Search PubMed⌕ Search

Biomedical subjects

C Pariente

Publications and source records attributed to C Pariente.

At least 19 recordsLinked to original sources
PubMed2001

Circulating leptin levels after cardiopulmonary bypass in children.

OBJECTIVE: To characterize the dynamics of circulating leptin in children after cardiac surgery with cardiopulmonary bypass (CPB), which is known to induce a systemic inflammatory response. DESIGN: Investigative study. SETTING: University-affiliated tertiary care hospital. PARTICIPANTS: Eight children (age range, 3 months to 13 years) undergoing CPB to correct congenital heart disease. INTERVENTIONS: The time courses of leptin and cortisol levels were determined. Serial blood samples were collected from the arterial catheter or from the CPB circuit preoperatively; on termination of CPB; and at 2, 4, 8, 12, 18, and 24 hours postoperatively. Plasma was recovered immediately, divided into aliquots, and frozen at -70 degrees C until use. Leptin was measured by a human leptin radioimmunoassay kit. MEASUREMENTS AND MAIN RESULTS: Leptin levels during CPB decreased to 50% of pre-CPB levels (p < 0.01). After termination of CPB, levels increased gradually and peaked at 12 hours postoperatively (10 P.M. to 1 A.M.). Cortisol levels were inversely correlated to leptin levels (p = 0.016). CONCLUSION: CPB is associated with acute changes in circulating leptin levels. These changes parallel those in cortisol, showing an inverse relationship between leptin and cortisol, suggesting a relationship between the neurobiology of these systems that could be important for the neuroendocrine response to CPB. A prognostic role of leptin and its relationship to cortisol after CPB warrant further study.

Adolescent↗
PubMed2001

Circulating leptin and the perioperative neuroendocrinological stress response after pediatric cardiac surgery.

OBJECTIVE: Leptin may be involved in the acute stress response, regulating inflammatory parameters of major importance after cardiopulmonary bypass (CPB) surgery. Critically ill patients demonstrated significant increases in leptin levels in response to stress-related cytokines (tumor necrosis factor, interleukin [IL]-1) and abolishment of the circadian rhythm of leptin secretion. We characterized the pattern of leptin secretion in the acute postoperative period in children undergoing cardiac surgery and compared the changes in leptin levels with concomitantly occurring changes in cortisol levels, IL-8, and clinical parameters. DESIGN: Investigative study. SETTING: University-affiliated tertiary care hospital. PARTICIPANTS AND INTERVENTIONS: Twenty-nine consecutive patients, aged 6 days to 15 yrs, operated upon for the correction of congenital heart defects were studied. Surgery in 20 patients (group 1) involved conventional CPB techniques, and 9 (group 2) underwent closed-heart surgery. The time courses of leptin, cortisol, and IL-8 levels were determined. Serial blood samples were collected preoperatively, on termination of CPB, and at six time points postoperatively. Plasma was recovered immediately, aliquoted, and frozen at -70 degrees C until use. MEASUREMENTS AND MAIN RESULTS: The leptin levels in group 1 decreased during CPB to 51% of baseline (p <.001), then gradually increased, reaching 120% of baseline levels at 12-18 hrs postoperatively (p <.001), returning to baseline levels at 24 hrs (p <.01). In patients undergoing closed-heart surgery (group 2), leptin levels displayed a pattern resembling the first group: they decreased during surgery to 71% of baseline levels (p =.002) and showed a tendency to return to baseline thereafter. All group 1 patients' cortisol levels increased significantly during the first hour of surgery, then decreased, returning to baseline levels at 18-24 hrs postoperatively. There was a significant negative correlation between leptin and cortisol levels (r = -2.8, p <.01). In group 2, cortisol levels increased during and after surgery, peaking 4 hrs postoperatively and decreasing thereafter. IL-8 levels determined in 15 group 1 patients increased significantly during CPB, peaked at the end of surgery, and then decreased but remained slightly elevated even at 48 hrs postoperatively. There was a significant correlation between cortisol and IL-8 levels (r = 2.55, p <.05). Children with leukocytosis, tachycardia, and hypotension had lower leptin levels and less variation over time as opposed to those with an uncomplicated course. CONCLUSIONS: CPB is associated with acute changes in circulating leptin levels. These changes parallel those in cortisol, demonstrating an inverse relationship between leptin and cortisol. Further studies of the prognostic and therapeutic roles of leptin after CPB should be investigated.

