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H Dechaud

Publications and source records attributed to H Dechaud.

At least 19 recordsLinked to original sources
PubMed1992

[Sub-capsular hematoma of the liver during pregnancy: a case report].

A sub-capsular haematoma of the liver is a rare but very serious complication of pregnancy. We report a case of a primipara whose pregnancy was first complicated by hypertension, then by a haematoma of the liver at the 28th week of amenorrhoea. It was diagnosed because of the clinical symptoms associated with the hypertension and a pain in the right hypochondrium and nausea. The diagnosis of haematoma of the liver was made before rupture and confirmed by ultrasound of the liver and by tomodensitometry made it possible to avoid operating on the liver during the laparotomy that was carried out to terminate the pregnancy. Regular X-ray follow-ups showed that the lesion had regressed in six months. MRI investigation of the parenchyma of the liver showed no cause of the lesions. If there is even the slightest suspicion of a haematoma of the liver in pregnancy, ultrasound nowadays should be carried out because it is indispensable to make the diagnosis.

Adult↗
PubMed1992

[The combined stimulation test sulpiride-TRH in the investigation of prolactin secretion].

We have studied the response of prolactin (PRL) secretion to the test combining i.m. sulpiride in the dose 1 mg/kg followed by 200 micrograms i.v. of TRH, in 12 normal women and 37 patients with hyperprolactinaemia. The response was expressed as a percentage rise in plasma PRL concentration (delta %) 20 minutes after the administration of sulpiride or TRH. In the controls the response in PRL secretion to sulpiride worked out at between 639 and 2,760%. When there was a pituitary adenoma or supra-sellar lesion the PRL response to sulpiride was always less than 481%. On the other hand the PRL response with TRH after sulpiride was not significantly different as between the controls (less than 175%) and the patients (less than 91%). We conclude: 1) the combined sulpiride and TRH test is useless for assessing hyperprolactinaemia; 2) the sulpiride test on the other hand makes it possible to show that hyperprolactinaemia cannot be stimulated and to suspect the presence in this case of a prolactin producing adenoma or a supra-sellar tumour.

Adenoma↗
PubMed1991

Glucocorticoid receptors in lymphocytes in anorexia nervosa.

OBJECTIVE: The aim was to explore the down-regulation of the glucocorticoid receptors during hypercortisolaemia in anorexia nervosa. DESIGN: Urine and plasma samples were obtained for cortisol determination and blood lymphocytes were isolated for receptor binding studies. PATIENTS: Sixteen anorexic patients, aged 16-27 years, with a mean +/- SEM body mass index of 14.2 +/- 2.0 (ranging from 11.1 to 17.4), and 15 normal women were studied. Six patients were reinvestigated after a significant weight gain. MEASUREMENTS: The binding capacity and affinity of the glucocorticoid receptors were measured with dexamethasone as ligand on lymphocytes. RESULTS: In patients, both total and free plasma cortisol concentrations were higher than in the normal women, as was their urinary free cortisol; the number of glucocorticoid receptors per cell (Ro) and the binding affinity (Kd) for dexamethasone were, however, not significantly different (Ro: 7687 +/- 1750 vs 7347 +/- 1285 sites/cell; Kd: 7.7 +/- 2.4 vs 7.4 +/- 1.7 nM at 24 degrees C). After weight gain (14 +/- 2 to 16 +/- 2 kg/m2), receptor numbers were 8421 +/- 2126 (pre) and 9011 +/- 500 (post) sites/cell, which are not significantly different (P greater than 0.2); the Kd was unchanged (9.3 +/- 2.6 vs 9.2 +/- 2.4 nM). CONCLUSIONS Hypercortisolaemia does not down-regulate the lymphocyte glucocorticoid receptors in anorexia nervosa and a post-receptor defect might be involved in peripheral tissue resistance to the effects of glucocorticoid hormones in undernutrition.

Adolescent↗
PubMed1991

[Inverse relationship between body mass index and fasting insulinemia with testosterone-binding protein in hirsutism].

To identify the factor(s) involved in the decreased of sex steroid binding-protein (SBP) in hirsute women, we have investigated which parameters were in correlation with SBP in a population of 90 hirsute women. We found no significant correlation of SBP binding capacity with the plasma concentrations of the main androgens. Conversely, SBP was in inverse and significant correlation with body mass index and with the fasting insulin plasma level. These findings confirm that nutritional status must be considered in the physiopathology of hyperandrogenism in women. The control of overweight may be a goal for treating hirsutism in some patients.

