Neointimal thickening after balloon denudation is enhanced by aldosterone and inhibited by spironolactone, and aldosterone antagonist.

OBJECTIVE: The aim was to examine the effects of aldosterone and of an aldosterone antagonist, spironolactone, on neointimal thickening in a rabbit model of balloon injury. METHODS: Eighteen rabbits underwent aortic and iliac balloon injury and were randomised to subcutaneous infusion of aldosterone (70 micrograms.kg-1.d-1) or vehicle solution for 28 d. Eighteen other rabbits were randomised to receive daily subcutaneous injections of spironolactone (50 mg.kg-1.d-1) or of vehicle for 7 d before injury and for 28 d after the procedure. All animals were then killed just after measurement of plasma renin activity and of arterial pressure. Vessels were fixed and five cross sections were analysed per rabbit (three aortic; two from iliac artery). Mean values of neointimal area and of the neointimal area/medial area ratio were calculated. RESULTS: Aldosterone treatment was associated with a decrease in renin activity and a non-significant increase in mean arterial pressure. Aldosterone significantly augmented the neointimal thickening in the iliac artery [0.42(SEM 0.07) v 0.24(0.03) mm2, P < 0.05] but not in the aorta [0.63(0.08) v 0.59(0.12) mm2, NS]. Spironolactone significantly inhibited intimal thickening, both in the iliac artery [0.09(0.02) v 0.29(0.01) mm2, P < 0.001] and in the aorta [0.31(0.03) v 0.59(0.06) mm2, P < 0.001]. Spironolactone administration was associated with an increase in renin activity and a decrease in mean arterial blood pressure. CONCLUSIONS: Aldosterone administration enhances neointimal thickening after injury and spironolactone, an aldosterone antagonist, is a potent inhibitor of neointimal thickening in the same model. This suggests a role for aldosterone in the pathophysiology of neointimal proliferation after balloon injury and for aldosterone antagonists in its prevention.

A double blind controlled study of the hormonal and clinical effects of bromocriptine in the polycystic ovary syndrome.

Previous studies on the efficacy of bromocriptine for the treatment of patients with the polycystic ovary syndrome failed to include control groups. This study, therefore, was undertaken to determine the clinical and endocrine effects of bromocriptine and a placebo (given in a random double blind fashion) in 55 patients with PCOS. The plasma levels of estrone, estradiol, testosterone, androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate, 17-hydroxyprogesterone, and serum PRL and gonadotropins (LH and FSH) were measured before treatment. In addition the serum PRL response to TRH and the serum LH and FSH response to GnRH were determined. The effects of acute administration of bromocriptine (2 X 2.5 mg at 12-h intervals) on serum gonadotropins and their response to GnRH were studied to explore the possibility that this test might predict the response to chronic bromocriptine treatment. Bromocriptine then was given at an initial dose of 1.25 mg twice daily. If no clinical improvement occurred 2.5 mg were given twice daily for at least 6 months. Hormonal measurements and dynamic tests were repeated after 3 and 6 months of therapy. The endocrine profile of the two groups was not different before treatment. The clinical results were not better in the treatment group than in the placebo-treated patients: therapy was successful (restoration of ovulatory cycles of less than 35 days duration) in 12 of 28 patients taking bromocriptine vs. 8 of 27 taking placebo. Slight improvement (1 or 2 ovulations) occurred in 3 of 28 vs. 3 of 27, and failure (no clinical change) in 13 of 28 taking bromocriptine vs. 16 of 27 taking placebo, respectively. Serum PRL fell significantly in the bromocriptine group, and there was a significant fall in the serum LH response to GnRH in both groups. No hormonal measurement or response predicted the clinical response to treatment. The only significant effect of chronic bromocriptine therapy (5 mg/day) in patients with the polycystic ovary syndrome was to lower the serum PRL concentration.

Serum alpha-inhibin levels in polycystic ovary syndrome: relationship to the serum androstenedione level.

