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Biomedical subjects

G Copinschi

Publications and source records attributed to G Copinschi.

At least 55 records · Page 3Linked to original sources

Somatomedins and steroids.

Somatomedin levels measured by radioreceptor assay, competitive protein-binding assay or radioimmunoassay are normal in hypercortisolism; the decrease of somatomedin activity consistently found in this condition is due to an increase in circulating somatomedin inhibitors resulting in an inhibition of somatomedin action. Progestagens could possibly have a direct stimulatory effect on somatomedin-C (Sm-C) production. During puberty, the increase of Sm-C is correlated with the increase in plasma estradiol and testosterone. In young subjects, relatively low doses of estrogens and of testosterone enhance Sm-C secretion, and in adult menstruating women, a positive relationship is found between testosterone and Sm-C values. An inhibitory effect of estrogens on Sm-C is observed with higher doses and/or in older subjects. Thus, somatomedin levels might be modulated by variations of sex steroids.

Estrogens↗

Prolonged pulsatile administration of ovine corticotropin-releasing hormone in normal man.

The 24-h profiles of plasma ACTH and cortisol were determined at 15-min intervals in five normal men basally and during iv bolus injections of 25 micrograms ovine corticotropin-releasing hormone (oCRH) every 4 h for 72 h. Each oCRH injection was followed by a distinct elevation of plasma ACTH and cortisol levels, with a return to basal values before the next injection. The characteristics of the ACTH and cortisol pulses induced by 25 micrograms oCRH (i.e. 0.3-0.4 micrograms/kg) were similar to those observed in other studies with 1 microgram/kg human CRH. There was no significant blunting of oCRH-induced hormonal increments in the course of the 72-h study. On each oCRH injection day, the mean 24-h cortisol level was higher than that in the basal study, but there was no increase in the mean 24-h ACTH level. During the 72-h oCRH study, the preinjection ACTH and cortisol levels exhibited a diurnal variation, indicating persistence of the circadian periodicity of pituitary-adrenal activity. There was a diurnal variation of oCRH-induced ACTH increments, with highest responses at 0700 h. A small but not significant reverse trend was apparent for cortisol increments. Spontaneous pulses of ACTH and cortisol occurred throughout the 3 days of oCRH injections, and the total number of spontaneous and oCRH-induced pulses was similar to the number of spontaneous pulses observed in the basal study. All oCRH-induced and more than 90% of spontaneous cortisol pulses occurred concomitantly with an ACTH pulse. The variability of pulse increments was greater for ACTH than for cortisol. In conclusion, prolonged pulsatile administration of oCRH did not induce pituitary desensitization and did not suppress the endogenous circadian and pulsatile ACTH and cortisol variations.

Adrenocorticotropic Hormone↗

Modulation of immunoreactive somatomedin-C levels by sex steroids.

Among 28 menstruating women tested once randomly during the cycle, somatomedin-C (Sm-C) values were lower in the 10 women in normal follicular phase than in the 10 women in normal luteal phase or the 8 women with hyperandrogenism. Among these 28 subjects, Sm-C showed a positive correlation with testosterone and a positive correlation of borderline significance with oestradiol. A positive correlation was also evidenced between Sm-C and in progesterone among the 20 women of this group who were not hyperandrogenic. In 5 other normal women investigated daily throughout an entire menstrual cycle, Sm-C concentrations were higher during days +4 to +9 of this cycle (luteal phase) than during days -3 to -8 (follicular phase). In another group of 21 healthy women, Sm-C values were increased during medroxyprogesterone acetate (150 mg trimestrially) treatment. In 7 normal men, Sm-C decreased during ethinyl-oestradiol (1 mg daily for 5 days) administration. These findings suggest that circulating Sm-C levels are modulated by variations of sex steroids which occur during the menstrual cycle as well as by pharmacological doses of oestrogens and progestagens.

Adult↗

Diurnal hypersecretion of growth hormone in depression.

A 24-h profile of plasma GH concentrations was obtained together with polygraphic recordings of sleep in 16 men suffering from a major depressive disorder (8 unipolar and 8 bipolar) and in 8 age- and sex-matched normal men. None of the patients had any physical illness. All were studied after a drug-free period of at least 15 days. Blood was sampled every 15 min. The amount of GH released in every significant secretory spike was estimated using a computer program. Both unipolar and bipolar depressed patients secreted more GH than normal men (mean +/- SD, 441 +/- 189 micrograms/24 h for unipolar depressed men; 357 +/- 143 micrograms/24 h for bipolar depressed men vs. 172 +/- 101 micrograms/24 h for normal men (P less than 0.01). This hypersecretion occurred during waking hours rather than during sleep. The increase in daytime GH release was more marked in unipolar depressed patients. During sleep, depressed patients and normal men secreted similar amounts of GH despite an overall reduction in slow wave stages in depressed patients. An early sleep GH increase was found in all but one of the normal men, but was absent in seven of the eight unipolar depressed patients, who had, instead, a presleep increase in between 2100-0000 h. No consistent disturbance of the temporal association between sleep onset and GH secretion was found in bipolar depressed patients.