Adolescent↗
PubMed2001

Serum leptin levels increase following acute myocardial infarction.

Leptin is secreted into the circulation and communicates the peripheral nutritional status to specific hypothalamic centers. Recent studies suggest that leptin may be involved in the acute response to stress, and that its interaction with the hypothalamo-pituitary-adrenal axis and the inflammatory cytokine system may be of clinical importance. Since these systems are activated during acute myocardial infarction (AMI), we studied leptin and cortisol levels during hospitalization in 30 consecutive patients admitted for AMI. The results show that leptin reached its peak on the second day of hospitalization, with a 2-fold increase from its baseline level on admission (p < 0.02). On day 3, leptin levels declined, and were 46%, 9%, and 6% above baseline on days 3, 4 and 5, respectively. The mean cortisol level was elevated on day 1 and decreased toward normal levels thereafter (p < 0.001). The cortisol level did not correlate with leptin concentration throughout the study. These findings suggest that leptin may have a role in the metabolic changes taking place during the first days after an AMI.

Aged↗
PubMed2000

Pregnancy and amyloidosis: II. Suppression of amyloidogenesis during pregnancy.

The observation of a deleterious effect of pregnancy on kidney function in amyloidosis of familial Mediterranean fever suggests that pregnancy may enhance amyloidogenesis. To determine whether pregnancy may indeed affect amyloidogenesis, pregnant mice were made amyloidotic by administration of amyloid-enhancing factor (AEF) and AgNO3 at different points in time from conception, and amyloid- deposition was studied with the crush-and-smear technique. A possible effect of exogenous female sex hormones (beta-estradiol and progesterone) on amyloidogenesis was studied by administration of these hormones during amyloid induction in nonpregnant female mice. Amyloidogenesis was found to be significantly suppressed in mice during pregnancy. The reduction was possibly related to the effect of pregnancy on the inflammatory stimulus (AgNO3) and not on the administered AEF. Exogenous estrogen and progesterone failed to inhibit amyloidogenesis in nonpregnant mice. These findings suggest that pregnancy may suppress amyloidogenesis in mice. The suppression is caused by an anti-inflammatory effect of pregnancy. Estrogen and progesterone are probably unrelated to this finding.

Amyloidosis↗
PubMed1996

Insulin-like growth factor I and its binding proteins 3 and 4 are increased in Human inflammatory synovial fluid.

OBJECTIVE: To measure insulin-like growth factor I (IGF-I) and its binding proteins (IGFBP) in human synovial fluid (SF), as IGF-I resistance in the chondrocyte was implicated in the pathogenesis of inflammatory arthritis. METHODS: Ten patients with inflammatory arthritis and 7 controls were evaluated. IGF-I and IGFBP-3 were measured by radioimmunoassay while all IGFBP were evaluated by Western ligand blotting. RESULTS: Serum IGF-I did not differ between patients and controls (22.3 +/- 2.9 vs 22.0 +/- 3.0 nmol/l), while significantly higher values were found in inflammatory SF compared with noninflammatory SF (14.7 +/- 1.5 vs 10.2 +/- 1.2 nmol/l; p = 0.05). IGFBP-3 and IGFBP-4 were the most prominent bands found in inflammatory SF by Western ligand blotting. The 24 kDa IGFBP-4 band appeared faintly in 2 noninflammatory effusions and was nearly absent in others. IGFBP-3 levels in sera from the 2 groups did not differ (2.9 +/- 0.3 vs 2.5 +/- 0.3 mg/l), but were significantly higher in inflammatory compared with noninflammatory effusions (1.5 +/- 0.2 vs 0.9 +/- 0.2 mg/l; p = 0.05). CONCLUSION: The pattern of IGFBP in SF differs in inflammatory versus noninflammatory joints.