To date, only one study has demonstrated increased serum inhibin levels in women with polycystic ovary syndrome (PCOS). Moreover, no relationship between serum inhibin and either FSH or androgen levels has been noted. This lack of data could be due to 1) the heterogeneity of PCOS and the small sample size of previous studies, and/or 2) the complexity of circulating inhibin molecular forms, which hinders the precise evaluation of bioactive inhibin. In the present study, alpha-inhibin levels were assayed in the serum of 61 healthy women and 72 PCOS patients by means of an alpha-alpha enzyme-linked immunosorbent assay. Serum alpha-inhibin levels together with LH and androstenedione (A) levels were significantly increased in PCOS women (mean +/- SD, 1.45 +/- 0.55 vs. 0.94 +/- 0.36 U/mL in controls; P < 0.001). Moreover, simple and partial regression analysis demonstrated that serum A levels were positively and independently correlated to serum alpha-inhibin (r = 0.32; P < 0.01) and LH levels (r = 0.48; P < 0.001) in PCOS. The respective influences of alpha-inhibin and LH on A variability were 20% and 80%, as determined by multiple regression analysis. In conclusion, in agreement with recent in vitro data, our in vivo results argue for a role of inhibin in the hyperandrogenism of PCOS together with, but independently from, that of LH. Further studies are needed to determine whether this effect is produced by inhibin A and/or B.

Clinical and biological phenotypes in late-onset 21-hydroxylase deficiency.

We analyzed data from 20 patients with late-onset 21-hydroxylase deficiency (LOHD). Three clinical phenotypes could be distinguished among the 18 women. Seven (39%) presented with clinical features suggesting polycystic ovarian disease (PCOD). However, despite androgen levels similar to those of patients with typical PCOD, high serum LH to FSH ratios were not consistently found. Seven other women (39%) presented with isolated hirsutism, suggesting idiopathic hirsutism. The remaining 4 women (22%) had no manifestations of androgen excess and were considered to have the cryptic form of LOHD. Serum 17-hydroxyprogesterone (17-OHP) and androgen levels were similar in the 3 phenotypes, suggesting that the clinical expression of LOHD in women is modulated by individual factors, such as androgen sensitivity. The 2 men were detected by family study and were clinically normal. Since clinical diagnosis of LOHD is impossible, we concentrated on hormonal data with the aim of providing guidelines for the biological diagnosis of LOHD. Assay of basal serum 17-OHD at 0800 h in both sexes and in the early follicular phase in women was sufficient to establish the diagnosis of LOHD in most patients. If doubtful results are obtained, i.e. serum 17-OHP levels between 2 and 5 ng/ml, an ACTH test must be performed. Post-ACTH serum 17-OHP levels exceeding 10 ng/ml confirm the diagnosis of LOHD. Such results should avoid confusion with heterozygotes for 21-hydroxylase deficiency, whose frequency is high within the general population and may be even higher in patients with idiopathic hirsutism or PCOD.

Modification of human transcortin by tetranitromethane. Evidence for the implication of a tyrosine residue in cortisol binding.

The effect of tetranitromethane on the cortisol binding activity of human transcortin has been investigated. This reagent induced a decrease of activity concomitant with nitration of tyrosine residues. An oxidation of sulphydryl groups was also observed but had no implication on cortisol binding. The nitration was specifically oriented in the site at pH6 and with low concentrations of reagent; under these conditions, a single essential tyrosine per molecule of transcortin seems implicated in cortisol binding. The absence of denaturation in modified transcortin was checked by circular dichroism spectra and polyacrylamide gel electrophoresis. Site specificity was demonstrated by full protection with cortisol against inactivation.

Plasma levels of atrial natriuretic peptide at peak exercise: a prognostic marker of cardiovascular-related death and heart transplantation in patients with moderate congestive heart failure.

BACKGROUND: Conflicting data have been published concerning exercise performance and hormonal activation. Previous studies have demonstrated the prognostic information of plasma levels of neurohormones at rest in patients with congestive heart failure. No study has examined the prognostic information of plasma levels of hormones at peak exercise. METHODS: Fifty-five consecutive ambulatory patients with stable moderate congestive heart failure (New York Heart Association class II to III) performed a maximal symptom limited cardiopulmonary exercise test with the determination of peak oxygen consumption. Blood samples were drawn at rest and at peak exercise for the determination of plasma levels of atrial natriuretic peptide, aldosterone, and plasma renin activity. RESULTS: Hormonal activation was present at rest, and exercise significantly increased hormonal values. There was no correlation between exercise parameters and hormonal values either at rest or at peak exercise. After a median follow-up period of 724 days, in univariate and multivariate Cox analysis, the most significant independent prognostic marker was the plasma level of atrial natriuretic peptide at peak exercise. Patients with a plasma level of atrial natriuretic peptide > 38 pmol/L had an event rate of 48% compared with an event rate of 14.8% in the other subgroup (p < 0.01). CONCLUSIONS: In patients with stable moderate congestive heart failure, exercise increased hormonal values, but there was no relationship between hormonal activation and exercise performance. Plasma level of atrial natriuretic peptide at peak exercise was the most significant independent marker of cardiovascular-related death and of cardiovascular-related death and heart transplantation.

