Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153690 (bone metastases)
 6,382 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostaglandin E concentrations were measured in a patiet with breast carcinoma, hypercalcemia, undetectable parathyroid hormone (PTH) and no evidence of bone metastases. Catheterization of the drainage bed of her tumor documented production of E series prostaglandins. Treatment with the largest recommended doses of indomethacin for 10 days failed to lower her plasma prostaglandin E (PGE) concentrations or to correct the hypercalcemia, but it normalized urinary excretion of PGE. Subsequent chemotherapy reduced prostaglandin concentrations toward normal values concomitant with a reduction of clinically estimated tumor burden. During this period of time, serum calcium concentrations had no consistent relationship to the plasma PGE levels. We suggest that PGE merely reflected the tumor burden of this patient and did not directly contribute to the genesis of her hypercalcemia. The pertinent literature relating PGE and hypercalcemia is reviewed.
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PMID:Prostaglandin E and hypercalcemia in breast carcinoma: only a tumor marker? A need for perspective. 21 52

Rapid differential diagnosis of hypercalcaemia due to primary hyperparathyroidism or malignancy with or without bone metastases may be life saving. A parathormone infusion test (6 USP units/kg body wt X 20 min) enables a differential diagnosis within three hours by means of measurement of renal calcium excretion. In normal persons calcium excretion decreased from 147 +/- 90 to 79 +/- 54 mumol/h (x +/- s, n = 10). In primary hyperparathyroidism with hypercalcaemia the high calcium excretion remained unchanged: 716 +/- 162 mumol/h before and 804 +/- 130 mumul/h 120 minutes after the PTH infusion (n = 12). In patients with hypercalcaemia caused by bronchial carcinoma with (n = 5) and without (n = 1) bone metastases calcium excretion decreased from 552 +/- 182 to 163 +/- 114 mumol/h. As a consequence of these data this test is advisable when the indication for operation in cases with hypercalcaemia has to be reached within a few hours.
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PMID:[Differential diagnosis of hypercalcaemia by measurement of renal calcium excretion during parathormone administration (author's transl)]. 49 90

Plasma calcium was measured routinely as a part of profile screening of patients admitted to a geriatric department. Pathological hypercalcaemia was found in 1.33% of those screened, the cause being bone metastases (29%), hyperparathyroidism (21%), bronchial carcinoma without bone metastasis (18.5%), lymphosarcoma without bone metastasis (8%) and multiple myeloma (2.5%). There remained a further group of patients with hypercalcaemia and renal failure (21%) in whom diagnosis was often obscure. Where renal function was normal, discriminant analysis showed that the four main diagnostic groups were biochemically distinguishable. Discriminant analysis thus seems likely to be of practical value in the differential diagnosis of hypercalcaemia in elderly patients with normal renal function, but requires prospective validation.
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PMID:Hypercalcaemia in elderly hospital in-patients: value of discriminant analysis in differential diagnosis. 57 68

Bone marrow acid phosphatase has been reported to be a sensitive indicator of early bony metastasis from adenocarcinoma of the prostate. In order to evaluate this hypothesis, we measured bone marrow acid and alkaline phosphatase, lactic dehydrogenase, and calcium levels in a group of 84 patients with a variety of problems, including 18 with cancer of the prostate. We found that the bone marrow acid and alkaline phosphatase and lactic dehydrogenase were elevated and calcium was depressed in most patients. Among patients with prostate cancer, bone marrow acid phosphatase was not significantly different between those with or without bone metastases. In addition, the patients with prostatic cancer did not have higher levels of bone marrow acid phosphatase than subjects with other malignant and nonmalignant conditions. The level of acid and alkaline phosphatase, lactic dehydrogenase and calcium varied predictably with the aspiration technique used and was independent of sex, disease state or method of chemical determination. Due to this variation, we believe that bone marrow enzyme and calcium levels are of no value in the detection of metastases in patients with prostate cancer.
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PMID:Lack of usefulness of bone marrow enzymes and calcium in staging patients with prostatic cancer. 63 3

A patient with known transitional cell carcinoma of the bladder and hypercalcemia was evaluated for urinary prostaglandin levels when no bone metastases or elevated parathormone levels could be demonstrated. Urinary levels of prostaglandin E metabolite were assessed in relation to serum and urinary calcium levels during treatment. The serum calcium levels decreased from the 13.0 mg. per cent range whenever the rpimary tumor was manipulated (transurethral resection) or when other treatments directed at the tumor were used (radiation therapy and chemotherapy). Serum and urinary calcium levels, and urinary prostaglandin E metabolite decreased when 3 gm. aspirin were given daily. These data suggest that the somewhat unusual hypercalcemia in our patient was caused by a prostaglandin-secreting transitional cell carcinoma. Prostaglandin-secreting tumors are reviewed herein.
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PMID:Prostaglandin-mediated hypercalcemia in transitional cell carcinoma of the bladder. 66 Jul 46

