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Query: UMLS:C0153690 (bone metastases)
 6,382 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case of hypercalcemia secondary to metastasis to a benign parathyroid adenoma is reported. The patient had documented lung adenocarcinoma with multiple bone metastases and a mass in the lower anterior neck for at least 5 months before hypercalcemia and hypophosphatemia resistant to treatment developed. Autopsy revealed widespread metastatic disease including metastatic tumor invading a benign parathyroid adenoma. The analysis of four cases of metastatic cancer spread to a benign parathyroid adenoma reported previously revealed that two of them also had hypercalcemia during a late stage of the disease. There are data that the incidence of metastases to parathyroid gland might be as high as 11.9%, and the incidence of parathyroid adenomas in patients with cancer is significantly higher than in controls. The metastases to benign parathyroid adenomas might be another mechanism of hypercalcemia of malignancy.
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PMID:A case of adenocarcinoma of the lung associated with a neck mass and hypercalcemia. 191 81

Hypercalcemia is one of the most serious metabolic disorders associated with cancer. The incidence and clinical circumstances associated with hypercalcemia vary in different types of cancer. Hypercalcemia is the most frequent metabolic complication of breast cancer and is usually related to widespread osteolytic metastases; however, local and systemic humoral factors mediating bone resorption have been described. In some patients with breast cancer, hypercalcemia results from treatment with estrogens, antiestrogens, androgens, or progestins. Coexisting primary hyperparathyroidism rarely confounds the diagnosis. In patients with lung cancer, the incidence of hypercalcemia varies with histology and is often unrelated to bone metastases. Hypercalcemia may occur either late or early in the disease but is seldom a presenting symptom. In patients with cancers of the head and neck region, hypercalcemia is most often associated with advanced recurrent and terminal disease, presumably humorally mediated. In renal cell carcinoma, hypercalcemia is also an adverse prognostic indicator, commonly mediated by humoral factors. On the other hand, almost all patients with multiple myeloma have extensive osteolytic bone destruction and hypercalcemia is frequently a presenting symptom. Hypercalcemia is uncommon in most lymphomas; however, it is usually a prominent feature of adult T-cell lymphomas and also occurs in some large cell, diffuse B-cell lymphomas. Awareness of the setting in which hypercalcemia of malignancy occurs will lead to its prompt diagnosis and institution of appropriate therapy.
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PMID:Overview of cancer-related hypercalcemia: epidemiology and etiology. 218 51

Serum bone GLA-protein, a modern and sensitive marker of bone turnover, was measured in 15 patients with primary hyperparathyroidism, 18 patients with hypercalcemia of malignancy, 41 patients with bone metastasis without hypercalcemia, and 29 healthy subjects. Serum bone GLA-protein was increased in primary hyperparathyroidism (17.6 +/- 3.9 ng/ml) and normal in hypercalcemia of malignancy (5.2 +/- 2.8 ng/ml; p less than 0.001 vs hyperparathyroidism) and in normocalcemic patients with bone metastases. In primary hyperparathyroidism parathyroid hormone correlated positively with urinary calcium excretion (p less than 0.05) and with urinary hydroxyproline excretion (p less than 0.001). The sensitivity of serum bone GLA-protein measurements in differentiating between primary hyperparathyroidism and hypercalcemia of malignancy was 91% and the specificity 84%. Thus this marker appears to be a useful tool for the differential diagnosis of hypercalcemias.
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PMID:Serum bone GLA-protein in hypercalcemia of primary hyperparathyroidism and malignancy. 232 Dec 72

A class of drugs called diphosphonates have been used for several years in benign disorders of ossification such as Paget disease. Recently, these compounds have been applied to treating hypercalcemia of malignancy and painful bone metastases. We have used one of the oral diphosphonates, etidronate disodium, to palliate pain in 12 patients suffering from multiple bone metastases from prostate cancer. All of the patients had progressive metastatic disease following earlier endocrine therapy. Ten of 12 (83%) patients had a positive subjective and clinical response to treatment with oral etidronate disodium. Daily narcotic usage and pain intensity (measured by a zero to 10 pain scale) both decreased significantly on the etidronate protocol. There were no side effects associated with the drug in our patients.
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PMID:Treatment of painful prostatic bone metastases with oral etidronate disodium. 246 Sep 88

