Iodine toxicity

Iodoquinol should be taken with meals to limit gastrointestinal toxicity. It should be used with caution in patients with optic neuropathy, renal or thyroid disease, or nonamebic hepatic disease. The drug should be discontinued if it produces persistent diarrhea or signs of iodine toxicity (dermatitis, urticaria, pruritus, fever). It is contraindicated in patients with intolerance to iodine. 

Kanakiriya S, De Chazal I, Nath KA, Haugen EN, Albright RC, Juncos LA. Iodine toxicity treated with hemodialysis and continuous venovenous hemodiafiltration. Am J Kidney Dis 2003 41 702-8. 

Thyrotoxicosis related to iodine toxicity in a child with burns occurred after alternate-day povidone-iodine washes (16). 

Glick PL, Guglielmo BJ, Tranbaugh RF, Turley K. Iodine toxicity in a patient treated by continuous povidone-iodine mediastinal irrigation. Ann Thorac Surg 1985 39(5) 478-80. 

Baker DH (2004) Iodine toxicity and its amelioration. Experimental Biology and Medicine (Maywood, N.J.) 229 473 78. 

Iodine has not been shown to be essential to plants, and stimulatory effects on plant growth at low levels have not been reported. Mengel and Kirkby (1978) reported that a stimulatory effect of iodine was observed at 100 pg I L in nutrient solutions, whereas toxic effects in plants occurred at an iodine concentration of 500-1000 pg L b As the toxic concentration is higher than the soluble iodine content of soils, iodine toxicity is rare in plants under natural field conditions. However, a physiological disease of rice plants named Akagare has been reported (Yuita 1979), induced by excessive absorption of iodine from soil enriched with easily soluble iodine when land was converted for submerged paddy fields (Kabata-Pendias and Pendias 1992). 

Species differ widely in their susceptibility to iodine toxicity, but all species can tolerate iodine levels far in excess of their normative requirement. The main problem of iodine intoxication in farm animals is not poisoning but the iodine overload of humans through milk, dairy products and eggs (Anke et al. 1994, Burkhard et al. 2002). 

Iodide requirements in extreme preterm infants are particularly difficult to assess as they have very limited thyroidal iodine reserves (Etling, 1977 Costa et ai, 1986 van den Hove et at, 1999), and they are also susceptible to iodine toxicity and hypothyroidism if too much iodide is given (L AUemand et ai, 1987). There are no current pubhshed studies indicating the iodine requirements of extreme preterm infants, sick infants, or infants in the early neonatal period. Iodide requirements of these infants should therefore be assessed through carefully-controlled studies that avoid toxicity, but also test the efficacy of iodide supplementation in optimizing thyroid function. 

Is iodine insufficiency of current parenteral nutrition regimens potentially compromising the brain development of extreme and preterm infants when it is their only, or predominant, source of nutrition The determination of the iodide requirements of extreme preterm infants, and the safe levels of iodide supplementation necessary to achieve optimal blood levels, requires carefully piloted and designed clinical trials so that iodine toxicity is avoided. We have started this program of work (Ibrahim et al., 2003) and extended our knowledge through three further pilot studies in infants <30 weeks gestation. 

Blood iodine levels were elevated at subtoxic doses of iodine, indicating adequate exposure. Iodine toxicity manifested itself as reduced performance. Since iron supplementation prevented it, this toxicity may have resulted from an apparent interference of iodate or iodine, respectively, with iron uptake or utiftzation. NOELs for pigs were observed at 400 parts per million (ppm) calcium iodate added to hog mash calves were more susceptible with a NOEL of only 25 ppm. The toxic signs were attributed either to iron deficiency or to general iodine toxicity. 

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