The effect of magnesium chloride or magnesium sulfate infusion on circulating levels of immunoreactive calcitonin (iCT) was evaluated on nine occasions in three patients with metastatic medullary carcinoma of the thyroid. One patient was normocalcemic and had normal circulating levels of immunoreactive parathyroid hormone (iPTH), one patient was hypocalcemic and had surgical hypoparathyroidism, and one patient had mild to moderate hypercalcemia associated with bone metastases. The basal serum iPTH levels were undetectable in the latter two patients. In every instance magnesium administration produced a rapid and striking fall in circulating iCT and usually a detectable fall in serum calcium. During the hypermagnesemic state, serum iPTH fell from normal to undetectable in the patient with normal parathyroid function, while serum iPTH levels remained undetectable in the hypoparathyroid patient and in the patient with hypercalcemia associated with bone metastases. The results of these studies indicate that: (a) contrary to what has been reported in normal experimental animals, magnesium administration lowers circulating iCT in human subjects with thyroid medullary carcinoma and (b) the calcium-lowering effect produced by magnesium in patients with medullary carcinoma may, in part at least, be due to a redistribution of body calcium that is not mediated by the actions of either parathyroid hormone or clacitonin.
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PMID:Serum calcitonin-lowering effect of magnesium in patients with medullary carcinoma of the thyroid. 120 87

In a double blind randomised multicentre study the effect of intravenous clodronate plus hydration was compared with placebo plus hydration in the treatment of hypercalcaemia in breast cancer patients with bone metastases. The patients were treated either with hydration plus clodronate 300 mg/day or hydration plus placebo, up to 7 days or until serum ionised calcium was below 1.4 mmol/l. 25 patients received clodronate and 19 placebo. A significant difference in favour of clodronate was observed in the time to reach normocalcaemia (P = 0.004) and in the number of patients achieving normocalcaemia (P = 0.0003). 17 patients of 21 evaluable patients on clodronate achieved normocalcaemia compared with 4 of 19 patients on placebo. The only adverse event clearly associated with clodronate was symptomatic hypocalcaemia in 1 patient. Thus, clodronate seems to be a safe and highly efficacious drug for the treatment of hypercalcaemia in breast cancer patients.
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PMID:Intravenous clodronate for the treatment of hypercalcaemia in breast cancer patients with bone metastases--a prospective randomised placebo-controlled multicentre study. 138 38

Tumor-induced hypercalcemia and tumor-induced osteolysis are essentially due to a marked increase in osteoclast-mediated bone resorption, although the kidneys play an important contributory role in the genesis of tumor-induced hypercalcemia. Parathyroid hormone-like protein plays an essential role in tumor-induced hypercalcemia, and maybe in tumor-induced osteolysis, but other factors could also be responsible for the osteoclast activation secondary to the neoplastic infiltration of the skeleton. Treatment of tumor-induced hypercalcemia essentially consists of volume repletion and administration of potent anti-osteolytic drugs. The bisphosphonate pamidronate is particularly useful for that matter and a dose of 1.0 to 1.5 mg/kg can normalize serum calcium in about 90% of hypercalcemic cancer patients. The apparently low response rate of bone metastases to systemic antineoplastic therapy seems to essentially reflect the relative insensitivity of our current methods for assessing response in tumor-induced osteolysis. Newly developed biochemical markers of bone turnover could be particularly useful for that matter. Bisphosphonates are the most potent of the available inhibitors of osteoclast activity. Prolonged administration of oral pamidronate could reduce by almost one half the complications of tumor-induced osteolysis, and repeated 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, blinded trials and many questions remain unanswered concerning the optimal therapeutic schemes. Medical therapy of tumor-induced osteolysis by noncytotoxic means has nevertheless become a reality.
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PMID:Bone metastases and tumor-induced hypercalcemia. 151 Oct 19

Hypercalcemia may occur as a complication of haematological malignancies, in association with solid tumors with bone metastases, and with solid tumors in the absence of bone metastases. The latter syndrome, known as the humoral hypercalcemia of malignancy (HHM) shares many features with primary hyperparathyroidism. A parathyroid hormone-related protein (PTHrP) has been identified, isolated and cloned, which is most likely responsible for the calcium disturbances in HHM, PTHrP is a previously unrecognized hormone which has limited amino-terminal sequence homology with PTH and is the product of a separate gene. Tissue localization studies have identified PTHrP in squamous cell carcinomata, renal cortical carcinomata, in a proportion of breast cancers and in adult T-cell leukemia/lymphoma. In normal tissues, PTHrP has been immunohistochemically localized in keratinocytes, placenta and fetal parathyroid glands. In addition to its role in mediating hypercalcemia in cancer, PTHrP is likely to have an important endocrine role in the fetus, and perhaps a paracrine function in several organs.
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PMID:Hypercalcemia in cancer. 152 53

The collagen crosslinks, pyridinoline and deoxypyridinoline, are recently described markers of the rate of bone resorption. The urinary excretion of these compounds, expressed as a ratio to urinary creatinine, has been measured using ion-pair reversed phase high-performance liquid chromatography in 20 patients receiving oral pamidronate for bone metastases from breast cancer. Before treatment the ratio of pyridinoline and deoxypyridinoline to creatinine in urine (UPCR and UdPCR respectively) were each above normal in 16/20 (80%) patients. Urinary calcium excretion (UCCR) was elevated in 15/20 (75%). There was a strong correlation between UPCR and UdPCR, but neither of the crosslink measurements correlated well with UCCR. Urinary excretion of all three indices of bone resorption fell significantly during pamidronate treatment. The median values after 4 weeks treatment were 63% of baseline for UPCR, 45% for UdPCR and 26% for UCCR. From this preliminary study urinary pyridinoline and deoxypyridinoline excretion appear to be promising markers of bone resorption in advanced malignancy. Their role in response assessment and the advantages over UCCR measurements merit further study.
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PMID:Preliminary results of the use of urinary excretion of pyridinium crosslinks for monitoring metastatic bone disease. 158 5


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