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Biomedical subjects

M L'Hermite

Publications and source records attributed to M L'Hermite.

At least 55 records · Page 3Linked to original sources
PubMed1978

Thyrotrophin, prolactin and growth hormone responses to TRH in barbiturate coma and in depression.

The effects of 200 microgram thyrotrophin-releasing hormone (TRH) i.v. on thyrotrophin (TSH), prolactin (PRL), growth hormone (GH) and triiodothyronine (T3) were studied in eight patients with barbiturate coma due to attempted suicide, in the same patients after recovery, in eight depressive patients and in eight normal controls. The patients with barbiturate coma presented normal basal TSH and PRL, elevated basal GH and normal PRL but blunted TSH responses to TRH; their GH concentrations varied widely without consistent relation to TRH administration. The same patients after recovery from coma presented normal TSH and PRL, slightly elevated basal GH, and normal PRL but blunted TSH responses to TRH; in four of these patients, a clear-cut rise in GH (i.e. more than 10 ng/ml) occurred after TRH administration. The depressive patients presented normal basal TSH and PRL, slightly elevated basal GH, and normal PRL but blunted TSH responses to TRH; in four of these patients, a moderated rise in GH (less than 10 ng/ml) occurred after TRH administration. The increment in T3 concentrations 120 min after TRH was found reduced in the comatose patients only. Basal cortisol was measured in all the subjects and found elevated in the comatose patients only. It is concluded that the abnormal TSH and GH responses to TRH observed in patients with barbiturate coma are more likely related to depressive illness than to an effect of barbiturates at the pituitary level. Barbiturates might affect thyroid secretion.

Adolescent↗
PubMed1978

Alteration of feedback mechanism of estrogen on gonadotropin by sulpiride-induced hyperprolactinemia.

Four normally cycling women received an iv injection of 20 mg Premarin (conjugated estrogens equivalent to 20 mg estrone sulfate) on the seventh day of two consecutive cycles; the second experiment was performed under sulpiride-induced hyperprolactinemia (mean PRL level = 906 microU MRC standard 71/222 per ml; significantly 7.8 times greater than mean control level of 115 microU MRC standard 71/222 per ml, P less than 0.001). In comparison to the control experiment, sulpiride-induced hyperprolactinemia prevented the occurrence of any gonadotropin peak within the 84 h of estrogen administration; the negative feedback effect of estrogen on gonadotropin secretion was maintained and was even potentiated. These alterations of feedback mechanisms of estrogen were considered to be related to hyperprolactinemia itself rather than to sulpiride. Five other normally cycling women received iv injections of 100 microgram LRH on the 22nd day of a cycle under sulpiride-induced hyperprolactinemia since the onset of menstruation. Their mean LH response was somewhat greater (although not statistically significant) and their mean FSH response was considerably greater (P less than 0.001 at all times) than those of a control group of 10 women tested in their luteal phase. The results of these LRH tests under sulpiride-induced hyperprolactinemia give some support to the concept that hyperprolactinemia interferes at the hypothalamic or higher level with cyclic release of indogenous LRH.

Adolescent↗
PubMed1977

[The sella turcica and pituitary function in congenital hypothyroidism due to thyroid ectopia or hypogenesis (author's transl)].

Nine patients suffering from hypothyroidism due to thyroid ectopia or hypogenesis, with a large sella turcica, were examined at adolescence or during adult life. TSH, prolactin and growth hormone function were studied. Basal plasma TSH, evaluated in 5 cases, was raised and responded explosively to stimulation with TRH. The administration of L-dopa was not associated with any notable changes in TSH. In one case, the chronic administration of l-T3 resulted in a fall followed by normalisation in plasma TSH levels. Basal plasma prolactin, explored in 6 patients, was high in 4 females and normal in 2 males. TRH stimulation resulted in a marked increased in prolactin in the female cases and a moderate increase in the male cases. L-dopa caused a fall only in high prolactin values. Stimulation of GH by argininehydrochloride, insulin hypoglycaemia and L-dopa gave variable responses. In one case, substitutive thyroid hormone therapy restored the GH response to L-dopa and arginine hydrochloride to normal. Paradoxically, GH increase following stimulation with TRH.

Adolescent↗
PubMed1977

Serum prolactin levels during the menstrual cycle.

Serum prolactin has been measured in blood samples collected daily during 51 menstrual cycles using an homologous human radioimmunoassay for 17 cycles and an homologous ovine radioimmunoassay for 34 cycles. There was a progressive and significant increase in serum prolactin during the late follicular phase, with a maximal value concomitant to the LH peak. Serum prolactin levels were also significantly higher during the luteal phase than during early follicular phase. In some 70% of the individual cycles, the highest serum prolactin level was found at mid-cycle. Similar patterns were obtained with both radioimmunoassays. However, when using the same laboratory serum standard, the average serum prolactin level calculated for the entire cycle was 1.6 times higher with the homologous ovine assay than with the homologous human assay. The overall pattern of serum prolactin during the menstrual cycle resembles that reported for circulating 17beta-estradiol.

Animals↗
PubMed1977

Hypogonadism, galactorrhoea and hyper-prolactinaemia: Evaluation of pituitary gonadotrophins reserve before and under bromocriptine.

