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

The symptoms which are caused by hypercalcemia are variable and unspecific. In the elderly the functional capacity of homeostatic mechanisms is less than in young people and at the same time the prevalence of diseases which may cause hypercalcemia is greater. One should be aware of the possibility of hypercalcemia in patients presenting vague gastrointestinal and/or psychiatric complaints or symptoms. The prevalence of hypercalcemia in elderly women may well be 3%. Hypercalcemia leads to renal loss of salt and disturbances of renal function. An increasing inability to excrete the calcium overload is the result. Only in primary hyperparathyroidism renal function remains generally normal and moderately increased calcium levels may exist for years without serious consequences. Important causes of hypercalcemia in the elderly are hyperthyroidism, malignant disease and abrupt immobilization with previously elevated skeletal remodelling activity. Thiazide diuretics may precipitate the hypercalcemic state. Diagnosis is relatively simple and is based on a limited package of laboratory tests. Treatment should always begin with the restoration of the extracellular fluid volume. This is followed by inhibition of bone resorption by means of bisphosphonates or corticosteroids and treatment of the underlying disease.
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PMID:[Hypercalcemia in the elderly]. 218 Jan 40

The occurrence of acetylation phenotype has been studied in 76 patients with untreated hyperthyroidism. In 23 of these patients having the "fast" and in 42 having the "slow" acetylation phenotype the selected parameters of calcium-phosphate metabolism have been determined before, during and after propranolol therapy lasting six days. Propranolol was administered at a dose of 160 milligrams daily. A significant decrease in the blood serum level of calcium and urinary calcium excretion following propranolol administration was found only in patients with hypercalcemia and hypercalciuria. On the other hand, a significant decrease in the urinary excretion of hydroxyproline was observed in all the patients with hyperthyroidism treated with propranolol. The effect of propranolol on the measured parameters of calcium-phosphorus metabolism was similar in hyperthyroid patients with both "fast" and "slow" acetylation phenotypes, what suggests that it does not depend on the N-acetyltransferase activity.
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PMID:[Acetylation phenotype and the changes in selected indicators of calcium-phosphate metabolism in patients with hyperthyroidism treated with propranolol]. 248 31

Measured levels of serum calcium, phosphate, alkaline phosphatase, and urinary hydroxyproline were measured and calcium-phosphate product was calculated in 20 hyperthyroid patients and 20 normal controls. Eleven of the patients took propranolol 160 mg per day for 28 days. We found that the serum level of calcium was higher than that of normal controls. The incidence of hypercalcaemia in hyperthyroid patients was 10%. The serum level of phosphate and the calcium-phosphate product increased (P less than 0.01). Elevation of alkaline phosphatase and bone alkaline phosphatase were also observed (P less than 0.01). The urinary hydroxyproline was also elevated (P less than 0.01). After treatment with propranolol serum calcium and triiodothyronine decreased (P less than 0.05). It is suggested that the major mechanism of hypercalcaemia and hyperphosphatemia in hyperthyroidism was increase of bone absorption stimulated by triiodothyronine. Propranolol decreased the serum level of calcium through decreasing triiodothyronine level and through beta-receptor blocking effect as well as its direct effect on bone.
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PMID:[Hypercalcemia and hyperphosphatemia in thyrotoxoicosis and the therapeutic effect of propranolol]. 263 74

The authors report on various diagnostic pitfalls on 102 patients having undergone exploratory cervicotomy for primary hyperparathyroidism. A false positive diagnostic error was made on 2% of the cases, bringing to 100 the number of patients with a confirmed diagnosis of primary hyperparathyroidism. False negative diagnosis was made on 4% of the patients: two late diagnoses leading to an acute toxic state and death postoperatively in both cases; two pure psychiatric variants leading to repetitive hospitalizations in psychiatry. Error in diagnosis because of a masking effect was made in 4% of the cases:--one association with a clear cell nephro--epithelioma--one association with a multiple myeloma--two associations with a benign monoclonal gammapathy. The absence of hypercalcemia, a diagnostic pitfall in the modern form of this disease was found in 7% of the cases. PTH hypersecretion which is virtually a constant finding in the normocalcemic form of the disease obviates in most cases the need of a bone biopsy and quantitative histomorphometric analysis. The association with another endocrinopathy was found in 12% of the cases (2 MEN I, 1 MEN II, 9 hyperthyroidism). Because of its high frequency in the aged (22% greater than 75 years) the diagnosis of this disease is difficult for its signs are mimicked as well by the aging process. The preoperative topographic diagnostic error is avoided since there doesn't seem to be any test which would preclude the normal surgical procedure of carefully exploring all 4 topographic sites of the parathyroid. Surgical errors can be numerous but minimized with the increasing experience of the operator. Histological errors are seen mainly in the normocalcemic variety where only electron microscopy can detect the typical signs of cellular hyperactivity.
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PMID:[Primary hyperparathyroidism. Apropos of 102 recent exploratory cervicotomies: diagnostic and clinical pitfalls]. 264 28

