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

Patients suffering from malignant disease will probably develop some metabolic abnormality of electrolytes. Hypernatremia is defined as an elevation of serum natrium over 150 mEq/l and caused by decrease of water intake, low level of ADH secretion and impaired response of kidney to ADH. Hyponatremia below 135 mEq/l of serum natrium is caused by SI-DAH, sick cell syndrome and increased loss of natrium from the kidney. On the other hand, hyperkalemia is defined as an elevation of serum kalium over 5.0 mEq/l and caused by acute tumor cell lysis syndrome, adrenal and renal insufficiency. Hypokalemia is caused by kalium loss from kidney and hypersecretion of mineral corticoid. Hypercalcemia is found in the high frequency among patients with malignant disease. Hypercalcemia is defined as an elevation of serum calcium over 11.0 mg/dl, although the most important aspect is the level of ionized calcium. The excess calcium causes defective urinary concentration with polydipsia, nausea and vomiting leading to volume depletion. At serum calcium levels about 13.8 mg/dl, there may be rapid deterioration or renal function, dehydration, coma and cardiac arrhythmias. Hypercalcemia is rarely the first manifestation of cancer. There are three principle pathogenic causes of malignant hypercalcemia, 1) hypercalcemia is a feature of several hematological cancers, including Burkitt's lymphoma, T cell leukemia, but most commonly with myeloma. The hypercalcemia in these myeloma patients is due to the secretion of an osteoclast activator, a lymphokine by the myeloma cells. 2) all patients with bony metastases have biochemical evidence of increased bone resorption. However, not all patients with bony metastases develop hypercalcemia. Probably the hypercalcemia is due partially to increased renal tubular reabsorption of calcium, mediated by a humoral factor, with activity similar to that of parathormone. 3) hypercalcemia in the patients without bony metastases is due to increased bone resorption caused by the ectopic secretion by the tumor. Mildly symptomatic patients will benefit from modest salt loading. They are dehydrated and replacement of the extracellular fluid is the first line of treatment. This may require 4-10 l normal saline/24 h. In addition, frusemide will increase calcium excretion. Calcitonin may be given subcutaneously or intravenously to refuse the mobilisation of calcium from bone. Glucocorticoids are unhelpful, but will prolong the effect of calcitonin. A diphosphonate is also useful.
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PMID:[Palliative therapy in cancer. 4. Palliation of the symptoms from a malignant tumor. (2)]. 169 56

During recent years the total number of patients undergoing surgery for hyperparathyroidism has markedly increased, but the annual number of cases with substantial hypercalcemia has remained unchanged. Parathyroid carcinoma and water clear cell hyperplasia cause more severe hypercalcemia than other kinds of hyperparathyroidism. Grave hypercalcemia due to hyperparathyroidism is more common among the elderly, but can occur during pregnancy and also among children. Occasionally, a patient with hyperparathyroidism can also have another cause of the hypercalcemia and does not become normocalcemic until adequately treated for both. The suspicion of grave hypercalcemia should arise due to its clinical features. Determination of serum calcium and intact parathyroid hormone concentrations establishes the diagnosis. The basic treatment of grave hypercalcemia is to rehydrate the patient and to restore the sodium losses. To further lower the serum calcium value we have found bisphosphonates to be very effective. The definitive treatment of grave hypercalcemia due to hyperparathyroidism is surgery. As a last resort, frail patients with grave hyperparathyroidism can undergo surgery under local anesthesia. Repeat operations can improve the prognosis of patients with metastatic parathyroid carcinoma. Selective venous catheterization with blood sampling for determination of intact parathyroid hormone can be helpful in localizing recurrent disease.
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PMID:Management of hyperparathyroid patients with grave hypercalcemia. 176 39

