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PubMedDate not supplied

[Potential reserve capabilities of the adenohypophyseal-adrenal cortex system in children with thymus hyperplasia and prospects for treatment].

The potentialities of the adrenocortical system and thymic condition after corticotropin use were studied in young children with thymic hyperplasia combined with pneumonia. The results of the hormonal status studies after zinc-corticotropin suspension load indicate the secondary adrenocortical hypofunction. Corticotropin use within 5 to 10 days in a dose of 1 E/kg body weight intramuscularly is adequate to obtain the thymic involution in thymomegaly.

Adrenal Cortex↗
PubMed1992

Structure and dynamics of adrenal mitochondria following stimulation with corticotropin releasing hormone.

The mitochondria of rat adrenals were investigated qualitatively and quantitatively in different functional states of the adrenal cortex. Following stimulation of the animals with corticotropin releasing hormone (CRH), the corticosterone serum levels reached a maximum 1 hour after stimulation with CRH. The amount of inner mitochondrial membrane within the zona fasciculata increased showing a biphasic time course, with a first maximum 2 hours and a second maximum 8 hours after stimulation. In contrast, a significant rise of mitochondrial volume occurred only 24 hours after CRH stimulation. Therefore, the dense vesicularization of mitochondrial cristae may constitute an early process to enhance the steroidogenic capacity of these cells. Within cells of the transition zone between zona glomerulosa and zona fasciculata, we could depict a special type of mitochondria with characteristic crescent-like cristae only seen after stimulation with CRH. This type of mitochondria may represent an intermediate form between mitochondria of zona glomerulosa and zona fasciculata underlining the impressive transformational capacity of adrenocortical mitochondria. After hypophysectomy, zona fasciculata cells contained mitochondria with tubular inner membranes, representing a hypofunctional state. In contrast, the hypofunctional state after hypophysectomy and the hyperfunctional state after stimulation of the adrenal cortex via CRH injection did not appear to correlate with the morphology of mitochondria from the zona reticularis and adrenal medulla.

Adrenal Cortex↗
PubMed1996

Perianaesthetic management of patients with endocrine disease.

Hyper- or hypofunctioning endocrine organs present a number of perianaesthetic challenges. This review covers some of the issues of perianaesthetic management of patients with primary or coexisting pathology of the following endocrine organs: The pancreas with diabetes mellitus as the most common endocrine cause of primary and secondary organ dysfunctions affecting anaesthetic care. Adrenal cortical pathology with excess or deficiency of adrenocortical hormones. Pheochromocytoma of the adrenal medulla with infrequent but challenging perianaesthetic problems. Thyroid gland diseases with hyper- or hypothyroidism. Parathyroid gland pathology with hypercalcaemia or hypocalcaemia. Disorders of the anterior and posterior pituitary gland. The carcinoid syndrome and more uncommon endocrinopathies such as adenomas from the gastroenteropancreatic endocrine tissues and the ovarian hyperstimulation syndrome are also reviewed briefly.

Anesthesia↗
PubMed1993

Effect of acupuncture on weight loss evaluated by adrenal function.

In order to understand the relationship between patients' adrenal function and simple obesity and effect of acupuncture on it, the obesity indices, lipid indices, fasting blood-glucose, noradrenaline, dopamine, adrenalin and cortisol were observed. The results indicated that patients with simple obesity had hypofunction of the sympathetic-adrenal system and the hypothalamus-pituitary-adrenal system. Acupuncture treatment not only affected weight loss but also enhanced functioning of the two systems, suggesting that the effect of acupuncture on weight loss may be produced by enhancing the functions of both the sympathetic-adrenal system and the hypothalamus-pituitary-adrenal system.

Acupuncture Therapy↗
PubMed2000

Deletion of tyrosine hydroxylase gene reveals functional interdependence of adrenocortical and chromaffin cell system in vivo.

