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

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

Hyperparathyroidism is associated with abnormalities in glucose tolerance and insulin secretion. To assess the effects of hyperparathyroidism on the control of diabetes mellitus, 56 patients with concomitant hyperparathyroidism and diabetes mellitus were studied before and after parathyroidectomy. Fifty patients (89.3%) had hypercalcemia, and six patients (10.7%) had normocalcemia associated with inappropriately elevated parathyroid hormone. After surgery, three of five patients with insulin-dependent diabetes mellitus showed more than a 50% reduction in insulin requirement. Thirty-nine of 49 patients with noninsulin-dependent diabetes mellitus were followed. Of these, three patients had restoration of normal blood glucose levels without any diabetic treatment including diet restriction. Diabetes control improved in eight parents, remained stable in 18, and deteriorated in 10 patients. In the remaining two patients, impaired glucose tolerance disappeared in one patient and progressed to frank diabetes in the other. Overall 60.7% of the patients improved or remained stable in their diabetes control after parathyroidectomy. We conclude that in patients with hyperparathyroidism, the coexistence of diabetes mellitus might be a further indication for parathyroidectomy. Physicians should be alerted to the possible change in diabetic regimen and the risk of hypoglycemia in patients with diabetes after parathyroidectomy.
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PMID:Effect of hyperparathyroidism on the control of diabetes mellitus. 353 62

A female patient with acromegaly, hypercalcemia, and Zollinger-Ellison syndrome was found to have a very high plasma concentration (average 2,300 pmol/liter; normal less than 50 pmol/liter) of growth hormone-releasing factor as measured by a radioimmunoassay to human pituitary growth hormone-releasing factor-1-44. The plasma concentration of growth hormone averaged 25 mIU/liter (normal less than 5 mIU/liter) and there was no rise following an intravenous 100 micrograms bolus of human pituitary growth hormone-releasing factor-1-44. Plasma growth hormone and growth hormone-releasing factor levels were unaffected by bromocriptine, insulin-induced hypoglycemia, and sleep. A long-acting somatostatin analogue lowered both the growth hormone-releasing factor and the growth hormone levels. Thyrotropin-releasing hormone stimulation and oral glucose tolerance tests produced significant increases in plasma growth hormone levels whereas the growth hormone-releasing factor level remained unchanged, suggesting that when normal somatotrophs are exposed to maximal growth hormone-releasing factor stimulation, thyrotropin-releasing hormone becomes a secretagogue of growth hormone from the pituitary. It is proposed that in the absence of a radioimmunoassay for growth hormone-releasing factor, a lack of growth hormone response to growth hormone-releasing factor in a patient with acromegaly is compatible with a source of ectopic growth hormone-releasing factor production.
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PMID:Growth hormone secretion dynamics in a patient with ectopic growth hormone-releasing factor production. 392 80

Plasma insulin dynamics were evaluated in 10 patients with primary hyperparathyroidism before and after parathyroidectomy and correction of hypercalcemia. Before surgery fasting plasma insulin concentrations and insulin responses to administered glucose, tolbutamide, and glucagon were significantly greater than postoperative values. Hyperinsulinemia was not associated with altered glucose curves during glucose or glucagon tolerance tests, but a relatively greater insulin response to tolbutamide resulted in an increased hypoglycemic effect following its administration. The glucose-lowering action of intravenous insulin was slightly impaired before treatment. Intramuscular injections of parathormone to six normal men for 8 days induced mild hypercalcemia and hypophosphatemia and reproduced augmented plasma insulin responses to oral glucose and intravenous tolbutamide. 4-hr intravenous infusions of calcium to another group of six normal men raised serum calcium concentrations above 11 mg/100 ml. This did not alter glucose or insulin curves during oral glucose tolerance but markedly accentuated insulin responses to tolbutamide and potentiated its hypoglycemic effect. When highly purified parathormone was incubated with isolated pancreatic islets of male rats, glucose-stimulated insulin secretion was unaffected. These findings suggest that chronic hypercalcemia of hyperparathyroidism sustains a form of endogenous insulin resistance that necessitates augmented insulin secretion to maintain plasma glucose homeostasis. This state is insufficient to oppose tolbutamide-induced hypoglycemia because of an additional direct, selective enhancement of hypercalcemia on pancreatic beta cell responsiveness to the sulfonylurea. The possible direct role of parathormone in these events has not been established.
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PMID:Plasma insulin disturbances in primary hyperparathyroidism. 512 11

Sufficient histologic and embryologic information is now available to allow for a reasonably satisfactory histogenic classification of ovarian neoplasms. The majority of these tumors are derived from germ cells, sex cord-mesenchyme or the germinal epithelium. A few, such as the Brenner tumor, must still be classed as being of "uncertain histogenesis," for the cell (or tissue) of origin is not yet known. It is now realized that many ovarian neoplasms previously considered to be endocrinologically inert may, on occasion, be associated with either estrogenic or androgenic activity. This applies particularly to Brenner tumors, mucinous cystadenomas and serous cystadenomas. The common factor associated with such endocrine activity is luteinization of the tumor stroma.Ovarian neoplasms usually manifest only local symptoms, but they may, on occasion, be associated with such unusual systemic effects as hypoglycemia, hypercalcemia or a hemolytic anemia.
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PMID:Ovarian tumors. Histogenesis and systemic effects. 574 84

