Biomedical subjects
Publications and source records attributed to T Ohzeki.
We report a case of anorexia nervosa in a man who had suffered hypogonadism from infancy. The study of the case adds an evidence to clarify roles of sex hormones in anorexia nervosa (Young, 1975).
Salivary testosterone (T) levels in male children and adolescents were measured and compared with plasma T. Salivary concentrations correlated well with plasma total T (r = 0.72) and even better with free plasma T (r = 0.89) in subjects with plasma T levels of pubertal or adult levels (greater than 1.0 nmol/l). In subjects with prepubertal or low plasma T (less than 1.0 nmol/l), there was neither a correlation with plasma total, nor with free T. In hCG tests (responder and nonresponder), salivary T reflected plasma levels faithfully. The results suggest that salivary T, which is suitable for repeated sampling, is a good marker of T secretion in pubertal males.
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Tritiated yohimbine binding was used to estimate platelet membrane alpha 2-adrenoceptor characteristics in normal subjects (n = 12) and patients with essential hypertension (n = 30), primary hyperaldosteronism (n = 10) and phaeochromocytoma (n = 10). There was a 20-fold increase in mean levels of resting norepinephrine and epinephrine in the phaeochromocytoma group. Total binding sites (Bmax) and dissociation constant (Kd) for 3H-yohimbine did not differ significantly among the four groups. Following curative surgery for phaeochromocytoma, plasma catecholamine levels were normalized but the Bmax remained unchanged. Following surgery for primary hyperaldosteronism, levels of plasma norepinephrine rose but Bmax was not changed. In all but the phaeochromocytoma patients, Bmax values correlated positively (r = 0.437, n = 48, P less than 0.01) with resting plasma norepinephrine. A significant negative correlation was observed between the change in plasma norepinephrine in response to postural change and resting Bmax. Treatment for 2-4 weeks with guanabenz or bethanidine induced a parallel fall in both Bmax and plasma norepinephrine. Treatment with reserpine was followed by a comparable fall in plasma norepinephrine, but Bmax values were unchanged. The findings support the view that platelet alpha 2-adrenoceptor density is functionally regulated in parallel with sympathetic nerve activity rather than circulating catecholamine levels, although it is not known which neuronal substance(s) may participate in this regulation.
Body weight and height of Japanese boys and girls aged 12-14 years were measured to calculate the prevalence of obesity, leanness and anorexia nervosa. In boys, the prevalence of obesity as well as leanness was significantly higher in the areas where population density was lower and among the boys who attended schools with smaller numbers of pupils. In the girls, these findings were similar to the boys. On the other hand, anorexia nervosa was found in girls only more commonly in the areas with higher population density and in the larger schools. These results suggest that higher prevalence of obesity in certain subjects may be associated with increased numbers of leanness but not with anorexia nervosa.
A neonatal case of hyperthyrotropinemia is described in association with pseudohypoparathyroidism (PHP). This girl was found to have high serum thyrotropin (TSH) on screening, though serum thyroid hormones were within the normal ranges throughout the observation. The patient's TSH remained above the normal limit until 5 years of age, when she suffered from hypocalcemic tetany and was diagnosed as type-1 PHP on the basis of responsiveness to parathyroid hormone. She also had stigmata of Albright's hereditary osteodystrophy. The results demonstrate that elevated TSH, although thyroid hormone concentrations are normal and medication is not indicated, may be one of the earliest diagnostic clues for PHP.
We report on a 6-year-old girl with Ullrich-Turner syndrome and anorexia nervosa. The diagnosis was made at 6 years and she became anorectic at 14 years. She had been treated with low doses of estrogen just before the onset of anorexia. In spite of remarkable decrease in food intake, her body weight was in the normal range compared to standard weight. Rohrer indices were also normal, probably due to abnormal habitus in individuals with the syndrome. The pathogenetic relationship between this disorder and the hormone treatment in the onset of anorexia nervosa is discussed.