Catecholamines are produced in the medulla of the adrenal gland and may participate in the intraglandular regulation of its cortex. We analyzed the adrenal structure and function of albino tyrosine hydroxylase-null (TH-null) mice that are deficient in adrenal catecholamine production. Adrenal catecholamines were markedly reduced, and catecholamine histofluorescence was abrogated in 15-day-old TH-null mice. Chromaffin cell structure was strikingly altered at the ultrastructural level with a depletion of chromaffin vesicles and an increase in rough endoplasmic reticulum compared with wild-type mice. Remaining chromaffin vesicles lined up proximally to the cell membrane in preparation for exocytosis providing a "string-of-pearls" appearance. There was a 5-fold increase in the expression of proenkephalin mRNA (502.8 +/- 142% vs. 100 +/- 17.5%, P = 0.016) and a 2-fold increase in the expression of neuropeptide Y (213.4 +/- 41.2% vs. 100 +/- 59.9%, P = 0.014) in the TH-null animals as determined by quantitative TaqMan (Perkin-Elmer) PCR. Accordingly, immunofluorescence for met-enkephalin and neuropeptide tyrosine in these animals was strongly enhanced. The expression of phenylethanolamine N-methyl transferase and chromogranin B mRNA was similar in TH-null and wild-type mice. In TH-null mice, adrenocortical cells were characterized by an increase in liposomes and by tubular mitochondria with reduced internal membranes, suggesting a hypofunctional state of these steroid-producing cells. In accordance with these findings, plasma corticosterone levels were decreased. Plasma ACTH levels were not significantly different in TH-null mice. In conclusion, both the adrenomedullary and adrenocortical systems demonstrate structural and functional changes in catecholamine-deficient TH-null mice, underscoring the great importance of the functional interdependence of these systems in vivo.

Adrenal Glands↗
PubMed1980

Familial Schmidt's syndrome.

Among the 17 offspring of a common father, overt adrenal and thyroid insufficiency developed in three brothers. In eight of the 12 siblings then examined, and also in one of the two mothers of this kindred, endocrine abnormalities were documented. Early compensated adrenal and thyroid hypofunction with organ-specific antibodies were found in asymptomatic relatives. Pernicious anemia, vitiligo, and alopecia were also seen. Age of clinical onset varied from 18 to 38 years. Familial investigations may identify asymptomatic persons at risk for the development of serious endocrine deficiencies.

Adolescent↗
PubMed1993

Effects of danazol on endometrial DNA synthesis in rats.

The suppressive effects of Danazol, an isoxazol derivative of the synthetic steroid 17 alpha-ethinyltestosterone, on endometrial DNA synthesis were investigated in rats by immunohistochemistry with bromodeoxyuridine (BrdU) and DNA-synthesizing enzyme assays. Rats treated with Danazol for 14 days at 17-19 weeks of age showed a decrease of plasma gonadotropins associated with ovarian hypofunction, persistent diestrus, and a smaller number of corpora lutea in ovary, resulting in no BrdU-immunoreactive (S-phase) cells in endometrial epithelium and lower activity of thymidine kinase in the uterus compared with control.

Adrenal Glands↗
PubMed2003

Endocrine diseases in dogs and cats: similarities and differences with endocrine diseases in humans.

Over several millennia, humans have created hundreds of dog and cat breeds by selective breeding, including fixation of mutant genes. The domestic dog is unique in the extent of its variation in height, weight and shape as well as its behavior. It is primarily the relatively long persistence of high levels of growth hormone (GH) release at a young age that accounts for the large body size in giant breeds of dogs. Several of the endocrine diseases of humans are also known to occur as similar entities in dogs and cats. With some variations, this is true for conditions such as diabetes mellitus and the hypofunction syndromes of the thyroid and adrenal cortex. Also, the hyperfunction syndromes of hypercortisolism and hyperparathyroidism in dogs and cats have many similarities with their human counterparts. The exception seems to be Graves' disease. This condition, which is due to production of thyroid-stimulating hormone (TSH)-receptor antibodies, has not been observed in dogs and cats. The very common form of hyperthyroidism in cats is due to toxic adenomas. In the 1980s it was discovered that in dogs exogenous progestins and endogenous progesterone can induce GH excess. This GH excess originates form the mammary gland and may give rise to acromegaly and insulin resistance. GH production by the mammary gland is not unique to the dog. It has become clear that cats and humans also express the GH gene in the mammary gland. There is increasing evidence that this locally produced GH not only plays a role in the morphologic changes of the mammary gland associated with the ovarian cycle and gestation, but that it is also involved in the development of breast cancer. In dogs, induction of mammary GH production by progestin administration allows for treatment of GH deficiency.

