How the sauna affects the endocrine system

The sauna induces changes in the secretion of hormones, some similar to changes induced in any other stress situation and others characteristic of exposure to the sauna. Noradrenaline is usually the only catecholamine raised by the sauna in people accustomed to it. The secretion of the antidiuretic hormone is increased and the renin-angiotensin-aldosterone system is activated. The concentrations of the growth hormone and prolactin, in particular, secreted from the anterior pituitary are increased in the circulation. The concentration of the immunoreactive beta-endorphin in blood may also increase which may reflect the feeling of pleasure or, on the other hand, discomfort induced by the sauna. The views on the effects of the sauna on the secretion of the ACTH and cortisol are partly contradictory, probably due to differing ways of taking the sauna bath. In Finnish sauna takers the concentration of cortisol in blood is not usually increased. The changes induced by the sauna in various hormone concentrations in the circulation are, however, normalized within a couple of hours after the heat stress.     

Adrenal insufficiency following traumatic brain injury in adults

PURPOSE OF REVIEW: Hypoadrenalism occurs in approximately 25% of patients soon after traumatic brain injury. Neurosurgeons or critical care physicians should be prepared to diagnose and treat this and other related hormonal deficiencies. RECENT FINDINGS: The severity of traumatic brain injury, location of basilar skull fractures and edema or hemorrhage within the hypothalamic-pituitary axis appear correlated with secondary adrenal failure. Primary hypoadrenalism also may occur due to injury-related systemic inflammation. Hypotension requiring vasoactive drug support, hyponatremia and hypoglycemia may be corresponding clinical signs. Evaluation of either primary or secondary hypoadrenalism should include measurement of basal and post-adrenocorticotropin stimulation cortisol blood concentrations. If the basal cortisol is under 15 microg/dl or increases by over 9 microg/dl after stimulation treatment should be considered. Intravenous hydrocortisone at 50-100 mg every 8 h or by continuous infusion is usually sufficient but may be supplemented with a mineralocorticoid if hyponatremia persists. All patients sustaining severe traumatic brain injury should be tested for endocrine failure (adrenal, thyroid and growth hormone) 3 months after injury. SUMMARY: Adrenal gland failure or the inability to produce adrenocorticotropin and other pituitary hormones may occur early after traumatic brain injury. Acute treatment of either cause of hypoadrenalism may correct associated hypotension, hypoglycemia, or hyponatremia.     

Thyroid hormone extraction by plasma exchange: a study of extraction rate.

How to obtain an optimal efficiency of plasma exchanges in the treatment of severe hyperthyroidism has not been defined. In order to evaluate how long the exchanges must be continued to be fully effective in extracting thyroid hormones, we evaluated the extraction rate by repeated plasma sampling in two hyperthyroid patients and three euthyroid subjects who underwent a total of seven exchanges. Plasma concentrations of thyroid hormones were also determined just before, just after, and 24 hours following the exchange. The hormonal removal rate did not fall dramatically during the exchange, so that its efficiency--in terms of hormone extraction--depends closely on its duration. The determination of plasma thyroid hormone concentrations after the exchange does not appear to be useful in evaluating the thyroid hormone loss since these concentrations may not change in spite of the hormonal extraction.     

Thyroid hormone resistance

General resistance to the action of thyroid hormones is characterized by increased levels of thyroid hormones and normal thyroid hormone binding proteins but clinical euthyroidism. There is a wide clinical spectrum ranging from patients with congenital goitre and signs of subclinical hypothyroidism to subjects with no physical abnormality. In the most affected patients special physical features have been described. Serum thyrotrophin (TSH) and the response to thyrotrophin releasing hormone (TRH) is mostly normal but may fluctuate being at times elevated and even markedly increased values may be encountered. Studies on lymphocytes and fibroblasts indicate that a decreased affinity of thyroid hormones for nuclear receptors, a decreased binding capacity of the receptors or some post-receptor mechanism may be responsible for these changes. Hitherto, six families, comprising 24 patients and seven single cases, have been described. The pedigrees are compatible with dominant inheritance. Selective refractoriness of the pituitary thyrotrophs to thyroid hormones has been described in five patients with hyperthyroidism. Excessive secretion of TSH is the cause of hyperthyroidism. In four of the cases reported TRH caused an exaggerated TSH response and TSH was partially suppressible by additional exogenous thyroid hormone. The response of TSH and the behaviour of the alpha- and beta-subunits of TSH distinguish this syndrome from TSH-induced hyperthyroidism due to pituitary tumours. The underlying mechanisms are unknown.     