Hypercalcaemia in malignancy is a major clinical problem. It contributes significantly to morbidity and mortality and can present difficult diagnostic and management dilemmas. Direct bony invasion by tumour cells rather than humorally mediated hypercalcaemia is probably the most common cause of malignant hypercalcaemia. Yet even in this situation the mechanism of bone resorption or the reason that the normal homeostatic mechanisms cannot cope with the calcium load are poorly understood. It is likely that the humoral and paracrine factors produced by tumours which result in hypercalcaemia or in osteosclerotic bone metastases, are interposing themselves into the normal regulatory processes and deranging them. Humoral hypercalcaemia of malignancy is an important model for studying these questions, and it also provides some insight into the normal regulation of bone turnover. This review will examine the animal models and human syndromes of malignant hypercalcaemia and show how animal models, although helpful, fail to delineate the relative importance of the various potential humoral factors. A most interesting recent development in this area is the description of a new hormone, the parathyroid hormone-related peptide, which may explain many of the cases of humoral hypercalcaemia of malignancy. It is also a useful model with multiple sites of action within the bone and calcium homeostatic process. The active hormonal form of vitamin D3, 1,25-dihydroxyvitamin D3, may also be involved in a small proportion of cases, but again it is a useful model of some of the factors that may operate. Of considerable interest are the tumour derived factors, such as the transforming growth factors, and the cytokines, such as tumour necrosis factors, interleukins, and haemopoietic colony stimulating factors. Prostanoids are seldom of major importance, but may be important in certain tumour types. Osteosclerotic metastases, although seldom associated with hypercalcaemia, may provide insight into osteoblast regulating factors. Treatment of hypercalcaemia is discussed to show ways in which response to treatment may shed light on underlying pathophysiological mechanisms. Most effective treatments have many potential modes of action, and further study of the interactions of these agents and tumour types may help to unravel some of the enigmas in this human syndrome. The major advances in this complex problem involve the realisation of the necessity of multiple sites of action, including renal calcium handling as well as relative increases in bone resorption and/or intestinal calcium absorption.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypercalcaemia of malignancy. 266 84

Hypercalcemia is a common and serious complication of neoplastic disease. It may occur in association with a variety of tumors and usually indicates a lack of tumor control. Early symptoms are nonspecific, involving several organ systems in a syndrome that may progress rapidly to death. The pathophysiology of hypercalcemia is complex and not fully understood. Research continues on local mechanisms of bone destruction at sites of bone metastases and the identification of humoral tumor-derived osteolytic factors. The therapeutic approach to hypercalcemia should be sequential, dictated more by clinical symptoms than by absolute calcium levels. The diversity of measures and agents used in the therapy of hypercalcemia of malignancy reflects the multiple mechanisms involved. The therapeutic maneuvers outlined usually yield temporary success and must be accompanied by specific antitumor therapy, the ultimate treatment for the hypercalcemia of neoplastic disease.
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PMID:Hypercalcemia in malignant disease. 676 Sep 66

Hypercalcemia of malignancy is most commonly due to the effects of parathyroid hormone-related peptide, which acts as a humoral factor to cause generalized osteoclast-mediated bone resorption and reabsorption of calcium by the kidney tubule, and may also act as a local resorptive factor adjacent to bone metastases. Local resorptive mechanisms are less common causes of malignant hypercalcemia than previously believed. Treatment begins with intravenous fluid rehydration, followed by a furosemide diuresis and the bisphosphonate pamidronate, 60-90 mg, intravenously. Gallium nitrate is an efficacious but inconvenient alternative to pamidronate. Calcitonin combined with pamidronate is a reasonable initial therapy for severe hypercalcemia to hasten normalization of the serum calcium. Steroids should be reserved for hypercalcemia due to tumor production of 1,25 dihydroxyvitamin D, or for steroid-responsive malignancies. Oral or parenteral bisphosphonates can be used to maintain normocalcemia. In addition to improving the morbidity of acute hypercalcemia, bisphosphonate therapy has been shown to reduce bone pain and pathological fractures in patients with bone metastases, and calcitonin also has a potent analgesic effect in these patients. Treatment for hypercalcemia should therefore be considered in the majority of patients in the palliative care setting.
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PMID:Hypercalcemia of malignancy in the palliative care patient: a treatment strategy. 754 27