Androgen-Binding Protein↗
PubMed1990

[Treatment of hirsutism with spironolactone and progestagen combination].

The antiandrogenic activity of spironolactone was used for treating hirsutism in 76 women, 29 of whom also had acne. Midcycle vaginal bleeding was observed in 21 patients under spironolactone 75 mg per day. This side-effect disappeared after a progestagen administered 10 days each month was added to the treatment. With this combination, spironolactone was well tolerated and effective in treating acne within the first months of administration, but in 61 percent of the patients at least 6 months were required to improve hirsutism.

Acne Vulgaris↗
PubMed1989

[Familial congenital adrenal hyperplasia caused by 11 beta-hydroxylase. Failure of prevention of sexual ambiguity and prenatal diagnosis].

In a sepharad family from Morocco, 2 children out of 4 had congenital adrenal hyperplasia with 11 beta-hydroxylase deficiency. The index case had a very severe genital masculinization (Prader V), diagnosed at 18 months of age. For the fourth pregnancy, dexamethasone was given from the 8th to the 24th week of amenorrhea, in order to prevent the virilization of a female fetus. The treatment was interrupted for 5 days, at the 20th week, because of amniocentesis. As the amniotic steroid concentrations were normal, the treatment was stopped. Nevertheless the neonate also has severe virilization of the external genitalia and postnatal hormonal studies confirmed the diagnosis of congenital adrenal hyperplasia due to 11 beta-hydroxylase deficiency. The reasons for the failure of the treatment are analyzed.

Adrenal Hyperplasia, Congenital↗
PubMed1988

[Changes in plasma binding protein of sex steroids and transcortin during the treatment of menopause with oral estrogens].

Sex steroid binding protein (SBP) and transcortin (CBG) plasma concentrations were measured in 15 postmenopausal women before and during oral administration of estradiol 2 mg plus estriol 1 mg given alone for one month and in sequential combination with noresthisterone 1 mg for the following months. The results were compared with those obtained in a group of 13 premenopausal women who were studied during the early follicular phase or during administration of estroprogestagens. The oral administration of estrogens slightly increased CBG levels (56.1 +/- 11.4 vs 46.0 +/- 5.2 mg/l, P less than 0.05) which in 4 patient were higher than in premenopausal women. The mean SBP level was lower in postmenopausal women than in premenopausal women (1.02 +/- 0.40 vs 1.35 +/- 0.38 micrograms/dl, P less than 0.02), and SBP correlated negatively and significantly with the body mass index (r = 0.794, P less than 0.02). On average, SBP increased twofold during the estrogen treatment. In 6 patients the concentrations of estrogen-stimulated SBP were higher than the upper limit for premenopausal women. Lowered SBP levels were normalized during estrogen therapy. During estrogen substitution in the postmenopausal women, the mean E2 to SBP ratio (an index of free estradiol) was within the normal limits for premenopausal women. These results demonstrate that SBP is highly sensitive to oral estrogens. The increase in SBP is associated with a free E2 index which is within the physiological range of premenopausal women. The risk(s) or benefit(s) associated with the increase in SBP during estrogen therapy in postmenopausal women deserve to be evaluated by further investigations.

Administration, Oral↗
PubMed1987

Effects of drug administration on gonadotropins, sex steroid hormones and binding proteins in humans.

The possible mechanisms by which the administration of drugs may alter the gonadal function in humans are considered in this review. Based on personal data, and on data published in the literature, the following events may occur: (1) blockade of gonadal steroidogenesis; (2) interaction of drug(s) with the steroid-binding protein system in plasma, and (3) interference of drug(s) at the level of the feedback control of gonadotropin secretion. Representative examples of the above mechanisms are as following: (1) Ketoconazole possesses inhibitory effects in vitro on cytochrome P-450. When given in adult males, it decreased the plasma concentrations of testosterone (T) and androstenedione and increased 17 alpha-hydroxyprogesterone levels, suggesting that this drug acts in vivo on gonadal steroidogenesis by blocking the 17,20-lyase. (2) Danazol is a progestagen with high affinity for sex steroid-binding protein (SBP); when given in high dosages in normal males, it increased rapidly the dialyzable fraction (percent protein unbound or free fraction) of T. This suggests that by interacting with the binding sites of SBP, danazol and/or its metabolites displace the fraction of T bound to SBP. However, in males as well as in females, the long-term administration of danazol decreased also the binding capacity of SBP, and consequently increased the free fraction of sex steroid hormones. (3) Dihydrotestosterone (DHT), the most active androgen in many target cells, given at therapeutic dosages to adult males, resulted in a decrease in plasma concentrations of luteinizing hormone (LH) and T, without any significant change in the percent of free T, even though the affinity of DHT for SBP is higher than that of T. This suggests that the main effect of DHT is to inhibit gonadotropin secretion at the central level. (4) Flutamide, a nonsteroidal antiandrogen, increased both LH and T levels, demonstrating its pure antiandrogenic activity on gonadotropin secretion. The consequence(s) of the effects of such drugs on the production, the metabolic clearance rate and the bioavailability of sex steroid hormones are discussed.

