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Biomedical subjects

P Garnier

Publications and source records attributed to P Garnier.

At least 19 recordsLinked to original sources
PubMed1992

Influence of calcitonin treatment on the osteocalcin concentration in the algodystrophy of bone.

Algodystrophy (AD) attacks all tissues in the affected region and results in the rapid demineralization of bones. Osteocalcin (OC) and alkaline phosphatase (AP) are markers of bone turnover. Calcitonin is the treatment of choice of AD. Two groups of patients were studied: Group I (n = 8)--acute stage of AD (before and during the calcitonin treatment), Group II (n = 5)--late chronic stage of AD. In the acute stage of AD both OC level and AP activity were increased. They were normal in the chronic stage of AD. During the calcitonin treatment OC level normalized after 14 days and then increased again. During the treatment, AP activity temporarily increased and then returned to the initial level. We confirm that an increased bone turnover is observed in the acute stage of AD. Discrepancy between OC level and AP activity reflects the local metabolic disturbances. Salmon calcitonin inhibits the algodystrophic process and probably contributes to the activation of the skeletal restoration.

Acute Disease↗
PubMed1990

Growth hormone (GH) and GH-releasing hormone response to ACTH 1-17 at different times of day. Evidence of a circadian stage dependence.

The effect of injection of ACTH 1-17 on the secretion of GH has been examined at three different circadian stages (07, 14 and 21 h) in the winter. Each week for six consecutive weeks the subjects were investigated before and after I.M. injection either of saline (controls) or 100 micrograms ACTH 1-17. Each subject was his own control. The peak plasma concentration of GH was always found 40 min after the injection. The larger absolute increase and the greater AUC curve were seen following the injections at 14.00 h and 21.00 h. The findings could not be attributed to an effect on GH-RH, since secretion of it remained unchanged during the test.

Adolescent↗
PubMed1990

Effects of oral contraceptives on carbohydrate and lipid metabolisms in a healthy population: the Telecom study.

In a cross-sectional study that aimed to identify risk factors for diabetes, 1290 consecutive, healthy, nonpregnant women of child-bearing age were examined in a center for preventive medicine. An in-depth interview about menses, use of oral contraceptives, and menopause was performed. Plasma glucose at fasting and 2 hours after a 75 gm glucose load, glycated hemoglobin A1c, fasting plasma insulin, total plasma cholesterol, and triglycerides were measured. Compared with nonusers taking no progestogens, oral contraceptive users (n = 431; 33.4%) were younger (p less than 0.001) and leaner (p less than 0.001). After adjustment for age and body mass index, oral contraceptive users had higher 2-hour plasma glucose (p less than 0.001), higher fasting plasma insulin (p less than 0.01), and higher triglycerides levels (p less than 0.01). Fasting plasma glucose, glycated hemoglobin A1c, and total cholesterol did not significantly differ between the two groups. In relation to dosage and types of steroid components, few differences have been found between high-dose and low-dose oral contraceptives or according to the estrogen-progestogen balance of the preparations. Use of oral contraceptives appears to induce an increase of insulin-resistance markers, which have recently been cited as risk factors for ischemic vascular diseases. These markers should be carefully monitored in oral contraceptive users.

Adult↗
PubMed1990

Oral contraceptives, insulin resistance and ischemic vascular disease.

From a large prospective study on diabetes risks, 1112 professionally active, non-menopausal, non-pregnant, healthy women were cross-sectionally analysed according to their use of oral contraception. After adjustment for age, weight and diabetes risk factors, those taking the pill, compared to those who did not, had significantly higher fasting serum insulin, triglycerides and 2-h 75 g OGTT blood glucose levels. The insulin-resistance markers which have recently been cited as ischemic vascular disease risk factors should be carefully monitored in pill users.

Adult↗
PubMed1990

Growth hormone secretion during sleep. II. Interrelationships between growth hormone secretion, insulin-like growth factor I and sex steroids.

