Superior vena cava syndrome caused by benign intrathoracic goitre.
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Aged↗
Biomedical subjects
L Vanhaelst
Publications and source records attributed to L Vanhaelst.
Defect in ACTH control persisting after removal of an ectopic source of ACTH.
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ACTH Syndrome, Ectopic↗
Asymptomatic atrophic thyroiditis.
Asymptomatic atrophic thyroiditis (AAT), one of the three variants of autoimmune thyroiditis, is characterized by the presence of serum antithyroid antibodies in good correlation with thyroid lymphoplasmocytic infiltrations. AAT affects 5-15% of the general population and is especially prevalent in elderly women. Patients with AAT have no goitre and are clinically euthyroid. While circulating thyroid hormones are always in the normal range, peak TSH and TRH and basal TSH values are increased in two thirds of the cases. There is a familial aggregation of AAT and a frequent association with other autoimmune diseases. Development of overt hypothyroidism in AAT patients is not rare. Preventive thyroid replacement therapy is indicated in patients with elevated basal TSH levels.
Aged↗
Autoimmune thyroiditis: a condition related to a decrease in T-suppressor cells.
Monoclonal antibodies recognizing specific antigenic determinants of peripheral T-lymphocytes (OKT3PAN), helper T-cells (OKT4IND) and suppressor T-cells (OKT8SUP) were used to study the immune regulation in autoimmune thyroiditis. An indirect immunofluorescence microscopy method was employed to quantify the number of different subtypes. In addition, B-lymphocytes were also studied using a fluorescent surface Ig detection technique. Patients with autoimmune thyroiditis--independent of their clinical status--show a decrease in the number of suppressor T-lymphocytes. This finding, in agreement with other functional tests, indicates that the autoimmune phenomenon is linked to a decreased T-suppressor activity.
Adult↗
Atrophic autoimmune thyroiditis: relationship between the clinical state and intrathyroidal iodine as measured in vivo in man.
The intrathyroidal iodine (ITI) was measured by means of the x-ray fluorescence method in 58 patients suffering from atrophic autoimmune thyroiditis (AAT). They were divided into 4 groups according to their basal T4, basal TSH, and the peak TSH response after TRH administration. Forty-eight normal subjects served as controls. A progressive fall of ITI was found, with less ITI in the first grade AAT patients as compared to the controls. A negative correlation between basal TSH and ITI could be shown. These data support the concept of a graded evolution of AAT, linking the clinical state to the ITI. The results also suggest that, with the hemagglutination techniques used for the determination of antithyroglobulin antibodies and antithyroid microsomal antibodies, positively at a dilution of 1:25 and 1:100, respectively, should be regraded as significant.
Autoimmune Diseases↗
Thyrotropin nyctohemeral pattern in primary depression: differences between unipolar and bipolar women.
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Adolescent↗
Hypothyroidism with normal thyroid hormone levels as a consequence of autoimmune thyroiditis and peripheral resistance to thyroid hormone.
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Aged↗
Grades of subclinical hypothyroidism in asymptomatic autoimmune thyroiditis revealed by the thyrotropin-releasing hormone test.
Serum levels of T4 T3, and TSH and peak TSH after TRH administration were determined in 60 female subjects affected with asymptomatic autoimmune thyroiditis (AAT), in 27 normal subjects, and in 8 myxoedematous patients used as controls. The AAT subjects were divided into 3 groups on the basis of their basal and peak TSH values. In the first group (grade I AAT), these parameters were similar to those of the normal controls; in the second (grade II AAT), basal TSH remained normal but peak TSH was significantly increased; and in the third (grade III AAT), both parameters were significantly increased. Serum T4 levels decreased progressively from group 1 to group 3, but all T4 values were within the normal range. T3 levels were similar in all groups. Peak and basal TSH values were highly correlated, except in grade II AAT. There seems to exist a graded process of subclinical hypothyroidism in AAT; a progressive pituitary TSH reserve is modulated by a progressive decrease in T4 levels still within the normal range.
Adult↗
Prolactin response to TRH in diabetic ketoacidosis.
The prolactin response to 200 microgram thyrotropin-releasing hormone (TRH) IV was studied in seven patients with diabetic ketoacidosis, at the start of the treatment, and again, in the same patients, five days after recovery, when the diabetes was well controlled. Normal basal prolactin concentrations and prolactin responses to TRH were found in both situations. There was no correlation between basal prolactin concentrations, or magnitude of prolactin responses to TRH, and any of the metabolic variables measured. These findings do no suggest a role for prolactin in the development of diabetic ketoacidosis.
Adult↗
Effect of cyproheptadine on thyrotrophin and prolactin secretion in normal man.
In order to investigate the effect of cyproheptadine, a compound with antiserotoninergic activity, on the secretion of thyrotrophin (TSH) and prolactin (PRL), the nocturnal secretory patterns of these hormones have been studied in 4 normal men in the basal state and after an oral treatment with the drug. In addition, the TSH and PRL responses to TRH of 6 women were compared in the basal conditions and after cyproheptadine treatment. The TSH nocturnal secretion was slightly modified by drug treatment. The response to TRH as well as the basal levels were comparable in the treated and non-treated subjects. In contrast, the PRL secretion measured through the nocturnal investigation was significantly inhibited by cyproheptadine administration as were the PRL basal levels in the TRH test. The PRL response to TRH was comparable in both situations.
