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Biomedical subjects

A Lacroix

Publications and source records attributed to A Lacroix.

At least 145 records · Page 8Linked to original sources

Gonadal dysfunction in adult men with congenital adrenal hyperplasia.

Two adult males are described with congenital adrenal hyperplasia (21-hydroxylase deficiency). Patient 1 was receiving therapy with cortisone acetate and presented with clinical features of glucocorticoid excess and uncontrolled adrenal androgen activity. It was established that the short-acting steroid which the patient was receiving was cleared so rapidly that endogenous ACTH secretion was not inhibited. Patient 2 presented with enlarged and painful testes in association with poor compliance with corticosteroid therapy. The histologic picture of the testis was compatible with 'Leydig cell hyperplasia'. However, successful response to dexamethasone therapy suggests that the testes harboured an adrenal rest. These observations highlight the need for careful follow-up and treatment of adult male patients with congenital adrenal hyperplasia.

Adrenal Hyperplasia, Congenital↗

[End-to-end mechanical circular anastomosis in digestive surgery (author's transl)].

The anastomotic clamp described may be used to perform end-to-end anastomoses in digestive surgery. After a description of the instrument and its mode of use in its most suitable application -- colo-rectal anastomosis -- the authors report the first results of their clinical experience in 13 anastomoses, which are highly satisfactory.

Colon↗

[The use of vasopressin during portal bypass (author's transl)].

Vasopressin was infused intra-arterially or intravenously during 12 portal bypass operations. In comparison with a control group (without vasopressin), there was a very significant reduction in blood loss and portal pressure, and a moderate increase in arterial blood pressure.

Blood Pressure↗

Seventy-two hour infusions of LHRH in normal men: gonadotropin and testicular steroid responses.

Four normal male subjects received LHRH by continuous infusion for 72 hrs at 1.4 microgram/min. Mean basal LH was 7.7 +/- 1.0 mIU/ml, increased to a maximum of 120 +/- 22.7 mIU/ml, and then declined to levels between 28--34 mIU/ml for the last 30 hrs of infusion; FSH rose from 3.7 to 11.4 mIU/ml (p less than 0.05) at 16 hrs and then returned to baseline. Testosterone levels rose by 50% at 12 hrs, and remained elevated throughout with maximum values between 6.6 and 12 ng/ml. Estradiol-17beta levels were 26.2 +/- 4.7 pg/ml basally, rose to 104 +/- 8 pg/ml and while levels declined therafter, they were significantly above baseline throughout the 72 hrs. Plasma androstenedione and dehydroepiandrosterone levels also showed significant increases. By contrast, transient elevations in pregnenolone and 17-hydroxypregnenolone levels probably corresponded to the nomral morning rise in plasma levels of these steroids; 17-hydroxyprogesterone rose from 1.3 +/- 0.15 to 3.9 +/- 0.26 ng/ml at 12 hrs and remained elevated through the infusion. An increase in 17-hydroxyprogesterone:testosterone ratio was observed in all subjects. Thus, chronic LHRH infusion effected a persistent increase in endogenous LH with, in turn, prolonged stimulation of gonadal steroid secretion.

17-alpha-Hydroxypregnenolone↗

Testicular activity in Cushing's disease.

Plasma testosterone levels were suppressed in 6 of 8 mature male patients with Cushing's disease, all of whom complained of loss of libido and decreased sexual potency. Gonadotrophin levels, both under basal conditions and in response to LH-RH, were generally normal. The testicular response to stimulation with hCG was brisk in the 2 patients examined. Oestradiol levels were slightly elevated in 2 patients and prolactin levels were normal in all patients. Thus, male patients with Cushing's disease demonstrated normal gonadotrophin levels in the presence of suppressed testosterone, or, viewed from a slightly different prospect, low testosterone levels despite normal gonadotrophins. Neither oestradiol nor prolactin excess appeared to account for the observations. Possible explanations for these findings include (a) a combination of impaired hypothalamic and testicular function, and (b) a resetting downwards of the level of testosterone that is seen as appropriate by the disordered bypothalamic-pituitary unit. Following correction of cortisol excess in Cushing's disease, testosterone levels rose into the normal range.

17-Hydroxycorticosteroids↗

LH and testosterone release in developing bulls following LH-RH treatment. Effect of gonadectomy and chronic testosterone propionate pre-treatment.

LH and testosterone release after LH-RH treatment was studied in male calves from 1 week to 8 months of age. Total LH release, LH peak values and duration of the discharge increased from 1 week to 4 months of age by 406, 453 and 110%, respectively. Significant decreases of 54, 48 and 24% were observed at 6 months of age compared to 4 months of age. This was followed by steep increases in those variables of 344, 129 and 69% at 8 months compared to 4 months. A testosterone response following an LH increase was first seen at 4 months of age when a weak discharge occurred in 2 out of 5 calves. In older calves strong and LH-correlated testosterone responses were always observed. In a second experiment the LH response to LH-RH was studied in 6 months old calves castrated 2 months previously. The total LH response was 61% greater than in intact controls. When animals were castrated and pre-treated briefly with testosterone propionate the response was increased by 183% and the time to reach the LH peak was increased by 360%. From these and other results a synthesis of endocrine events during the first year of life is proposed. In particular it seems that the period between 4 and 8 months of age is crucial since interactions between steroid feedback and pituitary sensitivity to LH-RH change and eventually reach an equilibrium.

Age Factors↗

Short-term variations in plasma LH and testosterone in bull calves from birth to 1 year of age.

LH and testosterone levels in bull calves were studied in the plasma samples collected sequentially at 15-min intervals every month during the first year of life. An episodic pattern of LH release occurred after birth and the frequency and magnitude of the LH peaks increased up to 4 months of age and decreased thereafter. A testicular response was not observed before this age. It is suggested that this episodic LH activity is responsible for the testicular development which then initiates puberty.

Aging↗

Calcium infusion and pentagastrin injection in diagnosis of medullary thyroid carcinoma.

Calcium infusion and pentagastrin injection were compared as tests to stimulate calcitonin secretion for the detection of medullary carcinoma of the thyroid. Plasma concentrations of immunoreactive calcitonin were measured by radioimmunoassay before and during both stimulation tests in 2 persons who had been found at operation to have medullary thyroid carcinoma, 1 relative in whom a cervical lymph node biopsy had shown medullary thyroid carcinoma and 36 asymptomatic relatives. The tests were carried out on separate days by intravenous infusion of calcium gluconate for 2 hours, to provide 3.75 mg/kg of elemental calcium per hour, and rapid intravenous injection of 0.5 microgram/kg of pentagastrin. Before stimulation immunoreactive calcitonin was undetectable in the plasma of 34 of the 36 asymptomatic persons; the 2 with elevated baseline concentrations of the hormone had a positive response to both tests. Seven others showed an increase in plasma immunoreactive calcitonin concentration only after pentagastrin injection. The two persons with initially elevated values and three of the seven with increased values after pentagastrin injection were found at subsequent operation to have focal medullary carcinoma and parafollicular cell hyperplasia; after the operation immunoreactive calcitonin was undetectable in the plasma, even after stimulation. Rapid injection of pentagastrin is more reliable than slow infusion of calcium as a stimulation test for the early detection of medullary thyroid carcinoma.

Adolescent↗