Animals↗
PubMed1984

Adrenal hypofunction and trisomy 18.

Three cases of trisomy 18 are described, each with evidence of diminished fetoplacental function, specifically reduced 24-hour maternal urinary estrogen. All three infants died within three months and showed gross and microscopic evidence of hypoplasia of the fetal adrenal cortical zone. This abnormality is consistent with and helps explain the increased incidence of obstetric intervention and prolonged pregnancy in this syndrome.

Abnormalities, Multiple↗
PubMed1989

Assessment of thyroid and adrenal function in patients with familial amyloidotic polyneuropathy.

This study was performed to evaluate thyroid and adrenal function in patients with familial amyloidotic polyneuropathy. Twenty-four patients without any clinical overt endocrinological dysfunction were studied. None of the patients showed laboratory evidences of hypo- or hyperthyroidism. A short ACTH-stimulation test was performed in 17 of the patients. A low cortisol response to ACTH stimulation, suggesting adrenocortical insufficiency, was found in four (24%) of the patients, and an intermediate response interpreted as suspected hypofunction was found in three (18%) patients. Low serum dehydroepiandrosterone sulphate levels, suggesting adrenal hypofunction, were found in six (25%) of the patients. We believe that the possibility of glucocorticoid insufficiency should always be considered in patients with familial amyloidotic polyneuropathy.

Adrenal Cortex↗
PubMedDate not supplied

Free urinary cortisol radioimmunoassay (application in the diagnosis of adrenal diseases).

The availability of a specific antiserum has made it possible to develop in our laboratory a radioimmunoassay for free urinary cortisol which is quite simple and rapid to perform. No preliminary procedures of chromatographic purification are necessary, and no correction for losses is required. Precision and accuracy tests are satisfactory. Seventeen normal subjects, 10 obese subjects, 18 patients with Cushing's syndrome, 4 hypopituitaric patients and 4 with Addison's disease were studied. The values of free urinary cortisol were compared with those of urinary 17-OHCS, plasma cortisol and, in some cases, the cortisol secretion rate. In normal subjects, the mean free urinary cortisol was 77.22 +/- 7.74 microgram/24 h, in obese subjects it was 112.05 +/- 13.64 microgram/24 h, and in patients with Cushing's syndrome it was at significantly higher levels with a mean value of 488.06 +/- 64.39 microgram/24 h. There was no overlap between the values obtained in the first two groups and those of subjects with adrenal hyperfunction, and the results were similar to those shown by the cortisol secretion rate. The same was not true for urinary 17-OHCS and plasma cortisol. Thus, the assay of free urinary cortisol, that is the free biologically active circulating fraction, may provide a relatively simple alternative to measurement of the cortisol secretion rate, as a single differential test for the diagnosis of conditions with adrenal hyperfunction. Less satisfactory were the results obtained in patients with primary and secondary adrenal hypofunction. Another limitation of the method is its relative non-specificity, since the results of 16 urinary samples measured without preliminary chromatography were 29.6% higher than those after previous chromatographic purification. However, in our experience, this overestimation does not affect the value of the method as a screening test for the diagnosis of Cushing's syndrome.

Addison Disease↗
PubMedDate not supplied

[Addison's disease: principal clinical associations and description of natural history of the disease].