Usefulness and limits of quick intraoperative measurements of intact (1-84) parathyroid hormone in the surgical management of hyperparathyroidism: sequential measurements in patients with multiglandular disease.

This study was designed to assess whether reliability of quick intraoperative assay of intact (1-84) immunoreactive parathyroid hormone (iPTH) could allow us to quit after removing one (or several) enlarged parathyroid gland(s) and obtaining a normal iPTH level. Intact iPTH was assayed during surgery before removal of enlarged parathyroid gland(s) and 5, 10, and 20 minutes afterward. Forty-seven patients entered the study: 40 with primary hyperparathyroidism (32 with uniglandular disease and eight with multiglandular disease) and seven with secondary hyperparathyroidism; all underwent bilateral neck exploration. Among 32 patients with uniglandular disease, five had normal basal intraoperative levels, 25 demonstrated a clear-cut drop from supranormal to normal levels, and two had elevated levels. Among the eight patients with multiglandular disease, two had undetectable levels and two had normal levels after removal of the first enlarged gland. The seven patients with secondary hyperparathyroidism demonstrated a decline in PTH levels, suggesting hormone clearance similar to that of patients with primary hyperparathyroidism. In conclusion, quick intraoperative assay with intact (1-84) iPTH (1) is not hampered by renal insufficiency, (2) may overlook a second enlarged gland after removal of a first adenoma and obtaining normal iPTH levels, and (3) should not be used as a substitute for bilateral neck exploration.

Essential hypertension: first reason for persistent hypertension after unilateral adrenalectomy for primary aldosteronism?

BACKGROUND: Despite cure of primary aldosteronism by surgical resection, hypertension persists postoperatively in 30% to 50% of patients. The aim of this study was to determine factors influencing long-term outcome of blood pressure after unilateral adrenalectomy for primary aldosteronism. METHODS: Records of 100 patients who underwent unilateral adrenalectomy for primary aldosteronism from 1970 through 1997 were reviewed. Patients were distributed in 2 groups according to whether blood pressure was normal (criteria of World Health Organization). Clinical, biochemical, and pathologic data were compared. RESULTS: All patients were biochemically cured. Blood pressure was normal in 56 patients and improved in 44 (mean follow-up, 69 and 59 months). Persistent hypertension correlated with age, known duration and seriousness of preoperative hypertension, family history of hypertension, no preoperative response to spironolactone, and contralateral adrenal hypertrophy. Gender, surgical approach, and pathologic findings were not predictive factors of blood pressure outcome. The prevalence of hypertension was almost the same in these postoperative patients as the prevalence of essential hypertension in a random population of the same age. CONCLUSIONS: Early unilateral adrenalectomy allows cure or improvement of hypertension in all patients with primary aldosteronism induced by unilateral excessive source of aldosterone secretion regardless of the pathologic findings. Persistent hypertension suggests that coexisting essential hypertension is present.

Screening heterozygotes for 21-hydroxylase deficiency among hirsute women: lack of utility of the adrenocorticotropin hormone test.

Heterozygosity for 21-hydroxylase deficiency (21-OHD) was investigated in 174 adult hirsute women by using the sum of the incremental responses of serum 17 alpha-hydroxyprogesterone (17 alpha-OHP) and progesterone (P) (delta 17 alpha-OHP + P), 60 minutes after a 0.25 mg intravenous (IV) bolus of synthetic adrenocorticotropic hormone (ACTH). The distribution of 17 alpha-OHP + P in hirsute women was bimodal, allowing two subgroups to be distinguished. In one subgroup including 137 patients, the mode was similar to controls and all values were lower than 3 ng/ml. Thirty-seven (21%) patients constituted another subgroup with values higher than 3 ng/ml and could a priori have been considered as heterozygotes for 21-OHD. However, human leukocyte antigen genotyping provided no conclusive evidence that this subgroup included exclusively heterozygotes for the 21-OHD.

Acute effects of bromocriptine on gonadotropin secretion in polycystic ovary syndrome.

