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Biomedical subjects

G Brabant

Publications and source records attributed to G Brabant.

At least 127 records · Page 7Linked to original sources
PubMed1995

Time series prediction of plasma hormone concentration. Evidence for differences in predictability of parathyroid hormone secretion between osteoporotic patients and normal controls.

Recent evidence links osteoporosis, a disease of bone remodeling, to changes in the dynamics of parathyroid hormone secretion. We use nonlinear and linear time series prediction to characterize the secretory dynamics of parathyroid hormone in both healthy human subjects and patients with osteoporosis. Osteoporotic patients appear to lack the periods of high predictability found in normal humans. Our results may provide an explanation for why an intermittent administration of parathyroid hormone is effective in restoring bone mass in osteoporotic patients.

Adult↗
PubMed1995

Regulation of the cell-cell adhesion protein, E-cadherin, in dog and human thyrocytes in vitro.

E-cadherin, a cell-cell adhesion protein specifically expressed at the basolateral membrane of thyrocytes, is variably dysregulated in thyroid carcinomas in parallel to the dedifferentiation of the tumors. No data are currently available on the regulation of E-cadherin in messenger RNA (mRNA) expression by physiological stimulators of thyroid proliferation and differentiation. The present study investigated the control of E-cadherin steady state mRNA levels and protein expression in primary cultures of dog and human thyrocytes under the influence of physiological regulators of thyroid differentiation and dedifferentiation using Northern blot analysis and immunohistochemistry. Following dedifferentiation by epidermal growth factor and fetal calf serum in primary cultures of dog and human thyrocytes, E-cadherin steady state mRNA expression was low but easily detectable. Stimulation of the cells by TSH (1 mU/ml) or forskolin (10 microM) induced an increase in E-cadherin mRNA levels with a maximal effect after 20 h. An up-regulation of E-cadherin protein levels are also observed by immunostaining with anti-E-cadherin antibodies. A concentration-response relation determined for TSH stimulation (10 microU/ml to 10 mU/ml) led to a concentration-dependent stimulation of E-cadherin mRNA levels and a parallel increase in protein expression with a minimal effective concentration of 10-30 microU/ml. These effects depend on protein synthesis as they are completely blocked by the presence of 10 micrograms/ml cycloheximide. Treatment with EGF did not markedly alter E-cadherin mRNA expression, whereas removal of insulin from the medium slightly decreased E-cadherin mRNA and protein levels. There is, therefore, a qualitative parallelism between the effect of the various factors on E-cadherin protein and mRNA levels. These results suggest that the cell-cell adhesion protein E-cadherin is under the control of the TSH-cAMP-dependent pathway and may play an important physiological role on the action of this pathway in proliferation and differentiation.

Animals↗
PubMed1995

Functional and morphological changes of the thyroid gland following 5 days of pulsatile TRH stimulation in male rats.

The aim of the present study was to evaluate in vivo the selective effects of a small increase in plasma TSH levels on thyroid function, proliferation and morphology. Chronically catheterized male Sprague-Dawley rats were stimulated i.v. over 5 days either with TRH (2 micrograms TRH in 100 microliters 0.9% (w/v) NaCl (TRH-P) or the NaCl carrier alone (P), both given as pulses every 2 h. Control groups were cotreated i.v. with 10 micrograms thyroxine (T4)/100 g body weight per day (TRH-P + T4) starting 2 days before pulsatile stimulation. TSH plasma levels were approximately doubled by TRH-P (P < or = 0.001), T4 plasma levels significantly increased (P < or = 0.001) but tri-iodothyronine plasma levels did not change compared with treatment with P. No significant changes between groups were found in thyroid weight and in intrathyroidal iodine content, but the percentage of 5-bromo-2'-desoxyuridine-labelled thyrocytes as a marker of proliferation in TRH-P-treated animals was significantly increased over P or TRH-P + T4 (P < or = 0.001). Ultrastructural analysis of the thyroid evaluated by electron microscopy revealed a significant increase in the number of lysosomes (P < or = 0.001). The size of the endoplasmic reticulum (ER) in relation to the cytoplasm was significantly increased when treated with TRH-P compared with P or TRH-P + T4 (P < or = 0.001). Post-embedding immunogold staining revealed Tg as a major product within ER cisternae. Immunogold labelling was moderate in controls and higher densities of gold particles were obtained in TRH-P-treated animals (P < or = 0.001). In conclusion, short-term pulsatile TRH stimulation increasing the plasma levels of immunoreactive TSH only twofold is capable of inducing hypertrophy of the thyrocytes by gross ultrastructural changes which are paralleled by an increase in circulating T4. These data underscore the dominant role of TSH on thyroid ultrastructure within the narrow boundaries of normal physiological regulation.