From 1967 to 1988 we studied 75 cases of Addison's disease (AD). An autoimmune etiology was found in 68%, while previous tubercular infection was demonstrated in 21% of the cases; minor causes were involved in 3%, and in 8% of the cases the disease remained of unknown origin. Autoimmune adrenalitis has become the most frequent cause of AD as a consequence of decreased tubercular infection. Autoimmune AD prevailed in children or in young people, and tubercular AD in adults. The finding of calcifications in adrenals and/or other organs was the specific diagnostic sign for the identification of tubercular forms. On the other hand, the finding of circulating adrenal autoantibodies (AA) and/or other organ specific autoantibodies was the fundamental diagnostic marker of autoimmune forms. In 72% of the cases autoimmune AD is associated with other organ-specific autoimmune diseases. Subjects with AA but without clinical signs of hypoadrenalism were considered to have "potential AD", because they showed a high risk of developing clinical hypoadrenalism. This condition develops over a long period characterized by different stages of subclinical adrenal hypofunction. Steroid cell autoantibodies (StCA) are frequently detectable in patients with autoimmune AD, in whom they are markers of autoimmune premature ovarian failure. The study of StCA-positive cases without hypogonadism will be important to clarify whether or not these autoantibodies could be markers of potential autoimmune hypogonadism.

Addison Disease↗
PubMed2001

Glucocorticoid hypersecretion following intracerebroventricular injection of ethylcholine mustard aziridinium ion in rats.

To investigate whether cholinergic hypofunctions in the brain influence hypothalamic-pituitary-adrenal activity, we examined the effects of cholinergic neurotoxin ethylcholine mustard aziridinium ion on basal and stress-induced levels of corticosterone in rats. Blood sampling from rats following intracerebroventricular injection of saline (5 microl, as a control) or this neurotoxin (5 nmol/5 microl) was performed over a day in one series, and was taken before, during and after an immobilization stress exposure in another series. Plasma levels of corticosterone and adrenocorticotropin were determined by the radioimmunoassay. The basal levels of plasma corticosterone and adrenocorticotropin over a day were significantly higher in the neurotoxin-treated rats, compared with the control rats (corticosterone, P<0.001; adrenocorticotropin, P<0.05). Further, relative adrenal gland weight of the neurotoxin-treated rats was significantly greater than that of the control rats (P<0.05). However, responses in plasma corticosterone level caused by the immobilization stress in the neurotoxin-treated rats were not different from those in the control rats. The present study demonstrated that damage to the cholinergic neurons in the brain increased hypothalamic-pituitary-adrenal activity over a day, probably due to freedom from inhibitory influences of the hippocampal cholinergic system, but that this damage did not influence stress-induced changes in plasma glucocorticoid level.

Adrenal Glands↗
PubMed1985

Corticotropin releasing factor (CRF): diagnostic implications.

Nine normal volunteers received an intravenous bolus injection of 50, 100, and 200 micrograms ovine Corticotropin releasing factor. There was no dose response relationship between the injected oCRF dosage and stimulated ACTH, beta-endorphin, and cortisol secretion. When human synthetic CRF was injected (50 and 100 micrograms i.v.) no significant difference compared to the oCRF induced ACTH stimulation was observed. In contrast to the lacking relationship between the CRF dosage and the biological response there was a clearcut dose response relationship between the amount of oCRF injected and the CRF immunoreactivity measured 15 minutes after injection with a specific oCRF radioimmunoassay. No serious side effects were observed when the 100 micrograms CRF dosage was used as standard dose in the CRF test in patients with diseases of the hypothalamo-pituitary-adrenal axis. In patients with Cushing's syndrome the CRF test is helpful for the differential diagnosis (ACTH dependent Cushing's disease, autonomous cortisol secretion due to an adrenal adenoma or carcinoma, ectopic ACTH syndrome). In addition the CRF test is of prognostic value after surgical or neurosurgical therapy of Cushing's syndrome. Furthermore secondary adrenal failure after operative therapy can be documented by the CRF test. In patients on corticoid therapy the degree of suppression of CRF induced ACTH secretion correlated to the dosage and the duration of corticoid therapy. The main suppressive effect of corticoids on the hypothalamo-pituitary-adrenal axis seems to take place at the pituitary level. In patients with secondary adrenal failure the analysis of ACTH secretion after CRF administration allows the differential diagnosis between hypothalamic and pituitary ACTH hyposecretion. In conclusion the administration of oCRF has been shown to be a well tolerated and useful tool in the differential diagnosis of the causes of hyper- and hypofunction of the hypothalamo-pituitary-adrenal axis. Though there was only 10% cross reactivity with synthetic human CRF, CRF immunoreactivity could be detected in 53 out of 55 pregnant females. The results of measuring endogenous CRF levels in patients with diseases of the hypothalamo-pituitary-adrenal axis are preliminary but endogenous CRF levels measured by the heterologous oCRF radioimmunoassay, correlated well to the clinical situation and the ACTH-levels. These results have to be verified with a homologous hCRF radioimmunoassay.

