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)

A male infant with secondary hypothyroidism is described. Within the first month after birth, the patient manifested feeding difficulties, lethargy, persistent jaundice, umbilical hernia, and large anterior and open posterior fontanels. The roentgenogram of the knee joints at 27 days showed absence of the distal femoral epiphyses. His serum thyroid-stimulating hormone (TSH) level was low despite decreased levels of triiodothyronine (T3) and tetraiodothyronine (T4) in serum. Assessment of the hypothalamic-pituitary hormone (TRH) nor growth hormone (GH) responses to L-arginine and insulin, while responses of both luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to luteinizing hormone-releasing hormone (LH-RH) and adrenocorticotropic hormone (ACTH) to insulin were within normal limits. The malady of the patient in this case was not detected by newborn screening for congenital hypothyroidism due to the fact that in the Aomori district of Japan thyroid screening involves only the measurement of TSH. Such measurement cannot detect cases of secondary or tertiary hypothyroidism such as our patient. Replacement therapy was initiated at 58 days and his physical and mental development has been regarded as normal since treatment.
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PMID:Congenital secondary hypothyroidism with low serum GH and prolactin levels in a 27-day-old male infant. 628 48

Cold intolerance and secondary amenorrhea developed in a patient who had meningoencephalitis 4 yr prior to study. A clinical diagnosis of hypothalamic hypothyroidism was made on the basis of low serum thyroxine and triiodothyronine levels, and low plasma thyrotropin concentrations, which were responsive to thyrotropin-releasing hormone (TRH). The secretion of the remaining pituitary hormones (growth hormone, prolactin, adrenocorticotropin and gonadotropins) was intact. Not only was thyroid function normalized by oral administration of TRH, but also menses resumed after adequate replacement therapy with thyroid hormone. These results imply that hypothyroidism in this patient was due to isolated dysfunction of hypothalamic TRH release.
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PMID:Hypothalamic hypothyroidism due to isolated thyrotropin-releasing hormone (TRH) deficiency. 643 93

These studies investigated the effect of aging on thyroid hormone regulation of beta-endorphin in rat corpus striatum and hypothalamus. In both brain areas, basal levels of beta-endorphin declined with age. In addition, age modified the response of beta-endorphin to thyroid hormone status. Hypothyroid rats aged 6 months (mature) exhibited a 67% mean decline in the level of beta-endorphin in the corpus striatum. Hypothyroid rats aged 20-24 months (senescent) exhibited no change in the level of beta-endorphin in the corpus striatum. Hypothyroid rats aged 6 months had a 28% mean decline in the level of hypothalamic beta-endorphin. There was no change in hypothalamic beta-endorphin content in hypothyroid senescent rats. Hyperthyroidism resulted in elevations of beta-endorphin in both the corpus striatum and hypothalamus in senescent, but not mature rats. Changes in beta-endorphin seen with age are at least in part thyroid hormone dependent. In addition, age is capable of modifying the response of brain tissue to thyroid hormone.
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PMID:Interaction of age and thyroid hormone status on beta-endorphin content in rat corpus striatum and hypothalamus. 720

Two opioid neuropeptides, methionine enkephalin (ME) and beta-endorphin (BE), and one tachykinin neuropeptide, substance P (SP), were quantified in 10 prolactin (PRL)-secreting human pituitary adenomas and in 10 control human pituitaries. Immunohistochemical techniques provided appropriate staining for PRL. Reversed-phase high performance liquid chromatography (RP-HPLC) was used to purify these three neuropeptides before their analysis, radioimmunoassay (RIA) was used for the quantification of SP-like immunoreactivity (SP-LI), and liquid secondary-ion mass spectrometry (LSIMS) was used for the qualitative and quantitative analysis of ME and a tryptic peptide of BE. This study shows that, for 90% of the cases studied here (excluding one hypothyroidism case), the tachykinin A neuropeptide SP-LI level is decreased, the POMC peptide BE level is not altered, and the proenkephalin A neuropeptide ME level is increased in these PRL-secreting tumors.
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PMID:Opioid and tachykinin neuropeptides in prolactin-secreting human pituitary adenomas. 853 94