Thyrotropin-releasing hormone and thyrotropin secretion

Thyrotropin (TSH) secretion is regulated primarily by thyroid hormones and thyrotropin-releasing hormone (TRH). Normally, TSH secretion is exquisitely sensitive to small increases and decreases in serum thyroid hormone concentrations when they occur as a result of alterations in thyroid secretion. Serum TSH responses to TRH are altered by even smaller decreases and increases in serum thyroid hormone concentrations. This sensitivity explains the value of measurements of basal serum TSH concentrations and serum TSH responses to TRH in the diagnosis of hypothyroidism and hyperthyroidism, respectively. How TRH secretion is regulated is unknown, but the direct inhibitory effect of thyroid hormones on the thyrotrophs minimizes the stimulatory effect of any chronic changes in TRH secretion that may occur. In patients with nonthyroid illness, however, the normal relationships between serum thyroxine and triiodothyronine concentrations and TSH secretion are altered. Slightly or moderately ill patients have decreases in extrathyroidal triiodothyronine production that are not followed by an increase in TSH secretion, although the sensitivity of the thyrotrophs to further reduction or to an increase in triiodothyronine concentration is maintained. More severe illness may result in impaired TSH secretion and thus in decreased thyroidal as well as decreased extrathyroidal thyroid hormone production. These alterations in thyrotroph sensitivity and secretion, so that TSH secretion is not increased when extrathyroidal triiodothyronine production is decreased and thyroid secretion is decreased in more severe illness, suggest that decreased thyroid hormone production is a beneficial adaptation to nonthyroid illness.     

Endocrine alterations in the aging male.

The recent increase in the elderly population, current health trends and awareness of age-related changes in the male endocrine system, have led to discussions about the role of the hormonal changes in the aging process in males. Better prevention and treatment of suboptimal health status and age-related diseases in aging men are based on an improved understanding of aging, particularly of the significance of age-associated hormonal changes. The aims of this study were 1) to evaluate the age dependence of the serum concentrations of the following important hormonal parameters in adult males using the IMMULITE 1 automated assay system (DPC, Los Angeles): testosterone, dehydro-epiandrosterone sulfate (DHEAS), estradiol (E2), sex hormone binding globulin (SHBG), lutropin (LH), follitropin (FSH), cortisol, prolactin, thyroid stimulating hormone (TSH), free triiodothyronine (fT3), free thyroxine (fT4) and the growth hormone-dependent parameters insulin-like growth factor (IGF-I) and IGF-binding protein-3 (IGFBP-3) and 2) to derive the following parameters: calculated free testosterone (cFT), ratio of calculated free testosterone to total testosterone (% cFT) and free androgen index (FAI). We found a significant decrease between the 21-30-year age group and the > 70-year age group for total testosterone (-42.4%), FAI (-65.5%), cFT (-60.0%), % cFT (-30.0%), DHEAS (-71.9%), E2 (-35.4%), TSH (-23.6%), IGF-I (-40.3%) and IGFBP-3 (-26.5%). Since the decreases in the FAI and cFT were greater than that of total testosterone and because these derived parameters reflect the biologically active fraction of testosterone, FAI and cFT are better markers for androgen deficiency in males. In contrast, a significant increase with age was observed for SHBG (+61.2%), LH (+40.0%), FSH (+98.3%) and cortisol (+54.2%). No significant alterations with age were observed for prolactin, fT3 and fT4. The study demonstrates that determining complete profiles of the androgenic, gonadotropic, adrenocortical, thyroid, pituitary and growth hormone/IGF endocrine axes in middle-aged and elderly men may be helpful in obtaining a correct clinical diagnosis for various hormonal disorders.     

Alterations in laboratory test results during adjuvant breast cancer treatment.

