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

The prevalence of diabetes mellitus in primary hyperparathyroidism is approximately 8% and that of primary hyperparathyroidism in diabetic patients is approximately 1%. Both values are about three-fold higher than the respective expected prevalences in general populations. Patients with both disorders are over 40 years of age and 80% are female; 22% have type 1 and 78% type 2 diabetes. Primary hyperparathyroidism presents first in approximately 20% of patients, and diabetes mellitus in 40%; both disorders present together, or within 1 year, in 40%. Approximately 40% of patients with primary hyperparathyroidism have impaired glucose tolerance. Insulin resistance is present in hyperparathyroidism and probably arises from a raised intracellular free calcium concentration which, by decreasing normal insulin-stimulated glucose transport, increases the requirement for insulin: if this insulin resistance progresses, impaired glucose tolerance and diabetes mellitus would result. Parathyroidectomy has been followed by regression of diabetes and of impaired glucose tolerance in some but not all patients. Early diagnosis of the second disorder is clinically desirable when one disorder is present. Hyperparathyroid patients should therefore be screened for impaired glucose tolerance and diabetes annually, and pre-operatively. Diabetic patients should be checked for hypercalcaemia at appropriate intervals; although only 1% of them may have hyperparathyroidism, this disorder if untreated is associated with hypertension, to which diabetic patients are already prone.
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PMID:Coincident diabetes mellitus and primary hyperparathyroidism. 1142 30

Population-based screening showed 2.1% prevalence of primary hyperparathyroidism (pHPT) in postmenopausal women. Individuals with total serum (s)-calcium levels of 2.55 mmol/L or more at screening were diagnosed with pHPT when subsequent analysis supported inappropriately elevated intact parathormone (PTH) levels in relation to even normal s-calcium levels. The arbitrary diagnostic criteria were validated by parathyroidectomy. Herein we reinvestigated biochemical signs of pHPT in women not diagnosed with pHPT due to s-calcium 2.50 to 2.54 mmol/L (group A, n = 160) at screening or due to appropriate PTH levels on two occasions after screening (group B, n = 70). Altogether, 99 women in group A and 47 in group B underwent reinvestigation 8.8 years after screening when they were 65 to 84 years old. The s-calcium levels averaged 2.56 mmol/L and had increased in group A (mean 0.04 mmol/L) and decreased in group B (mean 0.05 mmol/L). A total of 48 and 18 females (48%, 38%), respectively, met the previously validated criteria of pHPT. Altogether 21% of them were hypercalcemic (range 2.60-3.12 mmol/L). Subgroup analysis showed that PTH had not increased with time (n = 47) and that atherogenic blood lipids, but not glucose levels, were similar in pHPT patients and matched controls (n = 37). Assuming the existence of pHPT already at screening, the prevalence of pHPT could be adjusted to 3.4%. Even the most liberal diagnostic criteria utilized at pHPT screening seemed to underdiagnose the disease by inefficient cutoff limits for s-calcium and PTH. Because one-fifth of the women with pHPT progressed to hypercalcemia, long-term follow-up is advocated for those with s-calcium in the upper normal range.
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PMID:Primary hyperparathyroidism revisited in menopausal women with serum calcium in the upper normal range at population-based screening 8 years ago. 1204 63

Tumours of non-endocrine origin may exert deleterious effects by elaborating active principles which disturb body regulation. Systemic manifestations are fairly common with neoplasms of the lung, kidney, gastro-intestinal tract and thymus. The secretion of these tumours may have a known chemical structure (serotonin), may present hormone-like action (parathormone, antidiuretic hormone, insulinoid), or have well-defined biological properties (erythropoietin, gastrin-like principle). Tumours may stimulate endocrine glands by an unknown mechanism, producing disorders such as Cushing's syndrome, hypercalcemia, gynecomastia and hypoglycemia. Thymomas may be associated with autoimmune diseases. Tumours may extensively utilize or excrete some metabolite (glucose) or electrolyte (Na or K). Awareness of the systemic effects of various neoplasms may lead to an early diagnosis and proper treatment of these manifestations.
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PMID:SYSTEMIC EFFECTS OF NON-ENDOCRINE TUMOURS. 1420 55

Successful lithium treatment of manic disorders was reported in 1949 by John Cade. This marked the beginning of the pharmacological era in psychiatry. In spite of the emergence of alternative drugs with antimanic and moodstabilising properties, lithium remains the primary long-term treatment for preventing relapse of bipolar disorders. Among the adverse effects of lithium treatment are unintentional lithium intoxication, nephropathy, hypothyroidism, hypercalcemia, hyperparathyroidism, diarrhoea, tremor, weight gain, and effects on the fetus and the newborn child. Early detection or prevention of adverse effects, particularly lithium intoxication, is vital for safety. Therefore, P-lithium and P-creatinine are assessed every 4 months (and pre-lithium) while thyroid and parathyroid function, weight, 24 h consumption of liquids (or 24 h urinary output), B-glucose, and blood pressure are assessed annually (and pre-lithium). Urinary concentrating capacity and glomerular filtration rate are always measured after 5 years of lithium treatment, and always when clinically indicated. Patient education and annual reinforcement of his/her knowledge of pertinent aspects of the treatment and of risk factors for lithium intoxication are important aspects for ensuring safety.
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PMID:[Adverse effects of lithium treatment and safety routines]. 1519 Jul 55

