Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The first case of isolated thyrotropin (TSH) deficiency with Cushing's syndrome was reported. A 46-year-old female was admitted to our hospital because of fatigability, puffy eye-lids, leg edema and petechia. She was treated with thyroid hormone. A low free triiodothyronine continued. Serum TSH was undetectable and serum thyrotropin releasing hormone (TRH) was elevated. No response of serum TSH and normal response of serum prolactin after administration of exogenous TRH suggested the abnormalities of anterior pituitary gland. The secretion of growth hormone and gonadotropin were intact, but the secretion of adrenocorticotropic hormone (ACTH) was impaired. A high level of serum cortisol, no response of serum ACTH by metyrapone test and a tumor mass of abdomen detected by computed tomography led to the diagnosis of Cushing's syndrome. Histological examination of the tumor revealed adrenal adenoma. Twenty two months after the surgery, serum ACTH level was normalized, but the secretion of serum TSH to exogenous TRH was still absent. The results indicated that hypothyroidism in our patient was due to isolated TSH deficiency.
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PMID:A case of isolated thyrotropin deficiency with Cushing's syndrome. 263 42

We describe a patient with type I diabetes mellitus and hypothyroidism who developed frank adrenocortical insufficiency while receiving a high-dose ketoconazole therapy for keratitis caused by Acanthamoeba species. While impaired cortisol responses to corticotropin and mildly symptomatic hypoadrenalism have been described previously with ketoconazole therapy, to our knowledge, this case represents the first documented article of an actual adrenal crisis associated with this drug. Two reasons are postulated for the development of this complication in our patient: high-dose ketoconazole therapy given in divided doses during the day, and a possibly impaired central response to stress because of hypothyroidism. Our article points to the need to monitor patients treated with high-dose ketoconazole for adrenal insufficiency, particularly if associated illnesses are present that may impair an adequate stress response.
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PMID:Adrenal crisis in the setting of high-dose ketoconazole therapy. 270 31

The activity of plasma renin, concentration of serum aldosterone and plasma corticotropin were determined by a radioimmunoassay in 78 patients with diffuse toxic goiter with thyrotoxicosis of various degrees of gravity, im 21 patients with primary hypothyroidism and 25 controls in euthyroid condition. In the patients with thyrotoxicosis such investigations were conducted before and after a course of drug therapy. In thyrotoxicosis the activity of the renin-angiotensin-aldosterone system was raised, in hypothyroidism it was lowered, a degree of expression of appropriate changes being associated with the gravity of disease. In the patients with marked thyrotoxicosis after a course of drug therapy the indices of plasma renin activity and serum aldosterone concentration did not return to normal. Hypophyseal corticotropic function was raised in marked thyrotoxicosis, mild hypothyroidism and corresponded to the normal level in the patients with hypothyroidism of average gravity. Plasma ACTH concentration in the patients with marked thyrotoxicosis returned to normal after a course of drug therapy.
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PMID:[State of the renin-angiotensin-aldosterone system in thyroid pathology based on the results of radioimmunoassay]. 283 33

In conscious, chronically cannulated, unrestrained rats, systemic administration of catecholamines increases the plasma levels of beta-endorphin-like immunoreactivity (beta Ei). In euthyroid rats, this effect is mediated by both alpha 1 and beta-adrenergic receptors; the rise in plasma beta Ei caused by isoproterenol is blocked by 1 mg/kg propranolol, and the similar effects of norepinephrine and phenylephrine are blocked by 0.1 mg/kg prazosin. Both types of responses are completely suppressed by a 4-h pretreatment of rats with 0.1 mg/kg dexamethasone, indicating the anterior pituitary origin of the beta Ei released. Prior sectioning of the pituitary stalk does not significantly reduce the response to either phenylephrine or isoproterenol, suggesting that both agents act directly on the pituitary. Hypothyroidism induced by surgical thyroidectomy does not influence the beta Ei response to isoproterenol, which remains sensitive to block by propranolol or suppression by dexamethasone. However, neither norepinephrine nor phenylephrine is able to increase plasma beta Ei in the hypothyroid animals. Both isoproterenol and phenylephrine remain fully effective in rats made hyperthyroid by daily injections of 40 micrograms/kg T3 for 4 days. We propose that in unstressed rats catecholamines increase plasma beta Ei by a direct action on the anterior pituitary via either alpha 1- or beta-adrenergic receptors, and that expression of the alpha 1-, but not the beta-adrenergic response is regulated by thyroid hormones.
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PMID:Adrenergic regulation of beta-endorphin secretion from anterior pituitary in conscious rats: effects of thyroid state. 294 18

A comparison of the effect of PTU-induced hypothyroidism on the contents of immunoactive met-enkephalin and beta-endorphin in the pituitaries from rats aged 2 1/2, 12, and 18 months was made. In all ages, there was significant reduction of IR-met-enkephalin content in the anterior lobe and IR-beta-endorphin content in the neuro-intermediate lobe after PTU treatment. There was a significant age-related decrease in IR-beta-endorphin content in the anterior lobe. Rats of all three ages responded to PTU treatment with an increase in serum TSH level and a drastic reduction in serum T3 and T4 levels. The results indicate that there was no age-related difference in the change of pituitary opioid peptide contents in response to hypothyroidism.
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PMID:Hypothyroidism and pituitary contents of immunoactive met-enkephalin and beta-endorphin in male rats of different ages. 296 63