Androgens↗
PubMed1987

Increased luteinizing hormone sensitivity to dopaminergic inhibition in Graves' disease.

The effect of dopamine infusion (4 micrograms X kg-1 X min-1 from 9.00 to 13.00 h) on serum LH and FSH concentrations were studied in 15 patients (10 women, 5 men) with diffuse toxic goitre, and 10 healthy subjects (6 women, 4 men). Basal serum LH (17.0 +/- 0.8 IU/l) and oestradiol (women: 3.74 +/- 1.84; men: 3.05 +/- 0.77 pmol/l) were elevated in patients, whereas serum FSH and PRI were normal. Dopamine infusion did not modify serum FSH levels, but significantly depressed LH concentration in both hyperthyroid and healthy subjects. The LH decrement was more pronounced (P less than 0.01) in patients with Graves' disease (8.4 +/- 1.4 IU/l) as compared with controls (2.3 +/- 0.9 IU/l). There was a positive correlation between the maximum net decrease and the basal LH concentration (r = 0.95). The per cent decrease of LH levels in the hyperthyroid patients (54 +/- 4) was higher (P less than 0.001) than that in the controls. The finding of enhanced sensitivity to dopamine inhibition in thyrotoxic patients suggests that their inappropriately elevated serum LH levels may result in part from a reduced dopaminergic inhibition of LH secretion.

Adult↗
PubMed1986

Sex hormone binding globulin in women with anorexia nervosa.

In 29 women with anorexia nervosa, on a blood sample withdrawn at 0900 h before and during weight gain, the binding parameters of serum sex hormone binding globulin (SHBG) were measured by a solid phase method and the levels of testosterone, oestradiol and thyroid hormones were measured by radioimmunoassay. The binding capacity of SHBG was higher than the upper limit for normally menstruating women in 23 patients whilst its affinity for binding testosterone at 37 degrees C was normal (0.32-0.53 X 10(-9) mol/l). The mean levels of testosterone, oestradiol and free thyroxine were normal and the mean level of triiodothyronine was significantly (P less than 0.005) decreased. The binding capacity of SHBG did not correlate significantly with body mass index, percent weight lost, thyroid hormone or sex hormone levels. In 9 patients, an i.v. infusion providing 1200-1400 calories daily was given for 1 week. In these patients a significant decrease (P less than 0.005) in the binding capacity of SHBG (from 74.7 +/- 26.7 to 52.9 +/- 21.8 nmol/l) and a significant increase (P less than 0.001) in T3 levels (from 0.69 +/- 0.21 to 0.95 +/- 0.13 nmol/l) was observed. In 14 patients, when a weight gain of at least 5% was obtained, the binding capacity of SHBG fell into the normal range (25.6-62.9 nmol/l) while T3 levels rose to normal (0.85-2.30 nmol/l). These findings suggested that variations of calorie intake and/or body weight may influence the binding capacity of SHBG in the human.

Adolescent↗
PubMed1986

The 24-h cortisol secretory pattern in Cushing's syndrome.

