PubMed Health⌕ Search

Biomedical subjects

C Gervy-Decoster

Publications and source records attributed to C Gervy-Decoster.

10 recordsLinked to original sources
PubMed1997

Increased angiotensin II in ascites during severe ovarian hyperstimulation syndrome: role of early pregnancy and ovarian gonadotropin stimulation.

OBJECTIVE: To investigate the implications of the ovarian renin-angiotensin system (RAS) in the pathophysiology of the ovarian hyperstimulation syndrome (OHSS) in relation to gonadotropin stimulation and early pregnancy. DESIGN: A controlled clinical study comparing blood and simultaneously sampled peritoneal fluid (PF) from patients with severe OHSS and from controls without OHSS. SETTING: University Hospitals. PATIENT(S): Eleven patients with severe OHSS, 8 patients with ascites of other origin, 9 patients with a first-trimester pregnancy, and 15 patients stimulated with gonadotropins for IVF. MAIN OUTCOME MEASURE(S): Angiotensin II immunoreactivity was measured in blood and PF and analyzed by high-performance liquid chromatography (HPLC) in ascites from OHSS. RESULT(S): Angiotensin II immunoreactivity (pg/mL; mean +/- SE) was highest in the ascites from pregnant OHSS (1,669 +/- 418), reaching levels 5 times higher than in the plasma (331 +/- 61) and 100 times higher than in control ascites (17 +/- 6.7). Angiotensin II immunoreactivity was elevated in the PF during early pregnancy (211 +/- 68) and after gonadotropin stimulation (244 +/- 41) and was higher than in the plasma in both groups. Analysis by HPLC showed that the majority of Ang II immunoreactivity in the ascites of OHSS was because of true Ang II. CONCLUSION(S): Severe forms of OHSS, especially those associated with pregnancy, are consistently characterized by huge concentrations of Ang II immunoreactivity in the ascites, proved to be true Ang II by HPLC analysis. This may be due to the synergistic effects of exogenous and endogenous hCG on the ovarian RAS.

Adult↗
PubMed1997

Prorenin and active renin concentrations in plasma and ascites during severe ovarian hyperstimulation syndrome.

The pathophysiology of ovarian hyperstimulation syndrome (OHSS) remains unclear. Several lines of evidence indicate that OHSS is associated with a stimulation of the renin-angiotensin system (RAS), but its functional significance as well as its role in the pathogenesis of the syndrome are not yet determined. OHSS is associated with high plasma and ascitic concentrations of total renin, renin activity (RA) and angiotensin II (Ang II). Their ovarian or renal origin is, however, still a matter of debate. To clarify these issues further, total renin, active renin, prorenin, RA and aldosterone were measured in plasma and ascites of nine patients who developed severe OHSS after in-vitro fertilization. Blood and ascites were sampled simultaneously during therapeutic paracentesis. Total renin and prorenin concentrations were significantly higher in the ascites (mean concentration +/- SE respectively of 5920 +/- 1430 mIU/l and 5250 +/- 1350 mIU/l) than in the plasma (respectively 3060 +/- 740 mIU/l and 2000 +/- 460 mIU/l) (P = 0.020 and 0.017 respectively). Conversely, active renin and RA concentrations tended to be lower, although not statistically significantly so in the ascites (respectively 670 +/- 190 mIU/l and 47 +/- 11 ng Ang I/ml/h) than in the plasma (respectively 1060 +/- 370 mIU/l and 75 +/- 21 ng Ang I/ml/h). Aldosterone concentrations were significantly higher in the serum (2609 +/- 374 pg/ml) than in the ascites (2025 +/- 347 pg/ml) (P = 0.015). The concentration gradient between plasma and ascites for total renin and prorenin supports the hypothesis of their ovarian origin in ascites and, to a large extent, in plasma, while it is likely that the high plasma active renin and RA concentrations reflect a peripheral activation of the RAS. In conclusion, the present findings are consistent with a marked stimulation of both ovarian and renal RAS during OHSS.

Adult↗
PubMed1996

Periovulatory elevation of angiotensin II in the peritoneal fluid during the human menstrual cycle.

Local variations in the ovarian renin-angiotensin system were investigated in peritoneal fluid (PF) during normal menstrual cycles and after ovarian stimulation with gonadotropins. PF was collected either during laparoscopy or by transvaginal aspiration before ovocyte retrieval for in vitro fertilization. Renin activity (RA) and angiotensin II immunoreactivity (Ang II-ir) were assayed in PF and simultaneously collected blood. The level of Ang II-ir was higher in PF than in plasma throughout the cycle, where as RA was in the same range of magnitude in the two compartments. In PF, Ang II-ir reached levels 2-5 times higher in the periovulatory period (days 12-14 and 15-17 of the cycle) than those found during the other stages of the cycle, whereas plasmatic Ang II-ir remained stable. No significant change could be demonstrated in RA throughout the cycle in either PF or plasma. Ovarian stimulation induced a strong elevation of Ang II-ir in PF, but not in plasma. High performance liquid chromatography revealed that the majority of Ang II-ir in PF was true Ang II. In conclusion, these results show a periovulatory elevation of Ang II in PF during the cycle and a more pronounced rise after treatment with gonadotropins. These observations support the involvement of Ang II in the process of ovulation or fecundation.