Hypercalcemia is the most common paraneoplastic syndrome associated with cancer. This paper addresses the etiology and pathogenesis of hypercalcemia of malignancy and discusses the relative contributions of local and humoral effects on bone and renal calcium homeostasis. The roles of parathyroid hormone-related protein and other osteolytic cytokines are outlined. New biochemical markers that enable more specific monitoring of the response of bone metastases to treatment are introduced, including urinary excretion of the collagen crosslinks pyridinoline and deoxypyridinoline. The clinical management and prevention of hypercalcemia is systemically outlined, including indications for bisphosphonate, glucocorticoid, and calcitonin therapy. The results of recent trials of bisphosphonate therapy for the prevention of tumor progression and its subsequent problems such as bone pain, fracture, and hypercalcemia also are discussed.
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PMID:Hypercalcemia and bone resorption in malignancy. 763 18

Hypercalcemia of malignancy is due either to local osteolysis at the site of bone metastases or to production by the malignancy of parathyroid hormone-related peptide, which shares some of the effects of parathyroid hormone. We used a radioimmunoassay (antiserum specific to the amino-terminus) to measure serum parathyroid hormone-related peptide levels in controls (n = 61), chronic renal failure patients (n = 10), patients with primary hyperparathyroidism (n = 19), cancer patients with (n = 35) or without (n = 57) hypercalcemia and/or bone metastases (n = 53 and n = 39, respectively), and patients with hematologic malignancies (n = 15). We set the upper limit of normal of the parathyroid hormone-related peptide assay at 2.7 pmol/L. The peptide was undetectable in two-thirds of healthy controls. Renal failure did not interfere with the assay. Eighteen of the 19 patients with primary hyperparathyroidism had normal levels. In contrast, 82% of patients with humoral hypercalcemia of malignancy (i.e., without detectable bone metastases) had increased levels; in this subgroup there was a significant inverse correlation between serum levels of the peptide and phosphorus. Elevation of parathyroid hormone-related peptide levels was less common among hypercalcemic patients with metastatic bone disease (38%). Four of the seven hypercalcemic patients with hematologic malignancies had elevated parathyroid hormone-related peptide levels. In our overall study population, serum calcium levels were weakly but significantly correlated with parathyroid hormone-related peptide levels. In conclusion, elevated parathyroid hormone-related peptide in a patient with hypercalcemia suggests a malignant disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of parathyroid hormone-related peptide to the evaluation of hypercalcemia. 778 31

The development of bone metastases is a selective process in which the hematogenous dissemination of tumor cells into the bone marrow does not play a decisive role. In addition to the peculiarities of blood flow within the marrow sinuses, leading to an accumulation of circulating tumor cells, host organ specific factors (adhesion molecules, chemotactic signals, cytokines and growth factors) are pathogenetically involved. These factors are liberated from the bone matrix by osteoclasts, which are activated by a variety of osteotropic tumor factors. Thereby a tumor osteopathy develops, which by osteolytic bone destruction and tumor-enhanced remodelling may cause bone pain, pathological fractures and hypercalcemia of malignancy. So far only the late stage of macrometastases and the concomitant osteopathy can be diagnosed. Using immunocytological methods, tumor cells can now be detected in bone marrow aspirates during the early subclinical stage of tumor cell shedding. Tumor cell-positive bone marrow aspirates in general mean a worsening of the prognosis and may in breast cancer indicate those patients who are threatened by the development of bone metastases.
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PMID:[Pathogenesis of bone metastasis and tumor osteopathies]. 789 37


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