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Biomedical subjects

I Grégoire

Publications and source records attributed to I Grégoire.

14 recordsLinked to original sources
PubMed1997

The effectiveness of a professionally led support group for men with prostate cancer.

PURPOSE: This study investigated the effectiveness of support groups in: (a) helping patients and significant others voice their concerns about the physical and psychosocial implications of their disease in an emotionally supportive context, (b) enhancing patients' understanding of their disease and its treatments and side effects, and (c) facilitating more active involvement in their treatment. A total of 54 men and some family members participated in seven separate groups. Patients were invited to participate with a letter describing the goals of the support groups or were referred by nurses and doctors. METHOD: The participants met for a series of 10 weekly sessions each of 90 minutes duration. The meetings were led by a nurse and a psychologist, who together provided information on the medical aspects of the disease and its treatment, focused on the psychologic reactions to a diagnosis of cancer, and encouraged participants to adopt more active, health-promoting coping strategies. RESULTS: The participants were surveyed anonymously by questionnaire at the end of the tenth session on their views and attitudes about the support groups and their overall satisfaction. The results showed that participants in the support group felt they had a better understanding of their illness and perceived themselves as more involved in their treatment. They expressed that sharing their experiences with others gave them reassurance, helped alleviate their anxiety, and provided them with a more positive outlook. CONCLUSION: It was concluded that these findings furnished evidence of the effectiveness of support groups in facilitating perceptions of enhanced coping in men with prostate cancer.

Aged↗
PubMed1990

Reduction in testicular function in rats. I. Reduction by a specific gonadotropin-releasing hormone antagonist in fetal rats.

A gonadotropin-releasing hormone (GnRH) antagonist, when injected 24 h before sacrifice to rat fetuses, did not modify plasma testosterone concentrations in males on day 18 of gestation but it did on days 19, 20 and 21. This GnRH antagonist reduced plasma luteinizing hormone (LH) levels and increased pituitary LH content in both male and female 19-day-old fetuses from mothers adrenalectomized on day 14 of gestation. An inverse relationship between plasma testosterone and LH levels was noted in males and females, on days 19 and 21. These data suggest that the hypothalamic control of gonadotropic function is operating by day 19 of fetal life and that a negative feedback of testosterone on LH and probably GnRH release is also operating in rat fetuses on days 19 and 21 of gestation.

Adrenalectomy↗
PubMed1990

Reduction in testicular function in rats. II. Reduction by dexamethasone in fetal and neonatal rats.

Chronic administration of dexamethasone in drinking water to maternal rats from days 15 to 21 of gestation (1) reduced plasma testosterone concentrations in male fetuses between days 19 and 21 but not earlier on day 18 and abolished the prenatal peak of plasma testosterone which normally occurs on day 19 of gestation, and (2) suppressed the postnatal surge of plasma testosterone in male newborns 1.5 and 2 h after delivery at term by cesarean section. The administration of dexamethasone to male fetuses at birth induced 1 h later a slight but not significant increase in hypothalamic gonadotropin-releasing hormone (GnRH) and pituitary luteinizing hormone (LH) contents, reduced drastically plasma LH levels and completely prevented the postnatal surge of plasma testosterone which occurred normally in littermate controls. A rise in pituitary LH content, and a sharp reduction in plasma LH and testosterone concentrations were noted in 19-day-old male fetuses whose mothers were acutely treated with dexamethasone on day 18 of gestation. Similar evolutions for LH were observed in littermate females. These results suggest that the inhibitory effects of exogenous glucocorticoids on testosterone secretion could be mediated in both fetuses and newborns at least partially through suppression of the hypothalamic and pituitary secretion of GnRH and LH, respectively, and provide insight how stress or hormone imbalance may affect the development of this neuroendocrine system.

Animals↗
PubMed1987

Effect of pregnancy on plasma renin activity and glomerular synthesis of prostaglandins and thromboxane in rats.

Normal pregnancy in women and rats is characterized by an increased glomerular filtration rate. Because prostaglandin glomerular synthesis has been reported to be increased in 2 other circumstances with glomerular hyperfiltration (streptozotocin-induced diabetes and high protein dietary intake in Heymann nephrilis), we studied prostaglandin biosynthesis in glomeruli obtained from pregnant Wistar rats in comparison with non pregnant rats during the estrus cycle. Comparatively to the 3 first phases of the cycle, and wether or not arachidonic acid was present, PGE2 and PGF2 alpha production rates were found significantly higher in diestrus 2 (2-3 fold increase for both) at 15 days of pregnancy (2 fold increase for PGE2, 5-6 fold increase for PGF2 alpha) and at 21 days of pregnancy (5-6 fold increase for both). On the other hand synthesis of TXB2 was not increased during pregnancy nor during diestrus 2. Plasma renin activity (PRA) was increased during pregnancy. It is concluded that in presence of increased PRA, the increased synthesis of PGE2 may be the hormonal factor explaining, at least in part, the hemodynamic mechanism of glomerular hyperfiltration which has been previously described by micropuncture techniques and characterized by increased renal plasma flow, increased glomerular filtration pressure and decreased ultrafiltration coefficient.