Animals↗
PubMed1995

Implications of host pancreatic hormones in the restart of grafted liver.

Regulatory roles of insulin and glucagon in hepatic metabolism and function are well described. However, little is known about implications of host pancreatic hormones in primary function of grafted liver. This study aimed to investigate it in relation to hepatic mitochondrial function. Insulin, c-peptide, and glucagon in peripheral blood were monitored for 2 days in clinical liver transplantation by a continuous sampling technique to avoid influences of hormonal oscillation. In grafts with immediate function (n = 10), smooth increase of arterial ketone body ratio reflecting hepatic intramitochondrial redox state was accompanied by increased c-peptide and decreased glucagon, resulting in the increase of c-peptide/glucagon ratio. In other functioning grafts (n = 20), where ketone body ratio was rather lower, increased glucagon level, observed also during anhepatic phase, resulted in the slower increase of c-peptide/glucagon ratio. There were accompanied by increased free fatty acid and ketone body levels. In primary nonfunction (n = 4), rapid increase of c-peptide accompanied by hyperglycemia resulted in the accelerated increase of c-peptide/glucagon ratio, but ketone body ratio did not show any increase. Insulin/c-peptide ratio also showed a rapid increase. These findings suggest that the increase of insulin/glucagon ratio in portal blood, potentially influenced by recipient condition, is associated with the recovery of mitochondrial energy metabolism in survived hepatic grafts. However, this relationship does not work in failed grafts, where irreversible impairment of energy metabolism is attributed to graft itself.

Adolescent↗
PubMed1995

[Pulsatile hormone secretion for control of target organs].

Pulsatile secretion of hormones are observed in many endocrine systems. Here we discuss the significance of pulsatile patterns of hormone secretion for the regulation of endocrine target tissues in physiology and pathophysiology. New approaches to analyze endocrine rhythms are introduced that may enable to better define the temporal patterns of secretion relevant for the regulation of distinct processes in complex in vivo systems. This may lead to improved diagnostic and therapeutic strategies of endocrine diseases.

Animals↗
PubMed1994

Western blot analysis of thyrotropin receptor expression in human thyroid tumours and correlation with TSH-binding.

Expression of thyrotropin receptor (TSHr) was analyzed in normal human thyroids and differentiated thyroid tumours by Northern blotting of total RNA and by Western blotting of detergent-solubilized membrane proteins with an antibody specific for the extracellular domain of TSHr. Under nonreducing conditions TSHr stained as a 90-kDa protein in normal thyroid tissue. Expression varied in differentiated carcinomas from normal to not detectable in parallel to steady state TSHr mRNA levels and TSH binding in a TSH binding assay. The negative expression of TSHr in some patients with differentiated carcinomas may have consequences for the TSH suppressive treatments of these patients.

Binding Sites↗
PubMed1994

Pulsatile thyrotropin secretion in patients with Cushing's syndrome.