An increasing number of women is treated with adjuvant cyclophosphamide, methotrexate and 5-fluorouracil therapy for breast cancer. The effects of the chemotherapy on many laboratory tests are, however, inadequately known. This study investigates the effects of the treatment on various laboratory tests. Fifteen premenopausal women receiving adjuvant cyclophosphamide, methotrexate and 5-fluorouracil chemotherapy and optional radiotherapy were included in the study. Common hormonal, biochemical, hematological, protein and lipid laboratory tests were taken serially during a 10-month follow-up. Twelve women became amenorrheic. Their serum follicle stimulating hormone and luteinising hormone concentrations increased accordingly. Other serum hormones (testosterone, androstenedione, sex hormone-binding globulin, prolactin, dehydroepiandrosterone sulfate, cortisol, parathyroid hormone and thyroid hormones) changed only slightly. Hemoglobin concentration and white blood cell count decreased slightly. Serum alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, creatine kinase, angiotensin-converting enzyme, amylase, glucose, potassium, phosphate, urea and triglycerides concentrations increased slightly whereas serum bilirubin, haptoglobin, and immunoglobulin A and M decreased slightly. Serum alpha1-antitrypsin fluctuated around the baseline concentration. Other test results remained at their pretreatment concentrations. With the exception of increases in serum gonadotrophins, the changes observed were slight and the mean concentrations remained within reference limits. Therefore, cyclophosphamide, methotrexate and 5-fluorouracil adjuvant treatment is unlikely to complicate the diagnosis of other diseases.     

Endocrinology in aging

Aging is a time of reduced adaptability to metabolic perturbation. This is particularly true in endocrinology which, after all, is the science of chemically regulated biologic systems. There is no evidence that equilibrium concentrations of the principal hormones are altered with age. However, the systems utilized to reach those equilibria become progressively taxed, and new equilibria may be achieved reflecting that regulatory problem. Thus, with advancing age there are significant alterations in hormone production, metabolism, and action. Some of these changes may play a role in the pathophysiology of senescence, although the evidence for that is limited. The magnitude of age-related alterations is highly variable and sex dependent. Whereas only subtle changes occur in pituitary dynamics, adrenal gland physiology, and thyroid function, the changes in glucose homeostasis, reproductive function, and calcium metabolism are more apparent. In the elderly, the interpretation of endocrine tests should reflect the nutritional status of the patient and the presence of coexisting illnesses. In this review, we describe the principles of endocrinology in the geriatric population and elaborate on the changes in specific glandular functions with aging. We also define strategies of evaluation and management protocols appropriate for the elderly with suspected endocrine dysfunction.     

Hypothalamic-Pituitary Function in Diverse Hyperprolactinemic States

Prolactin secretion in normal adults is characterized by periods of episodic secretion which increase in magnitude during sleep. In this study, we report the 24-h mean prolactin concentrations, prolactin secretory patterns, and associated pituitary hormone function in nine patients (seven women and two men) with hyperprolactinemia of diverse etiologies. Four of the women and one of the men had clinically demonstrable pituitary tumors, one boy had a hypothalamic tumor, and the three other women had "functional" hyperprolactinemia. The 24-h mean prolactin concentrations derived from averaging the 20-min interval samples for 24 h ranged from 28.6 to 1,220 ng/ml. The plasma prolactin patterns in these patients showed persistence of episodic secretion in all and loss of the normal sleep-wake difference in plasma prolactin in seven of nine. Three of the patients with galactorrhea and comparable 24-h mean prolactin concentrations (58.3, 59.7, and 64.3 ng/ml) showed similar prolactin secretory patterns despite different etiologic mechanisms. Evaluation of the secretory patterns of luteinizing hormone (LH) in these patients showed loss of normal pulsatile LH release and a low 24-h mean LH concentration in the patient with the pituitary tumor, while the two patients without clinically demonstrable pituitary tumors ("post-pill" galactorrhea and "idiopathic" galactorrhea) showed normal LH secretory patterns and 24-h mean LH concentrations. The 24-h mean cortisol concentrations and secretory patterns were normal in five of the seven patients who had these parameters measured. The patient with the hypothalamic tumor had a low 24-h mean cortisol concentration and production rate and absent response to metyrapone. The patient with "idiopathic" galactorrhea had an elevated 24-h mean cortisol concentration but normal cortisol production rate and urinary 17-hydroxycorticoid excretion. Growth hormone secretion was abnormal in four of the patients (one with the hypothalamic tumor and three with pituitary tumors). Thyrotropin-releasing hormone (TRH) administration in four patients resulted in normal TSH release in two patients (one of whom developed galactorrhea after the test), an absent response in the patient with the hypothalamic tumor, and a blunted response in one of the women with a pituitary tumor. The two men had low 24-h mean plasma testosterone concentrations (69 and 30 ng/100 ml) and symptoms of impotence and loss of libido. Five of the women (four with pituitary tumors and one with Chiari-Frommel syndrome) had either low 24-h mean LH concentrations, abnormal LH secretory patterns, or both. These data indicate that patients with hyperprolactinemia encompassing a varied etiological range frequently show loss of the normal sleep-associated increase in prolactin secretion as well as abnormalities in the regulation of the other hypothalamic pituitary-regulated hormones. The finding that the abnormalities in LH, growth hormone, thyrotropin, and cortisol (adrenocorticotrophic) secretion were almost uniformly confined to the patients with the clinically demonstrable hypothalamic or pituitary tumors suggests that the size of the lesion is the critical factor.     