Animals↗
PubMed1987

[Perinatal influence of sex hormones on the differential activation of corticotrope function during stress in the male and female].

The stress-induced activation of the corticostimulating function of the pituitary gland was noted to vary according to sex in both the adult and the newborn. The pituitary response in testosterone or estradiol-injected females at the time of birth was similar to that of intact males, in contrast, the castration of the males performed just before the postnatal surge of plasma testosterone was unable to modify at the 8th day, the male characteristic evolution in response to ether inhalation. Present data suggest--in the male, prenatal differentiation of the neuroendocrine pathways involved in the pattern of ACTH release in response to ether inhalation, probably in correlation with the peak of plasma testosterone on day 19 of gestation--in the female, the existence of androgen--sensitive structures in early postnatal life. An alpha stimulatory effect of norepinephrine on these neuroendocrine pathways was suggested. Present report also discuss--the catecholaminergic control of CRF X producing neurons--the sex dependent AVP and/or oxytocin (OT) release induced by a stress--the AVP and OT potentiation of CRF-induced ACTH release.

Adrenocorticotropic Hormone↗
PubMed1987

[Pregnancy-induced hypertension and pre-eclampsia develop in spite of high circulating levels of cardionatrin].

Plasma cardionatrine was measured during pregnancy in 14 normotensive non pregnant women, 15 normotensive pregnant women, 35 pregnancy induced hypertension (PIH) and 10 preeclampsia (PE) and again 2 months after delivery in respectively 7, 15 and 7 cases together with plasma volume, PRA and plasma aldosterone. The plasma levels of cardionatrine are higher in pregnant normotensive women than in non pregnant normotensive women suggesting that pregnancy per se stimulates cardionatrine secretion. The higher levels of cardionatrine in PIH and specially in PE during pregnancy and the greater decrease of plasma cardionatrine after delivery in the hypertensive patients than in the normotensive controls exclude a deficiency of cardionatrine secretion in the pathogenesis of hypertension. These data rather suggest a compensatory role of cardionatrine in the prevention of blood pressure increase. Plasma volume was decreased in PIH (-17 p. 100) and in preeclampsia (-25 p. 100). The simultaneous high levels of cardionatrin may explain the inappropriate stimulation of the renin and aldosterone secretion in these hypovolemic hypertensive states.

Adult↗
PubMed1987

[Digoxin-like natriuretic factor, raised during normal pregnancy, is increased in pregnancy-induced hypertension and pre-eclampsia].

UNLABELLED: The increase of peripheral resistance in pregnancy induced hypertension (PIH) and in preeclampsia (PE) is not yet explained since previous studies have found that renin-angiotensin-aldosterone system is actually depressed, that adrenergic system is inconstantly stimulated and that vasodilating prostaglandins are inconstantly decreased. In order to get a better insight in the pathogenesis of PIH and PE, we have measured the 24 h urinary excretion of digoxin-like natriuretic factor (DLF) in 15 normotensive pregnant women (NP), in 29 women with PIH and in 6 women with PE under normal salt diet, without treatment. DLF have been measured by radio receptor binding assay. Normal values were established in 14 normotensive non pregnant (NNP). In NP, 24 h urinary excretion of DLF was significantly higher than in NNP (respectively 14.9 +/- 7.5 and 9.5 +/- 2.5 nmol/mmol of creatininuria, p less than 0.01). Comparatively to NP, 24 h urinary excretion of DLF was significantly higher in PIH (31.7 +/- 19 nmol/mmol of creatininuria) and in PE (40.7 +/- 16.3 nmol/mmol of creatininuria). In PIH and PE, there were simultaneously a decrease of plasma renin activity and plasma volume but no difference for plasma catecholamines. IN CONCLUSION: 1. the production of DLF is increased by normal pregnancy; 2. it is increased in PIH and PE in comparison with NP and may explain the increase of peripheral resistance.

Adult↗
PubMed1987

[Evaluation of maximal filtration capacity and renal functional reserve by an oral protein-loading test in adults and children].

After a protein load, the glomerular filtration increases to a maximum called maximal filtration capacity (MFC). The difference of this value with that observed in the fasting state defines the functional renal reserve (FRR). Fifty oral protein loads have been performed in 16 controls (13 adults and 3 children) and 31 patients with kidney disease or hypertension (22 adults, 9 children, 3 tests being performed twice). The load consisted in the adults of 80 g of various proteins. In the children the load consisted in the 100% of the protein intake recommended of the whole day. The urinary samples were made hourly during the 5 hours following the beginning of the meal. The MFC was not always observed during the 2 hours following the end of the meal. However the mean of the clearances measured during these 2 hours allowed an acceptable evaluation of the FRR in 42 out of 50 cases and had the advantage to reduce the errors linked to incomplete bladder voiding. In the adult controls the mean of hourly determined MFC is 156 +/- 27 ml/min, the mean of the clearances measured on the 2 hours following the meal is 136 +/- 21 ml/min and the fasting clearance 96 +/- 22 ml/min. The FRR is null in all patients with a nephropathy with a fasting clearance below 40 ml/min. It is modest or null in patients with acquired or congenital solitary kidney. Three out of five patients with proteinuria have MFC and FRR higher than the mean of the patients with comparable fasting clearances but without proteinuria suggesting that proteinuria is associated with a hyperfiltration state.

