Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypercalcemic crisis or severe hypercalcemia represents a life-threatening emergency. The most common cause is hypercalcemia of malignancy, although granulomatous diseases, previously undetected primary hyperparathyroidism, medication-induced hypercalcemia, and a few rarer causes may result in this endocrine emergency as well. The clinical presentation and prognosis depend on the acuity of the development of hypercalcemia, the degree of hypercalcemia, and the underlying cause. Certainly, patients with malignancy who develop hypercalcemia superimposed on their already debilitated state are more likely to have a poor outcome than a previously relatively healthy patient with thiazide-induced hypercalcemia, for example. The clinical presentation of patients with hypercalcemic crisis varies depending once again on the underlying cause and degree and rapidity of the hypercalcemia. Most patients experience some constitutional symptoms, neurologic symptoms, gastrointestinal symptoms, and renal manifestations of hypercalcemia. Immediate and effective therapy directed toward the pathophysiology of hypercalcemia is essential. General measures must be implemented to reverse the dehydration, to promote urinary calcium excretion, to avoid prolonged immobilization, and to identify the underlying cause of hypercalcemia. Specific measures directed at inhibiting bone resorption, increasing renal sodium and calcium excretion, and occasionally at decreasing intestinal absorption of calcium (or more specifically blocking vitamin D metabolism) should also be implemented. Obviously the more reversible the underlying cause of hypercalcemia, the more aggressive one should be with the therapy. The literature was reviewed to compile comparative data that practitioners may use in choosing among the various pharmacologic therapies available for the treatment of acute hypercalcemia. Despite all the advances in the field, hypercalcemic crisis still carries a significant mortality risk, although with appropriate therapy with the aforementioned general and specific measures, the calcium level can effectively be lowered in most patients.
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PMID:Hypercalcemic crisis. 780 96

Milk-alkali syndrome can be caused by ingesting large amounts of calcium carbonate. Coincident with the promotion of calcium carbonate as treatment for both dyspepsia and osteoporosis, milk-alkali syndrome is now a common cause of hypercalcemia severe enough to require admission to the hospital. The syndrome accounted for less than 2% of such admissions before 1990, but from 1990 through 1993, it was the cause of hypercalcemia for over 12% of these patients. Only primary hyperparathyroidism and hypercalcemia of malignancy (excluding multiple myeloma) are more common. The diagnosis of milk-alkali syndrome is made almost entirely based on the patient's history; careful attention to dietary practices and over-the-counter drug use is required, as numerous over-the-counter medications contain calcium carbonate. Modern assays for PTH demonstrate the expected suppression of PTH by hypercalcemia. Nonetheless, measurement of PTH must be performed in a timely manner as treatment with intravenous saline may result in hypocalcemia and elevated PTH soon after admission. Given the pathophysiology of milk-alkali syndrome compared to other causes of hypercalcemia, hypocalcemia with rebound hyperparathyroidism is probably unique to milk-alkali syndrome.
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PMID:Milk-alkali syndrome associated with calcium carbonate consumption. Report of 7 patients with parathyroid hormone levels and an estimate of prevalence among patients hospitalized with hypercalcemia. 789 47

We have treated 30 patients with hypercalcemia from 1984 to 1991. Twenty four out of 30 patients were associated with primary hyperparathyroidism and the other six were associated with malignancy. Of 24 cases primary hyperparathyroidism, 15 were due to single parathyroid adenoma, five to MEN 1 and one to familial hyperparathyroidism. In the other three cases, it was difficult to identify the cause of the hyperparathyroidism. Following conclusions were obtained: 1. Hypercalcemia shows no specific and characteristic symptoms, so it is essential to keep hypercalcemia in mind in diagnosis of patients with vague or general complaints. Malignancy associated hypercalcemia shows high serum calcium level and PTH level. When considering malignancy, it is easy to diagnose that it might be the cause of hypercalcemia. 2. When serum PTH is over 2000pg/ml (high sensitivity PTH assay) in primary hyperparathyroidism, the probability of swelling of multiple parathyroid glands should be considered in evaluation of localization study and surgery. When serum PTH is high or swelling of multiple glands is found. It is essential to evaluate the possibility of MEN 1.
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PMID:[Analysis of 30 patients with hypercalcemia]. 790 47