Pulsatile and circadian thyrotropin (TSH) secretion were studied in 16 healthy controls and in three patients with Cushing's syndrome who were studied twice (before and after treatment). Blood was sampled every 10 minutes over 24 hours for TSH (immunoradiometric assay [IRMA]). Mean 24-hour TSH in Cushing's syndrome was lower than in controls (0.4 +/- 0.2 v 1.7 +/- 0.7 mU/L, P < .001), related to a lower mean 24-hour TSH pulse amplitude (Desade: 0.16 +/- 0.15 v 0.44 +/- 0.20 mU/L, P < .001; Cluster: 0.17 +/- 0.14 v 0.39 +/- 0.20 mU/L, P < .001; mean +/- SD). TSH pulse frequency was unchanged with approximately 10 pulses/24 h. The nocturnal TSH surge was diminished relative to controls (median-0, range- -0.03 to 0.2 mU/L v 0.9 and 0.3 to 2.5 mU/L, respectively), related to a loss of the usual nocturnal increase in TSH pulse amplitude, but not of TSH pulse frequency. In the eucorticoid state, there was an increase of mean 24-hour TSH to 1.3 +/- 0.8 mU/L (P < .001) under normalization of the mean 24-hour TSH pulse amplitude. The nocturnal TSH surge also increased (median, 0.21; range, 0.15 to 0.4 mU/L) under restoration of the usual nocturnal increase in TSH pulse amplitude. In conclusion, Cushing's syndrome is associated with a decrease of mean 24-hour plasma TSH, related to a decrease of TSH pulse amplitude (not of TSH pulse frequency). The nocturnal TSH surge is decreased in Cushing's syndrome associated with a loss of the usual nocturnal increase of TSH pulse amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Growth hormone therapy in adults: rationales, results, and perspectives.

This review outlines the present knowledge of the rationales, clinical aspects, and perspectives of a therapy with recombinant human growth hormone (rhGH) in adults. In patients with hypopituitarism the effects of rhGH replacement have been extensively studied. Recent clinical trials show that rhGH treatment improves most alterations of body composition and psychological performance, but many of the metabolic actions of GH remain equivocal. Although side effects after short-term administration are usually mild, the risks of severe long-term adverse effects are still uncertain. A supplementation with rhGH is also suggestive in advanced age and obesity, but the clinical results are controversial so far. The anabolic actions of rhGH were exploited in several recent trials including patients who were severely ill, malnourished, on chronic haemodialysis, or on total parenteral nutrition. Although nitrogen-sparing effects of GH have been demonstrated in most cases, the data do not indicate a clinical benefit in terms of reduced mortality, improved outcome, or accelerated recovery. Therefore, recommendations for the use of rhGH do not have any rationale in these patients yet. The efficacy of rhGH in the treatment of reproductive or immunological disorders remains elusive and needs further investigation. In conclusion, the application of rhGH is still an experimental therapy which should be performed under close observation in well-controlled clinical studies.

Aging↗
PubMed1994

Is there low-dimensional chaos in pulsatile secretion of parathyroid hormone in normal human subjects?

In many biological systems information is transferred by hormonal ligands, and it is assumed that these hormonal signals encode developmental and regulatory programs in mammalian organisms. The specificity of the biological response on activation by a hormone has so far been located within the interaction of a specific conformation of the ligand with the corresponding receptor structure. According to these classical explanations, the constant circulating hormonal pool described by the rate of its production and metabolic clearance is a major determinant of this interaction. Recently it has become apparent that hormone pulses contribute to this hormonal pool. Phase-space analysis of dynamic parathyroid hormone (PTH) secretion allowed the definition (in comparison to normal subjects) of a relatively quiet "low dynamic" secretory pattern in osteoporosis, and a "high dynamic" state in hyperparathyroidism. We now investigate whether this pulsatile secretion of PTH in healthy humans exhibits characteristics of low-dimensional deterministic chaos. Our findings suggest that this indeed appears to be the case. PTH secretion thus seems to be a first example of a chaotic hormonal rhythm in human physiology.

Adult↗
PubMed1994

Pulsatile thyrotropin and prolactin secretion in a patient with a mixed thyrotropin- and prolactin-secreting pituitary adenoma.

The circadian and pulsatile thyrotropin (TSH) and prolactin (PRL) release was investigated in a patient with slight hyperthyroidism due to a mixed TSH- and PRL-secreting pituitary adenoma. Blood was withdrawn every 10 min for 24 h (before and after medical treatment); pulse characteristics were analyzed by Desade and Cluster programs (values as mean +/- SD). The inappropriately high mean 24-h TSH concentration of 3.55 +/- 0.31 mU/l was associated with a higher mean 24-h TSH pulse amplitude but unaltered mean 24-h TSH pulse frequency relative to healthy controls. The nocturnal TSH surge (absolute surge 0.5 mU/l, relative surge 16%) was low, related to a loss of the usual nocturnal increase of TSH pulse amplitude and TSH pulse frequency. Chronic treatment with octreotide resulted in a modest clinical and biochemical improvement of the hyperthyroid state; addition of bromocriptine at a later stage had no further beneficial effect. At the end of the follow-up period the mean 24-h TSH paradoxically had increased to 5.33 +/- 0.81 mU/l. The nocturnal TSH surge also increased (absolute surge 1.9 mU/l, relative surge 42%), but circadian changes in TSH pulsatility remained absent. In the untreated period the increased mean 24-h PRL concentration of 234 +/- 24 micrograms/l was associated with an increased mean 24-h PRL amplitude, whereas the 24-h PRL pulse frequency (N = 4) was lower relative to controls. No circadian PRL rhythm was present. After octreotide and bromocriptine treatment the mean 24-h PRL concentration and mean 24-h PRL pulse amplitude were unchanged, but a clear nocturnal increase of PRL now was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1994