Several hormonal alterations have been described in patients with chronic renal failure. However, there are few epidemiological studies on uremia-associated endocrine derangements, in particular in patients undergoing peritoneal dialysis (PD). A cross-sectional descriptive study was performed to assess the prevalence of hormonal dysfunctions affecting pituitary secretions in the whole population of patients in the PD unit of our hospital. The total population included 69 patients, 66 on continuous ambulatory PD and 3 on continuous cycling PD. There were 31 men and 38 women, the mean age was 55 years (range 23-82 years), and the mean duration of PD was 32 months (range 1-161 months). There were 27 (39.1%) patients with diabetes mellitus (7 type I and 20 type II). Clinical records were reviewed for hormonal alterations affecting the pituitary and its target glands. The whole population had available data on the pituitary-thyroid axis. The following diagnoses and prevalences were found: hypothyrotropic hypothyroidism 4 (5.8%), subclinical hypothyroidism 4 (5.8%), primary hypothyroidism 8 (11.6%), and low T3 syndrome 11 (15.9%). The remaining pituitary hormones were available in 20 patients. Hyperprolactinemia was found in 7 (35%) patients and abnormally increased growth hormone levels in 6 (30%). Gonadotropin levels were normal for the age of the women and showed a tendency to be increased in most of the men. Corticotropin levels were normal in all patients with available data. There was no relationship between the high prevalence of diabetes mellitus in our population and the remaining hormonal derangements found. These results suggest that there is a non-negligible prevalence of pituitary abnormalities in uremic patients undergoing PD.
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PMID:Pituitary dysfunctions in uremic patients undergoing peritoneal dialysis: a cross sectional descriptive study. 853 9

We report a 62-year-old male patient who had variant angina and isolated adrenocorticotropic hormone (ACTH) deficiency. His serum sodium concentration was low and vasopressin was inappropriately high for the low plasma osmolality. Serum free thyroxine (FT4) was low and thyroid stimulating hormone (TSH) was high with positive anti-thyroperoxidase antibodies, compatible with Hashimoto's thyroiditis. Treatment with Amrodipine and hydrocortisone relieved chest symptoms and hyponatremia, and hypothyroidism was also normalized. It is suggested that coronary artery spasm may be related to cortisol deficiency and/or inappropriately high vasopressin secretion and that hypothyroidism was ameliorated because the reduced responsiveness to TSH returned to normal due to hydrocortisone supplement.
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PMID:Variant angina in isolated adrenocorticotropin deficiency, inappropriate vasopressin secretion and Hashimoto's thyroiditis. 963 Feb 2

We describe a 51-year-old woman with long-standing young-onset primary hypothyroidism. Serum cortisol, adrenocorticotropin, and arginine vasopressin levels were normal, but urinary excretion of 17-hydroxycorticosteroid was decreased. Administration of a very small initial dose of thyroid hormone induced severe acute complications including fever, palpitation, and sweating associated with a rapid decrease in serum thyrotropin level, a dramatic increase in serum alkaline-phosphatase level, and a decrease in serum total cholesterol level. A week later, the late complications of nausea, severe hyponatremia, and eosinophilia occurred. Serum cortisol level decreased slightly but remained within normal limits during this hyponatremic period. This rare case suggests that increased sensitivity to thyroid hormone can occur in long-standing primary hypothyroidism with biphasic clinical course of acute thyrotoxic complications followed by severe hyponatremia resembling hypoadrenocorticism.
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PMID:Increased sensitivity to thyroid hormone replacement therapy followed by hyponatremia and eosinophilia in a patient with long-standing young-onset primary hypothyroidism. 1043 59

A set of data suggests that the thyroid gland plays a role in the bi-directional interaction between the electrophysiological and the endocrine components of sleep, e.g. the nonREM-REM-cycle and the patterns of nocturnal hormone secretion, respectively. In detail thyroid-stimulating hormone (TSH) and thyroxin (T4) show circadian rhythms. A specific relationship was observed between TSH and REM sleep. Blunted TSH levels were found in healthy elderly subjects and, probably due to overactivity of corticotropin-releasing hormone in patients with depression in comparison to young normal controls. Pulsatile administration of thyrotropin-releasing hormone induced a decrease of sleep efficiency and an earlier occurrence of the cortisol rise in normal controls. Slow wave sleep was reduced in patients with hypothyroidism in comparison to normal controls. The sleep EEG normalised after therapy.
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PMID:[Thyroid gland and sleep]. 1052 32