Adult↗
PubMed1996

Insulin-like growth factor-I and IGF binding protein-3 remain high after GnRH analogue therapy in girls with central precocious puberty.

OBJECTIVE: IGF-I rises in normal adolescence and in central precocious puberty (CPP), secondary to a rise in sex steroids and GH. The aim of this study was to examine changes in serum IGF-I and its major binding protein IGFBP-3 after pharmacological arrest of puberty. PATIENTS AND MEASUREMENTS: Ten girls diagnosed for CPP were evaluated before and during the first 3 months of GnRH analogue (GnRHa) therapy aimed at suppression of the gonadal axis. Serum IGF-I was measured by immunoradiometric assay (IRMA) and IGFBP-3 by both IRMA and Western ligand blotting (WLB). RESULTS: Serum IGF-I was markedly higher in patients with CPP as compared with age matched controls (48.8 +/- 6.5 vs 23.1 +/- 4.9 nmol/l, P < 0.01). While GnRHa therapy caused serum oestradiol levels to return to prepubertal levels in all 10 patients, serum IGF-I levels decreased only minimally after 1, 2 or 3 months of therapy (43.2 +/- 5.6, 42.3 +/- 6.4 and 44.1 +/- 7.2 nmol/l respectively). Serum IGFBP-3 levels as determined using IRMA were also higher in CPP compared with age matched controls (4.70 +/- 0.37 vs 3.71 +/- 0.42 mg/l, P < 0.01). These differences were also evident when measured by WLB. GnRHa therapy caused a small and insignificant decrease in serum IGFBP-3 levels after 1, 2 or 3 months of therapy (4.57 +/- 0.33, 4.48 +/- 0.4 and 4.42 +/- 0.3 mg/l respectively). CONCLUSIONS: The lack of suppression of both IGF-I and IGFBP-3, despite therapy which halts puberty and slows growth velocity, suggests that steroids may be involved in the induction of changes in the GH/IGF-I axis but not in their subsequent maintenance.

Blotting, Western↗
PubMed1995

Clinical, hormonal and sonographic predictors of successful RU-486-induced abortions.

To evaluate which method, clinical, hormonal or sonographic, can be used as the best predictor of successful RU-486-induced abortions, 20 healthy women with fetal cardiac activity, between 6 and 9 weeks from the last menstrual period and desiring abortion, were studied. Fourteen women (70%) successfully aborted, and 6 (30%) failed to abort within 7 days following therapy. A small hematoma, seen as a localized detachment of the gestational sac, was observed in the decidua capsularis in women who aborted successfully. A significant decrease in plasma levels of estradiol and progesterone (p < 0.04) and significantly increased cortisol levels (p < 0.001) in the plasma of the 14 patients who aborted were noted by the 7th day following treatment. No significant changes were observed in the 6 nonaborting patients. In conclusion, the differences in the early sonographic findings may be helpful in the early prediction of successful RU-486 administration.

Abortifacient Agents↗
PubMed1995

A cytosolic protein tyrosine kinase activity is induced by follicle stimulating hormone and insulin like growth factor-I in human granulosa cells.

Follicle stimulating hormone (FSH) induces estradiol (E2) production in rat, porcine and human granulosa cells with a concomitant increase in cAMP. In human granulosa cells insulin like growth factor-I (IGF-I) induces E2 production without cAMP accumulation. In the current study we report that IGF-I and FSH effects on aromatase activity both involve activation of a cytosolic soluble protein tyrosine kinase (CytPTK). This FSH and IGF-I stimulated CytPTK activity was blocked by AG-82 (a tyrosine kinase inhibitor) and by staurosporine (STS) (a non specific protein kinase inhibitor) at concentrations which inhibited E2 production. These new findings strengthen the concept of fail-safe mechanism in E2 production in human granulosa cells by an involvement of tyrosine kinase(s) activity downstream of cAMP formation and protein kinase A (PKA) activation.

