We recently isolated a cDNA encoding a short isoform of the corticotropin-releasing factor (CRF) receptor subtype, referred to as CRF_2α-tr, from the rat amygdala. The present study utilized in situ hybridization histochemistry to localize the distribution of CRF_2α-tr receptor mRNA in the rat brain. The results showed significant levels of hybridization in the lateral septum, central nucleus of the amygdaloid, cortico-amygdaloid nucleus, ventromedial hypothalamic nucleus (VMH), and frontal cortex. In the physiological study, antidepressive drugs increased the expression of CRF_2α-tr mRNA and the total binding activity to CRF in the rat amygdala. These results suggest that CRF_2α-tr may regulate the synthesis and secretion of CRF in the amygdala.

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Children with craniopharyngioma usually present with growth retardation and hypogonadism. They rarely develop precocious puberty. We describe here the case of a boy with craniopharyngioma who developed isosexual precocious puberty after partial surgical resection of the tumor. He was treated at first with cyproterone acetate (CA) for precocius puberty, but his bone age progressed markedly. Thus, LH-RH analog treatment was started. This regimen improved his secondary sexual development, but decreased his growth velocity from 7.2 cm/y to 2.8 cm/y. Then growth hormone treatment in addition to LHRH analog injection was started. Although the start of growth hormone (GH) treatment was delayed, his height has improved. No recurrence of the tumor has been recognized until now.

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We investigated the prevalence and clinical features of patients with eating disorders among juvenile-onset type 1 diabetes mellitus (DM). Among one hundred patients with type 1 DM, eating disorders were found in four females, two adolescent girls and two young women. In the four affected patients, three were diagnosed as having binge eating disorders and one as anorexia nervosa. The overall prevalence of eating disorders was 4.0% (4/100); that in females was 7.1% (4/56); that in adolescents and young adults was 4.8% (4/84); and that in adolescent females and young adults was 8.5% (4/47). Patients with eating disorders had irregular eating habits and showed antipathy to dietary restraint. In most cases, they had poor glycemic control associated with noncompliance with self-management of diabetes. They declared indifferent or false reports in self-monitoring of blood glucose and used inuslin omission and underdosing. On the basis of these findings, adolescent girls and young women with type 1 DM seemed to have risk factors for developing eating disorders. In cases suspected of having eating disorders, a flexible and individualized psychological approach would appear to be paticularly important.

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The objective of our study was to investigate the zinc (Zn) status and effects of Zn supplementation in relation to insulin-like growth factor-I (IGF-I), iron deficiency anemia and outcome of birth weight of newborn in pregnant women. The role of Zn and IGF-I in hematological abnormalities has remained unclear. Twenty-four Japanese women, when examined at the second trimester of pregnancy, had hemoglobin concentrations (Hb) below 11.0 g/dl and almost normocytic indices. We compared the hematological status and serum IGF-I levels before and after Zn supplementation. While Hb and RBC did not change, IGF-I and total iron binding capacity (TIBC) were increased significantly, and concentrations of erythropoetin were increased, but not statistically significant. There were significant positive correlations between increases in RBC and increases in IGF-I and TIBC in the Zn administration. Birth weights of newborn under 2500 g whose mother received zinc were 4.2%, against 7.1% in controls. Zn status to some extent can account for IGF-I and hematological abnormalities and the outcome of birth weight of the newborn in pregnant women.

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We investigated annual prevalence rate of complications found in 6,658 obese schoolchildren during checkups performed in Setagaya Ward between 1984 and 1998. The overall mean prevalence rate of blood lipid abnormalities, hepatic function abnormalities, fasting blood glucose abnormalities and blood pressure abnormalities was 34.2%, 12.9%, 1.6% and 2.8%, respectively, in boys. No gender difference was found except in hepatic function abnormalities, which were less than half as prevalent in girls as in boys. Recently (from 1995 to 1998), the prevalence rates of cholesterol abnormalities, low-density lipoprotein cholesterol (LDLC) abnormalities as well as an abnormal arteriosclerotic index (AI) have decreased significantly (from 35.6 to 9.0%, 56.7 to 23% and 28.9 to 15.2% in boys, respectively; and 26.1 to 8.1%, 37.8 to 23% and 25.2 to 12.2% in girls, respectively). The mean levels of cholesterol, LDLC, triglycerides and AI showed no significant difference, but tended to decrease. In conclusion, 1) Gender differences were observed only with regard to hepatic function abnormalities. 2) The prevalence of fasting blood glucose abnormalities was low, and oral glucose tolerance test (OGTT) seems to be necessary for screening. 3) Arteriosclerotic risk factors have recently tended to improve in spite of the increased prevalence of obesity in children.

