Madoka Arisaka

Effect of testosterone on bone density and bone metabolism in adolescent male hypogonadism

To assess the influence of gonadal steroid testosterone (T) on bone mineral status in males during puberty, we observed the response of cortical bone density and serum biochemical parameters of bone metabolism to T treatment in 12 adolescent patients with hypogonadotropic hypogonadism (11 with both gonadotropin and growth hormone deficiency and one with isolated gonadotropin deficiency). The 12 patients aged 15 to 21 years (Tanner stage I to II) were divided into two groups: group 1 (n = 6) given T treatment for 2 consecutive years, and group 2 (n = 6) without T treatment for the first year and then with T treatment for the second year. Cortical bone density measured in the radius was less than the age-matched mean value for normal subjects in all 12 patients (groups 1 and 2) at the start of the study. Bone density in group 1 increased significantly during the 2-year T treatment period, but did not increase in group 2 during the first year without T treatment, although an increase was observed during the subsequent year with T treatment. Among circulating biochemical factors such as osteocalcin, parathyroid hormone (PTH), 25-hydroxyvitamin D (25-OHD), and 1,25-dihydroxyvitamin D [1,25-(OH)2D], only osteocalcin showed an increase in response to T treatment in both groups. Levels of insulin-like growth factor-I (IGF-I) remained consistently low and did not change in any patients except one with isolated gonadotropin deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Testosterone on Radial Bone Mineral Density in Adolescent Male Hypogonadism

Gonadal function is considered to be important in both men and women for the maintenance of normal bone mineral content; failure of gonadal function causes osteopenia in adults (1). Furthermore, it is known that bone mineral density increases during puberty (2, 3 ) . In order to assess the effect of gonadal steroid on bone mineral density in adolescent males with osteopenia due to hypogonadism, we compared the changes in bone density in patients given testosterone replacement with those in patients without this replacement therapy. This study was approved by the ethics committee of our hospital.

Central diabetes insipidus in hypoxic brain damage

We describe two children who after cardiopulmonary arrest developed hypernatremia at the terminal stage. Urinary antidiuretic hormone concentration was very low, indicating central diabetes insipidus. These cases illustrate the necessity of alertness to the development of central diabetes insipidus in patients with severe hypoxic brain damage.

Chorea as an Initial Manifestation of Systemic Lupus Erythematosus A Case Report of a 10-year-old Girl

Neurological complications of systemic lupus erythematosus (SLE) are relatively common, but isolated chorea as the initial manifestation of SLE is very rare. We report a 10-year-old girl presenting with chorea, who developed clinical and lab oratory findings of SLE 10 months after the onset of chorea. In this case, mild depression of complement levels in serum, which had already been found in the early stage of the chorea, was the only abnormal laboratory datum. The low serum complement levels that precede the appearance of other clinical and laboratory findings may be helpful for the diagnosis of isolated chorea involvement in SLE.

Primary Hyperparathyroidism Case Report and Management

A 13-year-old girl presenting with abdominal pain, polyuria, polydipsia, and radiologically confirmed renal calculi was diagnosed as having primary hyper parathyroidism. Laboratory data revealed markedly elevated serum calcium, low phosphorus, and elevated parathyroid hormone. Other parathyroid function tests also confirmed the diagnosis of primary hyperparathyroidism. Ultrasound ex amination showed a small echogenic nodule in the parathyroid gland. Following a single gland resection, the extremely high serum calcium level promptly decreased to normal range, and it has remained normal.

Intrauterine Growth Retardation and Early Adolescent Growth Spurt in Two Sisters

Two sisters who presented with a similar growth pattern are described. They delivered with idiopathic intrauterine growth retardation and had an early adolescent growth spurt. The physical and endocrine findings suggested a potential relationship between intrauterine growth retardation and early puberty.

Osteoporosis in a boy with hypogonadotropic hypogonadism

SummaryWe describe a 16-year-old boy with idiopathic hypogonadotropic hypogonadism associated with osteoporosis. Osteoporotic lesions of the hands, skull and spine were shown by routine radiography. Single-photon absorptiometry at the distal radius confirmed a significant reduction of bone mineral density. The parathyroid hormone-vitamin D axis and calcitonin secretion showed no derangement. Reduced bone mineral density in association with relatively elevated levels of serum osteocalcin and alkaline phosphatase suggested an increased bone turnover (so-called high-turnover osteoporosis). Tetosterone therapy for 3 months significantly increased the radial bone mineral density.This case illustrates that testosterone deficiency during puberty seems to alter the bone mineral status, impairing bone mineralization and bone remodeling.

