ABSTRACT
UNLABELLED: To determine the effects of low dose radiation from 131I and 137Cs resulting from the Chernobyl disaster on the expression of endemic goiter in children, we studied children in regions with and without evidence of radiocontamination but comparable iodine insufficiency. We included 89 children in the study (radiocontaminated) region (SR) and 116 in the control region (CR) because they were either fetuses, infants, or pre-adolescents at the time of exposure. We evaluated thyroid dimensions by clinical examination and ultrasound; thyroid function by hormonal levels, and thyroglobulin measurement; histology of the thyroid by fine needle aspiration; and thyroid autoimmunity. SR subjects had 5 times the frequency of thyroid enlargement as those from CR, greatest in the younger patients. There were no instances of clinically apparent thyroid dysfunction. Antithyroid microsomal and antithyroglobulin antibodies were present in a markedly greater percentage of SR subjects. Fine needle biopsy demonstrated greater cellular proliferation in samples from SR. CONCLUSIONS: We have demonstrated findings of autoimmune thyroid disease at markedly increased frequency in a population of children with poor iodine nutriture who were exposed to low level radiation, compared to a more iodine deficient population not so exposed. These results suggest that low level radiation may induce thyroid gland changes in children who have inadequate iodine intake nutriture and reinforce the importance of adequate dietary iodine.
Subject(s)
Goiter, Endemic , Power Plants , Radiation Injuries , Radioactive Hazard Release , Adolescent , Autoimmunity , Child , Child, Preschool , Female , Goiter, Endemic/epidemiology , Goiter, Endemic/immunology , Goiter, Endemic/physiopathology , Humans , Infant , Iodine/deficiency , Male , Thyroid Function Tests , Ukraine/epidemiologyABSTRACT
Primary GH insensitivity (Laron syndrome) due to GH receptor deficiency (GHRD) is an autosomal recessive condition characterized by severe growth failure. Diverse alterations in the GHR gene have been reported in affected individuals. We report here the first family with GHRD from Russia, with two affected siblings and consanguineous parents. Analysis of blood spot DNA by polymerase chain reaction (PCR), denaturing gradiant gel electrophoresis, and nucleotide sequencing indicated that these siblings are homozygous for a nonsense mutation, R43X, in the GHR gene. The R43X mutation, which changes an arginine codon to a translational stop codon, occurs at a CpG dinucleotide mutational hotspot and has previously been identified in affected individuals of Mediterranean and Ecuadorian origin.
Subject(s)
Codon, Nonsense , Growth Disorders/genetics , Growth Hormone/physiology , Receptors, Somatotropin/genetics , Base Sequence , Child, Preschool , Genes, Recessive/genetics , Growth Disorders/physiopathology , Growth Hormone/genetics , Humans , Infant , Male , Molecular Sequence Data , Mutation , Pedigree , Protein Biosynthesis , Russia , SyndromeSubject(s)
Blood Glucose Self-Monitoring , Diabetes Mellitus, Type 1/drug therapy , Insulin/administration & dosage , Blood Glucose/analysis , Child , Delayed-Action Preparations , Diabetes Mellitus, Type 1/blood , Dose-Response Relationship, Drug , Drug Therapy, Combination , Fasting/blood , Humans , Insulin/blood , Time FactorsABSTRACT
The study confirmed the data on the absence of a stable compensation of diabetes mellitus in most patients with the insulin-dependent form of disease under domestic conditions. It was extremely difficult to maintain the state of compensation without active participation of patients instructed in therapeutic measures and control of disease. Therefore the most urgent problems of modern diabetology are to train patients, to encourage their participation in a therapeutic process and to provide facilities for determination of glycemia under domestic conditions.