Markers of bone metabolism during short-term administration of thyroxine in healthy volunteers.

We investigated the influence of L-thyroxine (L-T4) treatment over 3 weeks on biochemical markers of bone turnover in 12 healthy young men (age 25.6 +/- 1.4 years, BMI: 22.6 +/- 2.5 kg/m2). Serum parameters indicating bone formation [bone Gla protein (BGP), carboxyterminal propeptide of type I procollagen (PICP), and bone-specific alkaline phosphatase (BAP)] and bone resorption [cross-linked carboxyterminal telopeptide of type I collagen (ICTP) and the urinary excretion of pyridinoline (Pyr) and deoxypyridinoline (D-Pyr)] were measured before and after three weeks of treatment with 300 micrograms L-T4/d. T3 and T4 significantly increased and TSH decreased to almost undetectable levels even when measured with a third generation TSH assay. Markers of bone formation showed variable responses with a small but significant increase in BGP but not in PICP or BAP. In contrast, all parameters of bone resorption increased significantly with a good correlation between D-Pyr excretion and the serum parameter ICTP (r = 0.78, p < 0.0001). These changes in bone-turnover markers were not necessarily paralleled by comparable increments of other markers of tissue thyrotoxicosis (SHBG, pulse rate, VO2), suggesting a variability in tissue sensitivity. These rapid responding parameters, especially in the easily obtainable serum parameter ICTP, might be valuable tools in the evaluation of several states of thyroxine excess.

Adult↗
PubMed1993

E-cadherin: a differentiation marker in thyroid malignancies.

Loss of E-cadherin (uvomorulin), a Ca(2+)-dependent cell adhesion molecule required for normal epithelial function, has been attributed a pathogenetic role in tumor invasion. The expression of E-cadherin was studied in normal and neoplastic follicular epithelium of the human thyroid by Northern blot analysis and immunofluorescence on frozen tissue sections. In the normal thyroid (n = 10) and in benign thyroid disorders (n = 21; toxic diffuse goitre; multinodular goitre; follicular adenomas), E-cadherin mRNA levels were equally high and the follicles were generally stained, mainly along the lateral surface of the epithelial cells, by the anti-E-cadherin monoclonal antibody. In anaplastic thyroid carcinomas (n = 6) E-cadherin expression was very low or lacking. In papillary carcinomas (n = 23), E-cadherin mRNA levels varied from nearly normal to highly reduced, which roughly correlated with the overall immunofluorescence intensity. However, the immunostaining also revealed a heterogeneous "all-or-nothing" expression of E-cadherin among adjacent cells in the same tumor. In the follicular carcinomas (n = 9), E-cadherin mRNA levels were in general rather high but the immunostaining varied considerably. A few papillary and follicular tumors lacked immunoreactive E-cadherin in spite of high mRNA levels. In oxyphilic (Hürthle) cell tumors, comprising both adenomas (n = 4) and carcinomas (n = 2), E-cadherin immunoreactivity was reduced and distributed intracellularly rather than at the cell surface. The expression of E-cadherin in relapsing thyroid carcinomas and in tumors with metastatic spreading was, irrespective of the histiotype, low or lacking. Sequential Northern analysis revealed a close correlation between the expression levels of E-cadherin and the thyrotropin receptor. Together, the data suggest that in human thyroid malignancies both gene expression and posttranscriptional control of E-cadherin may be impaired.

Adenoma↗
PubMed1993

Hypothyroid-like regulation of the pituitary-thyroid axis in stable human immunodeficiency virus infection.