Two hypotheses have been postulated as to the pathogenesis of hypogonadotropinemia in anorexia nervosa; one is starvation and weight loss and the other is a psychological factor to influence gonadotropin secretion. Our patient suffered from very rare concurrence of Turner's syndrome and anorexia nervosa and a study of this experiment in nature provided important evidences concerning decreased secretion of gonadotropins in the eating disorder. The patient was diagnosed as Turner's syndrome when she was 6 years old. Her gonadotropin levels were elevated to the castrated ranges (LH 61.8 IU/l; FSH 175.8 IU/l) after 8 years of age. She was noticed to be anorectic at the age of 13 years. Serum levels of the pituitary gonadotropins were lowered (LH 2.9 IU/l; FSH 3.0 IU/l) and their responses to luteinizing hormone-releasing hormone were decreased beneath the normal prepubertal limits. After one year of the anorectic period, she recovered the weight though her gonadotropin levels remained in the very low ranges (LH 2.7 IU/l; FSH 2.5 IU/l). The results suggest that hypogonadism in anorexia nervosa is not solely caused by nutritional deficiency but rather by other factors such as psychological abnormalities.
1. The baroreflex-mediated changes in plasma norepinephrine (NE) and heart period (RR interval) to phenylephrine (PE)-evoked pressor and nitroprusside (NP)-evoked depressor stimulations were studied in 19 patients with chronic essential hypertension, 12 with borderline hypertension and in 11 age-matched normal controls. 2. Intravenous infusion of PE at a rate of 0.25-1.0 microgram/kg/min induced dose-related increases in mean arterial pressure (MAP) and in RR interval and a decrease in plasma NE. Similarly, NP infusion at a rate of 0.1-0.4 microgram/kg/min evoked the opposite changes in each variable. The reflex sensitivity was defined as the slope of linear regression between the changes in RR interval and MAP (RR/MAP) and between those in plasma NE (% of the baselines) and MAP (%NE/MAP). 3. Both RR/MAP and %NE/MAP for pressor and depressor stimulations were reduced below values found in normal subjects, in both chronic and borderline hypertensives. 4. The values of %NE/MAP was negatively related to the basal plasma NE during falls in blood pressure (r = -0.401, P less than 0.05). 5. The %NE/MAP may be a useful index of the sympathetic component of baroreflex sensitivity. A decrease in %NE/MAP in hypertensive and borderline hypertensive patients suggests a blunted sensitivity of the sympathetic constrictor reflexes.
The concentration of plasma free dopamine (PDA) is said to be much lower than that of other catecholamines and its physiological significance remains unclear. Our recent studies using a newly developed radioenzymatic method disclosed the fairly distinctive features of PDA in patients with various types of hypertension. PDA was also confirmed as a variable responsive to postural change, dietary sodium loading and dopamine receptor antagonist. The results suggest that PDA could be a sensitive marker to represent the peripheral dopaminergic function, which might play an inherent role as a physiological regulator responsible for the cardiovascular and endocrine system.
Functional relationships between platelet alpha 2-adrenoceptors and sympathetic nerve activity were studied in patients with essential hypertension (n = 23), primary aldosteronism (n = 10), and normal subjects (n = 12). The maximum number of binding sites (Bmax) and the dissociation constant (Kd) of 3H-yohimbine on platelet membranes and resting plasma norepinephrine (NE) were similar among these groups of subjects. In all subjects combined, Bmax values were correlated positively (r = 0.471, p less than 0.01) to resting plasma NE and negatively (r = -0.531, p less than 0.01) to the changes in plasma NE when subjects were moved from lying to standing. A 2-4 week treatment with guanabenz or bethanidine induced a parallel fall of both Bmax and plasma NE, whereas administration of reserpine caused a similar fall of plasma NE but Bmax remained unchanged. Kd values were not changed after any of these treatments. The results support the view that platelet alpha 2-adrenoceptor density is functionally regulated in parallel with sympathetic nerve activity rather than plasma NE per se. This hypothesis seems quite reasonable when it is extended to the presynaptic alpha 2-adrenoceptors; otherwise, the negative feedback function on NE release should be lessened and contradictory to its physiological role.