Since its introduction as a clinical entity in 1992, the Brugada syndrome has progressed from being a rare disease to one that is second only to automobile accidents as a cause of death among young adults in some countries. Electrocardiographically characterized by a distinct ST-segment elevation in the right precordial leads, the syndrome is associated with a high risk for sudden cardiac death in young and otherwise healthy adults, and less frequently in infants and children. Patients with a spontaneously appearing Brugada ECG have a high risk for sudden arrhythmic death secondary to ventricular tachycardia/fibrillation. The ECG manifestations of Brugada syndrome are often dynamic or concealed and may be unmasked or modulated by sodium channel blockers, a febrile state, vagotonic agents, alpha-adrenergic agonists, beta-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of glucose and insulin, hypo- and hyperkalemia, hypercalcemia, and alcohol and cocaine toxicity. In recent years, an exponential rise in the number of reported cases and a striking proliferation of articles defining the clinical, genetic, cellular, ionic, and molecular aspects of the disease have occurred. The report of the first consensus conference, published in 2002, focused on diagnostic criteria. The present report, which emanated from the second consensus conference held in September 2003, elaborates further on the diagnostic criteria and examines risk stratification schemes and device and pharmacological approaches to therapy on the basis of the available clinical and basic science data.
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PMID:Brugada syndrome: report of the second consensus conference: endorsed by the Heart Rhythm Society and the European Heart Rhythm Association. 1565 31

An 89-year-old male patient on hemodialysis presented clouding of consciousness caused by hypoglycemia during taking an anti-diabetic agent. His somnolent state continued in spite of glucose dispensation, and parental nutrition was started by a nasogastric tube because he couldn't have peroral ingestion. Though his blood glucose level recovered normal, his consciousness disorder was suspended, and he showed remarkable hypercalcemia. He was dosed with elcatonin, and the parental nutrient was changed to the other one that contained less vitamin D and calcium, and so his serum calcium level diminished slowly but he showed drowsiness about a month long. After resumption of peroral ingestion, his consciousness restored to the former condition rapidly. This case suggests that careful observation is needed in less active dialysis patients with parental nutrition because nutrient-contained vitamin D and calcium, which doesn't harm patients without renal insufficiency, may cause hypercalcemia.
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PMID:[Hypercalcemia complicated with status nervosus in an elderly patient on hemodialysis during parental nutrition]. 1574 2

Since its introduction as a clinical entity in 1992, the Brugada syndrome has progressed from being a rare disease to one that is second only to automobile accidents as a cause of death among young adults in some countries. Electrocardiographically characterized by a distinct ST-segment elevation in the right precordial leads, the syndrome is associated with a high risk for sudden cardiac death in young and otherwise healthy adults, and less frequently in infants and children. Patients with a spontaneously appearing Brugada ECG have a high risk for sudden arrhythmic death secondary to ventricular tachycardia/fibrillation. The ECG manifestations of Brugada syndrome are often dynamic or concealed and may be unmasked or modulated by sodium channel blockers, a febrile state, vagotonic agents, alpha-adrenergic agonists, beta-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of glucose and insulin, hypo- and hyperkalemia, hypercalcemia, and alcohol and cocaine toxicity. In recent years, an exponential rise in the number of reported cases and a striking proliferation of articles defining the clinical, genetic, cellular, ionic, and molecular aspects of the disease have occurred. The report of the first consensus conference, published in 2002, focused on diagnostic criteria. The present report, which emanated from the second consensus conference held in September 2003, elaborates further on the diagnostic criteria and examines risk stratification schemes and device and pharmacological approaches to therapy on the basis of the available clinical and basic science data.
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PMID:Brugada syndrome: report of the second consensus conference. 1589 65