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Four hypogonadotropic men with GH deficiency impregnated their wives a total of seven times and fathered six normal children during the course of HCG-HMG treatment. One pregnancy resulted in an artificial abortion because of severe maternal hypertension. After cessation of GH therapy, HCG was administered at 3,000 IU i.m., 2 or 3 times a week for 6 months followed by the addition of 75 IU of HMG to each dose of HCG for 3 months. This regimen of HCG alone for 6 months and the combination of HCG and HMG for 3 months was repeated. In all of the patients, serum testosterone levels increased to the normal adult range within 6 months. The patients had sperm counts of 24-100 × 10⁶/mL before they married. In conclusion, men with hypogonadotropic hypogonadism and GH deficiency were able to achieve spermatogenesis and to father children following our method of HCG-HMG treatment. Long-term HCG-HMG treatment is effective, even if a pretreatment HCG test is negative.

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Increased bone turnover and loss of bone mass in adult patients with hyperthyroidism is well documented, but bone manifestations in children with hyperthyroidism are poorly understood. We evaluated cortical bone mineral density (BMD) and bone metabolic markers in two boys and five girls, aged 5.7~16 yrs (12.2 ± 3.7 yrs) with hyperthyroidism before and during treatment. BMD (ΣGS/D) was assessed by computed X-ray densitometry in the second metacarpal bone of the left hand. The %BMD (percentage for expected ΣGS/D of age- and sex-matched standard) before treatment was 90.5 ± 8.5% (M ± SD), which was lower than normal children (p<0.05). After 6 months of treatment, %BMD increased to 95.9 ± 9.5%, showing partial restoration. Basal levels of urinary N-telopeptides of collagen type 1 (NTx) before treatment were markedly high, but decreased rapidly during treatment towards the normal range. We also found a transient rise in NTx on day 4 of treatment before the decrease. Basal levels of serum bone alkaline phosphatase were as high as the upper limits of the reference ranges in pubertal children, slightly decreasing for the first two weeks of treatment, increasing transiently for a few months and declining thereafter. We demonstrated decreased BMD in children with hyperthyroidism for the first time. Bone resorption rapidly ameliorated, and accelerated bone formation persisted for a few months after normalization of thyroid function, while BMD improved at 6 months' evaluation, as reported in adult patients. We also found a transient increase in bone resorption markers and initial suppression of bone formation markers before the amelioration. A longer period of follow up with more patients is needed to clarify how the mechanism of bone metabolism is affected by thyroid function.

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An eleven-year-old Japanese boy was admitted to our hospital for evaluation of decreased growth velocity (0.7 cm/year) of two years. He also suffered from poor appetite, cold intolerance and slow body movements. Physical examination revealed myxedematous face and dry and cold skin but no goiter. His height was 138.8 cm (-1.0 SD), body weight 38.0 kg (+16.5%), and body temperature 35.4°C. His serum free-thyroxine (f-T4) was 0.06 ng/dl, free-triiodothyronine (f-T3) was 100 pg/dl, while TSH was 254.4 μU/ml. He was positive for anti-microsome antibody (AMA), anti-thyroglobulin antibody (ATA), thyrotropin-binding inhibitor immunoglobulins (TBII) and thyroid stimulation blocking antibody (TSBAb). Thyroid 24-hour radioiodine uptake was less than 1%. This patient was therefore diagnosed as having atrophic autoimmune thyroiditis (AAT), and replacement therapy with l-thyroxine was initiated. We also analyzed the HLA haplotypes and thyroid function of his family. The patient's HLA haplotypes were A2, A4, B62, B46, Cw1, Cw4, DR4 and DR8. All of his family members had normal thyroid function, but his mother was positive for anti-microsome antibody. We describe a rare case of AAT with positive TBII and TSBAb in a prepubertal boy. Accumulation and comparison of similar cases may facilitate our understanding of the autoimmune mechanisms in the pathogenesis of childhood AAT.

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