Administration, Oral↗
PubMed1985

Comparison of 1 alpha-OH-vitamin D3 and high doses of calcium carbonate for the control of hyperparathyroidism and hyperaluminemia in patients on maintenance dialysis.

27 patients on hemodialysis (dialysate aluminium less than 0.7 mumol/l for 2 years, and 2 mumol/l before) whose plasma Ca and PO4 were adequately controlled for already 6 months by high doses of CaCO3 alone (mean +/- SD: 9 +/- 5 g/day), were randomly divided into 2 groups, a control group (c group) which was kept on the same treatment, and a group in which CaCO3 was reduced to 3 g/day but in which plasma Ca was kept normal due to 1 alpha-OH-vitamin D3 administration (1 microgram/day at the beginning, 0.3 microgram/day after 6 months; 1 alpha group) whereas plasma phosphate was kept below 6.0 mg/dl because of Al(OH)3 (2.7-5 g/day). Initially, the 2 groups were comparable as regards the plasma concentrations of total and ionized Ca, phosphate, alkaline phosphatases, medium and C-terminal parathyroid hormone (PTH) and aluminium, but the control group had lower plasma 25-OH-vitamin D (25-OHD.) After 6 months, the same difference in plasma 25-OHD was found with comparable plasma concentrations of total and ionized calcium as well as of medium and C-terminal PTH (beta error 1%). However, plasma concentration of phosphate and the plasma Ca phosphate product, as well as the plasma aluminium were higher in the 1 alpha group whereas their PCO3H- was lower. Although the alkaline phosphatase values were not significantly different between the 2 groups, they increased only in the control group because of 1 patient who developed a vitamin-D-deficient osteomalacia (plasma 25-OHD 3 ng/ml), which was subsequently cured by physiological doses of 25-OHD3. The incidence of transient hypercalcemia (15 vs. 21 episodes) and worsening of soft tissue calcifications (3 in each group) was the same in the 2 groups.

Adult↗
PubMed1985

Critical role of oxalate restriction in association with calcium restriction to decrease the probability of being a stone former: insufficient effect in idiopathic hypercalciuria.

The probability of being a stone former (PSF) was calculated in 3 groups of idiopathic calcium stone formers [with normocalciuria (NC), dietary hypercalciuria (DH) and idiopathic hypercalciuria (IH)] in 4 conditions: while on a free diet; on a calcium- and oxalate-restricted diet during 4 days; after an oxalate load, while on a 1.5-gram calcium diet, and after an oxalate load while on a calcium-restricted diet. Combined calcium and oxalate restriction significantly decreased PSF only in NC and DH whereas the decrease was not significant in IH because of a concomitant significant increase in oxalate excretion. Increase of PSF with the oxalate load was significantly greater during a calcium-restricted diet than during the 1.5-gram calcium diet in all groups of patients (4, 6 and 12 times greater in NC, DH and IH, respectively). These data show the critical role of oxalate restriction when calcium is restricted in order to decrease the PSF. This combined restriction is however not sufficient in idiopathic hypercalciuric patients to decrease their PSF.

Calcium↗
PubMed1984

[Primary hyperparathyroidism. Lack of effect of cimetidine on plasma levels of parathyroid hormone and calcium].

Because of the contradictory results formerly published as regards the effect of cimetidine in primary hyperparathyroidism, we have studied the effect of cimetidine at the daily dose of 1200 mg in 14 cases of primary hyperparathyroidism. The diagnosis was ascertained in all cases by the coexistence of an otherwise unexplained hypercalcemia and of a concomitantly elevated plasma concentration of immunoreactive parathyroid hormone (PiPTH) measured by 2 different antibodies and confirmed in 10 cases by surgical neck exploration. In 5 cases with severe hypercalcemia (greater than 12.0 mg/l) cimetidine was discontinued after 5 days because of its lack of effect on both plasma concentrations of calcium and PiPTH, and the patients were successfully operated. In 8 cases with milder hypercalcemia, cimetidine was given for 1.5-6 months. There was no significant change in both plasma concentrations of calcium (PCa) and PiPTH but a regression analysis showed that PCa was negatively correlated to time with a correlation coefficient which would have become significant if the follow-up had been 9 months. In the last patient severe hypercalcemia was controlled by simultaneous administration of phosphate, indomethacin and cimetidine without concomitant decrease of PiPTH; and 6 weeks after cimetidine discontinuation no significant increase of PCa and PiPTH occurred. These data show that cimetidine has no clinically therapeutic value in primary hyperparathyroidism.

Adolescent↗