The industrialized countries around the world are experiencing an epidemic of childhood obesity. The level of fatness of a child at which morbidity increases acutely and/or later in life is determined on an individual basis. Overall, however, childhood obesity substantially increases the risk of subsequent morbidity whether or not obesity persists into adulthood. The genetic basis of childhood obesity has been elucidated to some extent through the discovery of leptin, the ob gene product, and the increasing knowledge of the role of neuropeptides such as pro-opiomelanocortin, neuropeptide Y and the melanocyte-concentrating hormone receptors. Environmental and exogenous factors are the main contributors to the development of a high degree of body fatness early in life. Studies involving twins suggest that approximately 50% of the tendency toward obesity is inherited. There are numerous disorders, including a number of endocrine disorders, such as Cushing's syndrome and hypothyroidism, and genetic syndromes, such as Prader-Labhard-Willi syndrome and Bardet-Biedl syndrome, that can present with obesity. A simple diagnostic algorithm allows for differentiation between primary and secondary obesity. Among the most common sequelae of primary childhood obesity are hypertension, dyslipidemia, back pain and psychosocial problems. It is somewhat ironic that the definition of obesity in childhood is not an easy one. Direct measurements of body fat content, such as hydrodensitometry, bioimpedance, or dual-energy X-ray absorptiometry, are useful tools in scientific studies. Body mass index (BMI) is, however, now generally accepted to be a good clinical measure for the definition of obesity in children and adolescents. In preadolescent boys, BMI also relates to muscle mass and should be used for the definition of fat mass with great caution. An increased risk of death from cardiovascular disease in adults has been found in patients whose BMI had been greater than the 75th percentile as adolescents. Therapeutic strategies include psychological and family therapy, modification of lifestyle and behavior, and nutritional education. The role of regular exercise and exercise programs is emphasized, while surgical procedures and drugs used in adult obesity are still not generally recommended for obese children. Obesity is the most common chronic disorder in industrialized countries, and its impact on individual lives as well as on health economics must be recognized by physicians and the public alike. This review aims to increase awareness of the health burden and economic dimension of the epidemic of childhood obesity that is occurring around the globe.
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PMID:Obesity in childhood and adolescence: clinical diagnosis and management. 1183 96

ACTH deficiency gradually develops in patients with growth hormone deficiency (GHD) who have abnormalities of the pituitary stalk on magnetic resonance imaging (MRI) following perinatal complications. We report here a rare case of GHD manifesting ACTH deficiency in middle age. A 48-year-old male patient was admitted to our hospital due to fever and hyponatremia. He was diagnosed as GHD and hypothyroidism at the age of 9, and had received lysine treatment until age 20, which was then replaced by thyroid hormone. He was not mentally retarded, but was the shortest in his class throughout his schooldays, reaching a final height of 148 cm. Hormonal examination revealed the presence of hypoadrenalism as indicated by poor responses of plasma cortisol to intravenous administration of corticotropin-releasing hormone (CRH) and insulin-induced hypoglycemia. Plasma ACTH responded well to CRH, but not to insulin-induced hypoglycemia, indicating that his hypoadrenalism was of hypothalamic origin. MRI showed an invisible pituitary stalk and relatively small pituitary gland. Since he had a perinatal abnormality, the damage around the pituitary and GHD could have originated from birth. In the literature, around 60% of GHD patients with pituitary stalk abnormalities develop hypoadrenalism due to ACTH deficiency, and more than 90% of such cases are diagnosed by age 30. We suggest that the appearance of hypoadrenalism should be carefully monitored in GHD patients with pituitary stalk abnormalities even after they reach middle age.
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PMID:Late onset of adrenocortical failure in GH deficiency with invisible pituitary stalk: a case report of a 48-year-old Japanese man and review of the literature. 1208 Dec 44


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