The serum levels of insulin-like growth factor I (IGF I), dehydroepiandrosterone sulfate (DHAS), testosterone (T) and estradiol (E2) have been measured in 78 prepubertal and 57 early pubertal patients referred for short stature, at the same time when their secretion of GH was evaluated both during nocturnal sleep and by two conventional stimulation tests. According to the results of GH measurements they were considered as having a normal secretion of GH (group I), a complete GH deficiency (group II), a partial GH deficiency (group III), low responses to stimuli with normal secretion during sleep (group IV) or a nocturnal neurosecretory dysfunction (group V). Though widely scattered, the IGF I levels showed the following characteristics: a significant increase at puberty from 0.77 to 1.29 U/ml (p less than 0.001) in the so-called endocrinologically normal patients of group I, not in the other groups; in the prepubertal patients of group I, a correlation of IGF I with chronological age (r = 0.47, p less than 0.005) and bone age (r = 0.52, p less than 0.002); significantly reduced IGF I levels in patients of group II having complete GH deficiency (p less than 0.001); no significant differences between prepubertal patients with partial or atypical GH deficiency from groups III, IV, V and prepubertal patients from group I; lower pubertal levels in groups III, IV, V than in pubertal patients from group I (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

[Growth hormone deficiency (hGH) in 1 case of terminal renal insufficiency treated with chronic hemodialysis].

The authors report the clinical history of a seventeen years old boy with renal failure treated with chronic haemodialysis since eleven and a half years of age. Growth velocity was 1.5 cm/year. The stature was below 5 SD as compared to the mean for the age. Hormonal measurements showed a complete growth hormone (hGH) deficiency and hyperparathyroidism. Thyroid, adrenal and gonadic secretions were normal, but the responses of TSH and prolactin to TRH were abnormal, showing an hypothalamic disturbance. hGH treatment, with thyroxin substitution, enhanced growth velocity up to 4 cm/year. Respective influences of hGH treatment, puberty and hyperparathyroidism on the incomplete correction of growth velocity are discussed.

Adolescent↗
PubMed1990

[Relation of the secretion of growth hormone (GH), somatomedin C/IGF I (IGF I) and steroids before and after the beginning of puberty in patients of short stature].

Somatomedin C/IGF I, dehydroepiandrosterone sulfate (DHAS), testosterone (T) or estradiol (E2) have been measured in 154 patients of a previous study in which growth hormone (GH) responses to classical pharmacologic stimuli and spontaneous growth hormone secretion during sleep were compared in short children before and at the beginning of puberty. Five groups were identified: Group I, normal growth hormone secreting children; group II, completely growth hormone deficient; group III, partially growth hormone deficient; group IV, with normal sleep secretion and low responses to stimuli; group V, with the reverse situation. The somatomedin C/IGF I levels were widely dispersed. In group I, the mean +/- SEM levels of somatomedin C/IGF I were 0.77 +/- 0.047 U/ml before puberty and 1.36 +/- 0.142 U/ml in early pubertal patients, with a relation to age (r = 0.52, p less than 0.001). The difference between prepubertal and pubertal patients was significant. In groups II to V, there was no pubertal rise of somatomedin C/IGF I. In group II, the mean IGF I level was 0.48 +/- 0.05 U/ml, significantly lower than in prepubertal patients of group I. In groups III, IV and V, it was 0.7 +/- 0.069 U/ml, 0.8 +/- 0.059 U/ml, and 0.73 +/- 0.059 U/ml respectively, not different from prepubertal patients of group I, but significantly lower than in early pubertal patients of the same group. In prepubertal patients, somatomedin C/IGFI was slightly but highly significantly correlated to the growth hormone sleep secretion (r = 0.27, p less than 0.001) and to dehydroepiandrosterone sulfate (r = 0.36, p less than 0.001), but growth hormone and dehydroepiandrosterone sulfate were not correlated together.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Height↗
PubMed1990

[The relation between the secretion of growth hormone (GH), somatomedin C/IGF I (IGF I) and steroids before and after the onset of puberty in patients of small stature].

Somatomedin C/IGF I, dehydroepiandrosterone sulfate (DHAS), testosterone (T) or estradiol (E2) have been measured in 154 patients of a previous study in which growth hormone (GH) responses to classical pharmacologic stimuli and spontaneous growth hormone secretion during sleep were compared in short children before and at the beginning of puberty. Five groups were identified: Group I, normal growth hormone secreting children; group II, completely growth hormone deficient; group III, partially growth hormone deficient; group IV, with normal sleep secretion and low responses to stimuli; group V, with the reverse situation. The somatomedin C/IGF I levels were widely dispersed. In group I, the mean +/- SEM levels of somatomedin C/IGF I were 0.77 +/- 0.047 U/ml before puberty and 1.36 +/- 0.142 U/ml in early pubertal patients, with a relation to age (r = 0.52, p less than 0.001). The difference between prepubertal and pubertal patients was significant. In groups II to V, there was no pubertal rise of somatomedin C/IGF I. In group II, the mean IGF I level was 0.48 +/- 0.05 U/ml, significantly lower than in prepubertal patients of group I. In groups III, IV and V, it was 0.7 +/- 0.069 U/ml, 0.8 +/- 0.059 U/ml, and 0.73 +/- 0.059 U/ml respectively, not different from prepubertal patients of group I, but significantly lower than in early pubertal patients of the same group. In prepubertal patients, somatomedin C/IGF I was slightly but highly significantly correlated to growth hormone sleep secretion (r = 0.27, p less than 0.001) and to dehydroepiandrosterone sulfate (r = 0.36, p less than 0.001), but growth hormone and dehydroepiandrosterone sulfate were not correlated with each other.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Height↗
PubMed1989

Epidemiological features of glycated haemoglobin A1c-distribution in a healthy population. The Telecom Study.