Adult↗

The 24-hour profile of adrenocorticotropin and cortisol in major depressive illness.

The 24-h profile of plasma ACTH and cortisol levels was determined in 18 men suffering from major depressive illness (8 with unipolar depression and 10 with bipolar depression) as well as in 7 age-matched normal men. Blood was sampled every 15 min. The circadian variation and episodic fluctuations were analyzed for each individual profile. Both unipolar and bipolar depressed patients had higher 24-h mean cortisol levels (P less than 0.01) than normal men, but no significant difference in 24-h mean ACTH level was found. The nadir of cortisol secretion occurred almost 3 h earlier in older normal subjects and patients with unipolar depression, regardless of age, than in younger normal subjects. This shift paralleled a similar advance of the ACTH nadir. Early timing of the quiescent period of ACTH-cortisol secretion was also found in several patients with bipolar depression, but did not reach significance at the group level. The hypercortisolism in the depressed patients was associated with an increase in the magnitude, but not the number, of cortisol secretory episodes. About 90% of the cortisol pulses could be related to a concomitant ACTH pulse in normal subjects as well as in both groups of depressed patients. However, concomitant ACTH and cortisol pulses were less correlated in magnitude in depressed patients than in normal subjects. These results indicate that major depressive illness is associated with disturbances of pituitary-adrenal function. The early timing of the nadir of ACTH-cortisol secretion suggests that disorders of circadian time keeping may characterize major endogenous depression.

Adrenocorticotropic Hormone↗

Relations between immunoreactive somatomedin C, insulin and T3 patterns during fasting in obese subjects.

Plasma glucose, immunoreactive somatomedin-C (Sm-C), GH, insulin (IRI) and T3 were measured daily in 20 obese subjects before and during a 9-day fast. Control levels of Sm-C were normal and exhibited no significant correlation with any of the other parameters investigated. During fasting there were no consistent variations in GH, but significant decreases occurred in blood glucose, IRI, T3 and Sm-C levels. While individual Sm-C patterns varied widely, as a group the fasting Sm-C values showed a positive correlation with the fasting IRI and T3 levels, and with control body weight. These findings suggest that the decrease in Sm-C which occurs during caloric deprivation may be the result of concomitant decreases occurring in T3 and IRI levels.

Adolescent↗

Evolution of the delta 4-adrenal androgens responsiveness in childhood during insulin test.

Serum 11-beta-hydroxy-androstenedione (11OHAD), androstenedione (AD) and cortisol (F) were estimated during an i.v. insulin test in 2 large groups of normal prepubertal children and in normal adults. The results revealed that the basal level and responsiveness of AD were much lower in both groups of children than in adults whereas the corresponding 11OHAD data were similar or superior to those of adults. This suggests that during childhood the limited amount of adrenal AD is preferentially switched to the 11-hydroxylation step. Comparison of hormonal data observed in adults after i.v. insulin (mild ACTH stimulation) and a maximal stimulating dose of synacthen showed that the sensitivity of delta 4-3 keto-androgens pathway is inferior to that of F.

Adrenal Glands↗

Exploration of hirsutism: elements for a strategy.

50 women complaining of hirsutism were investigated in order to establish an optimal strategy for hirsutism exploration. Basal hormonal evaluations were of great value, especially serum testosterone and, to a lesser degree, DHA-S and LH. LH response to LHRH stimulation appeared of little diagnostic value. ACTH stimulation tests may be useful in detecting enzyme deficiencies in patients with normal basal values. The origin of hyperandrogenism can hardly be detected by the inhibition tests. However, these tests allow to determine whether the androgen secretion is still under ACTH and/or LH control.

Adolescent↗

Effects of "jet lag" on hormonal patterns. IV. Time shifts increase growth hormone release.