Thirty-two women presenting with polycystic ovary syndrome (PCO) were studied on 3 consecutive days. On day 1, plasma androstenedione, testosterone, dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), 17-hydroxyprogesterone (17-OHP), estrone (E1), estradiol, serum prolactin (PRL), and PRL response to thyrotropin-releasing hormone were determined. On day 2 the patients were given two placebos at 1-hour intervals; then serum PRL, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) and the LH and FSH responses to LH-releasing hormone (LH-RH) were determined. On day 3 the patients were given two 2.5-mg tablets of bromocriptine (BRCR) at 12-hour intervals; then serum PRL, LH, and FSH and the LH and FSH responses to LH-RH were again determined. After BRCR, mean values of basal serum PRL (P less than 0.001), LH (P less than 0.05), and FSH (P less than 0.001) and the FSH response to LH-RH (P less than 0.01) fell with respect to the values determined on day 2. Our group of patients was heterogeneous regarding the effects of BRCR upon the LH response to LH-RH. Of 32 women undergoing the trial, 17 did not respond to BRCR (change of the LH response to LH-RH less than 33% with respect to day 2). They were called "nonresponders." Among the 15 who responded to BRCR, 10 decreased their LH response greater than or equal to 33% ("decreasers") and 5 increased their LH response greater than or equal to 33% ("increasers"). Decreasers had mean values of serum PRL, plasma E1, DHEA-S, and 17-OHP higher than nonresponders (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

[Determination of serum transcortin levels by electroimmunodiffusion (author's transl)]. / Dosage de la transcortine sérique par électro-immunodiffusion

The isolation of transcortin in a pure form made possible the preparation of a monospecific anti-human transcortin rabbit serum. Serum transcortin levels were measured by electroimmunodiffusion. Experimental results expressed as errors by the calculating of interserial reproducibility were 4.74 per 100. The mean value was significantly different for men (36 subjects: 39.7 +/- 3.6 mg/l) from women (36 subjects: 42.1 +/- 3.9 mg/l). The transcortin determination was performed in pregnancy serum and in serum of women during oestroprogestative treatment. Some studies were performed in pathological cases (hyper- and hyperthyroidism, hyper- and hypocorticism, Kahler disease, ascitic cirrhosis).

Plasma levels of endothelin-1 at rest and after exercise in patients with moderate congestive heart failure.

Plasma levels of endothelin-1 are increased in patients with severe congestive heart failure related to various etiologies. However, conflicting data have been published in patients with moderate congestive heart failure. Moreover, the effect of exercise on plasma levels of endothelin-1 is not precisely known. We determined the plasma levels of endothelin-1 in a homogenous group of patients with idiopathic dilated cardiomyopathy in stage II of the New York Heart Association functional classification at rest and at peak exercise. In this group of patients, plasma levels of endothelin-1 were increased compared to a control group (2.9 +/- 0.27 vs. 1.96 +/- 0.24 pmol/l, P < 0.01, mean +/- S.E.M.), as were plasma levels of atrial natriuretic peptide (26.3 +/- 6.3 vs. 2.95 +/- 0.7 pmol/l, P < 0.001), plasma renin activity (12.6 +/- 2.98 vs. 1.75 +/- 0.23 ng/ml per h, P < 0.001) and plasma levels of aldosterone (217 +/- 29.3 vs. 154 +/- 18.8 pg/ml, P < 0.05). In contrast to the other hormones, exercise did not increase plasma levels of endothelin-1. There was no correlation between plasma levels of endothelin-1 and plasma levels of atrial natriuretic peptide, and no correlation between left ventricular ejection fraction, peak oxygen consumption and hormonal values. In conclusion, plasma levels of endothelin-1 are increased in a homogeneous group of patients with idiopathic dilated cardiomyopathy and moderate congestive heart failure. Endothelin-1 could participate in the progression of heart failure. Exercise did not increase the plasma levels of endothelin-1 in contrast to the other hormones.

Response of atrial natriuretic factor to surgical pericardial drainage in patients with chronic pericardial effusion.

