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

Hypercalcemia with and without clinical manifestation appears to be diagnosed with increasing frequency. If hypercalcemia persists with no other obvious reasons, hyperparathyroidism can be suspected with a high degree of certainty. Surgical treatment requires confidence, patience and a thorough knowledge of the embryologic peculiarities and anatomic variations of these glands. In 88 percent of our 71 patients, a solitary benign parathyroid adenoma was diagnosed by light microscopy. Parathyroid four-gland hyperplasia was found in 5.6 percent of the patients and multiple adenoma in 3 percent. The cause of hypercalcemia was not found in 3 percent. All patients treated with parathyroidectomy responded well, with calcium levels returning to normal. Our results confirm that this conservative approach to parathyroidectomy without multiple gland biopsy is the better and more acceptable method of dealing with hyperparathyroidism. Multiple gland dissection biopsy, chest exploration and parathyroid implantation are necessary only in very difficult cases.
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PMID:Hyperparathyroidism. A review. 746 14

Five young patients with primary hyperparathyroidism were treated in our hospital. Male to female ratio was 3 to 2 and the mean age was 12.2 years old. Hypercalcemia due to a single adenoma of the parathyroid gland was found in all cases. They showed various clinical symptoms, such as abdominal pain, nausea, convulsions and disturbance of walking. Parathyroid tumors usually could be easily identified with ultrasonography or CT scan or thyroid subtraction scintigraphy. But in two cases parathyroid tumor was not found during operation. Angiography and/or venous sampling were performed and they showed the right localization.
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PMID:[Primary hyperparathyroidism in young patients]. 775 82

Parathyroid crisis is an unusual form of primary hyperparathyroidism characterized by life-threatening hypercalcemia. We encountered nine patients with primary hyperparathyroidism, who showed various clinical symptoms including psychoneurotic symptoms, as a result of marked hypercalcemia. The average age of the patients was 49 (29 to 77), with an even distribution between men and women. Marked hypercalcemia (16.1 +/- 2.0 mg/dl) was accompanied by high levels of parathyroid hormone. Physiological saline solution, furosemide and calcitonin were administered to the nine patients for ten to thirty-fore days, respectively, in order to correct hypercalcemia and dehydration, and then parathyroidectomy was performed. Postoperative courses were uneventful, and the psychoneurotic symptoms improved markedly. No renal or cardiac dysfunction was observed. Since surgery (parathyroidectomy) is effective for the present condition, it seems important to quickly relieve dehydration and to operate early rather than to offer prolonged treatment by medication.
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PMID:[Parathyroid crisis]. 775 86

Generalized parathyroid hyperplasia with superimposed clonal tumor growth is the most frequent expression of the MEN 1 trait and must be corrected surgically. The Zollinger-Ellison syndrome is an indication for early and aggressive control of hypercalcemia. If gastrin secretion is normal, early parathyroid surgery is usually not required; and to delay the operation will facilitate location of all parathyroid glands, a requisite for successful surgery. The best surgical approach is an extensive primary dissection including thymectomy, followed by total parathyroidectomy with autogenous parathyroid grafting. Parathyroid disease in MEN 2 is less frequent and of later onset. It usually takes secondary consideration to the cure of the C-cell neoplasm. Several other less common hereditary syndromes with parathyroid involvement are reviewed.
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PMID:Management of hyperparathyroidism in the multiple endocrine neoplasia syndromes and other familial endocrinopathies. 791 26

Parathyroid crisis occurring in primary hyperparathyroidism is characterized by extremely high circulating levels of parathyroid hormone and acute onset of severe hypercalcemia. We describe a 62-year-old woman with parathyroid crisis probably due to an intratumoral hemorrhage. Renal dysfunction reduced the effectiveness of preoperative management and continued to deteriorate for 5 days after parathyroidectomy. The normalization of serum calcium after parathyroidectomy delayed and it took 6 days. Maintenance of renal function is important for pre- and postoperative courses of the present case. The rapid decrease in serum parathyroid hormone after parathyroidectomy was followed by a rapid and transient (about fivefold) increase in serum alkaline phosphatase with peak value on the 10th postoperative day. This indicated that reversal phase from bone resorption (accelerated by parathyroid hormone) to bone formation lasted about 10 days under the conditions of the present case.
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PMID:The time course of renal function and bone turnover in parathyroid crisis due to intratumoral hemorrhage. 795 Jan 56

