocrit and oxygenation of haemoglobin all contribute to analytical variability of red cell folate, [1] making coefficients of variation for red cell folate assays close to twice those of serum folate assays. The cost of red cell folate is between 40% and 55% higher than that of serum folate in the private sector and the South African National Health Laboratory Service (NHLS) respectively. We recently carried out a retrospective analysis of red cell and serum folate requests in the Tshwane metropolitan(Pretoria) area. Of the almost 21 000 tests requested over an eight-year period, 2% demonstrated folate deficiency. This relatively low prevalence most likely reflects the success of the mandatory food fortification programme implemented in South

CASEA 21-year-old woman presented with a 5-day history of loss of appetite, malaise, nausea, and vomiting. On examination, she appeared acutely ill, with jaundice and right-sided hypochondrial tenderness. The stigmata of chronic liver disease were absent, and the results of her neurologic examination were typical. She had previously been well except for bouts of somnolence with occasional emesis during the previous year. There was no history of recent travel, alcohol or illicit drug use, or liver disease in her family. Viral hepatitis was considered the most likely diagnosis, but the patient's clinical deterioration necessitated hospital admission a day later. The results of serology tests for acute infection with hepatitis A virus, hepatitis B virus, or Epstein-Barr virus were negative, and the complete blood count revealed a macrocytic anemia. Liver function tests revealed the following: total bilirubin, 136 mol/L [upper reference limit (URL),