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Biomedical subjects

L Vanhaelst

Publications and source records attributed to L Vanhaelst.

At least 73 records · Page 4Linked to original sources
PubMed1987

Postnatal development of growth hormone and prolactin cells in male and female rat pituitary. An immunocytochemical light and electron microscopic study.

Localization and ultrastructural maturation of prolactin (PRL) and growth hormone (GH) cells were studied in pituitaries from neonatal, immature (4-6 weeks old), and adult rats (2-3 months old) by light and electron microscopic immunocytochemistry. The distribution pattern of these cells did not change with age. Both cell types were concentrated laterodorsally, with PRL cells adjacent to the intermediate lobe and GH cells nearer the center of the pars distalis. Labeling density of the immunogold reaction was highest for both hormones in immature rats. In neonatal and immature rats, one PRL cell type with granules 200 nm in diameter was present. In adult rats, two types of PRL cells were present: one containing polymorphous granules measuring about 500 nm (prevalent in female rats), the other with spherical granules about 200 nm (prevalent in male rats). No changes were detected in GH cells during maturation.

Animals↗
PubMed1987

Thyroid hormone reserve in asymptomatic autoimmune thyroiditis.

Basal (B) and peak (P) serum levels of thyroxine (T4), free thyroxine (FT4), triiodothyronine (T3), free triiodothyronine (FT3), and TSH were measured before and after oral TRH (40 mg) administration in 79 subjects affected with asymptomatic autoimmune thyroiditis (AAT) and in 69 normal subjects. The area under the curve (AUC) and peak values of T4, FT4, T3 and FT3 were considered as parameters of thyroid hormone reserve. Intrathyroidal iodine (ITI) was measured by the X-ray fluorescence method. The AAT subjects were divided into three groups on the basis of their basal and peak TSH values. In group I, these parameters were similar to those in the normal controls; in group II, basal TSH remained normal but peak TSH was significantly increased, and in group III both values were significantly increased. Group I differed from the controls by a decrease in P FT4 and AUC FT4, whereas in groups II and III B FT4 was also significantly lowered. T3 levels were similar in all groups except in group III, in whom they dropped. ITI was already lower in group I than in the controls. Its decline went further in groups II and III. An inverse correlation with significant r values was evidenced between log B and P TSH on one hand and log B FT4, P FT4 and AUC FT4 on the other. When group III was excluded, log P TSH was positively correlated with log B T3, P T3, AUC T3, and AUC F T3.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Effect of carvedilol on ambulatory blood pressure, renal hemodynamics, and cardiac function in essential hypertension.

A randomized, double-blind, placebo-controlled study was set up to study the effects of acute and chronic administration of carvedilol, a vasodilatory beta-blocker in essential hypertension. Acute administration of a single dose of 50 mg of carvedilol reduced systolic and diastolic blood pressure, without inducing reflex tachycardia. Renal blood flow was preserved; accordingly renal vascular resistance was significantly reduced. A significant reduction of glomerular filtration rate and filtration fraction was observed. Plasma renin activity (PRA) and plasma aldosterone were not changed. Chronic carvedilol treatment produced a significant fall in systolic and diastolic office and ambulatory blood pressure, heart rate, cardiac output, PRA and plasma aldosterone. Blood pressure variability was not changed. Renal blood flow, glomerular filtration rate and filtration fraction also remained unchanged; renal vascular resistance decreased significantly. It is concluded that carvedilol possesses definite antihypertensive and renal vasodilating properties, both acutely and after chronic treatment.

Adrenergic beta-Antagonists↗
PubMed1985

Effect of 1,25-dihydroxyvitamin D3 and nifedipine on prolactin release in normal man.

In normal man 1,25 (OH)2-vitamin D3 [1,25 (OH)2D] increases both basal and TRH-stimulated prolactinemia; this effect is completely reversible by the calcium antagonist nifedipine. Similarly the 1,25 (OH)2D-induced hypercalcemia is totally inhibited by nifedipine. These findings suggest that both biological effects of 1,25 (OH)2D are mediated by calcium-dependent mechanisms.

Adult↗
PubMed1985

Clonidine-suppression test in epinephrine secreting pheochromocytoma: report of a case.

A patient is described in whom the diagnosis of pheochromocytoma was suspected on clinical grounds. He had normal urinary and plasma norepinephrine levels, with normal suppression of plasma norepinephrine by clonidine. However, plasma and urinary epinephrine levels were above normal, and plasma epinephrine was not suppressed but increased by clonidine. Selective venous sampling showed marked unilateral adrenal epinephrine excess. A large epinephrine secreting pheochromocytoma was surgically removed. This case suggests that, in pheochromocytomas releasing predominantly epinephrine, normal norepinephrine release from axon terminals of sympathetic postganglionic neurons is maintained and is suppressed by clonidine administration. It further reaffirms the value of plasma epinephrine estimations in the diagnosis of pheochromocytoma and indicates that normal suppression of plasma norepinephrine by clonidine does not preclude the presence of a predominantly epinephrine secreting tumor.