Adult↗
PubMed1994

Angiotensin II immunoreactivity is elevated in ascites during severe ovarian hyperstimulation syndrome: implications for pathophysiology and clinical management.

OBJECTIVE: To investigate the ovarian renin-angiotensin system (RAS) during severe ovarian hyperstimulation syndrome (OHSS). DESIGN: Simultaneous sampling of blood and ascitic or peritoneal fluid (PF) during therapeutic paracentesis or laparoscopy. SETTING: University Hospital. PATIENTS: Twelve patients were investigated: three patients presenting severe OHSS, three patients with a spontaneous first trimester pregnancy, three normally cycling women during the early luteal phase, and three patients with ascites of nonovarian origin. MAIN OUTCOME MEASURE: Renin-like activity and angiotensin II (ANG II) immunoreactivity were measured simultaneously in the plasma and the ascites or PF. RESULTS: Angiotensin II immunoreactivity was much higher in the ascites or PF than in corresponding plasma during severe OHSS, first trimester pregnancy, and in the early luteal phase, while it was lower in ascites of nonovarian origin. Renin-like activity and ANG II immunoreactivity were the highest in the ascites of severe OHSS and in the PF from part of the patients with a spontaneous first trimester pregnancy. CONCLUSIONS: The present findings argue for the ovarian origin of the elevated renin-like activity and ANG II immunoreactivity in the ascites of severe OHSS and suggest a stimulatory role of hCG on the ovarian RAS whether during severe OHSS or first trimester spontaneous pregnancy. The vasoactive peptide ANG II may contribute to the maintenance of the ascites in severe OHSS but is probably not responsible for the formation of the ascites. The efficiency of paracentesis during severe OHSS could be explained at least partially by the removing of great amounts of ANG II from the peritoneal cavity.

Adult↗
PubMed1993

Enzymatic, metabolic and secretory perturbations in pancreatic islets of thyroidectomized rats.

In thyroidectomized rats, the activity of FAD-linked glycerophosphate dehydrogenase was severely diminished in liver homogenates but not affected significantly in pancreatic islet homogenates, whilst the activity of 2-ketoglutarate dehydrogenase was decreased modestly in both liver and islet homogenates. Likewise, in intact islets of thyroidectomized rats, the generation of 3HOH from [2-3H]glycerol was not decreased, and the ratio between oxidative and total glycolysis not significantly lower than in islets from sham-operated rats, at least in the presence of a high concentration of D-glucose. Nevertheless impaired oxidation of both D-[3,4-14C]glucose and D-[6-14C]glucose was observed in islets of thyroidectomized rats, the relative magnitude of such a decrease being more pronounced at a low than at a high D-glucose concentration. Such metabolic anomalies coincided with a lower level of plasma insulin and decreased output of insulin by islets incubated at low (2.8 mM), but not higher, concentrations of D-glucose. It is concluded that hypothyroidism does not mimic the deficiency in islet FAD-linked glycerophosphate dehydrogenase activity found in rats with inherited or acquired non-insulin-dependent diabetes.

Blood Glucose↗
PubMed1993

Human, bovine, canine and rat thyroglobulin promoter sequences display species-specific differences in an in vitro study.

The proximal promoter regions of the thyroglobulin gene from man, beef, dog and rat were compared by transient expression in primary cultured dog thyrocytes. All four promoter regions were able to control properly the expression of a reporter gene in response to cyclic AMP stimulation. Surprisingly, despite extensive sequence conservation, the transcriptional activities of these four mammalian thyroglobulin promoters were differently affected by equivalent mutations. Homologous sequence elements from these promoter regions also exhibited distinct binding characteristics in mobility-shift experiments conducted in the presence of nuclear proteins from bovine thyroids. Our observations show that the highly conserved thyroglobulin promoters may exhibit unexpected functional differences in a specific assay and indicate that some of the molecular mechanisms involved in the control of thyroglobulin gene expression have evolved differently within mammals.

Animals↗
PubMed1993

Selenium and the thyroid: how the relationship was established.

Several hypotheses concerning consequences of selenium deficiency on iodine metabolism can be proposed on the basis of experimental studies in rats and from epidemiological and experimental studies in humans. By decreasing intracellular GSH peroxidase activity, selenium deficiency may increase hydrogen peroxide (H2O2) supply and lead over several weeks to the thyroid atrophy observed in myxoedematous cretins. By improving thyroid hormone synthesis and by decreasing peripheral thyroxin (T4) deiodination, selenium deficiency could protect fetal brain T4 supply and thus prevent neurologic cretinism. Selenium deficiency may protect against iodine deficiency by decreasing T4 metabolism--and thus iodide leakage and--perhaps also by increasing H2O2 supply and thyroid hormone synthesis and thus thyroid efficiency.

Animals↗