Primary liver cell carcinoma (PLC) is common in Africa. It represents the commonest malignancy in the Nigerian males. White reports of paraneoplastic syndrome associated with PLC abound from the Western World--a geographic area of low incidence of the tumour--there is a paucity of information from the African continent generally, and specifically from Nigeria. This prospective study analyses the relative incidences of recognized syndromes in fifty Nigerians with PLC. Alpha-foetoproteinemia (51%) and hypercholesterolaemia (33%) are common while hypoglycemia (9%) and hypercalcaemia (4%) are uncommon. No case of porphyria cutanea tarda was encountered. Our findings are compared with reported incidences in the literature. The pathogenetic mechanisms of these syndromes are briefly reviewed.
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PMID:Paraneoplastic syndromes in primary liver-cell carcinoma: experience in Ibadan, Nigeria. 617 79

This report describes a 31-year-old woman with evidences of selective adrenocorticotropic hormone deficiency associated with a remarkable pituitary lesion, lymphoid hypophysitis. Clinical manifestations of secondary hypocortisolism, which first appeared during the immediate postpartum period following normal pregnancy, included progressive weakness and mental aberrations, fasting hypoglycemia, transient hypercalcemia, and striking ECG changes. Sudden death resulted from cardiorespiratory collapse. Microscopic examination of the anterior pituitary disclosed focal fibrosis and extensive lymphocytic infiltrations with a marked reduction of basophils; immunostaining techniques demonstrated a selective loss of corticotropin-secreting cells. The histopathology of the pituitary and its association in this case with lymphoid thyroiditis suggest that selective damage to corticotrophs was due to an autoimmune process.
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PMID:Lymphoid hypophysitis with selective adrenocorticotropic hormone deficiency. 625 May 7

Tumours may give rise to systemic complications, among others by the release of specific substances. The accompanying symptoms are referred to as paraneoplastic syndromes. These complications have a marked effect on the course run by the disease. A number of common syndromes which are easy to diagnose, are discussed in a survey of the literature, namely: cachexia, anorexia, fever, hypercalcaemia, hypoglycaemia, anaemia and coagulation defects. Attention is paid to the occurrence of the syndromes in man and dogs, the relationship with specific forms of tumour, the pathogenesis and some forms of possible therapy.
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PMID:[Systemic complications of tumors]. 635 48

Clinical and biochemical data are presented on 18 children with severe hyperinsulinaemic hypoglycaemia born to non-diabetic mothers. Thirteen presented within three days of birth, three by 20 months and two aged nine years. Diagnosis of hyperinsulinism (HI) was made in a single blood sample by showing inappropriate plasma insulin levels (23 +/- 3 mU/l) for glycaemia (1.2 +/- 0.1 mmol/l), with low blood ketone body, lactate, alanine and glycerol levels. All children showed increased glucose disappearance rates (KG 7.6% +/- 0.06) and glucose requirement (range, 9-25 mg/kg/min) and an exaggerated glycaemic response to glucagon when hypoglycaemic. Confirmatory tests included measurement of plasma insulin levels during leucine and arginine tolerance tests, during hypercalcaemia and after fish insulin. Coeliac angiograms were performed in three cases. Clinical progress could be divided into five categories. Four cases recovered normal insulin control spontaneously (transient neonatal HI); two children responded and remain on diazoxide therapy, two responded to diazoxide after partial pancreatectomy (diazoxide responsive HI); in three cases resolution of hypoglycaemia resulted from resection of isolated adenoma (insulinoma); total pancreatectomy was needed in five cases (nesidioblastosis) and two children were victims of drug administration (drug induced HI). This analysis allows the definition of a practical approach to diagnosis and management of this major clinical problem.
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PMID:Hyperinsulinaemic hypoglycaemia in infancy and childhood: a practical approach to diagnosis and medical treatment based on experience of 18 cases. 639 78

The authors investigated the effect of acute hypercalcaemia induced by a 2-hour intravenous infusion of calcium gluconate (8.9 mg Ca2+/kg b. w.) on the lactotrophic secretory reserve assessed by the test with insulin hypoglycaemia (delta PRL) and the effect of an intravenous bolus of 50 IU synthetic salmon calcitonin on the lactotrophic secretory reserve assessed by means of the TRH test (delta PRL). Acute hypercalcaemia inhibits PRL levels stimulated by insulin hypoglycaemia (p less than 0.01) as well as delta PRL (p less than 0.01). Calcitonin reduces PRL levels at rest and TRH stimulated levels (p less than 0.05 and p less than 0.01, respectively) as well as delta PRL (p less than 0.01). The prolactin inhibiting effect of calcitonin resembles markedly the effect of hypercalcaemia. The exact mechanism of these changes and the physiological impact of calcitonin on the regulation of PRL secretion is not known.
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PMID:Hypercalcaemia and calcitonin inhibit prolactin secretion. 644 27


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