HbA1c was measured in 3240 healthy non-diabetic adult individuals in a working population. There was no difference in HbA1c between sexes. The distribution of HbA1c was approximately normal with a slight difference between mean and median values at all ages in both sexes. HbA1c increased with deterioration of glucose tolerance and with all the known risk factors for diabetes (age, obesity, family history of diabetes, history of a large newborn delivery); age but not body mass index appeared as a factor influencing HbA1c independently. In women, HbA1c levels rose particularly at the age of menopause but the use of oral contraceptives or oestrogens made no difference. In both sexes, HbA1c was higher in smokers than in non-smokers. No consistent seasonal variation was observed. Haematologic factors had a negligible influence on HbA1c level. HbA1c was more highly correlated with fasting plasma glucose than with 2 h-plasma/glucose (r = 0.20 vs 0.11). In a stepwise multiple regression analysis, age followed by fasting plasma glucose were the only two significant factors associated with the level of HbA1c. These data indicate that HbA1c is influenced only by factors closely linked to diabetes.

Adult↗
PubMed1989

Effects of glucagon on systemic and splanchnic circulation in conscious rats with biliary cirrhosis.

To elucidate the relationship between the haemodynamic changes and glucagon in cirrhosis, we infused physiologic and supraphysiologic doses of this hormone in conscious rats with portal hypertension due to biliary cirrhosis. Cardiac output and splanchnic organ blood flows were measured by the radioactive microsphere method before and 30 min after glucagon infusion at doses of 2, 5 and 10 ng/min. Serum glucagon increased from a basal level of 92 +/- 17 pg/ml (mean +/- S.E.) to 399 +/- 89, 1151 +/- 136 and 2064 +/- 328 pg/ml, respectively, in sham-operated rats, and from 743 +/- 75 pg/ml to 1497 +/- 197, 1583 +/- 356 and 2957 +/- 649 pg/ml, respectively, in cirrhotic animals at 2, 5 and 10 ng/min doses. In both groups, cardiac output did not change after glucagon infusion at 2 and 5 ng/min doses, suggesting that factors other than glucagon are primarily responsible for the systemic hyperdynamic circulation in cirrhosis. Portal tributary blood flow increased significantly after glucagon infusion in sham-operated rats by 34 and 65% at doses of 5 ng/ml and 10 ng/ml, respectively, and in cirrhotic rats by 29% at a dose of 10 ng/ml. However, portal tributary blood flow did not change after glucagon infusion at the physiologic dose of 2 ng/min. This study shows that glucagon infused at a physiologic dose does not increase splanchnic blood flow, although it increases portal tributary blood flow at supraphysiologic doses. The discrepancy between blood glucagon levels and splanchnic haemodynamic responses suggests that glucagon plays only a minor role and that other factors are primarily responsible for the hyperdynamic state of the splanchnic circulation in rats with biliary cirrhosis.

Animals↗
PubMed1989

Receptors and neurohormones in human pituitary adenomas.

In order to go further into the pathogenesis of human pituitary adenomas, we studied receptors for neurohormones (thyroliberin, TRH; dopamine, DA; somatostatin, SRIH), for estradiol and epidermal growth factor (EGF) thought to influence hormone secretion and/or cell growth. The following results were obtained: (1) the receptors listed above, with the exception of EGF receptors in the adenomas, are present in normal pituitary tissue and in prolactin (PRL)- and growth hormone (GH)-secreting adenomas; (2) they are functional and their affinities are not different in normal or tumoral tissues; (3) their density is variable and depends on the type of secreting adenoma (GH or PRL), the size of the tumor and the plasma level of the hormone which is secreted, and (4) in nonsecreting adenomas, only TRH receptors are found with characteristics identical to those observed in secreting adenomas. We also showed that TRH is contained in normal and tumoral pituitary tissues. TRH and SRIH are released in vitro from adenomatous cells in large amounts, suggesting their possible synthesis by the pituitary. In both cases a local regulation is observed. TRH release is stimulated in the presence of DA while SRIH is inhibited in the presence of TRH. This neuropeptide release may be implicated in the pituitary hormone regulation through a paracrine or an autocrine mechanism. Thus, the neurohormone receptors found in pituitary adenomas should be dependent on a more complex regulation than it has been envisaged till now.

