This study provides further information on the prevalence of thyroid dysfunction and autoimmune thyroid diseases in an iodine sufficient area. In addition, it suggests that more than half of the patients with unsuspected hypothyroidism were negative for autoantibodies and that the excessive iodine intake may be involved in causing latent hypothyroidism.

The prevalence of thyroid dysfunction in relation to iodine intake was studied in adults (n = 1061) in five coastal areas of Japan that produce iodine-rich seaweed (kelp). The prevalence of hyperthyroidism (TSH < 0.15 mU/L) was similar in these areas, whereas that of hypothyroidism (TSH > 5.0 mU/L) varied from 0-9.7%. The relative frequency of above normal iodide concentration in the morning urine (> or = 75 mumol/L) [high urinary iodide (UI)] varied from 3.7%-30.3%. Together with previously reported results of a noncoastal city, the frequency of high UI correlated significantly with that of hypothyroidism with negative thyroid autoantibody (r = 0.829, n = 6, P < 0.05) but not with positive thyroid autoantibody (r = 0.278, NS) or with that of hyperthyroidism (r = 0.038, NS). Hypothyroidism was more prevalent in thyroid autoantibody-negative subjects with high UI (group II, 12.1%) than with normal UI (group I, 2.3%) (P < 0.001). The TSH [21.9(6.5-73.7)mU/L] (mean +/- SD) and thyroglobulin [288 (182-456) micrograms/L] levels in group II were significantly higher than the respective levels in group I [9.6(3.7-25.3)mU/L and 123 (38-399) micrograms/L] (P < 0.05). Free T4 of group II (9.9 +/- 3.9 pmol/L) was significantly lower than in group I (14.2 +/- 3.9 pmol/L) (P < 0.05). These results indicate that 1) the prevalence of hypothyroidism in iodine sufficient areas may be associated with the amount of iodine ingested; 2) hypothyroidism is more prevalent and marked in subjects consuming further excessive amounts of iodine; and 3) excessive intake of iodine should be considered an etiology of hypothyroidism in addition to chronic thyroiditis in these areas.

Transient hypothyroxinemia in infants born to mothers with Graves' disease is a unique disorder first reported by us in 1988. Most mothers of these infants have had no treatment, are diagnosed as having thyrotoxicosis during the last trimester, or were not well controlled during pregnancy. These infants are believed to have transient central hypothyroidism, the mechanisms of which have not been elucidated. We measured TSH-receptor antibody activities in maternal serum and blood thyroxine (T4) (free thyroxine, FT4) and TSH levels in blood dried on filter paper at 1, 3, and 5 d of age in 114 infants born to mothers with Graves' disease. The 114 infants were retrospectively divided into three groups according to the clinical course and thyroid function data: group G, neonatal thyrotoxicosis; group T, transient hypothyroxinemia; and group E, euthyroid. In group T, the dried blood T4 (FT4) level from cord blood and/or 1 d of age blood was 6.0 +/- 2.3 microg/dL (0.92 +/- 0.52 ng/dL), a value significantly higher than that at 5 d of age (3.6 +/- 1.0 microg/dL; 0.38 +/- 0.18 ng/dL) (p = 0.025 in T4, p = 0.042 in FT4). In contrast, these levels were significantly lower at birth relative to 5 d in group G (p = 0.0001 in T4) and not significantly changed in group E. The TSH level of cord blood and/or 1-d-old blood in group T was significantly lower than that of group E (p = 0.0006). Moreover, the TSH levels in response to thyrotropin-releasing hormone were blunted in most infants in group T. Bone maturation was not delayed in group T, compared with euthyroid infants. The higher blood T4 (FT4) levels at birth, relative to 5 d in group T, suggested that the fetal T4 level was higher than that of the newborn period. The fetal T4 level might have been elevated owing to transfer of T4 from mother to fetus during the last trimester when the mother's thyroid function was elevated and consequently the fetal pituitary-thyroid axis was suppressed. Although the serum T4 (FT4) levels were decreased after birth, TSH levels were not elevated, probably because the pituitary-thyroid axis was suppressed. This may be the reason for the transient hypothyroxinemia with a normal TSH level in infants born to mothers with poorly controlled Graves' disease. Weak maternal thyroid-stimulating antibody activities and differences in sensitivity of the thyroid gland to TSH-receptor antibodies may contribute to this unique disorder.

We isolated 872 strains of mumps virus from naso-pharyngeal secretions in seven different districts of Japan from January 2000 to July 2001. Among them, 57 strains were geno-typed by nucleotide sequencing in part of the hemagglutinin-neuraminidase (HN) and small hydrophobic (SH) protein regions. Four different genotypes (B, G, K, and L) of mumps virus were co-circulating in Japan and the distribution of genotypes varied in geographically different districts. Two new clusters designated as genotypes K and L had more than 7% nucleotide variation in the SH gene. Among the 57 strains, 11 were classified as B, 35 as G, three as K, and eight as L, which was mainly isolated in Tokyo. We also examined 104 stains isolated in a clinic in Mie prefecture from 1993 to 2003. Genotype B was the indigenous strain and genotype K was introduced in 1994. Genotypes B and K co-circulated in the 1990s and were replaced by genotype G in 2000. There was no significant change in neutralizing test antibody titers against genotypes B, G, K, and L using seven post-vaccination sera with Hoshino strain (genotype B) and these four genotypes had a different antigenicity from genotype A. We should continue to watch on mumps virus molecular epidemiology.

Abstract. To assess the daily iodine intake in a population study, we have compared the validity and degree of reliability of the urine iodide/creatinine ratios and iodide concentrations of casual samples as a representative index of daily urine iodide excretion. The morning urine samples were obtained from apparently healthy 2,956 men and 1,182 women residing in Sapporo, Japan, and urine iodide was measured by an iodide selective electrode. The iodide/creatinine ratio was higher in women than in men, increasing more steeply with age in women than in men, due to a concomitant decrease in the urine creatinine level with age. The iodide concentration showed no age-related change. Similarly the daily urine iodide excretion measured in 22 control subjects by collecting 24-h urine specimens did not vary with age, while the iodide/creatinine ratio of these subjects increased with age. The correlation coefficient(r) of the iodide concentration with daily iodide excretion in the 95 observations of the 22 subjects was 0.832 (P<0.001), higher than that of iodide/creatinine ratio with daily iodide excretion (0.699, P<0.001). The 95% range of the iodide concentration in morning urine samples in the population (n=4,138) was 9.0-70.3 µmol/L with a mean of 27.1 µmol/L. These results indicate that in a population with a large difference in age, an age-associated decrease in the urine creatinine concentration should be considered for the evaluation of the iodide/creatinine ratio and the measurement of the iodide concentration in morning spot urine sample may also be useful for the estimation of daily iodide excretion, and that the Japanese subjects here have a high iodine intake, with considerable variation. nient procedure especially in large population studies, and it has been suggested that the ratio between the concentration of iodine and creatinine in casual urine samples shows the daily urinary excretion of iodine [1][2][3] . It has been shown that urinary creatinine excretion varies with age, sex, body size, and the nutritional state [4][5][6], and these factors might have a strong influence on the iodine/creatinine ratio.We have conducted screening for thyroid diseases, and intended to investigate the possible