Alkaloids↗
PubMed1994

Insulin-like growth factor-I (IGF-I) and IGF-binding protein-2 are increased in cyst fluids of epithelial ovarian cancer.

Expression of insulin-like growth factor-I (IGF-I), its receptor, and IGF-binding proteins (IGFBPs) by epithelial ovarian cancer cells and its mitogenic effect on these cells in vitro suggest that IGF-I may have a role in the regulation of human ovarian cancer. To examine this role in vivo, we explored the IGF-I/IGFBP system in sera and cyst fluids of women undergoing surgery for simple and other benign cysts (n = 20) and borderline (n = 5) and invasive malignant epithelial neoplasms (n = 11). The IGF-I level was significantly higher in cyst fluid from invasive malignant compared to cyst fluid in benign neoplasms (16.1 +/- 2.2 vs. 7.3 +/- 1.2 nmol/L; P = 0.002). Although benign cysts contained almost no IGFBP, high IGFBP-2 levels were detected in malignant cysts regardless of histological type. Serum IGFBP-2 levels were also higher in women with invasive malignancy than in benign controls (1.32 +/- 0.32 vs. 0.53 +/- 0.07 relative units; P = 0.004). IGFBP-2 was higher in cyst fluids than in the corresponding sera, implying local production of this protein. Estradiol was high in fluid from invasive malignant cysts of postmenopausal women and correlated with IGF-I in the cyst fluid. Levels of IGF-I, IGFBP-2, and estradiol in cyst fluid could discriminate between benign and malignant neoplasms, except for the endometrioid-type tumors (n = 2). Our data support a role for IGF-I in the proliferation of ovarian cancer and suggest that IGF-I and estradiol interact in regulating this malignancy.

Adult↗
PubMed1994

Induction of aromatase in human granulosa cells by both follicle stimulating hormone and insulin-like growth factor-I involves tyrosine phosphorylation.

Evaluation of the intracellular signalling mechanisms of follicle stimulating hormone (FSH) and insulin-like growth factor-I (IGF-I) was performed in luteinized and non-luteinized human granulosa cells. A severalfold increase in estradiol production from androstenedione was induced by both hormones in these cells, while only FSH led to a concomitant increase in cAMP. IGF-I bound specifically to its receptor in these cells. Specific tyrosine kinase inhibitors (tyrphostins) blocked the effects of both FSH and IGF-I on aromatase activity without altering FSH-induced cAMP accumulation. These findings demonstrate an involvement of a tyrosine kinase pathway in the intracellular signalling mechanism of the IGF-I effect on aromatase activity. Furthermore, since FSH induction of aromatase activity can be blocked by a tyrosine kinase inhibitor without affecting the level of cAMP production, it can be suggested that tyrosine kinase(s) act downstream of cAMP production and protein kinase A activation.

Adenylyl Cyclases↗
PubMed1993

Serum insulin-like growth factor-binding protein-2 (IGFBP-2) is increased and IGFBP-3 is decreased in patients with prostate cancer: correlation with serum prostate-specific antigen.

Insulin-like growth factors (IGFs) are potent mitogens that stimulate the growth of prostate cells. In serum, IGFs circulate bound to IGF-binding proteins (IGFBPs), which modulate their proliferative action. We studied the electrophoretic pattern of IGFBPs in the serum of patients with prostate cancer and in individuals with increased serum levels of prostate-specific antigen (PSA) in the absence of prostate malignancy. Serum IGFBP-2 was dramatically increased in patients with metastatic prostate cancer compared with healthy controls (23.83 +/- 6.93% vs. 2.95 +/- 0.52% of total serum IGFBPs; P < 0.02). A moderate rise in IGFBP-2 was also observed among patients with increased PSA without malignancy. In contrast, a decrease in serum IGFBP-3 was detected in most patients with metastatic prostate cancer (68.2 +/- 9.1% vs. 95.4 +/- 0.9% of total serum IGFBPs; P < 0.02) and was more pronounced in advanced cases. A highly significant correlation between serum IGFBP-2 and PSA levels was found (r = 0.62; P < 0.002), with a significant negative correlation between serum PSA and IGFBP-3 (r = -0.63; P < 0.002). We suggest that IGFBPs may be involved in growth modulation of prostate malignancy and that alterations in their serum levels may serve as a marker for prostate cancer.

