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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Review of medical records in 600 consecutive cases of primary hyperparathyroidism revealed 10 patients with a documented history of iodine 131 (131I) treatment. In seven cases 131I had been given because of Graves' disease and in three cases for ablation of thyroid remnants after tumor operations. All but one of the patients were women. Their age at the time of 131I treatment ranged from 21 to 72 years, and the interval to detection of hypercalcemia was between 3 and 27 years. It is noteworthy that all patients treated for Graves' disease had absorbed radiation doses large enough to cause permanent hypothyroidism, and half of them showed complete absence of the thyroid gland at subsequent operation for hyperparathyroidism. Furthermore, parathyroid adenomas had developed at the sites of thyroid remnants in cases with 131I ablation after tumor operations. Our findings support other observations indicating that not only external radiation but also radiation from 131I is a risk factor for development of hyperparathyroidism, and it is emphasized that age at the time of radiation treatment may be of decisive importance in this context.
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PMID:Hyperparathyroidism after treatment with radioactive iodine: not only a coincidence? 258 8

This study deals with the relationship between the occurrence of hypercalcemia and the administration of prophylactic doses of vitamin D in children with hypothyroidism, before and during L-thyroxine (LT4) treatment. The goal of the study was to determine the dosage of vitamin D necessary to prevent rickets without inducing hypercalcemia. There was a 23% prevalence of hypercalcemia at the time of the diagnosis of hypothyroidism by screening whereas it was 21% in the children who were not given vitamin D during the first 3 months of LT4 treatment. This figure was significantly higher in those who were given vitamin D during the first 3 months of treatment and reached 70%. However, one of the 19 children not given vitamin D presented with biological signs evoking vitamin D deficiency. In conclusion, in hypothyroid infants, vitamin D should be administered carefully during the first 6 months of treatment and restricted to children at risk for developing vitamin D deficiency.
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PMID:[Prophylaxis of vitamin D deficiency in hypothyroidism in the newborn infant]. 260 8

Endocrine abnormalities in lymphomatoid granulomatosis are rare and have never been a major determinant of the clinical course. We describe three patients who illustrate that a wide range of endocrine dysfunction (hypoadrenalism, hypercalcemia, hypothyroidism, diabetes insipidus and hypogonadism) may be encountered in this disorder. Moreover, such endocrine manifestations may be the major feature at presentation, the treatment of which may significantly influence the subsequent clinical outcome.
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PMID:Endocrine dysfunction in lymphomatoid granulomatosis. 276 22

Adrenocortical insufficiency causes difficulty in diagnosis and morbidity out of proportion to its rarity, because of the non-specific, multi-system nature of the clinical features. Most of these are due to cortisol deficiency. Prominent features are well-known ones such as weight loss and asthenia, and hypoglycaemia. Less prominent in recent accounts are those due to failure of cellular sodium export and to vasopressin excess, which are frequent and clinically significant. For this reason, the clinical features of isolated ACTH deficiency, isolated glucocorticoid deficiency and Addison's disease overlap greatly. In addition, cortisol deficiency has secondary endocrine effects, e.g. glucocorticoid-reversible hypothyroidism, hyperprolactinaemia and hypercalcaemia. Further overlap between the various steroid insufficiency syndromes occurs because of the association of various organ-specific autoimmune endocrinopathies with Addison's disease. Over 80% of Addison's disease is of the autoimmune type, though almost any systemic destructive process can cause similar steroid insufficiency. Demonstration of adrenal insufficiency requires various combinations of tetracosactrin adrenal stimulation tests, and hypoglycaemia or equivalent tests, if the cause is ACTH deficiency but the correct test can only be chosen to suit a firm clinical diagnosis. The treatment of adrenocortical insufficiency is described.
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PMID:Adrenocortical insufficiency. 300 80

Lithium has been established as a useful drug for the treatment of mood and behavior disorders. In addition to its therapeutic role in psychiatric disease it is important to recognize that it has diverse effects on endocrine function. These include the development of hypothyroidism and goiter in up to 10% of patients. Hyperthyroidism is a rare but reported side effect. Other abnormalities include hypercalcemia, diabetes insipidus, and altered carbohydrate metabolism. Depending on the clinical situation it is usually not necessary to discontinue lithium treatment, but appropriate intervention to correct the resulting endocrine abnormality may be indicated. This review emphasizes that psychiatrists and clinicians caring for patients given lithium need to be aware of the possible endocrine effects of this drug.
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PMID:Effects of lithium on the endocrine system: a review. 329 7

Endocrinologic disorders occasionally manifest themselves by their associated or induced cutaneous abnormalities. In some instances the initial and most prominent complaints of the patient are related to alterations in the skin, and thus the dermatologist will at times be the first physician consulted. In this article we describe the cutaneous lesions that occur in patients with acromegaly, hypopituitarism, hypothyroidism, hyperthyroidism, diabetes mellitus, glucagonomas, hypercalcemia, hypoparathyroidism, and fibrous dysplasia. In addition, we also discuss the role of the skin in vitamin D metabolism. Whenever possible and where known, we have attempted to point out the pathophysiologic mechanisms that account for the cutaneous changes.
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PMID:Endocrine-skin interactions. Cutaneous manifestations of pituitary disease, thyroid disease, calcium disorders, and diabetes. 332 73