Concomitance of hyperthyroidism and hyperparathyroidism is rare and only forty-nine well documented cases could be found in the literature. In the present study, only forty-three patients with adequate available clinical and laboratory data are reported. Hypercalcemia was found in all the patients and five of them (12%) had acute hyperparathyroidism. Two patients were also pregnant and had pancreatitis. Hypercalcuria was found in 73% and hypophosphatemia in 55% of the patients. Eleven patients (26%) had renal concretions. Skeletal roentgenograms showed abnormalities in 63% of the patients. Elevated serum level of alkaline phosphatase was present in 64% of the patients. However, there seemed to be no correlation with the severity of the skeletal lesions. Thyrotoxicosis commenced before that of Hyperparathyroidism in twenty-three patients (53%) whereas in the remaining twenty patients it was impossible to determine which disease began first. The etiologies of hyperparathyroidism as well as the differential diagnosis of parathyroid-related and nonparathyroid-related hypercalcemia are discussed. Microscopically, 74% of the patients had a single adenoma; 16% had hyperplasia of one to three parathyroid glands. One patient had an adenoma in combination with hyperplasia of one parathyroid gland, one had an adenoma and three hyperplastic glands, one had adenomas of two parathyroid glands in combination with hyperplasia of one parathyroid gland, and the other one had carcinoma of a parathyroid gland.2+ Finally, if a thyrotoxic patient still has hypercalcemia when becoming euthyroid after antithyroid therapy, coexisting hyperthyroidism should be considered and an operation should be performed as surgical treatment cured both diseases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Primary hyperparathyroidism and coexisting hyperthyroidism--review of the literature. 267 Jan 39

A patient with concomitant primary hyperparathyroidism and Graves' disease with hyperthyroidism was observed during treatment with carbimazole. His serum free calcium levels was initially elevated (6.3mg/dl, normal 4.5-5.3 mg/dl) whereas his serum magnesium level was depressed (1.6 mg/dl, normal 1.7-2.8 mg/dl), but immunoreactive parathyroid hormone levels were only slightly increased (96 pg/ml, normal less than 86 pg/ml). During therapy with carbimazole, the patient became euthyroid and serum free calcium levels decreased to 6.0 mg/dl whereas serum magnesium levels increased to 2.3 mg/dl, and parathyroid hormone increased to values clearly indicative of hyperparathyroidism (185 pg/ml). A subtotal thyroidectomy and parathyroidectomy corrected both diseases in this case. These observations suggested that hyperthyroidism per se causes a decrease in serum magnesium levels and also potentiates the osteoclastic effects of parathyroid hormone resulting in an exacerbation of hypercalcemia which in turn produced a relative inhibition of hormone secretion by the abnormal parathyroid tissue.
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PMID:Concurrent hyperthyroidism and hyperparathyroidism: influence of hyperthyroidism on serum magnesium, free calcium and parathyroid hormone. 279 61

The abnormalities of calcium-phosphorum metabolism observed in hyperthyroidism (tendency to hypercalcaemia with subsequent functional hypoparathyroidism, increase in serum alkaline phosphatase and in hydroxyprolinuria) essentially result from excessive mobilization of bone calcium and phosphates by the thyroid hormones themselves. Histomorphometric studies have shown that the skeletal repercussions of hyperthyroidism are almost constant. There is, in particular, excessive bone remodelling due to increased bone-forming and bone-resorbing cellular activities. However, since bone resorption is quantitatively more stimulated than bone formation, the physiological bone loss is accelerated and is only partly repaired by re-establishment of the normal thyroid function.
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PMID:[Phospho-calcium and bone metabolism in hyperthyroidism in adults]. 293 96

A review is given on S-angiotensin-converting enzyme (SACE) and its clinical value, based upon 327 sarcoidosis patients and 1,274 patients with various disorders. SACE was elevated in 55% of the sarcoidosis patients, although with a higher frequency in those with active disease. Erythema nodosum was associated with normal initial SACE, subsequently rising, and sarcoid hypercalcaemia was consistently followed by elevated SACE. In non-sarcoid patients, elevated SACE was observed in only 10 cases. The sensitivity and specificity were 0.55 and 0.99, respectively, and the positive and negative predictive values were 0.95 and 0.90, respectively. Elevated SACE pointed strongly towards the presence of sarcoidosis, although reservations must be made in patients with liver disorders, diabetes mellitus, hyperthyroidism, asbestosis or silicosis which are rather common disorders also associated with elevated SACE. Normal SACE does not exclude sarcoidosis.
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PMID:Angiotensin-converting enzyme activity in sarcoidosis and other disorders. 303 89

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

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


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