Aged↗
PubMed1992

Ambiguous genitalia due to partial activity of cytochromes P450c17 and P450c21.

We describe a patient with male pseudohermaphrodism who has normal basal serum concentrations of cortisol and high basal levels of progesterone and 17 hydroxyprogesterone. Serum concentrations of androstendione, dehydroepiandrosterone sulfate and testosterone were low. On adequate human chorionic gonadotropin (HCG) stimulation, no rise in serum androstendione, dehydroepiandrosterone sulfate or testosterone concentrations was observed. After ACTH stimulation there was an excessive rise in progesterone and 17 hydroxyprogesterone with no rise in androstendione, dehydroepiandrosterone sulfate, testosterone, deoxycorticosterone or cortisol. These clinical and laboratory data suggest that the patient has a combined defect in both cytochromes P450c17 and P450c21. The genes coding for these cytochromes are on different chromosomes, 10 and 6, respectively. Unlike isolated 21 hydroxylase deficiency where all identical HLA siblings suffer from the disease, HLA typing of the patient's family revealed a healthy brother with identical HLA. This suggests that the gene coding for P450c21 on chromosome 6 is not affected and that the lesion might be on a common enzyme which donates an electron to both cytochromes, most probably a flavoprotein.

17-alpha-Hydroxyprogesterone↗
PubMed1992

The effect of gonadotropin-releasing hormone agonist on the ovarian response and in vitro fertilization results in polycystic ovarian syndrome: a prospective study.

OBJECTIVE: To assess the effect of gonadotropin-releasing hormone agonist (GnRH-a) on pituitary suppression, subsequent ovarian response, and results of in vitro fertilization (IVF) treatments in polycystic ovarian syndrome (PCOS) patients. DESIGN: Randomized prospective study. SETTING: In vitro fertilization program and endocrinologic institute. PATIENTS: Thirty patients with PCOS; 16 received GnRH-a, and 14 did not receive GnRH-a. INTERVENTIONS: Ovum pick-up and embryo transfer. MAIN OUTCOME MEASURES: Response to GnRH-a test, serum and follicular fluid (FF) hormonal measurements, steroid levels, and aromatse activity in granulosa cell (GC) culture, and results of IVF. RESULTS: Pituitary responsiveness was abolished in all patients 14 days after GnRH-a administration, and early luteinization was prevented. Steroid levels in FF did not differ between the two groups. In GC culture, progesterone (P) levels were higher in patients without the GnRH-a (3,704 +/- 1,232 nmol/L versus 2,117 +/- 235 nmol/L; P less than 0.05) as were androstenedione (A) levels (5.3 +/- 1.0 nmol/L versus less than 3.5 nmol/L; P less than 0.05). However, aromatase activity and IVF results were similar in the two groups. CONCLUSIONS: Administration of GnRH-a in patients with PCOS decreases P and A production by the GC cells and prevents early luteinization. It does not affect the IVF results.

Female↗
PubMed1992

The role of insulin-like growth factor-1 (IGF-1) and IGF binding protein-1 (IGFBP-1) in the pathogenesis of polycystic ovary syndrome.