233 SD rats weighing 100 approximately 120 g were divided randomly into 6 groups. The animals in group I and group II received 0.1 mg/kg selenium in the form of sodium selenite only and served as the negative control and positive control, respectively. Animals in groups III, IV and V were fed with selenium as Se-enriched malt supplemented diets (0.3, 1 and 3 mg/kg), and group VI with selenium by using sodium selenite supplemented diets (3 mg/kg). Animals of groups II approximately VI were induced hepatoma by diethylnitrosamine (100 mg/l) for 16 weeks, then drunk with sterilized water for 2 more weeks. Subsequently, the effects of Se-enriched malt and sodium selenite on hepatoma nodules, relative liver weight, the liver function indices including alanine aminotransferase (ALT), alkaline phosphatase (ALP), albumin (ALB), total bilirubin (TBIL), and the tumor markers, named as gamma-glutamyltranspeptidase (GGT), alpha-fetoprotein (AFP), insulin-like growth factor-II (IGF-II) were recorded. The calcium concentration, glucose content in plasma and values of the hormones regulating blood glucose, such as insulin, glucagons and thyroid hormones (3,5,3'-tetraiodothyronine, T(3); 3,5,3'5'-tetraiodothyronine, T(4)) were observed as well. At the same time, the correlations between the concentration of plasma glucose and related hormones were also analyzed. The results indicated that Se-enriched malt showed a better chemopreventive efficiency in decreasing the number of hepatoma nodules, relative liver weight and the contents of AFP, GGT, IGF-II, ALT, ALP and TBIL in the plasma, and delaying the descent of hormones in the serum, names as insulin, glucagons, T(3) and T(4) than those feeding with sodium selenite. Effect of Se-enriched malt excelled sodium selenite in the aspects of deadening the descent of glucose concentration in the plasma and the rise of calcium concentration in the serum of the rats with hepatoma induced by diethylnitrosamine. The values of glucose and calcium were significantly related to those items fore-named. In conclusion, the function of Se-enriched malt in deadening the lesion and delaying the development of hepatoma of rats induced by diethylnitrosamine was better than that of sodium selenite. Hypoglycemia and hypercalcemia were significantly correlated with the multifactors mentioned above.
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PMID:Effect of selenium-enriched malt on hepatocarcinogenesis, paraneoplastic syndrome and the hormones regulating blood glucose in rats treated by diethylnitrosamine. 1626 26

We used the mouse nephrin promoter to express a constitutively active Galphaq [Galphaq(Q>L)] transgene in mice. As previously reported, the transgene was expressed in kidney, pancreas, and brain, and the kidney phenotype was characterized by albuminuria and reduced nephron mass. Additional studies revealed a second phenotype characterized by polyuria and polydipsia. The polyuric phenotype was not caused by abnormal glucose metabolism or hypercalcemia but was accompanied by reduced urinary concentrating ability. Additional studies found that 1) water restriction was associated with an appropriate increase in serum vasopressin levels in transgenic (TG) mice; 2) the urinary concentrating defect was not corrected by administration of desamino-d-arginine vasopressin (DDAVP); and 3) papillary length was similar in TG and non-TG mice. To examine the renal response to DDAVP at the molecular level, we monitored aquaporin 2 (AQP2) and vasopressin V2 receptor (V2R) mRNA levels in mouse kidney. Consistent with the known effects of vasopressin, administration of DDAVP caused a decrease in V2R mRNA levels and an increase in AQP2 mRNA levels in both TG and non-TG animals, suggesting an appropriate renal response to DDAVP in the TG mice. To determine whether the urine concentrating abnormality was the result of primary polydipsia, water intake by TG mice was restricted to the amount ingested by non-TG animals. After 5 days, urinary concentrating ability was similar in TG mice and non-TG littermate controls. These data are consistent with the notion that expression of the Galphaq(Q>L) transgene in the brain induced primary polydipsia in the TG mice.
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PMID:Galphaq-dependent signaling cascades stimulate water-seeking behavior. 1660 48

Alterations in electrolyte balance have been claimed to play a role in the pathophysiology of coronary heart disease; however, the relationship between the electrolyte pattern and other clinical variables immediately after an acute vascular event is unclear. The aim of the present study was to test whether electrolyte and microelement changes characterize the acute phase in patients with different degrees of glucose tolerance admitted to the hospital shortly after an acute cardiovascular or cerebrovascular ischemic event. Two hundred consecutive patients with either myocardial infarction or stroke (SP group), stratified by degree of glucose tolerance, were studied within six hours of admission, and compared against 125 patients admitted for conditions other than acute vascular ischemia (CP). Routine laboratory parameters and serum Na, K, Cl, Mg and Ca concentrations were determined in all patients and compared to those recorded within six months before the admission. Relative to CP and independently of confounding factors including glucose tolerance status, the SP group showed significantly higher plasma glucose and insulin concentrations, higher creatinine and a modified serum electrolyte pattern characterized by significantly lower potassium and magnesium levels and by hypercalcemia and hyperphosphatemia. Irrespective of glucose tolerance, the first hours following an acute vascular event are characterized by marked insulin resistance with a consistent shift in the serum electrolyte pattern. This pattern is the physiological consequence of the attendant compensatory hyperinsulinemia. Its significance for the evolution of ischemic damage remains to be established.
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PMID:Acute vascular events and electrolytes variations in elderly patients. 1667 13


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