Thyroid function and regulation were studied in 14 consecutive male outpatients with asymptomatic human immunodeficiency virus (HIV) infection (CDC II/III, n = 8) or AIDS (CDC IV, n = 6) who were free of concomitant infections and hepatic dysfunction, and in eight healthy, age- and weight-matched male controls. Blood was sampled every 10 minutes over 24 hours for measurement of thyrotropin (TSH). Thereafter, thyroid hormones and TSH responsiveness to thyrotropin-releasing hormone (TRH) were measured. Triiodothyronine (T3) and thyroxine (T4) did not differ between HIV-infected patients and controls, but HIV patients had lower thyroid hormone-binding index ([THBI] HIV patients, 1.01 +/- 0.02; controls, 1.11 +/- 0.03; P < .02), free thyroxine (FT4) index (94 +/- 3 v 110 +/- 4, P < .01), FT4 (11.8 +/- 0.4 v 14.3 +/- 0.4 pmol/L, P < .01), and reverse triiodothyronine (rT3) values (0.18 +/- 0.01 v 0.26 +/- 0.02 nmol/L, P < .001) and higher thyroxine-binding globulin ([TBG] 20 +/- 1 v 16 +/- 1 mg/L, P < .02) values. Mean 24-hour TSH levels were increased in HIV patients (2.39 +/- 0.33 v 1.44 +/- 0.16 mU/L, P < .05), associated with increased mean TSH pulse amplitude and TSH responsiveness to TRH. No differences were observed between asymptomatic HIV-seropositive and AIDS patients. In conclusion, there is a hypothyroid-like regulation of the pituitary-thyroid axis in stable HIV infection, which differs distinctly from the euthyroid sick syndrome in non-HIV-nonthyroidal illnesses.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Quality of life in patients with Addison's disease: effects of different cortisol replacement modes.

This study compares the impact of different modes of cortisol replacement therapy on the health perception and general well-being in patients with primary adrenocortical failure. 14 adults (8 female, 6 male) with Addison's disease on chronic cortisol replacement participated in the study. In a randomized double-blind cross-over design, all patients were treated with 3 modes of cortisol replacement for one week each (mode I: 20 mg hydrocortisone (HC) at 0700 h and 10 mg HC at 1900 h; mode II: 30 mg HC at 0700 h and placebo at 1900 h; mode III: placebo at 0700 h and 30 mg HC at 1900 h). Following the third week, the replacement modes were repeated in a different random order. For quality-of-life assessment the patients completed three different questionnaires (Addison-questionnaire, Basler Befindlichkeits-Skala, Beschwerde-Liste) and were interviewed about their general contentment at the last day of each treatment week. General well-being in terms of subjective contentment was best established during mode I (in 64% of patients) and less often stated with mode II (in 29%) and III (in 14%) (p < 0.05 mode I vs III). With the twice-daily replacement (mode I), sum scores of all questionnaires were changed towards improvement compared to both once-daily regimens (p < 0.05 vs mode II and III), but did not reach normal values of healthy subjects. Differences between mode II and III were insignificant. We conclude that quality of life in Addison patients is mainly influenced by the mode of cortisol replacement therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Addison Disease↗
PubMed1993

Temporal patterns of alpha 1-receptor stimulation regulate amplitude and frequency of calcium transients.

The pulsatile release of neurotransmitters and many hormones might encode specific biological information according to temporal pattern. We tested this hypothesis by applying pulsed alpha 1-adrenoceptor stimulation to single aequorin-injected hepatocytes. The amplitude of free Ca2+ transients induced by rapid phenylephrine pulses (20-s interpulse interval) and continuous stimulation was similar (approximately 640 nM) but increased to approximately 1,000 nM as the interpulse interval was increased to 120 s. The same overall response was maintained despite a 13-fold reduction in average phenylephrine concentration. Some regimes of pulsed phenylephrine stimulation could give a higher frequency of pulsed phenylephrine stimulation could give a higher frequency of free calcium oscillations than continuous stimulation, or more rapid stimulation when some agonist pulses failed to elicit a free Ca2+ transient. For the same average phenylephrine concentration (0.3-0.6 microM), pulsed regimes could result in significantly higher frequencies and integrated responses than constant application. The lags between phenylephrine pulses and free Ca2+ transients reduced as the period between pulses increased. The amplitude and lag data are consistent with a refractory period of 18 s and a recovery phase with a time constant of approximately 100 s, perhaps corresponding to dephosphorylation of alpha 1-adrenoceptors phosphorylated by protein kinase C during each free Ca2+ transient.