Increase in bone density during testosterone therapy in adolescent hypogonadism

Sir: Abundant evidence links decreased bone density with oestrogen-deficient status in women, and increases in bone density have been noted after oestrogen therapy [7]. Osteopenia in male hypogonadism, especially in adolescent boys, and concomitant androgen therapy has been only rarely reported [3, 5]. Recently, we investigated the effect of testosterone therapy on bone density in a boy with hypogonadotropic hypogonadism. A 17-year-old boy with Tanner stage I external genitalia was diagnosed as having an idiopathic isolated gonadotropin deficiency based upon the results of both a luteinizing hormone-releasing hormone test and a human chorionic gonadotropin (HCG) loading test. There was no anosmia. Plasma testosterone response to HCG stimulation (HCG 3000 units/m 2 for 3 days) rose from 10 ng/dl (basal level) to 90 ng/dl (peak level). Plasma somatomedin C concentration was 1.5U/ml (normal = 1.35-3.0). The patient s skeletal age was 13 years. Serum calcium, phosphorus, carboxyterminal parathyroid hormone, calcitonin, and vitamin D metabolites (25-hydroxy vitamin D and 1,25-dihydroxy vitamin D) were all within normal limits. Bone mineral density evaluated by single-photon absorptiometry at the non-dominant distal radius was decreased: 0.50g/cm 2 (normal 0.59 +_ 0.05). Testosterone enanthate 125 mg every 3 weeks (total four times) led to a significant increase in bone density to 0.57 g/cm 2. During puberty, a marked increase in bone density occurs and this is thought to be due to increased sex steroid secretion [1, 2, 4, 6]. Androgen deficiency during puberty seems to be a risk factor for osteopenia in adolescent boys and young male adults [1, 4, 5]. As shown by our patient, testosterone replacement at the appropriate age stimulates the pubertal increase in bone density and increases the skeletal resistance to mechanical forces. References

Hyponatremia in central partial diabetes insipidus due to postoperative hypothalamic tumor

We report the case of a 4-year-old boy with a postoperative hypothalamic tumor, who exhibited unusual water and electrolyte disturbance. This developed as a late manifestation during the course of central diabetes insipidus (DI), which started when the patient was 2 years old. Clinically, hyponatremia and DI appeared alternatlely within 1 day. The hyponatremia (lowest value Na+ 115 mmol/l) was associated with afebrile convulsions. Assessment of fluid status revealed that the patient had a reduced capacity for arginine vasopressin (AVP) secretion (partial DI), which was not physiologically regulated and which was not concomitantly sufficient to produce maximally concentrated urine and allow the production of maximally diluted urine. This defective osmoreceptor function in association with the previously existing reduced capacity for AVP release seemed to be responsible for the fluid disturbance in the patient. The administration of nasal 1-desamino-8d-arginine vasopressin (DDAVP) only when urine output was increased, instead of regular administration at a fixed time, prevented both worsening of hyponatremia and development of DI.

Atrial natriuretic peptide and fludrocortisone therapy in congenital adrenal hyperplasia

In treating patients with congenital adrenal hyperplasia (CAH), sufficient mineralocorticoid (9a-fludrocortisone acetate) in addition to glucocorticoid therapy should be prescribed, but care should be taken to avoid overdose which could cause sodium and fluid retention (1 -3). This condition can be detected by regular blood pressure monitoring or measurement of serum sodium concentration, but these indices do not appear to be sufficiently sensitive. Recent studies of atrial natriuretic peptide (ANP) in man have demonstrated that plasma ANP increases in parallel with sodium and water load, and that elevated ANP plays an important hormonal role in overcoming the sodium retention induced by mineralocorticoids (4-6). The present study was carried out to clarify whether the plasma ANP level could be used to indicate the effect of fludrocortisone therapy on sodium and water balance in patients with CAH.