Twenty patients with hypogonadism (19 women with amenorrhoea and 1 man with impotence and infertility), galactorrhoea and hyper-prolactinaemia (range: 36 to 344 ng/ml) were studied. The radiological study of the sella turcica, including in all cases hypocycloidal tomograms, allowed classification of the patients into 3 groups: group I (n = 4) had a grossly enlarged sella turcica, group II (n = 12) had localized alterations indicating the probable existence of a prolactin-secreting microadenoma ("microdeformation") while group III patients presented no radiological abnormality. Before treatment, all the patients were submitted to a complete evaluation of the function of their anterior pituitary, including the LH and FSH responses to iv administration of Gn-RH. All the group I patients had low basal LH levels and a blunted response to Gn-RH. The basal LH and in response to Gn-RH were normal in most of the group II patients and in all of the group III patients. An exaggerated FSH response to Gn-RH was observed in 6/12 patients with microdeformation (group II) but not in groups I and III patients. A low LH and a blunted LH response to Gn-RH is highly suggestive of the existence of a pituitary prolactin-secreting adenoma in case of amenorrhoea and hyper-prolactinaemia patients; a normal response does not however rule out such a diagnosis. The reasons for a exaggerated FSH response to Gn-RH in patients with suspected prolactin-secreting microadenoma remain to be investigated though this pattern can also occur in other cases of amenorrhoea. Hence the Gn-RH test might contribute to the assessment of the hypothalamo-pituitary axis of patients with hyper-prolactinaemia. Six patients treated for 4 months with bromocriptine (CB-154) were submitted to re-evaluation of their pituitary gonadotrophins reserve. All the women experienced restoration of menses with 39 days of treatment and the male patient regained potency. It was observed that bromocriptine treatment and subsequent normalized prolactin levels in the 4 group II women tested were associated with normalization of their previously exaggerated FSH response to Gn-RH; LH responses were also diminished in these cases. These data are compatible with the hypothesis that hyper-prolactinaemia per se could interfere with the endogenous secretion of Gn-RH at the hypothalamic level. In one patient with grossly enlarged sella turcica and a previous lack of an LH and FSH response to Gn-RH, bromocriptine treatment restored a normal gonadotrophins response, confirming that, in this case, the alteration of this response was indeed due to a prolonged lack of endogenous Gn-RH secretion.

Adolescent↗
PubMed1977

[Oestriol effect upon prolactinaemia in postmenopausal women (author's transl)].

Six postmenopausal women were treated at two ocasions with an oral dose of, respectively, 2 mg and 6 mg oestriol per day for 14 days; at least one month interval separated the two treatment periods. Blood was collected for prolactin measurement (homologous human radioimmunoassay) every other day during each treatment period as well as during a 14 days control period in the same subjects. Mean prolactin level during oestriol administration, regardless of the dose, was statistically not significantly different from that observed during the control period.

Administration, Oral↗
PubMed1976

Pituitary and extrapituitary effects of somatostatin in normal man.

The effects of synthetic linear somatostatin on basal circulating levels on several pituitary and pancreatic hormones, and of glucose and free fatty acids (FFA) were studied in 6 normal men after an overnight fast. A priming intravenous infusion of 250 mug of somatostatin in 18 sec was followed by a constant infusion of 500 mug over a period of 60 min. A decrease in plasma values of GH, prolactin, TSH, insulin and glucagon and in blood glucose was observed during somatostatin infusion, while FFA levels increased progressively. Plasma IRI and blood glucose increased rapidly when the somatostatin infusion was stopped, while FFA decreased progressively; GH, prolactin, TSH and glucagon remained low as compared to basal levels for one hour after the end of the infusion, i.e. until the end of the experiment. A slight but significant increase of LH and ACTH was observed after the end of the infusion.

Adrenocorticotropic Hormone↗
PubMed1976

Effects of testosterone on gonadotrophin responses to synthetic LH and FSH releasing hormone (LRH) in normal men.

LRH tests were performed in 6 adult men with intravenous injections of 25 mug, before and one week after an intramuscular injection of 250 mg testosterone oenanthate (Testoviron Depot). One week after intramuscular injection of Testoviron the tonic secretion of LH was completely suppressed, but the reactivity or the reserve capacity of LH secretion, as tested by LRH, remained unchanged. In contrast, the tonic secretion of FSH and the reactivity of FSH secretion to LRH were both partly suppressed. Three months after the Testoviron injection, the basal levels of LH were still significantly lower than the control values, but the basal levels of FSH were identical to the control values. These data indicate that, in man, the feedback action of testosterone on gonadotrophin secretion could be exerted, at least for LH, at the hypothalamic level rather than at the pituitary level . No significant effects of LRH were noted on the circulating levels of growth hormone and sugar. There was a distinct rise in serum prolactin, which was occasionally significant, within 30 min after LRH injection; this is considered to be without physiological significance.

Adult↗
PubMed1975

[ Study of prolactin and blood gonadotropins in amenorrheas-galactorrhea. Dynamic exploation in 13 cases].

A study of the secretion of prolactin and plasma gonadotrophins was carried out comparatively in 3 groups of patients: histologically confirmed prolactin adenoma (group 1), idiopathic or iatrogenic amenorrhoea/galactorrhoea syndrome (group 2), empty sella turcica syndrome (group 3). The last group differs fundamentally from the two previous by the presence of a normal basal LH and FSH levels and normal LH-RH stimulation. Prolactin is not increased. It may be suppressed by L-dopa and stimulated by TRH. There exist no differences, apart from neuroradiological criteria, between the other two groups. The level of LH is slightly decreased but the response to LRH is positive, this effect often being more clear on FSH. Prolactin levels are raised, this no doubt explaining the negative response to TRH and chlorpromazine stimulation. Suppression by L-dopa is positiive, reflecting the absence of autonomy of prolactin adenomata. The water load test is unsatisfactory. There exists at the present time no method sufficiently discriminating to exclude the presence of a tumour at the origin of an amenorrhoea-galactorrhoea syndrome.

Adenoma↗