Adrenergic alpha-Agonists↗
PubMed1993

Renal effects of atrial natriuretic peptide in cirrhotic rats with and without captopril pretreatment.

Compared to healthy humans in most patients with cirrhosis and renal sodium and water retention, effects of atrial natriuretic peptide (ANP) on sodium and water excretion are reduced. It has been postulated that this impaired response to ANP is caused by renal vasoconstriction, induced by high levels of angiotensin II. To further investigate this issue, we studied renal hemodynamics (glomerular filtration rate, GFR, single nephron GFR, SNGFR, renal blood flow, RBF) and urinary sodium excretion (UNaV) in rats with CCl4-induced cirrhosis of the liver, before and during ANP infusion. The same parameters were determined in cirrhotic rats after a 4-day pretreatment with the angiotensin-converting enzyme (ACE) inhibitor captopril before and during ANP. Results were compared to those obtained in 2 control groups of healthy rats, one of them pretreated with captopril. Rats with cirrhosis had a significantly reduced GFR, SNGFR, RBF, UNaV and an elevated plasma renin activity compared to healthy controls. ANP caused a significant rise in UNaV (+198%) but no significant change of GFR, SNGFR and RBF in cirrhotic rats. Captopril-pretreated rats with cirrhosis had a significantly higher RBF (+26%) and 24-hour urinary sodium excretion (+52%) but no significant differences in GFR and SNGFR compared to cirrhotic rats without captopril pretreatment. Administration of ANP to cirrhotic rats pretreated with captopril resulted in a significant rise in GFR (+56%), SNGFR (+42%), RBF (+29%) and UNaV (+159%) compared to cirrhotic rats with ANP alone. In healthy rats, there was no additional effect of a combined therapy with captopril and ANP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Pulsatile thyrotropin release in patients with untreated pituitary disease.

Pulsatile and nocturnal TSH secretion was investigated in 16 healthy controls (group A) and 19 patients with untreated pituitary disease [7 were euthyroid without suprasellar extension (group B), 6 were euthyroid with suprasellar extension (group C) of pituitary lesions, and 6 were hypothyroid with or without suprasellar extension (group D)]. Pulse analysis was performed using Desade and Cluster algorithms. No changes were observed among groups A-D in mean 24-h TSH pulse amplitude [values given as mean +/- SD; Desade, 0.4 +/- 0.2 vs. 0.7 +/- 0.4 vs. 0.6 +/- 0.4 vs. 0.5 +/- 0.2 mU/L (P = NS); Cluster, 0.4 +/- 0.2 vs. 0.7 +/- 0.4 vs. 0.5 +/- 0.3 vs. 0.4 +/- 0.2 mU/L (P = NS)] or in the mean 24-h TSH pulse frequency (approximately 10 pulses/24 h). The mean 24-h TSH concentration was highly correlated to the mean 24-h TSH pulse amplitude in controls (r = 0.93; P < 0.001) and patients (r = 0.63; P < 0.01), but not to the mean 24-h TSH pulse frequency. The nocturnal TSH surge was similar in controls and euthyroid patients without suprasellar extension (group A, 1.0 +/- 0.6; group B, 1.3 +/- 1.3 mU/L; P = NS), but was decreased in euthyroid patients with suprasellar extension (group C, 0.3 +/- 1.0 mU/L; P < 0.05) and hypothyroid patients (group D, 0.4 +/- 0.4 mU/L; P < 0.05). The decreased nocturnal TSH surge was associated with a loss of the usual nocturnal increase in TSH pulse amplitude, whereas the usual nocturnal increase in TSH pulse frequency was maintained. In conclusion, 1) mean 24-h TSH pulse amplitude and frequency are unchanged in untreated patients with pituitary disease; and 2) patients with central hypothyroidism as well as euthyroid patients with suprasellar extension of pituitary lesions had a decreased nocturnal TSH surge associated with a loss of the usual nocturnal increase in TSH amplitude, but not TSH pulse frequency.

Adult↗