Twenty-four-hour GH profiles were obtained in five normal male volunteers before travel, 1, 11, and 21 days after the Brussels-Chicago flight (time shift, 7 h); and 1, 11, and 21 days after the return flight. The westward and eastward travels involved, respectively, periods of 23 and 33 h of sleep deprivation. One year later, two of the five volunteers were submitted, in the laboratory, to an investigation mimicking the conditions of sleep deprivation undergone in the course of the eastward travel and involving two 24-h periods of blood sampling. Blood samples were drawn every 15 min, and sleep was polygraphically monitored. The amounts of GH secreted were quantified, and their relationship with the different sleep stages was analyzed. Time shifts, whether caused by "jet lag" or by sleep deprivation in the laboratory, had two effects on GH secretory patterns. First, a marked increase in GH release, due to an augmentation of the magnitude, rather than the number, of secretory spikes was observed, independently of sleep disturbances. Return to basal levels was slower after westward than after eastward travel and took at least 11 days. Second, 1 day after the eastward transportation as well as immediately after 33 h of sleep deprivation, the major GH spike, which occurred in early sleep in the other studies, was shifted to late sleep. In these investigations, the only consistent alteration of sleep was a reduction in the amount of rapid eye movement (REM) stage. The occurrence of GH spikes in sleep was significantly associated with slow wave (SW) stage. However, total amounts of GH secreted during sleep were negatively correlated with the total duration of REM stages rather than positively correlated with the total duration of SW stages. A spike by spike analysis showed that the amount of GH secreted correlates best with the ratio (SW - REM) to (SW + REM), which relates the amount of REM preceding the spike to the amount of SW during the spike and thus constitutes an indicator of the status of the REM-non-REM oscillation.

Adaptation, Physiological↗

Immediate and delayed alterations of adrenocorticotropin and cortisol nyctohemeral profiles after corticotropin-releasing factor in normal man.

Intravenous injections of 50 micrograms corticotropin-releasing factor (CRF) to four normal men at 0900 and 2300 h were followed by significant plasma ACTH and cortisol elevations, without changes in GH and PRL concentrations. The responses were more easily assessed late in the evening than in the morning, when they were superimposed upon the spontaneous hormonal variations. The initial hormonal response was always followed by a period of decreased hormonal values compared to control patterns. The normal pituitary-adrenal response to CRF was blunted or abolished by prior administration of dexamethasone. These data suggest that exogenous administration or CRF-induced endogenous production of glucocorticoids modulates the sensitivity of corticotropic cells to the action of CRF. Since normal ACTH and cortisol secretory episodes are likely to obscure the effects of CRF, stimulation tests for clinical purposes should be performed during the quiescent period, i.e. late in the evening.

Adrenocorticotropic Hormone↗

The relationship between episodic variations of plasma prolactin and REM-non-REM cyclicity is an artifact.

The concept of concomitance between nadirs and peaks of plasma levels of PRL and, respectively, rapid eye movement (REM) and non-REM stages in sleep was reevaluated using 24 nighttime profiles of plasma PRL collected at 15-min intervals and the corresponding polygraphic recordings of sleep. The subjects were 5 healthy young male adults. Data were examined using the methodology described in the original report, consisting of averaging across individual nights PRL levels during REM and non-REM sleep stages as well as using a detailed spike by spike analysis of each individual pair of hormonal and sleep profiles. We showed that in our subjects, there was no relation, other than a purely random one, between episodic PRL fluctuations in plasma and REM-non-REM cycles.

Adult↗

Seasonal, circadian and episodic variations of human immunoreactive beta-MSH, ACTH and cortisol.

The 24-hour profile of plasma levels of immunoreactive beta-MSH (IR-beta MSH), ACTH and cortisol was obtained at 15-min intervals in six normal males in summer and winter. In the radioimmunoassay used, dilution curves of human beta-MSH and human beta-LPH were not parallel. A seasonal variation in basal pituitary-adrenal secretion, with higher levels in winter than in summer, was demonstrated. A circadian rhythm was found to be significant for ACTH, IR-beta MSH and cortisol in all investigations. Whereas ACTH and cortisol patterns were largely concordant in all studies, there was a significant desynchronization of the circadian rhythm of IR-beta MSH as compared to ACTH in five cases. Eighty-three percent of the secretory spikes of cortisol but only 68% of the IR-beta MSH spikes were concomitant with an ACTH spike. Correlations between maximal levels of concomitant spikes were higher during the quiescent period of pituitary-adrenal secretion (22.00--04.00) for ACTH-cortisol whereas for ACTH-IR-beta MSH, highest correlations were found during the active early morning secretory phase (04.00--10.00). For the three plasma constituents studied, longer apparent half-lives were found to occur when the basal level before spiking was already elevated, suggesting that ACTH, beta-LPH and cortisol are secreted in bursts superimposed on a continuous basal secretion. Absolute increments of concentration appeared to be relatively independent of the level before spiking. It is suggested that the dissociations between ACTH and IR-beta MSH fluctuations in plasma observed here result from in vitro proteolysis of beta-LPH.

Adrenocorticotropic Hormone↗

Symptomatic hypopituitarism revealing a primary empty sella turcica.

A 64-year-old nulliparous woman presented with clinical signs of thyroid and adrenocortical insufficiency. Subsequent hormonal investigations demonstrated a failure of all anterior pituitary functions. Pneumotomo-encephalography revealed a large arachnoid herniation, leading to the diagnosis of primary empty sella turcica syndrome with secondary panhypopituitarism. This unusual observation emphasizes the necessity of ruling out an empty sella turcica syndrome in patients with pituitary insufficiency.

Empty Sella Syndrome↗