How does long term exposure to base stations and mobile phones affect human hormone profiles?

ObjectivesThis study is concerned with assessing the role of exposure to radio frequency radiation (RFR) emitted either from mobiles or base stations and its relations with human's hormone profiles.Design and methodsAll volunteers' samples were collected for hormonal analysis.ResultsThis study showed significant decrease in volunteers' ACTH, cortisol, thyroid hormones, prolactin for young females, and testosterone levels.ConclusionThe present study revealed that high RFR effects on pituitary–adrenal axis.     

Mechanisms for pituitary tumorigenesis: the plastic pituitary

The anterior pituitary gland integrates the repertoire of hormonal signals controlling thyroid, adrenal, reproductive, and growth functions. The gland responds to complex central and peripheral signals by trophic hormone secretion and by undergoing reversible plastic changes in cell growth leading to hyperplasia, involution, or benign adenomas arising from functional pituitary cells. Discussed herein are the mechanisms underlying hereditary pituitary hypoplasia, reversible pituitary hyperplasia, excess hormone production, and tumor initiation and promotion associated with normal and abnormal pituitary differentiation in health and disease.     

Altered interaction between triiodothyronine and its nuclear receptors in absence of cortisol: a proposed mechanism for increased thyrotropin secretion in corticosteroid deficiency states

Thyroid hormones occasionally appear less effective when administered alone to patients with panhypopituitarism, and manifestations suggestive of hypothyroidism have been reported in patients suffering from untreated Addison's disease. In the latter condition, thyrotropin secretion is increased: this occurs already after as little as 2 days of temporary withdrawal of therapy with substitution doses of corticosteroids while circulating levels of thyroid hormones remain within normal limits. Therefore, a possible role of cortisol in interaction between triiodothyronine and its nuclear receptors was examined at the level of circulating lymphocytes obtained from patients with primary or secondary adrenocortical failure. The affinity of these receptors was found to be decreased, by more than 50% on average, in the absence of cortisol treatments. This change was promptly corrected upon resumption of therapy. The number of binding sites was not significantly modified. The influence of cortisol on thyroid hormone receptors discussed here might account for the clinical observations mentioned above.     

Immediate and Long-term Effects on Hormone Levels Following Bites by the Burmese Russell's Viper