Ca2+ binds to a parathyroid cell Ca2+ receptor, which is G protein-coupled and activates inositol triphosphate production. Mutations in the Ca(2+)-sensing receptor gene cause familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism. Chronic hypocalcemia increases parathyroid hormone messenger RNA levels and parathyroid cell hyperplasia. Parathyroid cells in vitro are heterologous in their response to Ca2+. The concept of a higher Ca2+ set-point in secondary hyperparathyroidism is controversial. Calcitriol is more effective than the less hypercalcemia analogues in decreasing parathyroid hormone messenger RNA and immunoreactive parathyroid hormone levels, and its kinetics are well established. Phosphate and estrogens regulate the parathyroid independently of 1,25 dihydroxyvitamin D3 and Ca2+. The physiology of the effects of endothelin and insulin-like growth factors on the parathyroid need to be established. Important advances are being made in understanding the regulation of parathyroid hormone synthesis and secretion, which are relevant to both normal physiology and the pathogenesis and treatment of diseases such as the secondary hyperparathyroidism of renal failure and osteoporosis.
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PMID:New aspects in the control of parathyroid hormone secretion. 807 41

Tumor-induced hypercalcemia (TIH) and tumor-induced osteolysis (TIO) are essentially due to a marked increase in osteoclast-mediated bone resorption. Parathyroid-hormone-like protein plays an essential role in TIH, and maybe in TIO, but other substances, such as growth factors or cytokines, could contribute to the osteoclast activation and osteoblast inhibition secondary to the neoplastic infiltration of the skeleton. Treatment of TIH essentially consists of volume repletion and administration of potent anti-osteolytic drugs. Intravenous administration of the bisphosphonate clodronate or pamidronate is particularly useful for this. Pamidronate at a dose of 1.0-1.5 mg/kg as a single 4- to 24-h infusion can normalize serum calcium in about 90% of hypercalcemic cancer patients. The apparently low response rate of bone metastases to systemic antineoplastic therapy seems essentially to reflect the relative insensitivity of our current methods for assessing response in TIO. Quantitative evaluation of pain and of newly developed biochemical markers of bone turnover could be particularly useful for early assessment of response. Prolonged administration of oral pamidronate could reduce by almost one-half the complications of TIO, and iterative bisphosphonate infusions could induce a dramatic relief of bone pain in one-third and a sclerosis of lytic lesions in one-fourth of the cases. These data must, however, be confirmed in randomized blind trials and many questions remain unanswered concerning the optimal therapeutic schemes. Despite these limitations, medical therapy of TIO by non-cytotoxic means has already become a reality.
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PMID:Medical treatment of tumor-induced hypercalcemia and tumor-induced osteolysis: challenges for future research. 814 98