Adenoma↗
PubMed1989

Normal and growth hormone (GH)-secreting adenomatous human pituitaries release somatostatin and GH-releasing hormone.

Neuropeptides such as vasoactive intestinal peptide, LHRH, or TRH have been found in rat pituitary tissue and could act via paracrine or autocrine actions in this tissue. In this study we investigated whether normal human pituitary tissue and GH-secreting human pituitary adenomas could release somatostatin (SRIH) and GHRH. Fragments from three human pituitaries and dispersed cells from six GH-secreting adenomas (four adenomas were studied for GHRH release and five for SRIH release) were perifused using a Krebs-Ringer culture medium, and the perifusion medium was collected every 2 min (1 mL/fraction for 5 h). GH, GHRH, and SRIH were measured by RIA under basal conditions and in the presence of 10(-6) mol/L TRH or SRIH. Both normal pituitaries and GH-secreting pituitary adenomas released SRIH and GHRH. SRIH release commenced 90-180 min after initiation of the perifusion, at which time GH secretion had decreased significantly. TRH stimulated SRIH release from normal pituitary tissue and inhibited SRIH release from adenoma tissue. GHRH was present at the start of the perifusion, but rapidly disappeared. However, SRIH stimulated GHRH release from normal pituitary tissue, but not from adenoma tissue. Significant amounts of GHRH and SRIH were released during the experiments, suggesting their local synthesis. These results indicate that pituitary cells can release hypothalamic peptides. The liberation of these neuropeptides is regulated, and moreover, their regulation differs between normal and adenomatous pituitaries.

Adenoma↗
PubMed1989

The effects of treatment combining an agonist of gonadotropin-releasing hormone with growth hormone in pubertal patients with isolated growth hormone deficiency.

The final height of patients treated with growth hormone for isolated growth hormone deficiency has, up to now, been subnormal, with a mean below -2 SD in the series reported, an insufficient height at the onset of puberty and a more or less accelerated bone maturation during puberty being two important factors of the poor results. A long-acting analogue of gonadoliberin, Trp6-GnRH, has been given to GH-treated patients with isolated growth hormone deficiency at the time they reached pubertal stage 2, in combination with unchanged doses of GH, for one year in 11 and for two years in 7 of them. It resulted in an increase in the height age/bone age ratio and a reduction of the height insufficiency for bone age. The increase was slight but significant after one year, and fair after two years, in spite of reduced annual growth rate. Post-analogue follow-up in 5 patients with continued GH treatment showed a good development of growth and of puberty. It is concluded that combination of the long-acting Trp6-GnRH analogue and GH for 1-2 years in patients with isolated growth hormone deficiency whose puberty starts with a very insufficient height may be an appropriate way to improve their growth parameters. Studies with increased doses of GH or increased frequency of injections could help to optimize the results. Several years of follow-up are needed for demonstrating the results on final height.

Adolescent↗
PubMed1989

[Neurohormones coming from the normal and tumoral human anterior pituitary. Secretion and regulation in vitro].

Several neuropeptides, classically associated with the hypothalamus have been found in the anterior pituitary and their local synthesis has been hypothesized. Using normal and tumoral human pituitaries we found in the tissue itself different neuropeptides (TRH, SRIH, GHRH) and dopamine in variable quantities according to the nature of the tissue. They were all present in normal pituitaries while only stimulatory neurohormones like TRH and GHRH were found in tumoral tissue implying an imbalance between the stimulatory and inhibitory control of hypophyseal hormones (PRL and GH) in pituitary adenomas. Fragments from normal pituitaries and dispersed cells from GH, PRL and nonsecreting adenomas, were perifused for 4 hours in a Krebs-Ringer medium collected every 2 min and GH, PRL, TRH, GHRH and SRIH were measured by RIA under basal conditions and in the presence of 10(-6) mol/L DA, TRH or SRIH. Neuropeptides and DA were characterized by HPLC. Both normal and tumoral pituitaries released TRH, SRIH and GHRH in large amounts suggesting their local synthesis. There was an in situ regulation between SRIH and GH as their secretion profile was negatively correlated, GH secretion decreasing while SRIH secretion was increasing. Moreover the release of TRH was stimulated 5 to 20 folds by DA, while PRL decreased at the same time. Pulses of TRH and SRIH had differential effects on GHRH and SRIH release according to the nature of the tissue as TRH stimulated SRIH release from normal pituitary while it inhibited SRIH release from adenoma. These results indicate that anterior pituitary cells can release neuropeptides which are probably endogenously synthesized and have a local regulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1989

[Determination of EGF receptors (epidermal growth factor) in the placenta and breast tumors].