Studies of anterior pituitary function were made in victimsof a bite by the Burmese Russell's viper, who had required admissionto a renal unit. Twenty patients at the stage of the acute illness were studiedusing a single blood sample for several hormone assays. Noneshowed normal levels of all hormones measured. As acute severeillness can have a profound effect on the levels of these hormones,it is only possible to conclude that the results were compatiblewith although not diagnostic of anterior pituitary failure. Twelve survivors were assessed at eight to 226 weeks after envenoming,by hormone measurement in a basal sample, and a combined pituitaryreserve function test with TRH, GnRH, and insulin hypoglycaemia.All but one showed some deficit in pituitary hormone secretion.Seven had already been started on thyroid replacement therapyor corticosteroids. Three survivors were assessed in the acute stage and later andeach had similar findings on both occasions. Three survivorswho were followed up and assessed with a combined pituitaryreserve function test on two occasions had similar results eachtime. There was no sign of recovery. It seems that severe envenoming may be associated with anteriorpituitary failure. Results from five autopsies showed that thelesion was haemorrhagic anterior pituitary necrosis. An additionalmechanism may be direct action of the venom upon the functionof anterior pituitary cells. We conclude that severely affectedvictims should be considered at risk of pituitary insufficiency.     

Effect of carbamazepine, phenytoin and phenobarbitone on serum levels of thyroid hormones and thyrotropin in humans.

Patients on long-term treatment with either of the stereochemically related antiepileptic drugs phenytoin (DPH) or carbamazepine (CBZ) had similar changes in serum thyroid hormone concentrations. T4, FT4, FT4 index, T3, FT3, FT3 index and rT3 were reduced, whereas T3U and TSH were not significantly different from the reference group levels. Long-term phenobarbitone treatment had no convincing effect on the investigated parameters when used alone, but possibly potentiated the effect of CBZ. In patients starting on CBZ, T4 fell to a stable 70% of the basal level after 1--2 weeks. T3 decreased transitorily to 85% of the basal level. TSH showed a complementary but somewhat delayed transitory increase. T3U and TBG did not change significantly. The effect of CBZ and DPH can be explained by interference with thyroid hormone binding to TBG combined with enzyme-induced increased metabolic clearance rate of thyroid hormones without homeostatic maintenance of premedication levels of FT4 and FT3. We suggest that the regulated factor maintaining euthyroidism in these patients is the total quantity of thyroid hormones being degraded in the tissues per unit time. We conclude that serum concentrations of FT4 and FT3 do not reflect thyroid status adequately under all circumstances.     

Central hypothyroidism and hyperthyroidism

Thyroid function is maintained by tonic secretion of TSH by the pituitary. TSH secretion, in turn, is dependent on hypothalamic TRH production. Therefore, diseases of the hypothalamus and pituitary are frequently associated with TSH deficiency, producing central hypothyroidism. All patients with hypothalamic or pituitary disease should have thyroid function tests including a serum TSH by radioimmunoassay (RIA). In central hypothyroidism the TSH RIA is inappropriately low in relationship to the degree of hypothyroxinemia but is not always undetectable. In fact, because of the production of biologically inactive TSH, the TSH RIA may be in the high range of normal. Therapy of central hypothyroidism includes the management of associated pituitary hormone deficiencies, particularly secondary adrenal failure, and neurologic defects. A rare cause of hyperthyroidism is excessive TSH secretion. This may be due to a TSH-secreting pituitary tumor or to a functional disturbance in TSH secretion. TSH-secreting pituitary tumors are often large and locally invasive. Selective pituitary resistance to thyroid hormone is the most common cause of functional TSH-induced hyperthyroidism. It is important to rule out generalized thyroid hormone resistance before use of antithyroid drugs or thyroid surgery in patients suspected of this disorder. This is because antithyroid treatment is contraindicated in generalized thyroid hormone resistance.     

Suppression of Pituitary TSH Secretion in the Patient with a Hyperfunctioning Thyroid Nodule

10 patients with a single hyperfunctioning thyroid nodule each were studied for pituitary thyrotropin (TSH) suppression. They were judged to be euthyroid on clinical grounds. The total thyroxine (T(4)D), free thyroxine (FT(4)), total triiodothyronine (T(3)D), and free triiodothyronine (FT(3)) were normal in most of the patients. Incorporation of (131)I into the hyperfunctioning thyroid nodules was not suppressed by the administration of physiological doses of T(3). Basal serum TSH concentrations were undetectable (<0.5 - 1.0 muU/ml) in all patients. The metabolic clearance of TSH in one patient before and after excision of the thyroid nodule was unchanged (40 vs. 42 ml/min) whereas the calculated production rate was undetectable before the operation (<29 mU/day) and normal after (103 mU/day). These data, in one patient, suggest that the undetectable concentration of TSH in these patients is a result of suppressed TSH secretion rather than accelerated TSH clearance.In eight patients, basal serum TSH concentrations failed to increase after the intravenous administration of 200 mug of thyrotropin-releasing hormone (TRH); minimal increases in serum TSH concentrations were observed in two patients. The suppression of TSH was evident despite "normal" concentrations of circulating thyroid hormones. The observation that normal serum concentrations of T(4)D, FT(4), T(3)D, and FT(3) may be associated with undetectable basal serum TSH concentrations and suppressed TSH response to TRH was also found in four hypothyroid patients given increasing doses of L-thyroxine and sequential TRH stimulation tests.     