Hypercalcemia is most commonly associated with primary hyperparathyroidism and malignancy due to parathyroid hormone-related protein (PTHrP). Primary hyperparathyroidism is characterized by excessive secretion of parathyroid hormone in association with hypercalcemia. The modern presentation of primary hyperparathyroidism is as an asymptomatic disorder. Diagnostic tools such as bone mineral densitometry, bone histomorphometry, and the measurement of markers of bone turnover, as well as other clinical assessments, have all led to the development of guidelines to help direct decisions for parathyroid surgery or for medical management. Hypercalcemia of malignancy is often distinguishable from primary hyperparathyroidism by the presence of an obvious tumor. Primary hyperparathyroidism is excluded by the immunoradiometric assay for parathyroid hormone, which is suppressed. A number of clinical characteristics of hypercalcemia of malignancy can be explained on the basis of the tumor product, PTHrP, which directly causes hypercalcemia in many cases. Assays for PTHrP show elevated levels in patients in whom hypercalcemia is associated with the classic syndrome. Recent recognition that PTHrP is found ubiquitously in virtually all normal tissues and that it is possibly involved in a number of normal physiologic processes, apart from its pathologic role, provides an exciting basis for future research.
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PMID:Primary hyperparathyroidism and parathyroid hormone-related protein. 806 Jul 69

A radioimmunoassay for circulating levels of the pyridinoline cross-linked carboxy-terminal telopeptide of type 1 collagen (1CTP) was developed and can be available as a kit on a commercial base. Using the kits, we evaluated basically and clinically the assay. The assayed values were reproducible and the assay can detect as low as 0.5 ng/ml of 1CTP. In healthy volunteers, circulating level was high under age 24 and over age 46. In patients with bone metastasis, serum levels elevated even in its early stage and correlated well with clinical status. In other bone diseases, such as primary hyperparathyroidism, hyperthyroidism, post-gastrectomy, hypercalcemia of malignancy and myeloma, serum levels elevated according to their clinical conditions. In patients with chronic renal failure, serum levels were high, suggesting decrease of renal clearance of 1CTP. The circulating 1CTP levels seemed to reflect well clinical bone destructive status. A high correlation between serum 1CTP level and urinary pyridinoline (r = 0.884) was shown, whereas essentially no correlation was observed between bone formation markers such as osteocalcin and alkaline phosphatase. Thus, the measurement of circulating 1CTP seems to be a simple and sensitive method to monitor bone destruction.
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PMID:[Radioimmunoassay for the pyridinoline cross-linked carboxy-terminal telopeptide of type 1 collagen (1CTP)--some basic aspects of the RIA kit and clinical evaluation in various bone diseases]. 827 4

The principal pathophysiologic alteration in severe hypercalcemia accompanying hyperparathyroidism and malignancy is enhanced osteoclastic bone resorption. Hypercalcemia impairs renal mechanisms that lead to sodium and calcium excretion; PTH and PTHrP acting on renal tubules enhance further calcium reabsorption. Although rehydration is often necessary as an initial therapy of hypercalcemia, the cornerstone of therapy is to inhibit osteoclastic bone resorption. The bisphosphonates, plicamycin, gallium, and calcitonin all inhibit osteoclastic bone resorption. Calcitonin is the most rapidly acting agent. Toxicities of calcitonin are minimal, yet its therapeutic efficacy is limited by lack of potency and tachyphylaxis. The second-generation bisphosphonates such as pamidronate represent a class of compounds that are extremely effective in inhibiting the metabolic function of the osteoclast. Given in a single infusion, a significant majority of patients will have normalization of corrected serum calcium lasting, on average, 1-2 weeks. Therapeutic benefit will be of greater duration because most patients remain only minimally symptomatic until corrected serum calcium rises above 11.5 mg/dL. Side effects of low-grade fever, hypophosphatemia, hypomagnesemia, and hypocalcemia may occur. Gallium nitrate is a potent inhibitor of bone resorption and may be of increased clinical value when more efficient administration protocols can be developed. Plicamycin, available for two decades, has cumulative toxicities and is less potent than the aminobisphosphonates. Renal insufficiency often accompanies severe hypercalcemia. The nephrotoxicity of gallium nitrate and plicamycin should preclude their use when there is moderate impairment of renal function, and amino bisphosphonates become the treatment of choice in these patients. Although several authors have advocated individualized approaches to the management of hypercalcemia, the potency and duration of action of the aminobisphosphonates make them a reasonable treatment choice for most patients with symptomatic hypercalcemia. Most importantly, the most effective therapy for hypercalcemia is to recognize and treat the underlying disease. Acute primary hyperparathyroidism requires surgery. The effective treatment of hypercalcemia of malignancy allows the introduction of tumor-specific therapy, limits morbidity, and shortens and deintensifies hospitalization. At times, the most appropriate and compassionate decision (particularly in patients with malignancy who have exhausted all therapeutic options and have relentless bone pain) is to withhold therapy for hypercalcemia. Future therapies directed at the osteoclast, such as more potent later-generation bisphosphonates; inhibitors of osteoclast attachments and inhibitors of peptides, which stimulate osteoclastic bone resorption, may permit safe, easily administered, outpatient therapies that will improve the quality of life for hypercalcemic patients.
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PMID:Pathophysiology and management of severe hypercalcemia. 832 91