Receptors for Epidermal Growth Factor (EGF) have been identified in different types of tumors and they are often associated with other characteristics which are related to a bad prognosis. A technic has been established to measure membrane receptors in human placenta, which is appropriate for the study of tumors. Preparations of placental membranes were incubated either with increasing amounts (0.1 to 3.0, 10(-9) M) of EGF labeled with 125I (method by saturation) or with 0.2, 10(-9) M labeled EGF and increasing concentrations (0 to 1.6, 10(-9) M) of cold EGF (method by competition). The KD obtained with both technics are not significantly different: 0.85 and 0.77, 10(-9) M respectively, as well as the maximum binding capacity: 5.9 and 4.4 pmol/mg protein respectively. A preliminary study in breast tumors showed that 2 out of 9 contained significant amounts of receptors (58 and 114 fmol/mg protein). One of these two tumors held both estradiol and progesterone receptors. In the other 7 tumors without EGF receptors only one did not contained any estradiol or progesterone receptors. Further studies are needed to evaluate the relationships between EGF/sex hormone receptor status and the degree of breast tumor malignancy.

Breast Neoplasms↗
PubMed1988

Growth hormone secretion during sleep. I. Comparison with GH responses to conventional pharmacologic stimuli in pubertal and early pubertal short subjects. Effects of treatment with human GH in patients with discrepant measurements of GH secretion.

Growth hormone (GH) was measured in 215 short children (147 males and 68 females, 123 prepubertal, 92 at early pubertal stages), comparing GH responses to classical pharmacologic stimulation tests and spontaneous GH secretion during sleep. GH secretion during sleep, but not GH responses to stimuli, was higher in early pubertal than in prepubertal subjects. The patients were classified into five groups, according to the agreement between GH responses to stimuli and GH secretion during sleep: group I, normal GH-secreting children; group II, completely GH-deficient; group III, partially GH-deficient; group IV, with normal secretion during sleep and low responses to stimuli; group V, with the reverse situation. 30% of the patients were in groups IV and V, both at prepubertal and early pubertal stages. 46 patients of groups II-V were treated with extracted human GH(hGH). The growth rate was enhanced in groups IV and V, to the same extent as in groups II and III. Four points can be concluded: (1) the rise of GH secretion during sleep is an early event at the onset of puberty; (2) the discrepancy between the GH responses to classical stimuli and GH secretion during sleep are of pathological significance; (3) disturbances of GH secretion might be diagnosed by measuring GH secretion during sleep rather than by using conventional stimulation tests; (4) a trial course of hGH treatment could be proposed in patients with both kinds of discrepancies between GH responses to stimuli and GH secretion during sleep.

Adolescent↗
PubMed1988

Endocrine and immunological findings in cryptorchid infants.

In cryptorchid infants, significantly decreased mean levels of plasma testosterone and luteinizing hormone (LH) were found between the ages of 30 and 120 days. The levels of testosterone and LH were significantly correlated. No significant difference was found between infants with bilateral or unilateral cryptorchidism. After 120 days there was no longer any significant difference between cryptorchid infants and controls. No significant change in plasma follicle-stimulating hormone (FSH) was found. These data suggest that subnormal secretion of LH could be the primary abnormality in a proportion of boys with so-called common cryptorchidism. Our studies using LH-releasing hormone and human chorionic gonadotropin stimulation tests in older infants and children agree with the data obtained by measurement of basal plasma hormone levels during the first months of life. Anti-gonadotroph antibodies were found in the sera of approximately 50% of the cryptorchid children and infants studied, using an immunofluorescence technique. A study of 17 mothers and their infants gave concordant results in 16 pairs, 9 with and 7 without antibodies. This lead us to speculate on the possible role of maternal autoantibodies as a cause of partial gonadotrophin deficiency in the perinatal period and thus of testicular maldescent. As cryptorchidism is a syndrome, these findings do not mean that a similar mechanism is operative in all cases. However, these data do suggest that alternatives to the classical anatomical view of the descent and nondescent of the testes should be considered.

Age Factors↗