Adrenal Gland Neoplasms↗
PubMed1985

Natural history of primary myxedema.

It is generally admitted that primary myxedema in adults is the outcome of autoimmune atrophic thyroiditis. The present review traces the natural history of this process from its incipient biologic and genetic anomalies up to its protracted asymptomatic course, clinical development, and eventual lethal complications. The apprehension of preclinical hypothyroidism may change a clinician's outlook on early diagnosis and therapy.

Autoantibodies↗
PubMed1984

Ectopic adrenocorticotropin production: disappearance after removal of inflammatory tissue.

A patient presented with the clinical and laboratory features of the ectopic ACTH syndrome. No ACTH-producing tumor was found, and bilateral adrenalectomy was performed to correct the hypercortisolism. Six months later, the removal of a pseudotumor containing only fat and inflammatory tissue resulted in normalization of both basal plasma ACTH levels and the ACTH feedback response to cortisol infusion. It is suggested that the leukocytes in the inflammatory tissue were the source of the ectopic ACTH production.

ACTH Syndrome, Ectopic↗
PubMed1983

Effect of fluoxetine, a serotonin reuptake inhibitor, on the pituitary-thyroid axis in rat.

Fluoxetine, a specific serotonin reuptake inhibitor, was administered i.p. either acutely or chronically (2 and 10 mg doses), and intraventricularly to normal rats. Basal TSH levels were measured and the pituitary TSH reserve was estimated by direct determination of pituitary TSH content and/or by a TRH test. Thyroxine (T4) and triiodothyronine (T3) serum levels were also measured. The acute administration elicited only a decrease in T4 levels, whereas the chronic administration resulted in a decrease in both T4 and T3 levels. The 10 mg acute and chronic administrations induced an increase in basal TSH and in pituitary TSH reserve. Intraventricular administration only prevented the initial stress-induced decline of serum TSH levels. The major effect of the drug seems to be stimulation of TSH synthesis and release via the inhibition of T4-mediated thyroid-pituitary feedback. Additionally, fluoxetine could exert a minor direct central stimulatory effect on TSH secretion.

Animals↗
PubMed1983

Effect of 1,25-dihydroxyvitamin D3 on plasma prolactin in patients with renal failure on regular dialysis treatment.

Basal plasma prolactin (PRL) has been measured in 6 patients with chronic renal failure 3 months before and at monthly intervals during a 3 months 1,25-dihydroxyvitamin D3 [1,25 (OH)2-D] treatment. Plasma PRL decreased rapidly during, 1,25 (OH)2-D treatment, while it remained unchanged during the 3-months control period. There was no correlation between PRL and parathyroid hormone (PTH; measured either with carboxy- or amino-terminal assays) and several other parameters. A direct effect of 1,25 (OH)2-D on PRL secretion may exist.

Adult↗
PubMed1983

Thyroidal release after oral administration of TRH in normal subjects.

The oral administration of 40 mg TRH to 17 normal volunteers induced a greater TSH response in females than in males, contrasting with an identical pattern of total T3 and T4 (TT3, TT4) and of free T3 and T4 (FT3, FT4). TSH peaked at 180 min while thyroid hormones (total and free) reached their maximum at 360 min. The drop in the T4 to T3 ratio (total and free hormones) observed at 360 min is consistent with an initial preferential T3 secretion. At 360 min the thyroglobulin (Tg) levels were still in the basal range while at 24 h a significant increase was observed, essentially in female subjects. Thus T3, T4 and Tg seem to be sequentially secreted by the thyroid in response to a prolonged TSH stimulus.

Administration, Oral↗
PubMed1983

Measurement of thyroxine conversion to triiodothyronine using human lymphocytes. A useful and simple laboratory technique.

The deiodination of T4 to T3 has been studied after incubation of whole lymphocytes with different T4 concentrations, followed by a T3 radioimmunological determination performed on unextracted samples. The lymphocytes were isolated from blood from normal volunteers of both sexes and different age classes as well as from myxedematous subjects and patients with low T3 syndrome. The T3 production, in normal subjects, expressed as pmol/10.10(6) cells was 0.41 +/- 0.75 (T4 = 4.10(-7) M, n = 12), 1.43 +/- 0.14 (T4 = 4.10(-6) M, n = 26) and 1.65 +/- 0.29 (T4 = 8.10(-6) M, n = 11). There was no sex or age-related difference. In 3 myxedematous patients the T3 production was lower than the corresponding value obtained in normal subjects. The T3 production in patients with low T3 syndrome was lower than in controls (p less than 0.001); an inverse correlation was found between the T3 production and the serum rT3 levels, whereas no correlation could be found with serum T3 levels.

Adult↗