Measurement of parathyroid hormone-related peptide (PTHrP) associated with that of parathyroid hormone, allows to establish, in most cases, diagnosis of hypercalcemia of malignancy and more exactly of patients with Malignancy Humoral Hypercalcemia (MHH). Because of the variety of molecular forms of PTHrP, linked to its catabolism, its immunoassay remains difficult. After a study evaluating the methodological reliability, we measured the contribution of PTHrP to the hypercalcemia by 2 assays: a N-terminal RIA and a 1-72 IRMA in samples from 47 control subjects, 10 patients with chronic renal failure (IRC), 13 patients with primary hyperparathyroidism (HPT), and 48 patients with solid tumors classified by their level of calcemia: 48 normocalcemia and 23 hypercalcemia. We noted a strong correlation (r = 0.92) between the two assays. They do not show increases in renal insufficiency; they have a good diagnostic discrimination between HPT, normal subjects and patients with MHH. Elevated levels of PTHrP are similar in both assays. However, IRMA appears to be more sensitive and more practical than RIA. Moreover, it shows the best correlation between serum calcium and phosphorus in patients with MHH.
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PMID:[Performances of two kits for parathyroid hormone-related peptide (PTHrP) assay in the additional study of malignant hypercalcemias]. 874 2

The bisphosphonates have been investigated over the past two decades for the treatment of various diseases of bone and calcium metabolism that are characterized by increased bone resorption, including osteoporosis, Paget's disease, primary hyperparathyroidism, hypercalcemia of malignancy and metastatic bone disease. The bisphosphonate alendronate was recently approved by the U.S. Food and Drug Administration as a therapy for postmenopausal osteoporosis. This agent is currently the bisphosphonate of choice for clinical use. In postmenopausal osteoporosis, alendronate has been shown to increase bone mineral density and to decrease the rate of new fractures. Adverse effects are not usually a problem when 10 mg per day of alendronate is given with at least 6 oz of water 30 minutes before ingestion of the first food or beverage of the day.
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PMID:Alendronate: a bisphosphonate for treatment of osteoporosis. 890 Mar 45

Double-phase parathyroid gland scintigraphy, using technetium Tc 99m sestamibi, correctly identified the existence and location of a parathyroid adenoma in a dog with primary hyperparathyroidism. The parathyroid adenoma was removed surgically 2 days after scintigraphy. An area of focal radionuclide uptake persisted in the region corresponding to the left external parathyroid gland in the delayed-phase image. Delayed-phase images from 3 healthy dogs and a dog with hypercalcemia of malignancy caused by lymphoma did not reveal an area of persistent radiotracer uptake. Double-phase parathyroid gland scintigraphy, using 99mTc-sestamibi, is a simple, rapid, noninvasive test, which can be used for detection and localization of parathyroid adenomas in hypercalcemic dogs. It also can help to differentiate these dogs from dogs with hypercalcemia of malignancy.
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PMID:Use of technetium Tc 99m sestamibi for detection of a parathyroid adenoma in a dog with primary hyperparathyroidism. 892 Oct 31

The purpose of the present study was to review the literature with respect to the prevalence of hypercalcaemia in normal and in hospital populations. Pertinent studies were selected from the MEDLINE database (1980 to March 1995) and through the bibliographies of selected articles. Hypercalcaemia is one of the most common metabolic disorders in malignant diseases and develops in 3-30% of such patients. Hypercalcaemia of malignancy is the most common cause of hypercalcaemia followed by primary hyperparathyroidism in hospital populations. The most common cause in normal populations is primary hyperparathyroidism followed by transient hypercalcaemia. The prevalence of hypercalcaemia shows a large variation in hospital populations ranging from 0.17% to 2.92%. The prevalence in normal populations varies between 1.07% and 3.9% and, surprisingly exceeds the level in hospital populations. The discrepancies between prevalences may be due to varying referral patterns, different distribution of specialities causing different hospital populations and different definitions of hypercalcaemia. Hypercalcaemia presents a diagnostic problem. The percentage of cases of hypercalcaemia that are actually diagnosed has been observed to be as low as 25% in hospitals, in which laboratory results remain unreported unless requested. But even when presented, 20-50% of the cases are overlooked.
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PMID:Prevalence of hypercalcaemia in normal and in hospital populations. 977 94


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