The objective of this study was to elucidate the relationship and role of insulin-like growth factor-1 (IGF-1), IGF binding protein-1 (IGFBP-1), insulin and luteinizing hormone (LH) in the pathogenesis of polycystic ovary syndrome (PCOS). In a pilot study, serum concentrations of IGF-1 were determined in women with PCOS (n = 10), hypopituitarism (n = 12) and normal controls (n = 10). In the main study, serum concentrations of IGF-1, IGFBP-1, insulin and LH in women with anovulation associated (n = 23) and not associated (n = 47) with PCOS were determined. Serum concentrations of IGF-1 were not different in women with PCOS, anovulatory non-PCOS and healthy women but were low in those with hypopituitarism. Mean serum IGFBP-1 in PCOS (33.8 +/- 21.2 micrograms/l) was decreased compared with anovulatory non-PCOS (60.0 +/- 22 micrograms/l) (P = 0.0001), and correlated negatively with insulin concentrations (r = -0.67, P = 0.0006). Patients with PCOS could be separated into those with high LH and those with high insulin levels. It was concluded that women with PCOS have normal serum IGF-1 concentrations but IGFBP-1 levels, regulated by insulin, are low. Hyperinsulinaemia and raised LH are independently capable of stimulating ovarian androgen production. Growth factors may have an important role in the pathogenesis of PCOS.

Adult↗
PubMed1992

Insulin-like growth factor-I (IGF-I) may not be essential for ovarian follicular development: evidence from IGF-I deficiency.

Insulin-like growth factor-I (IGF-I) stimulates growth and differentiation in follicular granulosa cells (GC). To examine whether this effect is prerequisite to human folliculogenesis, a patient with Laron-type dwarfism (IGF-I deficiency secondary to GH receptor abnormality) was examined while undergoing in vitro fertilization treatment. Despite low levels of IGF-I in serum and follicular fluid (less than 3 and less than 2 nmol/L) and very high levels of IGF-I-binding protein, the patient developed normal ovarian follicles. After the administration of GnRH analog (GnRHa) and human menopausal gonadotropin in a dose similar to that used in normovulatory women, estradiol (E2) levels reached above 5000 pmol/L on the day of hCG administration, and mature fertilizable oocytes were retrieved during ovum pickup. The patient's GC E2 production, tested in a primary culture, did not respond to IGF-I after 4 days of incubation, while control cultures showed a significant increase. Only after a priming period of 7 days did IGF-I have a significant effect on E2 production, as observed in the patient's GC culture. This delayed response suggests that the patient's GC were not exposed in vivo to IGF-I. Our data support the view that IGF-I is not required for normal follicular development, but is, rather, a nonessential modulator of FSH action.

Adult↗
PubMed1992

Insulin-like growth factor-I and follicle-stimulating hormone suppress insulin-like growth factor binding protein-1 secretion by human granulosa-luteal cells.

Local regulation of insulin-like growth factor binding protein-1 (IGFBP-1) production in the human ovarian follicle was investigated using cultured human granulosa-luteal cells. Both insulin-like growth factor-I (IGF-I) and follicle-stimulating hormone (FSH) exerted a dual effect on granulosa cells: while estradiol (E2) production was increased by both stimulants, the addition of either of the two hormones led to a reduction in IGFBP-1 secretion by more than 50%. Inhibition of IGFBP-1 production in response to IGF-I was dose-dependent,with the highest effect observed at 5 nM IGF-I. A significant correlation was found between the increase in E2 and inhibition of IGFBP-1 secretion in response to IGF-I. These observations may suggest a novel mechanism, at the follicular level, by which FSH and IGF-I amplify the IGF-I effect in the ovarian follicular cells.

Carrier Proteins↗
PubMed1991

Reversible male infertility in late onset congenital adrenal hyperplasia.

We have studied a male patient who presented with secondary infertility. His eldest daughter suffers from late onset congenital adrenal hyperplasia. Based on his hormonal profile, adrenal and gonadal stimulation tests, semen analyses and testicular biopsy he was diagnosed as suffering from the same disease as his daughter. Steroid treatment yielded improvement in all the parameters mentioned above. Four months later his wife became pregnant and he fathered a child. Suppression of gonadotropin secretion due to overproduction of adrenal androgens would appear to be the reason for the failure of testicular maturation and spermatogenesis in this patient. We conclude: 1) glucocorticoid treatment is indicated in infertile males suffering from nonclassical 21-hydroxylase deficiency; 2) Late onset congenital adrenal hyperplasia should be suspected in any male infertility of unknown origin.

17-alpha-Hydroxyprogesterone↗