No abstract

Iodine is a key component of the thyroid hormones which are crucial for brain development. Adequate intake of iodine in pregnancy is important as in utero deficiency may have lifelong consequences for the offspring. Data on the iodine status of UK pregnant women are sparse, and there are no such data for pregnant women in the South East of the UK. A total of 100 pregnant women were recruited to a cross-sectional study carried out at the Royal Surrey County Hospital, Guildford, at their first-trimester visit for an ultrasound scan. The participants provided a spot-urine sample (for the measurement of urinary iodine concentration (UIC) and creatinine concentration) and 24 h iodine excretion was estimated from the urinary iodine:creatinine ratio. Women completed a general questionnaire and a FFQ. The median UIC (85·3 mg/l) indicated that the group was iodine deficient by World Health Organisation criteria. The median values of the iodine:creatinine ratio (122·9 mg/g) and of the estimated 24 h iodine excretion (151·2 mg/d) were also suggestive of iodine deficiency. UIC was significantly higher in women taking an iodine-containing prenatal supplement (n 42) than in those not taking such a supplement (P,0·001). In the adjusted analyses, milk intake, maternal age and iodine-containing prenatal supplement use were positively associated with the estimated 24 h urinary iodine excretion. Our finding of iodine deficiency in these women gives cause for concern. We suggest that women of childbearing age and pregnant women should be given advice on how to improve their iodine status through dietary means. A national survey of iodine status in UK pregnant women is required.

Background We have investigated the association between serum copper, zinc and selenium concentrations, dietary intake, and demographic characteristics, including individual coronary risk factors, in healthy subjects.

A neurological syndrome characterized by levodopa unresponsive bradykinesia, retropulsion with falls backwards, dysarthria, gait disturbance, dystonia, and emotional lability was identified in 13 male opiate addicts following the prolonged intravenous use of ephedrone (methcathinone), a central nervous stimulant prepared from pseudoephedrine, potassium permanganate, and vinegar. The natural history, response to treatment, and clinical features has been studied, and MR and dopamine transporter SPECT brain imaging were carried out. Pubic hair was sampled for manganese. The clinical and radiological picture closely resembled previous reports of chronic manganese poisoning and increased mean manganese level in pubic hair observed for at least 1 year after cessation of ephedrone. Odor identification was intact. Cognitive assessment showed a mild executive dysfunction and a mild depression. DaTSCANs were all normal. The neurological syndrome bears some similarities to PSP but differs from Parkinson's disease. Delayed neurological progression despite discontinuation of ephedrone occurred in one-third of cases. Ephedrone poisoning should be considered as a possible cause of secondary Parkinsonism in young adults, particularly from Eastern Europe.

Tellurium (Te) demonstrates properties similar to those of elements known to be toxic to humans, and has applications in industrial processes, which are rapidly growing in importance and scale. It is relevant, therefore, to consider the tellurium physiology, toxicity, and methods for monitoring the element in biological and environmental specimens. Animal studies suggest that up to 25% of orally administered tellurium is absorbed in the gut. There is a biphasic elimination from the circulation with loss of about 50% within a short period, t1/2 = 0.81 d, and slower elimination of the residual Te, t1/2 = 12.9 d. Following a single ip, injection the largest proportion is in the kidney and bone, but with repeated oral administration, Te is found in the heart > > kidney, spleen, bone, and lung. Formation of dimethyl telluride is a characteristic feature of exposure, and gives a pungent garlic-like odor to breath, excreta, and the viscera. The main target sites for Te toxicity are the kidney, nervous system, skin, and the fetus (hydrocephalus). Te can be reliable measured in different specimens by several analytical techniques. Recent work has employed hydride generation atomic absorption spectrometry. Topics for further investigation are proposed.