Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty patients were followed-up for an average of 3 years after treatment for urinary bladder calculi. In 10 of these (20%) altogether 20 metabolic or endocrine diagnoses were revealed at follow-up: hypercalcaemia, 8; hyperuricosaemia, 4; high parathormone, 3; hyperuricosuria, 2; hypercalciuria, 2: hyperoxaluria, 1. About half of the patients also had other diagnoses, dominated by outflow obstruction at the prostatic level, followed by neurogenic bladder disorder. Fifteen had developed new bladder calculi. Urography revealed upper tract calculi in 12 patients, but 11 of these were free from metabolic disorder. Significant bacteriuria was common (24%). Our conclusion is that a follow-up is to be recommended after treatment of bladder calculi. It should include cystoscopy and screening for endocrine/metabolic disorders.
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PMID:Follow-up of patients treated for urinary bladder calculi. 222 95

A case of osteitis fibrosa cystica or brown tumor of bone in a patient presenting with acute spinal cord compression that was suggested initially by needle aspiration biopsy of the spine is described. Following the aspiration biopsy, excision of vertebral lesions, cord decompression, and spinal fusion were successfully performed. A parathyroid adenoma was subsequently identified and also resected. Along with the diagnosis of malignancy, the presence of hyperparathyroidism with osteitis fibrosa cystica should be considered in a patient presenting with lytic lesions in bone, especially if they are associated with hypercalcemia. Serum parathormone level determination is usually diagnostic of hyperparathyroidism, but this test has a 7-10-day turnaround time. Preoperative needle aspiration biopsy is a safe and rapid method of diagnosing osteitis fibrosa cystica and may be of critical importance in a patient with acute and progressive symptoms such as cord compression.
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PMID:Osteitis fibrosa cystica (brown tumor) of the spine with cord compression: report of a case with needle aspiration biopsy findings. 229 20

We have investigated 13 families, each of which have one member with infantile hypercalcaemia/Williams-Beuren syndrome (IHWBS), for either a germ cell mutation of, or an association with, the calcitonin-CGRP gene. Restriction fragment mapping studies of the calcitonin-CGRP gene using five restriction enzymes (TaqI, Bg/II, PvuII, PstI, and SacI) and region specific probes failed to show any abnormalities of this gene complex. NO association of IHWBS with polymorphism of the calcitonin-CGRP/parathormone locus was found. Therefore, although the aetiology of IHWBS may be caused by a new dominant mutation, there is no evidence to implicate major rearrangements of the calcitonin-CGRP and parathormone genes.
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PMID:The calcitonin-CGRP gene in the infantile hypercalcaemia/Williams-Beuren syndrome. 248 8

We present a newborn baby with a diagnosis of neonatal severe primary hyperparathyroidism, based on the concomitant presence of hypercalcemia, hypophosphatemia and elevated values of parathormone. A national and international review on the subject is made and the differential diagnosis of this rare entity is discussed.
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PMID:[Severe neonatal primary hyperparathyroidism: presentation of a case and review of the literature]. 248 14

Correlative imaging by dual-isotope thallium/technetium subtraction scintigraphy, computed tomography, and magnetic resonance imaging demonstrated a pathologically proven parathyroid adenoma in a 62-year-old man with known neurofibromatosis, who presented with hypercalcemia and an elevated parathormone level. The association between neurofibromatosis and primary hyperparathyroidism is discussed.
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PMID:Parathyroid adenoma associated with neurofibromatosis: correlative scintigraphic and magnetic resonance imaging. 250 Feb 92

This study evaluates the use of calcium carbonate in chronic renal failure. Forty-eight patients (25 male, 23 female, mean age 54.3 years, six pre-dialysis. 12 CAPD, 30 haemodialysis) on phosphate restriction and requiring aluminum hydroxide (mean 2.4 +/- 0.8 g/day) to control serum phosphate, were converted to an equivalent dose of calcium carbonate (2.5 +/- 0.6 g/day). None received vitamin D analogues. Three months post-conversion there was a significant decrease in mean (+/- SEM) serum phosphate (1.86 +/- 0.08 versus 1.66 +/- 0.05 mmol/l P less than 0.01) and serum aluminum (28.3 +/- 5.4 versus 13.2 +/- 3.0 micrograms/l, P less than 0.0001): calcium/phosphate product was unchanged. Post-conversion there was an increase in serum bicarbonate, (20.6 +/- 0.5 versus 22.1 +/- 0.6 mmol/l, P less than 0.01) and serum calcium (2.32 +/- 0.02 versus 2.45 +/- 0.03 mmol/l, P less than 0.0001). No change in serum creatinine, alkaline phosphatase or parathormone occurred. No adverse effects were reported but nine (18%) patients became hypercalcaemic (2.7 to 2.93 mmol/l), eight of whom responded to dose reduction. Hypercalcaemia did not correlate with pre-conversion serum calcium, parathyroid hormone, alkaline phosphatase or aluminium. Calcium carbonate is an effective alternative to aluminium-based phosphate binders. It produces a beneficial increase in serum calcium and bicarbonate and a significant decrease in serum aluminium. Hypercalcaemia is unpredictable but is easily reversible in the majority of patients.
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PMID:The use of calcium carbonate to treat the hyperphosphataemia of chronic renal failure. 251 82