Adrenal Gland Diseases↗
PubMed1990

Effects of repetitive administration of corticotropin-releasing hormone combined with lysine vasopressin on plasma adrenocorticotropin and cortisol levels in secondary adrenocortical insufficiency.

To examine the functioning of the hypothalamo-pituitary-adrenocortical axis in secondary adrenocortical insufficiency, we administered 100 micrograms synthetic human CRH, iv, plus 10 U lysine-8-vasopressin (LVP), im, three times daily for 3 consecutive days. The changes in plasma ACTH and cortisol levels during the administration and the response to an insulin tolerance test (ITT) conducted before and after the administration were determined. In three patients with isolated ACTH deficiency, basal plasma ACTH and cortisol levels were undetectablly low, and there was no response noted in the ITT or during CRH-LVP administration throughout the observation period. In four patients with adrenocortical insufficiency who had undergone successful transsphenoidal microadenomectomy for Cushing's disease and in six patients who had undergone curative unilateral adrenalectomy for Cushing's syndrome, basal plasma ACTH levels were low, but responded considerably to both stimulation tests. Along with the 3 days of CRH-LVP stimulation, however, neither the peak nor the time-integrated ACTH response was significantly enhanced, because of the variability of the responses among the patients. Compared with the ACTH response on the last day of CRH-LVP stimulation, the subsequent ITT tended to induce a lower ACTH response in the post-Cushing's disease patients and a higher response in the post-Cushing's syndrome patients. Regarding the plasma cortisol levels, the basal, peak, and integrated responses tended to increase daily during CRH-LVP administration. Conversely, the ITT after repetitive CRH-LVP administration induced a higher cortisol response than the test before CRH-LVP administration in the post-Cushing's disease patients. No serious complications were noted in any of the patients during or after the treatment. The present findings indicate that 1) repetitive administration of CRH in combination with LVP is a safe and valuable provocation test to examine the pituitary ACTH reserve and the integrity of the pituitary-adrenocortical axis; 2) isolated ACTH deficiency is usually due to a defect at the pituitary level; 3) with respect to adrenocortical responsiveness, post-Cushing's disease patients show a better accumulation of the provocative effect than do post-Cushing's syndrome patients; and 4) both hypothalamic and pituitary dysfunction are responsible for adrenal hypofunction in patients after hypercortisolemia, but post-Cushing's syndrome patients (especially those with a short period of hypercortisolemia) appeared to have less impairment of hypothalamic ACTH-releasing activity than post-Cushing's disease patients.

Adrenal Cortex↗
PubMed2005

[Diagnosis of autoimmune thyroid disease].

