Dependent on the species, feedstuffs and plants differ considerably in their iodine content. Among the I-poorest feedstuffs there are grain concentrates, extracted soybean and rapeseed oil meals, mixed feed (without I-containing mineral mixture) and grasses. The I content of the plants decreases with proceeding growth. The I intake of ruminants via vegetable feed and drinking water is affected by the distance of the site from the seaside and the geological origin of the soil material. Ruminants get considerably less iodine via feedstuffs and water in the southern territory of the GDR than in the central and northern areas. Therefore, mineral mixtures for cattle and sheep are supplemented with 18 mg KIO3 per kg mixture in the southern districts. The I analysis of 205 charges of mineral mixtures revealed only a mean I content of 7 (3.8-11.3) mg per kg mixture.

Animal Feed↗

PubMedDate not supplied

Severe hepatotoxicity during valproate therapy: an update and report of eight new fatalities.

Since our last report on valproate (VPA)-related hepatotoxicity in 1988, 8 other children have died of VPA-associated liver failure in Germany and Switzerland. We compared the clinical course of these children with that of 6 children with a reversible outcome of severe hepatotoxicity related to VPA. Thirty-five percent of patients with fatal liver failure were normally developed, 23.5% were receiving VPA monotherapy, and 35.3% were aged < or = 2 years. The initial clinical symptoms of VPA-related hepatotoxicity were nausea, vomiting, apathy or coma, and increasing seizures in more than 50% of patients, in combination with febrile infections at onset of symptoms. As compared with the series of German patients reported in 1988, one third of the fatalities occurred after the first 6 months of therapy as compared with 6% in the 1988 series. Clinical symptoms and laboratory findings were the same in patients with reversible and with fatal outcome. Early or immediate withdrawal of VPA after the first signs of VPA-associated hepatotoxicity may be responsible for the increased number of children who recovered after VPA-related severe liver failure. The pathogenesis of liver failure during VPA treatment remains unknown; metabolic defects and cofactors such as polypharmacy or infections have become increasingly likely to contribute by depleting intracellular CoA. Worldwide, 132 patients have died of VPA-associated liver failure and/or pancreatitis. Because a group at risk for fatalities with VPA cannot be defined precisely, patients treated with VPA and their families must be made well aware of the clinical symptoms of hepatotoxicity such as apathy, vomiting, or increased seizure frequency, especially in the presence of febrile infections. Laboratory tests and clinical controls during the first 6 months of therapy should not be neglected.

Adult↗

PubMedDate not supplied

[The significance of health risks caused by outdoor pollution, demonstrated by cross-sectional studies of pseudocroup in Baden-Württemberg].

In the FRG the question of health effects by ambient (outdoor) air pollution is often considered with respect to respiratory diseases in children, especially group syndrome. Therefore, the results of a cross-sectional study in Baden-Württemberg are discussed as an example for the role of "outdoor pollution" at presently observed concentrations. In the study that was performed in Stuttgart, Tübingen/Reutlingen and Freudenstadt, the parents of 8.420 children at the age of 6 years participated (response rate 93%). Their reports on diseases were additionally validated and completed by the paediatricians concerned. The "crude" prevalence for the age group 0-6 years is about 9% each for croup syndrome and obstructive bronchitis. This is strongly influenced by sex, disposition in the family, education and nationality of the parents. In contrast, influences of ambient air pollution are less clear or missing. Pollution measurements on a sufficient spatial scale were only available for Stuttgart, where logistic regression showed after adjustment for the relevant confounders only that croup syndrome was slightly increased in streets with high traffic load. For childhood asthma (prevalence 1.5%) a correlation with traffic-dependent pollutants (NO2, NO, CO) and traffic load is found. These results are compared with those from North Rhine Westphalia, and their limitations are discussed.

Air Pollutants↗

PubMedDate not supplied

Progressive cerebral degeneration of childhood with liver disease (Alpers Huttenlocher disease) with cytochrome oxidase deficiency presenting with epilepsia partialis continua as the first clinical manifestation.

A previously healthy and normally developed 17-year-old young female presented with a sudden onset of focal motor seizure status that proved to be refractory to anticonvulsive treatment. Severe encephalopathy with visual impairment leading to blindness, mental deterioration, and predominantly left spastic tetraparesis developed progressively. Hepatic disease evolved 4 months after onset of the first symptoms and led to death in hepatic failure 1 month later. Diagnostic studies revealed an elevated protein and lactate in the cerebrospinal fluid, slow-wave and intermittently continuous spike-wave activity in the EEG, and a complex i.v. (cytochrome-C oxidase) deficiency in the muscle biopsy. MRI scans revealed signal abnormalities in the occipital lobe, thalamus, and basal ganglia only after 3 months. Histopathological findings in liver biopsy and in postmortem brain examination displaying widespread predominantly right cortical spongiosis, neuronal loss and astrocytosis were consistent with the clinically suspected diagnosis of progressive neuronal degeneration of childhood with liver disease (PNDC) or Alpers Huttenlocher disease. This rare disorder of unknown origin is usually seen in infants and young children and is rarely reported in adolescence.

Adolescent↗