Previous studies have demonstrated the importance of atrial transmural pressure in the secretion of atrial natriuretic peptide. These studies have been performed in patients with pericardial effusion and hemodynamic compromise. The response of atrial natriuretic peptide to the drainage of chronic pericardial effusion without clinical evidence of tamponade is unknown. We studied 13 patients with chronic abundant pericardial effusion but without hemodynamic compromise. Blood samples for hormonal determinations were drawn before and after surgical pericardiocentesis. Right atrial pressure was measured during the procedure. Drainage induced a significant increase of atrial natriuretic peptide (from 12 +/- 3.9 to 105 +/- 22.8 pmol/l, P < 0.001, mean +/- S.E.M.), correlated with the fall in right atrial pressure (from 7.65 +/- 1.18 to 4.31 +/- 1.46 mmHg, P < 0.05, r = 0.68, P = 0.01). This increase was inversely correlated with the rise of mean blood pressure after surgery (from 84 +/- 2.37 to 100 +/- 5.3 mmHg, P < 0.05, r = 0.65, P < 0.02). Plasma renin activity decreased after drainage (from 8.12 +/- 2.57 to 3.27 +/- 0.65 ng/ml/h, P < 0.05). Surgery induced an increase of plasma levels of aldosterone (from 811 +/- 241 to 1199 +/- 249 pmol/l, P < 0.05), which were reduced after pericardiocentesis (371 +/- 102 pmol/l, P < 0.02). In patients with chronic abundant pericardial effusion, surgical pericardiocentesis induced a significant increase of atrial natriuretic peptide, correlated with a fall in right atrial pressure. The increase of atrial natriuretic peptide was similar than in patients with tamponade, despite a moderate fall in right atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

[21-hydroxylase autoantibodies as a marker of adrenal involvement in patients with autoimmune endocrinopathies]. / Intérêt du dosage des anticorps anti-21 hydroxylase comme marqueur de l'atteinte surrénale dans les endocrinopathies auto-immunes.

Autoantibodies against 21-hydroxylase are common in idiopathic Addison's disease. The objective of this study was to determine the frequency of these antibodies in different endocrine autoimmune diseases with or without adrenal insufficiency and to follow up their evolution. We have used a radiobinding assay based on 125-I labeled 21-hydroxylase (21-OH-AB, RSR, UK). Serum samples with 21-hydroxylase antibodies levels equal or greater than 1.0 U/ml were considered as positive. We found these autoantibodies in 21/23 idiopathic Addisonian patients, in 0/18 patients with isolated hypothyroïdism, in 0/6 patients with isolated Grave's disease, in 2/14 patients with isolated ovarian failure, in 1/27 patients with 2 ou more associated autoimmune diseases without adrenal insufficiency. The comparison between patients with or without adrenal insufficiency has shown, for this assay, a sensibility of 91 %, a specificity of 96 %. The 21-hydroxylase autoantibodies were followed up in 4 patients with Addison's disease and showed progressive decreasing levels. We can not exclude that the addisonian sera might become negative for these antibodies after the total destruction of adrenal cortex. In conclusion, the presence of 21-hydroxylase autoantibodies is highly specific for idiopathic Addison's disease and the level of these antibodies decrease with disease duration.

[Urinary excretion of 17-ketosteroids studied by gas chromatography in the healthy adult: distribution of values]. / Excrétion urinaire des 17-cétostéroïdes étudiés par chromatographie gazeuse chez l'adulte sain: distribution des valeurs

The level of different urinary 17-ketosteroids were assayed using a method requiring an enzymatic hydrolysis and a solvolysis, a separation by gas-chromatography on OV 225 (cyanopropylsilicone) and a detection by flame ionisation. The method has been discuted. Statistical study of the results obtained in 89 healthy and ambulatory subjects (divided in 4 groups according to sex and age) has shown a log-normal distribution of urinary excretions.

[Atrial natriuretic hormone and endocrine functions]. / Hormone natriurétique auriculaire et fonctions endocrines.

The atrial natriuretic hormone (ANP) is a cardiac hormone which gene and receptors are widely present in the body. Its main function is to lower blood pressure and to control electrolyte homeostasis. Its main targets are the kidney and the cardiovascular system but ANP interacts with many other hormones in order to regulate their secretion. The adrenal glands are the first endocrine target. Steroidogenesis, especially mineralocorticoid synthesis, is inhibited by ANP, but glucocorticoid production seems to be depressed too. As ANP synthesis is enhanced by the latter, it suggests a regulatory loop. Moreover ANP inhibits the thyroid synthesis whereas its production is enhanced by thyroid hormone. The hypothalamo-hypophyseal axis is another important target. ANP inhibits ACTH release and arginine vasopressin secretion. Vasopressin enhances ANP synthesis while GH decreases it. Finally the endocrine effects of ANP strengthen the cardiovascular and renal effects of the hormone, antagonizing the salt and water retention due to aldosterone and AVP. Because of a local production, ANP may also act as a paracrine hormone that influences the function of many endocrine systems (ovarian function for instance). In the central nervous system, ANP acts as a neurotransmitter in order to regulate pituitary and vegetative functions. Plasma ANP levels are impaired in several endocrine diseases : the plasma hormone levels increase in hypercortisolism, hyperaldosteronism, thyrotoxicosis and inappropriate antidiuretic hormone secretion; it decreases in hypothyroidism. In case of Addison's disease, ANP may be used to assess the quality of mineralocorticoid treatment, in association with the other biological criteria.