The changes in met-enkephalin and beta-endorphin contents in the pituitary in PTU-induced hypothyroidism were studied in the rat. After 2 weeks of PTU-treatment, both IR-met-enkephalin and IR-beta-endorphin contents in the pituitary were significantly reduced. Gel filtration chromatography followed by radioimmunoassay showed that the immunoactivities in the peaks of precursors, met-enkephalin, beta-lipotropin and beta-endorphin were all lower in the pituitaries from the PTU-treated rats. In another experiment, some of the PTU-treated rats were injected daily with 500 micrograms T3/kg b.w. In the hypothyroid rats, IR-met-enkephalin and IR-beta-endorphin contents were decreased in both the anterior and neurointermediate lobes. Only the changes in the anterior lobe were reversed by T3 treatment. In conclusion, while the effects on the anterior lobe are probably due to a deficiency in thyroid hormones, the mechanism for the decrease of opioid peptide contents in the neurointermediate lobe is still unclear.
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PMID:T3 reverses the changes in met-enkephalin and beta-endorphin contents in the anterior lobe, but not the neuro-intermediate lobe of the pituitary of rats rendered hypothyroid by PTU-treatment. 297 Oct 9

A patient with isolated corticotropin deficiency demonstrated hyperresponsiveness of both thyrotropin and prolactin after protirelin stimulation. Following glucocorticoid replacement therapy, responses decreased to normal. Since true primary hypothyroidism may occur in association with cortisol-deficient states, it is necessary to reserve final evaluation until after glucocorticoid replacement. The finding of combined thyrotropin and prolactin hyperresponsiveness to protirelin suggests a related glucocorticoid feedback function.
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PMID:Abnormal thyrotropin and prolactin levels in untreated corticotropin deficiency. 298 27

The responsiveness of lipolysis to the stimulatory agonists noradrenaline, corticotropin and glucagon and to the inhibitory agonists N6-phenylisopropyladenosine, prostaglandin E1 and nicotinic acid was investigated with rat white adipocytes incubated with a high concentration of adenosine deaminase (1 unit/ml). The cells were obtained from fed or 48 h-starved euthyroid animals or from fed or starved animals rendered hypothyroid by 4 weeks of treatment with low-iodine diet and propylthiouracil. Hypothyroidism increased sensitivity to and efficacy of all three inhibitory agonists in their opposition of noradrenaline-stimulated lipolysis. Starvation decreased sensitivity to all three inhibitory agonists when opposing basal lipolysis. Hypothyroidism decreased sensitivity to noradrenaline, glucagon and corticotropin by 37-, 4- and 4-fold respectively and decreased the maximum response to these agonists by approx. 50%, 50% and 75% respectively. Starvation reversed decreases in maximum response to these agonists in hypothyroidism. Starvation in the euthyroid state increased sensitivity to glucagon and noradrenaline, but did not alter sensitivity to corticotropin. Cells from hypothyroid rats were relatively insensitive to Bordetella pertussis toxin, which substantially increased basal lipolysis in the euthyroid state.
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PMID:Sensitivity of adipocyte lipolysis to stimulatory and inhibitory agonists in hypothyroidism and starvation. 302 50

The endocrine status of patients receiving proton radiation for tumors of the upper clivus was reviewed to evaluate the effect of high dose treatment on the pituitary gland. The fourteen patients had chordomas or low grade chondrosarcomas and were all treated by the same techniques. The median tumor dose was 69.7 Cobalt Gray Equivalent (CGE) with a range from 66.6 to 74.4 CGE. (CGE is used because modulated protons have an RBE of 1.1 compared to 60Co). The daily fraction size was 1.8-2.1 CGE. The median follow-up time is 48 months, ranging from 30 to 68 months. All treatments were planned using a computerized multi-dimensional system with the position of the pituitary outlined on the planning CT scan. Review of the dose distribution indicated that the dose to the pituitary ranged from 60.5 to 72.3 CGE, with a median of 67.6 CGE. One female patient had decreased thyroid and gonadotropin function at the time of diagnosis and has been on hormone replacement since that time. The other three females were all pre-menopausal at the time of radiotherapy. At this time four patients (3 males and 1 female) have developed endocrine abnormalities 14 to 45 months after irradiation. All four had evidence of hypothyroidism and two have also developed corticotropin deficiency. The three males had decreased testosterone levels; the female patient developed amenorrhea and hyperprolactinemia. All four are asymptomatic with ongoing hormone replacement.
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PMID:Endocrine function following high dose proton therapy for tumors of the upper clivus. 313 12

The contents of immunoreactive somatostatin (IR-SRIF) and beta-endorphin (IR-beta-EP) in 12 brain regions were examined in rats exposed neonatally to propylthiouracil (PTU) through the mother's milk. Since the dose of PTU used in this study is lower than the usual dose employed to induce hypothyroidism, a milder form of neonatal hypothyroidism resulted. This conclusion is supported by the only mild subnormal growth of rats to adulthood and serum T4 and T3 concentrations in the normal range. Adult rats treated with PTU neonatally had significantly higher IR-SRIF contents in several brain regions compared to controls, whereas IR-beta-EP levels were not significantly different (significant increase only in the thalamus) in most regions. The results indicate that even mild hypothyroidism during early postnatal development causes permanent impairment of brain function, which manifests itself in part by an altered brain content of IR-SRIF.
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PMID:Immunoreactive somatostatin and beta-endorphin content in the brain of mature rats after neonatal exposure to propylthiouracil. 612 58


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