The 24-h plasma cortisol profile was obtained at 20-min intervals in 18 patients with Cushing's syndrome (10 with Cushing's disease, 5 with adrenal adenoma, 2 with ectopic ACTH secretion and 1 of questionable aetiology). The mean cortisol level was maximum in the case of ectopic ACTH secretion. The coefficient of variation of cortisol levels was subnormal in all except 2 subjects. Periodogram calculations, providing a best-fit curve (B F C) for each profile, showed that the existence of a significant baseline variation is a frequent feature. In certain cases, it is compatible with the persistence of a true circadian rhythm (2 patients with Cushing's disease; 1 patient with adrenal adenoma). The alteration of plasma cortisol pulsatility is much more pronounced in patients with adrenal adenoma than in patients with Cushing's disease. This is consistent with the hypothesis of a predominantly tonic secretion blunting the episodic hormone release. In 9 patients with Cushing's disease, the plasma cortisol pattern was suggestive of a combination of episodic cortisol release under CRF control and of continuous cortisol secretion due to constant stimulation from an autonomous ACTH source. Two cases were possibly of hypothalamic origin, as suggested by the presence of enhanced cortisol pulsatility and of a normal circadian amplitude. The analysis of the 24-h profile of plasma cortisol in Cushing's syndrome contributes to our understanding of the physiopathological mechanisms underlying this disorder and may help the diagnosis of its aetiology.

Adrenocorticotropic Hormone↗
PubMed1985

Determination of plasma testosterone by mass fragmentography using [3,4-13C]testosterone as an internal standard.

The combination of glass capillary gas chromatography--mass spectrometry is especially suitable for the recognition of compounds. The use of [3,4-13C]testosterone as internal standard, mass fragmentography and isotope ratio measurement have been applied to the quantitative determination of testosterone in plasma. This paper describes the method, using tert.-butyldimethylsilylmethoxime and di-heptafluorobutyrate derivatives. The calibration graph in isotopic dilution is examined. The results obtained are compared with the results obtained by radioimmunoassay. The sensitivity of the method is judged from the lower limit of detection: 4.5 pg. The precision, and inter- and intra-assay are calculated.

Dehydroepiandrosterone↗
PubMed1985

Daily variations of plasma sex hormone-binding globulin binding capacity, testosterone and luteinizing hormone concentrations in healthy rested adult males.

In this study the daily variations of plasma sex hormone-binding globulin (SHBG) binding capacity were measured together with plasma testosterone and luteinizing hormone (LH) concentrations in 7 healthy rested adult males. Plasma SHBG-binding capacity demonstrated a significant circadian rhythm (acrophase = 2.06 p.m.; mesor = 0.35 +/- 0.6 ng testosterone bound/100 ml; amplitude = 17% of the mesor). Plasma testosterone also showed a circadian rhythm (acrophase = 7.02 a.m.; mesor = 4.38 +/- 0.67 ng/ml; amplitude = 18% of the mesor). The free testosterone index (or the ratio between plasma testosterone and SHBG-binding capacity) was not correlated with plasma LH levels. In our hands this last parameter did not vary according to a circadian pattern. These data are discussed in terms of a feedback mechanism controlling the pituitary-testis axis regulation.

Adult↗
PubMed1985

Beta-lipotropin and cortisol responses to an intravenous infusion dexamethasone suppression test in Cushing's syndrome and obesity.

An i.v. infusion dexamethasone (Dex) test was used to investigate the ACTH feedback response in 9 normal subjects, 12 obese patients, and 11 patients with Cushing's syndrome. Dex phosphate was infused iv for 4 h, starting at 1100 h (1 mg/h). Plasma concentrations of beta-lipotropin (beta LPH) and cortisol were measured every 20 min between 0900 and 1600 h, then every 2 h until midnight and at 0900 h the next day. In normal subjects and obese patients, plasma beta LPH and cortisol concentrations fell rapidly to less than 40 ng/liter and 3 micrograms/dl, respectively, at the end of Dex infusion. Subsequent values remained low through 0900 h the next day. In 7 patients with Cushing's disease, basal plasma beta LPH and cortisol concentrations declined by greater than 50% during the Dex infusion. In these patients, rapid escape from suppression occurred between 1600 and 2400 h; by 0900 h the following day, beta LPH and cortisol levels were higher than 100 ng/liter and 10 micrograms/dl, respectively. In 3 patients with adrenal tumors, beta LPH concentrations were low, and cortisol concentrations did not decline during the Dex infusion. In 1 patient with ectopic ACTH secretion, beta LPH concentrations were high and were not suppressed by the Dex infusion. We conclude that the iv infusion Dex suppression test can distinguish patients with Cushing's syndrome from normal or obese subjects and can aid in the etiological diagnosis of Cushing's syndrome.