[Application of adsorption chromatography to the colorimetric determination of urinary estrogens in late pregnancy (author's transl)]. / Application de la chromatographie d'adsorption sur XAD-2 au dosage colorimétrique des estrogènes urinaires de fin de grossesse.

A new extraction procedure of urinary estrogens, based upon adsorption chromatography on Amberlite XAD-2, was deviced for a selective and complete extraction of these components. Estrogens were then quantified, without preliminar hydrolysis, by the colorimetric Kober reaction, modified by Ittrich. The reliability of this method has been established by comparison with four other methods.

[comparison of the effects on phosphocalcic metabolism and bone of 3 protocols of vitamin D administration in the elderly]. / Comparaisons des effets sur le métabolisme phosphocalcique et sur l'os de trois protocoles d'administration pendant un an de la vitamine D chez la personne âgée.

According to recent studies, vitamin D deficiency may contribute to the osteoporosis observed in elderly subjects, with reduced intestinal calcium absorption and secondary hyperparathyroidism. Vitamin D deficiency is often present in elderly people, due to inadequate diet and confinement at home. The administration of either oral vitamin D in doses of 4,000 IU per day, or six-monthly intramuscular injections of ergocalciferol 600,000 IU, combined with a daily intake of at least 1 g of calcium brings back to normal both 25 OH D concentrations and parathyroid hormone levels. When pursued for one year, these treatments also maintain the formation of cortical bone, as shown by the metacarpal index. As for the concentration of 25 OH D, it seems that 60 to 75 nmol/l are necessary to restore calcium homeostasis. The dietary habits of elderly people are such that a supplement of medicinal calcium is required. Finally, we regard the parenteral form of ergocalciferol as being preferable to the oral form at that age for better compliance with treatment.

[Phosphocalcium metabolism in the elderly. Study of 101 subjects living in an institution]. / Etude du métabolisme phosphocalcique de la personne âgée chez 101 sujets vivant en institution.

Calcium and phosphorus metabolism was studied in 101 institutionalized subjects over 70 years of age (mean: 82.5 years). The study was performed in serum and urine; it included parathyroid hormone and calcidiol (250HD3) assays and radiological examination of bones with determination of Meunier's index and metacarpal cortical index. Calcidiol concentrations did not vary with age but were higher in people who left the institution and in men. In contrast, there was a significant age-group related increase of parathyroid hormone concentrations. This increase was accompanied by an increase of parathyroid hormone activity, as shown by a parallel fall in phosphorus reabsorption rate. These findings are in agreement with current pathogenetic theories on senile osteoporosis. Invalid subjects had higher urinary calcium and serum parathyroid hormone levels and a lower cortical index. Paradoxically, there was less vertebral collapse as evaluated by Meunier's index, which may suggest that very old patients develop progressive cortical bone hyperresorption entirely independent of sequelae from their former trabecular osteoporosis.

[Posttraumatic neurogenic hyponatremia with late onset]. / Hyponatrémie neurogène post-traumatique de révélation tardive.

Ten months following a severe head injury, a 26-year-old man developed a syndrome of inappropriate secretion of antidiuretic hormone (ADH) with a grand mal seizure occurring after an increased intake of non alcoholic beverages. The water loading test was negative but the sorbitol infusion test was positive. In the basal state, plasma concentration of ADH was inappropriate to plasma osmolality. ADH has also been measured during dynamic tests (infusions of sorbitol and of normal saline; complete and partial water restriction; propranolol and diphenylhydantoin treatments). In spite of the poor sensitivity of these measurements when ADH concentrations are low, our results indicate that the plasma osmolality threshold at which ADH secretion is inhibited was probably reset at a level lower than normal.