Autoimmune thyroid disease (AITD) is the most common organ specific autoimmune disorder usually resulting in dysfunction (hyperfunction, hypofunction or both) of the thyroid gland. The syndromes comprising autoimmune thyroid disease are many intimately related illnesses: Graves' disease with goitre, hyperthyroidism and, in many patients, associated ophthalmopathy, Hashimoto's thyroiditis with goitre and euthyroidism or hypothyroidism but also thyroid dysfunction occurring independently of pregnancy and in 5-6% of postpartum women and thyroiditides induced by different drugs and other environmental influences. The immunological mechanisms involved in these diseases are closely related, while the phenotypes probably differ because of the specific type of immunological response that occurs. The syndromes are connected together by their similar thyroid pathology, similar immune mechanisms, co-occurrence in family groups, and transition from one clinical picture to another within the same individual over time. In some patients, other organ specific and nonorgan specific autoimmune syndromes are associated with autoimmune thyroid disease, including pernicious anemia, vitiligo, myasthenia gravis, primary adrenal autoimmune disease, celiac disease, rheumatoid arthritis or lupus. Thyroid peroxydase, TPO, the primary enzyme involved in thyroid hormonogenesis, was initially identified in 1959 as the 'thyroid microsomal antigenn. It is uncertain whether TPO autoantibodies or TPO-specific T cells are the primary cause of thyroid inflammation, which can lead, in some individuals, to thyroid failure and hypothyroidism. TPOAbs are the hallmark of AITB and are present in almost all patients with Hashimoto's thyroiditis, in two-thirds of patients with postpartum thyroiditis and also in 75% of patients with Graves' hyperthyroidism. The antibodies are mainly produced by lymphocytic infiltrate in the thyroid gland and only to a small extent by regional lymph nodes or the bone marrow. Unlike antibodies against thyroglobulin (Tg), TPO antibodies are capable of inducing antibody-dependent cell-mediated cytotoxicity. Antibodies to TSH-R mimic the function of TSH, and cause disease by binding to the TSH-R and stimulating (or inhibiting) thyroid cells. The TSHR, a member of the G protein-coupled receptor family with seven membrane-spanning segments. Patients with autoimmune thyroid disease may have both stimulating and blocking antibodies in their sera, the clinical picture being the result of the relative potency of each species; blocking antibodies seem more common in Graves' patients with ophthalmopathy compared to those without this complication. The major T cell epitopes are heterogeneous and T cell reactivity against certain TSH-R epitopes has been present in high proportion in normal subjects. More diversified response to TSH-R, with heterogeneity of epitope recognition by TSAb, is predictive of likely remission after antithyroid drug treatment for Graves' disease.

Autoimmune Diseases↗
PubMed1983

Surgery of the endocrine glands in pregnancy.

The surgical endocrinology of the pregnant patient is special with respect to the additional hazards of maternal and fetal loss under the stress of pregnancy, labor, and delivery. The added threat of drug, radiation, radioisotope, anesthetic, and surgical management requires extra precaution in diagnostic and therapeutic manipulation, and limitations are imposed by appropriate reluctance to employ radioisotopes or external radiation in localizing or treating focal endocrine tumors. The state of pregnancy itself causes some endocrine hyperfunction that is normal, and the normal types must be distinguished from those that are pathologic, with consideration of the hormone values that would be pathologic in the nonpregnant state. The physician must be concerned with hyperfunctioning and hypofunctioning endocrine systems in their effect on the mother and their frequently reciprocal effects on the fetus in the maternal/fetal unit. The most directly life-threatening concerns of endocrine surgery in the pregnant patient are those of thyrotoxicosis, hyperparathyroidism, insulinoma, and, most particularly, pheochromocytoma. The severe consequences of unsuspected pheochromocytoma in the pregnant patient are evident in maternal and fetal mortality that approximates nearly 50%. The only reduction in the lethal consequences in the combination of pheochromocytoma and pregnancy can be made through continual suspicion and early diagnostic efforts with patients who manifest cardiovascular, neurologic, blood sugar, or blood pressure abnormalities in pregnancy. Some of the endocrine syndromes may not only affect and be affected by pregnancy but may be passed on through it to kindred in familial syndromes. The multiple endocrine adenopathies that are known are genetically expressed as autosomal dominant traits. Careful screening methods for case-finding among affected families is important follow-up to genetic counseling.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

The role of thyroid in clinical disorders of hypothalamo-pituitary adrenocortical axis--a prelminary communication.

The study of thyroid function in clinical conditions associated with the disorders of the hypothalamio-pituitary-adrenocortical axis indicated overt hypofunction of thyroid in all the three cases of Cushing's disease and subclinical hypo-or low normal function of thyroid in most of the cases of adrenogenital syndrome. It was suggested that hypo or low normal function of thyroid might facilitate excess elaboration of ACTH through CRF by swaying the balance of neurotransmitters at hypothalamus in favour of serotonin.

Adult↗