This 55-year-old woman presented with primary adrenal insufficiency that led to multiple endocrine gland dysfunctions. Despite symptoms suggestive of hypothyroidism, she had mildly elevated serum thyroid hormone levels associated with elevated thyrotropin levels, hyperprolactinemia, and mild hypercalcemia. These abnormalities corrected with corticosteroid replacement but could be reproduced, in part, when the corticosteroids were temporarily withdrawn. The findings in this patient suggest that physiologic concentrations of glucocorticoids modulate prolactin secretion and the pituitary-thyroid axis. Adrenal insufficiency should be considered in the differential diagnosis of hyperprolactinemia and hyperthyrotropinemia with or without associated hyperthyroxinemia.
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PMID:Reversible hyperthyrotropinemia, hyperthyroxinemia, and hyperprolactinemia due to adrenal insufficiency. 402 80

Juvenile-onset hypothyroidism was diagnosed in an adult mixed-breed dog examined because of quadraparesis. Unusual clinical signs attributable to juvenile-onset or congenital hypothyroidism included disproportionate dwarfism; enlarged, protruding tongue; mental dullness; and retention of a "puppy" coat, which was soft and fluffy, without guard hairs. Radiography of the vertebral column and long bones revealed multiple areas of delayed epiphyseal closure and epiphyseal dysgenesis. Myelography demonstrated several intervertebral disk protrusions in the cervical and lumbar regions. Hypothyroidism was confirmed on the basis of a low basal serum thyroxine concentration that failed to increase after the administration of thyroid stimulating hormone. Other laboratory abnormalities included nonregenerative, normocytic, normochromic anemia; mild hypercalcemia; and an impaired growth hormone (GH) secretory response after xylazine administration. At necropsy, the thyroid gland was small and weighed only 0.2g. Microscopic examination of the thyroid gland revealed a loss of glandular tissue, which was replaced by adipose tissue along its periphery. Gross or microscopic abnormalities were not noted in the pituitary gland, and immunohistochemical staining of the pituitary gland revealed a normal number of GH-containing acidophils. This suggests that primary hypothyroidism may result in an impaired secretion of growth hormone, and that pituitary dwarfism or GH deficiency may be difficult to differentiate from hypothyroid dwarfism on the basis of provocative GH testing alone.
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PMID:Juvenile-onset hypothyroidism in a dog. 405 23

Pharmacological treatment of hypertension can cause clinically significant alterations in endocrine function through effects on glucose homeostasis, thyroid and parathyroid hormones, adrenal steroid metabolism and reproductive/pituitary physiology. Long term use of thiazide diuretics causes deterioration in glucose tolerance, probably secondary to potassium depletion. Hypoglycaemic complications of beta-blockers (mainly the non-selective compounds) can be dramatic, especially in type I diabetics. Clonidine, diazoxide and calcium antagonists have all been associated with deterioration in glucose tolerance and their long term use should be avoided in type II diabetics if possible. Propranolol lowers T3 levels by decreasing the conversion of T4 to T3. Prazosin causes elevations in T4 and thyroid-stimulating hormone, while sodium nitroprusside use may result in hypothyroidism. Numerous agents are associated with sexual dysfunction, including methyldopa, reserpine, clonidine and spironolactone. Thiazide diuretics may cause hypercalcaemia, particularly in patients with hyperparathyroidism, by decreasing urinary calcium as well as directly influencing bone and gut calcium handling. Conversely, propranolol may decrease circulating parathyroid hormone levels and correct the hypercalcaemia seen in hyperparathyroidism. Awareness of drug-induced changes in endocrine function will facilitate the rational management of the hypertensive patient.
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PMID:Effects of antihypertensive drugs on endocrine function. 614 2

Hypothyroidism is known to affect calcium homeostasis by decreasing bone turnover and serum calcium level, and by increasing parathyroid hormone and 1,25-dihydroxyvitamin D concentrations. A 52-year-old hypothyroid woman is described who had hypercalcemia associated with elevated parathyroid hormone and 1,25-dihydroxyvitamin D levels, but decreased 24-hour urinary calcium excretion and ratio of calcium to creatinine clearance. These parameters normalized following thyroid hormone replacement therapy. Hypercalcemia appeared to result from a combination of reduced renal calcium excretion and a change in the "set point" for calcium feedback inhibition of the parathyroid glands. These data suggest that thyroid hormone has a direct effect on the parathyroid glands, regulating parathyroid hormone secretion, and on the kidney's ability to excrete calcium. It is recommended that parathyroid hormone, 1,25-dihydroxyvitamin D, and urinary calcium excretion values be interpreted in light of thyroid hormone status.
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PMID:Reversible hypocalciuric hypercalcemia associated with hypothyroidism. 654 73


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