Persistent or recurrent hyperparathyroidism in patients with chronic renal failure may be a frustrating problem. We report a case history of a peritoneal dialysis patient who underwent total parathyroidectomy with autotransplantation for secondary hyperparathyroidism, developed tertiary hyperparathyroidism, and in an attempt to control hypercalcemia underwent seven partial resections of the autotransplant. Subsequently, a total excision of the parathyroid autograft was performed, but the patient continued to have hyperparathyroidism and unexpectedly was found to have a hyperplastic fifth parathyroid gland identified by thallium-technetium subtraction scan. The fifth gland was removed, and a part was implanted in the right forearm; however, the autoimplant had to be completely removed because of rapidly developing hypercalcemia. Hypercalcemia was controlled, but elevated levels of parathormone persisted. Remaining parathyroid tissue could not be found.
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PMID:Diagnostic dilemma of an unsuspected hyperfunctioning accessory parathyroid gland after total parathyroidectomy with autotransplantation in a peritoneal dialysis patient. 255 22

Six cases of primary hyperparathyroidism due to hyperfunctioning intrathyroidal parathyroid glands are reported. In five cases, hyperparathyroidism was due to an intrathyroidal parathyroid adenoma; in the sixth case, hyperparathyroidism resulted from an intrathyroidal parathyroid carcinoma. All five patients with adenoma were female with ages ranging from 40 to 70 yr. The patient with carcinoma was a 55-yr-old male. In all five patients with intrathyroidal parathyroid adenoma, thyroidectomy was performed when an abnormal parathyroid gland could not be located in the neck during surgery for hyperparathyroidism. The patient with intrathyroidal parathyroid carcinoma presented with hypercalcemia and a palpable right thyroid mass. The differential diagnosis of intrathyroidal parathyroid adenoma includes thyroid follicular adenoma. In some cases, the possibility of medullary carcinoma of thyroid might also be considered. Immunocytochemical staining for parathormone (PTH), thyroglobulin, and calcitonin is valuable in establishing the correct diagnosis.
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PMID:The intrathyroidal hyperfunctioning parathyroid gland. 258 70

In a chance observation, a 74-year-old woman was found to have hypercalcaemia (3.0 mmol/l) and multiple skeletal osteolyses. A diagnosis of multiple myeloma was made after the demonstration of paraproteins in serum (IgG-kappa) and a 10% proportion of plasma cells in a pelvic crest biopsy. Oral chemotherapy with melphalan and prednisone failed to alter the calcium level. Simultaneous increase in alkaline phosphatase and reduction in serum phosphate concentration led to further tests: determination of peripheral venous parathormone concentration, ultrasound examination of the neck, thallium-technetium subtraction scintigraphy and selective venous parathormone measurements. The results demonstrated the coexistence of primary hyperparathyroidism. The calcium level became normal after surgical removal of a parathyroid adenoma.
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PMID:[Hypercalcemia in coexistent parathyroid adenoma and multiple myeloma. Problems of differential diagnosis]. 266 81

We studied the effects of acute modifications in plasma calcium on parathormone (PTH) secretion in 23 patients with primary hyperparathyroidism (PHPT). In 12 patients, PTH hypersecretion was autonomous, and basal plasma calcium concentration was positively correlated with maximal serum PTH(1-84) reached during Na2EDTA infusions. In 11 patients, PTH hypersecretion remained suppressible, but with elevated set point value, and basal plasma calcium concentration was positively correlated with set point. Thus, the degree of hypercalcemia seems mainly determined by the magnitude of maximal PTH secretion and set point error in autonomous and suppressible PHPT, respectively. We have previously suggested that high serum calcitriol levels might chronically inhibit PTH hypersecretion in PHPT. We showed that hyperparathyroid patients with renal stone presentation exhibited an abnormally high value of circulating calcitriol and a moderately elevated PTH activity, while patients with severe bone disease presentation displayed a low to normal calcitriol value and a dramatically increased PTH activity. The hypothesis was supported by a recent study from our Unit in one hyperparathyroid patient with severe bone disease and normal serum calcitriol level. Increment of serum calcitriol after daily intravenous Rocaltrol for 5 days directly suppressed PTH hypersecretion without change in plasma ionized calcium.
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PMID:Determinants of parathormone secretion in primary hyperparathyroidism. 269 19


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