To investigate the effects of dietary sodium on the peripheral dopaminergic mechanism, changes of unconjugated plasma dopamine(DA) and its related humoral factors were studied in 8 patients with essential hypertension(EH) and 8 age-matched normal controls(N) while they were receiving ordinary meals (Na, 130-180 mEq daily) followed by higher sodium (250-300 mEq daily) diets for a week. Plasma and urinary DA, norepinephrine(NE) and epinephrine(E) were measured by the highly sensitive COMT-mediated radioenzymatic procedure, which permits an accurate estimation of plasma DA as low as 5-6 pg/ml. Under high sodium diets, blood pressure and heart rate were not changed significantly in N and EH subjects. Urinary NE and E tended to decrease, while urinary DA increased significantly in both groups of subjects (p less than 0.05). There was a significant correlation between urinary sodium and DA (r = 0.590, p less than 0.001), but plasma DA failed to correlate significantly to urinary sodium or DA in all subjects. Plasma NE and E tended to decrease in both N and EH subjects, while plasma DA increased significantly (p less than 0.05) in EH from 7.2 +/- 0.8 pg/ml [mean +/- SEM] to 9.3 +/- 1.0 and slightly in N from 9.1 +/- 1.8 to 11.2 +/- 1.3. Plasma renin activity(PRA) and plasma aldosterone(PAC) were invariably decreased in all subjects, while plasma prolactin(PRL) remained unchanged. A significant correlation was observed between plasma DA and NE under ordinary meals (r = 0.733, p less than 0.01), but this correlation disappeared under high sodium diets. Plasma DA showed an inverse correlation to PAC (r = 0.351, p less than 0.05) under both dietary conditions. Upright posture induced a significant rise (p less than 0.05) in NE, E, DA, PRA and PAC with ordinary meals, but the responses of NE and PAC were apparently attenuated with high sodium diets. An intravenous injection of metoclopramide (MCP, 10 mg), a DA receptor antagonist, provoked a slight rise in plasma NE and DA with ordinary meals, of which responses were further enhanced with high sodium diets. MCP induced a definite rise in PAC and PRL in all subjects under both dietary conditions (p less than 0.01), while plasma E and PRA remained unchanged after MCP challenge. The results lend support to the view that unconjugated plasma DA could be a useful marker of peripheral dopaminergic activity, which might be a physiological regulator responsible for the suppression of aldosterone secretion and sympathetic nerve activity observed during high sodium intake.
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A case of hypodipsic hypernatremia in a 16-month-old Japanese boy is reported. Partial antidiuretic hormone deficiency was present. Computed tomography of the brain revealed absence of septum lucidum. No ophthalmological abnormality could be found. He had hyposmia, which has not been reported previously in association with hypernatremia due to hypodipsia. Forced fluid administration and nasal 1-deamino-8-d-arginine vasopressin treatment could maintain serum electrolyte levels within normal ranges. However, episodes of hypernatremia could not be completely avoided while he was treated with 1-deamino-8-d-arginine vasopressin and ad libitum oral fluid.
Urinary adenosine 3',5'-monophosphate (cAMP) excretion before and after administration of aqueous vasopressin (pitressin) and 1-deamino-8-D-arginine vasopressin (DDAVP) was measured in congenital nephrogenic and in vasopressin sensitive diabetes insipidus (VS-DI). Excretion of cAMP into the urine increased markedly in response to pitressin (676%) and to DDAVP (252%) in VS-DI. Nephrogenic diabetes insipidus (N-DI) could be divided into two categories (type 1 and type 2) in respect to urinary cAMP responsiveness. In type 1, cAMP excretion showed no definite change after stimulation with pitressin (102%) or DDAVP (127%). On the other hand, urinary excretion of cAMP was significantly elevated in response to DDAVP in familial cases of N-DI type 2 (1269%) without producing any concentrating effect on the urine. Two different defects are considered to be involved in the pathogenesis of N-DI.
Two cases of a brother and a sister with thyroid hormone unresponsiveness are described. They had large goiters and high levels of thyroid hormones in the face of clinical euthyroidism. The birth weight of the brother was low for his gestational age. He was also lean and exophthalmic, as is often seen in Graves' disease.
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