癫痫患者甲状腺激素水平及抗癲痫药物对其影响的研究

目的:研究癫痫患者甲状腺激素水平和抗癫痫药物对甲状腺激素水平的影响以及与抗癫痫效果之间的关系。方法:测定确诊的45例未服用过抗癫痫药物的癫痫患者的血清甲状腺激素水平并与30例健康对照组进行比较。再经卡马西平、苯妥英钠、丙戊酸钠三种抗癫痫药物分组单药治疗三月、六月、一年后对甲状腺激素水平的变化及与疗效之间的关系进行现(?)。结果:未服用抗癫痫药物的癫痫患者游离甲状腺素(FT_4)水平显著低于健康对照组,经苯妥英钠、卡(?)西平分别治疗三月、六月、一年后甲状腺激素(T_4)、FT_4、游离三碘甲状腺原氨酸(FT_3)显著低于治疗前水平。经丙戊酸治疗后的不同时间段各甲状腺激素水平与治疗前无显著性差异。甲状腺激素水平的(?)化与抗癫痫效果之间似无相关性。结论:癫痫的反复发作虽不经抗癫痫药物治疗亦存在FT_4水平的降低。苯妥英钠、卡马西平可明显造成癫痫患者的亚临床甲低(T_4、FT_4、FT_3降低)。丙戊酸钠对患者甲状腺激素水平无显著影响。甲状腺激素水平的变化与疗效之间无相关性。     

Functional state of the neuroendocrine system in men after myocardial infarction in the period of rehabilitation

The paper is devoted to systemic analysis of changes of the hypophyseal hormones, sex and adrenal glands, and thyroid in men in the course of a year after MI. A stable state of the hypophyseal-gonadal system the first 2 mos after MI was followed by a significant decrease in prolactin, testosterone levels and an increase in estradiol concentration. A marked decrease in STH, cortisol, TSH and thyroid hormone levels, and monotonously decreased ("leveled") circadian rhythm of secretion of practically all hormones were revealed. Functional exercise tests have shown switching over of the neuroendocrine system of MI patients to a special sparing regimen functioning at a qualitatively new hormonal-metabolic level rather than its depletion.     

Thyroid hormone modulation of the hypothalamic growth hormone (GH)-releasing factor-pituitary GH axis in the rat.

Both thyroid hormone and hypothalamic growth hormone (GH)-releasing factor (GRF) facilitate pituitary somatotroph function. However, the pathophysiological role of thyroid hormone in GRF secretion is less well understood. Thyrotoxicosis, induced by administration of thyroxine (T4) in rats, inhibited both pituitary GH levels and immunoreactive GRF secretion from incubated hypothalamus. At the highest dose of T4 given for 12 d, GRF secretion and pituitary GH decreased by 50 and 39%, respectively. Hypothyroidism induced by thyroidectomy (Tx) enhanced GRF secretion approximately twofold while depleting pituitary GH by greater than 99%. Both of these hypothalamic and pituitary effects were reversed by replacement of T4 but not human GH for 7 or 14 d. Human GH was as potent as T4 in restoring decreased body weight gains or serum insulin-like growth factor-1 levels in Tx rats. These results indicate that at both physiological and pathological concentrations in serum, thyroid hormone acts as an inhibitory modulator of GRF secretion, probably not involving a feedback mechanism through GH. A biphasic effect of thyroid hormone on pituitary GH levels appears to derive from the difference in primary target tissues of hyper- and hypothyroidism, the hypothalamus and the pituitary, respectively.