Both intermittent intravenous and intermittent oral calcitriol have been shown to be effective in the treatment of secondary hyperparathyroidism in hemodialysis patients and it has been claimed that intravenous calcitriol causes less hypercalcemia. However, there has been no published systematic comparison of the two routes of administration of intermittent calcitriol. Therefore in a prospective crossover study 11 (9 male) patients on maintenance hemodialysis were randomized to receive intravenous followed by oral calcitriol for 4 months each, or oral followed by intravenous calcitriol, commencing at 2 micrograms postdialysis three times per week. Initial serum immunoreactive parathyroid hormone (PTH) was 446 +/- 111 (normal < 65) pg/ml. Calcium-containing phosphate binders were not used. Calcitriol was ceased if hypercalcemia developed and restarted at 2 micrograms or 1 microgram when calcium returned to normal. Hypercalcemia was frequent (11 episodes in 8 patients on intravenous calcitriol and 10 episodes in 7 patients on oral calcitriol) and dose reduction to 1 microgram was necessary in 7 patients on intravenous and on 6 patients on oral. Serum PTH fell during both treatments. Parathyroid enlargement was seen in 10 glands from 4 patients, but no size reduction was demonstrated with treatment. There was no reduction in activity on quantitative metabolic bone scan. In summary, intermittent oral calcitriol and intermittent intravenous calcitriol were equally effective in reducing serum parathyroid hormone levels and at a dose of 2 micrograms postdialysis caused hypercalcemia with equal frequency.
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PMID:Comparison of intermittent oral and intravenous calcitriol in hemodialysis patients with secondary hyperparathyroidism. 826 78

Parathyroid-hormone-related protein (PTHrP) has significant homology with parathyroid hormone (PTH) in the amino-terminal region. We compared the effects of synthetic human PTHrP [hPTHrP(1-34)] on Na(+)-dependent phosphate transport with those of synthetic human PTH [hPTH(1-34)]. Intravenous administration of hPTHrP(1-34) in parathyroidectomized rats caused hypercalcemia, hypophosphatemia and phosphaturia to the same degree as hPTH(1-34). In kinetic studies using renal brush border membrane vesicles, the apparent Km and Vmax of phosphate transport were identical for the two peptides [hPTHrP(1-34): Km 27.6 +/- 0.8 microM, Vmax 3.78 +/- 0.04 nmol/mg protein, hPTH(1-34): Km 29.6 +/- 0.9 microM, Vmax 3.04 +/- 0.90 nmol/mg protein]. Both hPTHrP(1-34) and hPTH(1-34) at a supramaximal dose were equipotent in eliciting a 12-fold increase in cyclic adenosine 3',5'-monophosphate (cAMP) production in the kidney. These results indicate that, in addition to the similar effect of hPTHrP(1-34) and hPTH(1-34) on serum calcium levels and urinary phosphorus and nephrogenous cAMP excretion in vivo, these two peptides have similar effects of Na(+)-dependent phosphate transport in brush border membrane vesicles in vitro.
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PMID:Effect of parathyroid-hormone-related protein on sodium-dependent phosphate transport in renal brush border membrane vesicles in rats. Comparison with parathyroid hormone. 836 86

Parathyroid-like protein (PLP), or parathyroid hormone-related peptide, is a well-recognized mediator of paraneoplastic hypercalcemia (humoral hypercalcemia of malignancy syndrome). In this study we examined the expression of PLP by 40 invasive squamous cell carcinomas (SCCs) of the cervix and selected carcinomas of nonsquamous histology. Using a polyclonal antibody to human PLP, 93% of SCCs, including two tumors from patients with humoral hypercalcemia of malignancy syndrome, showed moderate to strong cytoplasmic immunoperoxidase staining for PLP. The strongest staining often was observed in areas of invasion associated with stromal desmoplasia. The small number of weak or negatively stained SCCs were all poorly differentiated tumors. Although native uninvolved squamous epithelium showed weak to moderate staining of the superficial layers, there was variable or full-thickness immunostaining in areas of dysplasia. Normal endocervical glands and stroma as well as cervical adenocarcinomas and neuroendocrine carcinomas were negative. In situ hybridization studies showed abundant PLP mRNA within SCC in patients with hypercalcemia. However, PLP mRNA was of relatively low abundance in tumors of normocalcemic patients. Ultrastructural studies showed cytoplasmic, membrane-bound, granular inclusions in tumor cells from the hypercalcemic patients. Our data suggest that increased PLP gene transcription contributes to the increased production of PLP and the pathogenesis of humoral hypercalcemia of malignancy syndrome.
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PMID:In situ localization of parathyroid hormone-like protein and mRNA in intraepithelial neoplasia and invasive carcinoma of the uterine cervix. 840 15


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