Metabolic disturbances of Na, K, Ca and glucose as paraneoplastic syndrome were reviewed on the basis of recent progress of such areas. These abnormalities usually occur due to the production of hormones or other physiologically active substances by tumor tissues. Hyponatremia is the most common abnormality of Na metabolism in patients with cancers such as lung cancer, malignant lymphoma, thymoma and so on. Usual cause of hyponatremia as paraneoplastic syndrome is inadequate secretion of Antidiuretic Hormone (SIADH), which brings dilution hyponatremia associated with water intoxication. Recently hyponatremia due to abnormal secretion of atrial natriuretic peptide has been noted. Ca metabolism disturbance associated with cancer is usually observed as hypercalcemia and it is said that such hypercalcemia is seen in about 10% of cancer patients. Main cause of hypercalcemia associated with cancer is local osteolytic hypercalcemia (LOH) due to bone metastasis or humoral hypercalcemia of malignancy (HHM). The most common etiology of HHM is the production of Parathormone (PTH) related peptide (PTH-rP) massively secreted from cancer tissues. PTH-rP has been recently well investigated and its molecular, mRNA and gene structure have been already determined. The progress of this area is very rapid and PTH-rP will be assayed in the clinical laboratory in near future. As for glucose metabolism disturbance as paraneoplastic syndrome, hypoglycemia is the most common abnormality. This type of hypoglycemia has been noted in relation with excessive production of somatomedin.
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PMID:[Metabolic disturbance as paraneoplastic syndrome]. 182 8

Female Sprague-Dawley rats (100-120 g) were kept for 12 d on diets containing 250, 1500, or 9000 ppm Mg. Then subgroups were loaded with water, frusemide or magnesium and urine was collected over 6 h. Moderately Mg-deficient diet (250 ppm) induced moderate hypomagnesaemia (62.3% of controls), but did not result in hypercalcaemia or the formation of typical erythema. Nevertheless, pronounced nephrocalcinosis developed, as shown by increased renal wet and dry weight and elevated tissue concentrations of Ca, P and Mg, the calculous deposits probably consisting to a large extent of Ca3 (PO4)2. Despite these alterations, renal function remained unimpaired in Mg-deficient rats, as shown by normal urinary creatinine excretion and the unaffected ability of the kidneys to concentrate urine. Loading with water, frusemide or Mg increased urinary excretion of calcium in all three diet groups to a similar extent; hence no significant proof can be given that calculous deposits are mobilized under these conditions. Since comparable conditions may also be present under clinical conditions in man, special care should be given to maintain optimal Mg balance.
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PMID:Nephrocalcinosis without functional renal impairment in rats subjected to subacute moderate magnesium deficiency, and intervention studies on the mobilization of calcium deposits. 213 28

Primary disorders of water balance (central diabetes insipidus, congenital nephrogenic diabetes insipidus, and psychogenic polydipsia) should always be considered in the differential diagnosis of polyuria and polydipsia. In general, animals with these disorders have only one laboratory abnormality, a low urine specific gravity. The more common causes of polyuria and polydipsia (eg, hypercalcemia, chronic renal insufficiency, pyelonephritis, hyperadrenocorticism), in most instances, have specific and obvious abnormalities associated with the complete blood count (CBC), serum chemistry profile, and urinalysis. However, in some cases, a low urine specific gravity may initially be the only abnormality in these more common ruleouts. The workup for polyuria and polydipsia, especially in those cases with normal or near normal blood work, can be tedious, time consuming, confusing, and not without significant patient morbidity. This chapter will focus on the problems associated with diagnostic testing used to evaluate animals with disorders of water balance.
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PMID:Polyuria and polydipsia. Problems associated with patient evaluation. 213 78

In three experiments of 30 weeks' duration, 93 adult female Wistar rats received controlled amounts of calcium with food and water, to produce a state of either hypercalcemia or hypocalcemia. A systematic stereological analysis of the thyroid glands and a radioimmunological analysis of thyroxine, triiodothyronine, and thyrotropine were performed. In the hypercalcemic rats, a reactive hyperplasia of the parafollicular cells was established; this was accompanied by morphological and biochemical signs of hyperfunction of the follicular cells, despite a reduced central stimulation by thyrotropin. In the hypocalcemic animals, no quantitative morphological changes in the parafollicular cells were observed; however, morphological and biochemical signs of hypofunction of the follicular cells were obvious, despite stronger central stimulation by thyrotropin. It is concluded that the extrinsic regulation of follicular cells by the blood calcium level is stronger than the intrinsic regulation by hypothalamo-hypophyseal hormones.
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PMID:The effect of chronic hypercalcemia or hypocalcemia on the follicular and parafollicular cells in rat thyroid gland. 226 May 28