Adult↗
PubMed1985

Lack of beta-adrenergic role for catecholamines in the development of hyperglycemia and ketonaemia following acute insulin withdrawal in type I diabetic patients.

In order to evaluate the role of beta-receptor mediated effects of catecholamines in the metabolic deterioration following insulin withdrawal in insulin-dependent diabetic patients we have measured in 5 patients metabolic substrate and hormone concentrations during a 6 hours arrest of insulin infusion, without or with a simultaneous infusion of propranolol. During insulin deprivation plasma epinephrine and norepinephrine increased slightly (from 107 +/- 10 ng/L to 173 +/- 6 ng/L and from 307 +/- 37 ng/L to 518 +/- 77/ng/L respectively (p less than 0.05), cortisol decreased physiologically, but growth hormone and glucagon were not significantly modified. Free insulin decreased progressively from 12.2 +/- 2.5 mU/L to 5.4 +/- 1.1 mU/L (p less than 0.01). Blood glucose and ketone bodies rose sharply before any significant change in catecholamine levels. Plasma free fatty acids and blood glycerol increased progressively and their rise appeared somewhat temporally related to the variations of catecholamine levels. The addition of propranolol to insulin deprivation did not modify the changes in hormone concentrations in spite of a slightly greater rise of epinephrine (from 78 +/- 4 ng/L to 179 +/- 7 ng/L, p less than 0.05) and norepinephrine (from 395 +/- 80 ng/L to 679 +/- 153 ng/L, p less than 0.05). The rises of glucose and ketone bodies were unaffected whereas the increases of free fatty acids and glycerol were slightly blunted. In conclusion, we have no evidence for a beta-adrenergic mediated role for catecholamines in the development of hyperglycaemia and ketonaemia in non-stressed insulin deprived diabetic patients, and only small evidence for a permissive effect on lipolysis.

Adult↗
PubMed1985

[Evolution of plasma levels of SHBG (sex-hormone binding globulin) during ovulation induction using gonadotrophins].

The plasma levels of proteins bound to steroids come under the influence of the levels of estrogens. This is why we have studied the changes in plasma SHBG in sterile women who were being treated by gonadotropins (HMG-HCG). The plasma level of SHBG was worked out using Laurell's electroimmunoassay technique with an autoradiographic display using estradiol labeled with I.125. It only takes 48 hours contact with radio films. Out of 12 patients 9 responded to the treatment as demonstrated by the plasma levels of estradiol (E2) and progesterone (P). We have found that in these women there was a rise in plasma SHBG which was significant from the 7th day of the treatment onwards (3.7 +/- 1.7 mg/l as against 5.9 +/- 2.6 mg/l, p less than 0.01) and this reached nearly twice the base level when E2 reached its maximum level (6.4 +/- 2.7 mg/l). When treatment was stopped the plasma level of SHBG dropped to that of the follicular phase, but it was out of step with the plasma E2 levels. The index of free E2 as compared with E2/TEBG showed a close superimposition when compared with the levels of E2 obtained using a radioimmunological method. This fact reinforces the value of plasma E2 as the way of monitoring the effect of induction of ovulation. Our overall conclusion is that a marked and rapid change in the level of plasma E2 directly influences the level of plasma SHBG. The consequences for treatment are that it is important to respect as far as possible the physiological conditions that are present when induction of ovulation is undertaken.

Estradiol↗
PubMedDate not supplied

[Luteal insufficiency and elevation of sex-binding proteins by demegestone].

Demegestone, a norprogesterone derivative, was administered during the luteal phase in 6 normally ovulatory women and in 10 patients with luteal insufficiency. Demegestone decreased the LH surge and the plasma concentrations of estradiol and progesterone in the normally ovulatory women and did not modify the binding capacity of sex steroid binding protein (SBP). In the patients with luteal insufficiency, demegestone increased significantly SBP (0.94 +/- 0.24 vs 1.32 +/- 0.56 micrograms/dl, p less than 0.05) and decreased the free testosterone index (T/SBP) (38.8 +/- 33.3 vs 25.4 +/- 18.5, p less than 0.05). Transcortin, was unchanged during demegestone treatment in both groups of women. The results showed that demegestone did not exercise androgenic activity on SBP conversely to the nortestosterone derivatives which decrease SBP and confirmed that progesterone and norprogesterone derivatives influence positively the regulation of SBP.

Adult↗