Adult↗
Pituitary-thyroid axis during short term, mild and severe, iodine depletion in the rat.
To investigate the most early events occurring during the adaptation of the pituitary-thyroid axis to iodine depletion, two rat populations were submitted to 4 week low iodine regimens of different severity. The variations of the following parameters were studied: pituitary thyrotropin (TSH) concentration, serum thyroxine (T4), triiodothyronine (T3) and TSH, thyroid weight and thyroid iodine concentration. In the first population, mildly iodine depleted, serum and pituitary TSH remained unchanged. The weight of the thyroid increased by the 12th day. Serum T4 dropped by the 26th day. Serum T3 tended to increase during the whole observation period. In the second population, more severely iodine depleted, the increase in thyroid weight appeared by the 4th day. Serum T3 increased from day 13 to day 20, then returned to normal. Serum TSH increased and serum T4 decreased by the 20th day. These results suggest that, in the adaptation to iodine deficiency in the rat, autonomous thyroid regulatory mechanisms play a major role at the onset of goiter growth. On the other hand, most likely a combined effect of serum T3 and T4 triggers variations in pituitary TSH secretion.
Animals↗
A low T3 syndrome in diabetic ketoacidosis.
The pituitary-thyroid axis was investigated in nineteen euthyroid patients with severe diabetic ketoacidosis. A 'low T3 syndrome' was found, with the following characteristics: lowered serum concentrations of triiodothyronine (T3), increased reverse triiodothyronine (rT3), slightly low thyroxine (T4), normal thyrotrophin (TSH), slightly increased triiodothyronine uptake (RT3U) values, and a blunted TSH response to thyrotrophin-releasing hormone (TRH). These disturbances in thyroid-function tests required several days good control of the diabetes to be corrected, at least partially. The data suggest the presence of an abnormal extrathyroidal T4 metabolism as well as a pituitary defect. Caution is recommended in the interpretation of thyroid-function tests during and several days after the treatment of diabetic ketoacidosis.
Adult↗
Acute endocrine profile of sulpiride in the human.
Normal men and normally menstruating women received i.m. injections of 0.1 to 4.0 mg/kg sulpiride. This psychotropic drug induced a very rapid (already significant after 5 minutes) and sustained (still significant after 7 hours) elevation of prolactin (PRL) concentrations in all subjects with no consistent modification of LH and FSH. After injection of 4.0 mg/kg, there was similarly no modification of mean TSH concentrations in the women tested in the luteal phase, as well as of mean GH levels in men. Sulpiride prevented the inhibitory effect on PRL levels of 500 mg levodopa, administered orally simultaneously; levodopa administered 2 hours prior to sulpiride failed to counteract the PRL-stimulatory effect of sulpiride. Under chronic sulpiride-induced hyperprolactinaemia, levodopa exhibited however a very slight inhibitory effect on PRL concentrations. These data are in agreement with the hypothesis that sulpiride acts mainly at the pituitary level by blocking dopamine receptors of the lactotropes and support the concept that the menstrual cycle perturbations observed under chronic sulpiride administration result from hyperprolactinaemia itself or from a mechanism quite similar to that by which sulpiride induces hyperprolactinaemia.
Adolescent↗
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↗
Asymptomatic autoimmune thyroiditis and coronary heart-disease. Cross-sectional and prospective studies.
Cross sectional and prospective surveys of thyroid autoimmunity have been performed in two cohorts of men, 280 living in west Finland and 269 in east Finland. In both populations, aged 50 to 69 years at the first survey, risk factors for coronary heart-disease (C.H.D.) were common. The incidence of C.H.D. was shown to be related to the presence of thyroid antibodies. The results of the cross-sectional studies were not conclusive. The five-year follow-up study emphasised that in both areas asymptomatic thyroid autoimmunity, independently of other known risk factors, was a predictor of subsequent development of C.H.D. The importance of asymptomatic autoimmune thyroid-itis as a risk factor for C.H.D. increases with age.
Aged↗
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↗
Paradoxical modulation of thyrotrope responsiveness to TRH during the treatment of thyrotoxic patients: apparent absence of feed-back regulation.
Eight patients with active thyrotoxicosis have been followed up to one year after the onset of antithyroid treatment. At different time intervals during the investigation period, TRH tests were performed and total T4 and T3 basal levels were measured. The TRH-induced TSH release was delayed in all patients in spite of a normalization of the circulating levels of thyroid hormones. The delay varied according to the patients and lasted, in some cases, for as long as 24 weeks after the normalization of the thyroid hormone levels. Administration of thyroid hormones, together with methimazole, did not seem to prevent the pituitary thyrotropes responsiveness; moreover, it did not provoke an inhibition of the TRH-induced TSH release once the thyrotropes reactivity was fully restored. The feed-back mechanism does not seem to be the main modulator of the pituitary responsiveness to TRH in these circumstances.
Adolescent↗