Monosodium 4-amino-1-hydroxybutane-1, 1-diphosphonic acid (MK-217) is a bone resorption inhibitor implicated in the treatment of malignant hypercalcemia. This compound is very water soluble and has five ionizable groups with pKa values over the entire pH range. As a result, it is difficult to maintain a single species in solution for chromatographic separation. Since there is no chromophore in the molecular structure, UV detection is ineffective. The compound and its potential degradation products are separated by ion-pair chromatography using 0.01 M cetyltrimethylammonium bromide as the ion-pairing agent and a polymeric stationary phase. Detection is by fluorescence detection after postcolumn derivatization of the primary amine with ophthalaldehyde and mercaptoethanol (OPA-MERC). Optimization of the chromatographic separation and the postcolumn reaction has been carried out, and the method has been applied to the analysis of MK-217 in intravenous solutions and tablet formulations.
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PMID:HPLC analysis of an amino bisphosphonate in pharmaceutical formulations using postcolumn derivatization and fluorescence detection. 226 30

In fresh-water rainbow trout, Oncorhynchus mykiss (formerly called Salmo gairdneri), experimentally induced mild hypercalcemia results in release of immunoreactive stanniocalcin from the corpuscles of Stannius (CS) and stimulated synthetic and releasing activities of the glands as measured in vitro. Pulse-chase experiments showed that stanniocalcin (STC) is a 56-kDa glycoprotein, processed from a 64-kDa precursor, prostanniocalcin (PSTC). PSTC and STC are homodimeric molecules that are readily split into monomers in the presence of reducing agents such as 2-mercaptoethanol. The monomeric form of PSTC and STC contains an approximately 5- to 6-kDa glycomoiety. Neither this sugar residue nor the NH2-terminal amino acid sequences of PSTC or STC proved to contain antigenic sites for the antiserum used in this study. Two-dimensional gel electrophoresis indicated the presence of several isoforms of PSTC and STC molecules that may reflect different stages of maturation of the (pro)hormone.
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PMID:Rainbow trout corpuscles of Stannius: stanniocalcin synthesis in vitro. 233 96

In a piggery (approx. 60 sows) nearly all the weaned piglets (about 150) showed signs of poor development, reduced feed intake, increased water consumption, markedly dry and hard faeces, urine drinking, navel suckling and drowsiness over 6-8 weeks. In blood samples of 4 affected piglets a significant hypercalcaemia (values greater than 20 mg/dl)--combined with an at times marked hypophosphataemia--was measured. In the diet offered, a Ca content of 56.2 g/kg was estimated. An intoxication due to ochratoxin or due to excessive levels of quinoxaline or vitamin D was excluded by toxicological investigations of the diet. Contamination by Datura stramonium was also ruled out.
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PMID:[Clinical effects of an extreme Ca overdose in feed for growing piglets]. 237 89

Near drowning in the Dead Sea is a potentially lethal accident; the swallowing of the salty water causes acute combined hypercalcemia and hypermagnesemia, and this, rather than aspiration, is considered to be the main pathogenetic fator. The authors reviewed the electrocardiographic data of 37 patients who nearly drowned in the Dead Sea. Common findings in the acute phase included P wave changes, tendency for prolongation of P-R interval, prolongation of QRS complex, infra-His conduction disturbances, tendency for broadening and inversion of T wave, and the appearance of a prominent U wave. Three patients had potentially lethal ventricular tachyarrhythmias. The QaTc interval (beginning of QRS complex to apex of T wave, corrected for heart rate), the expected QaTc calculated from calcium blood level (QaTce), and their difference (DQaTc), were measured or calculated. The QaTc was found within normal limits and did not change during recovery from the Dead Sea water poisoning. The DQaTc correlated significantly with serum magnesium level (p less than 0.001). This correlation signifies that hypermagnesemia normalizes the QaTc interval, which is usually shortened by isolated hypercalcemia. Combined hypercalcemia and hypermagnesemia can be caused by swallowing excessively salty water. The potential cardiac complications require strict monitoring and electrocardiographic follow up study.
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PMID:Electrocardiographic manifestations of combined hypercalcemia and hypermagnesemia. 238 29


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