Yachiyo Nohara

Familial Neonatal Transient Hypothyroidism Due to Maternal TSH-Binding Inhibitor Immunoglobulins

IN 1960, Sutherland et al.1 reported on children with familial nongoitrous cretinism born of a hypothyroid mother with Hashimotos disease. Subsequently, Goldsmith et al.2 studied this family in de...

Primary Myxedema with Thyrotrophin-Binding Inhibitor Immunoglobulins: Clinical and Laboratory Findings in 15 Patients

In a screening of 43 patients with primary myxedema, 9 patients were found to have IgG that inhibits the binding of 125I-thyrotrophin to its receptor (thyrotrophin-binding inhibitor immunoglobulins). Preparations of IgG from these patients did not stimulate thyroidal cyclic adenosine monophosphate generation and blocked thyroid stimulation by thyrotrophin in vitro. Clinical and laboratory features of 15 patients with this inhibitor, including 6 who were previously known, were compared with those of patients without the inhibitor. The patients with inhibitor, 2 men and 13 women, had onset of their hypothyroidism from age 2 to 49 years, and thyroid uptake in these patients was significantly lower than that in patients without inhibitor. Transient hypothyroidism was seen in all 5 infants born to 4 mothers having potent inhibitor immunoglobulins. These clinical findings indicate that thyrotrophin-receptor-blocking antibodies play a pathogenic role in a group of patients with primary myxedema.

Comparison of atrophic and goitrous auto-immune thyroiditis in children: Clinical, laboratory and TSH-receptor antibody studies

We studied the clinical features, laboratory and thyroid functions and thyrotropin (TSH)-receptor and thyroid-stimulation antibodies in 21 patients with atrophic auto-immune thyroiditis (AAT) and 48 patients with goitrous auto-immune thyroiditis (GAT) of childhood onset. The clinical features of patient with AAT were cessation of growth and obesity, while asymptomatic enlargement of the thyroid gland was the sole symptom in most patients with GAT. Although the ages at diagnosis were comparable in both groups, the estimated ages at onset were much lower in patients with AAT than in those with GAT. Patients with AAT exhibited more severe hypothyroidism when evaluated by serum thyroxine (T4), tri-iodothyronine (T3), TSH, cholesterol levels and basal metabolic rates. The 24h123I-thyroidal uptake was significantly lower in patients with AAT than in those with GAT. None of the 19 patients with AAT possessed TSH-binding inhibitor immunoglobulins (TBII). On the other hand, 3 of the 32 GAT patients tested, possessed weak to potent TBII activities. Three TBII-positive patients with GAT also possessed thyroid-stimulation blocking antibodies. These findings suggest that: 1. Pathogenesis of AAT in children whose onset of hypothyroidism was before puberty is not due to TSH-receptor blocking antibodies, which are often found in patients with AAT of postpubertal onset. 2. AAT in children is considered not to be due to the later stage of GAT. 3. Some patients with GAT possessed TSH-receptor blocking antibodies. The aetiology and pathogenesis of AAT in children have yet to be elucidated.

Prolactin response to thyrotropin-releasing hormone in children with Turner's syndrome and hyperthyroidism

Plasma prolactin (PRL) response to synthetic thyrotropin-releasing hormone (TRH) was studied in 26 prepubertal and 19 pubertal children with constitutional short stature, 7 patients with Turners syndrome and 10 patients with hyperthyroidism. The mean basal concentrations of plasma PRL did not differ among groups. In prepubertal children PRL responses to TRH were comparable in both sexes, while pubertal children plasma PRL levels after TRH in females were significantly higher (P<0.05) than those in age-matched males. Plasma PRL levels after TRH in patients with Turners syndrome were significantly higher (P<0.05) than those in age-matched males, but were not significantly different from those in age-matched females. Plasma PRL response to TRH was markedly suppressed in patients with hyperthyroidism before treatment, but it returned to normal after treatment when patients became euthyroid. A significant correlation (P<0.05) between peak concentrations of plasma PRL after TRH stimulation and plasma T3 but not T4 levels was observed.These data suggest that a sex difference in TRH-stimulated PRL secretion appears around puberty and that plasma PRL response to TRH is suppressed in children with hyperthyroidism. The magnitude of plasma PRL response to TRH is closely correlated with the severity of hyperthyroidism when judged by plasma T3 but not T4 concentrations.

Effect of changes in basal metabolic rate on the circadian rhythm of human body temperature

Abstract In order to investigate whether changes in basal metabolic rate (BMR) influence the basic 24‐h rhythm of body temperature we examined daily variations of body temperature in eight hyperthyroid patients and two patients with anorexia nervosa. Although they exhibited high and low BMR, respectively, they demonstrated the temperature rhythm patterns similar to those in healthy control. These results suggest that both an increased and a decreased BMR may not modify the circadian rhythm of human body temperature.

Prolactin Response to Arginine in Children with Hyperthyroidism and Primary Hypothyroidism

Plasma prolactin (PRL) response to arginine was examined in 16 prepubertal and 18 pubertal children with constitutional short stature, 5 patients with hyperthyroidism and 4 patients with primary hypothyroidism. The mean basal concentration of plasma PRL was significantly higher (P<0.01) in primary hypothyroidism than in other groups. Arginine infusion elicited significant (P<0.05) rises in plasma PRL in all groups. The maximal increment of plasma PRL above the baseline level after arginine stimulation was significantly larger (P<0.05) in pubertal than in prepubertal females and was significantly smaller (P<0.05) in patients with hyperthyroidism than in age- and sex-matched controls. There was no sex difference in arginine-stimulated PRL secretion. These data suggest that arginine produces a significant increase in plasma PRL and the PRL response to arginine was greater in pubertal than in prepubertal children. Plasma PRL response to arginine is suppressed in children with hyperthyroidism and the basal plasma PRL is markedly elevated in primary hypothyroidism.