Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The short range tissue destruction of beta-emitting radioisotopes can be utilized in painful metastatic disease of the skeleton by employing a radionuclide that is specifically metabolized in or adjacent to these lesions. Sodium phosphate P 32 has been used for this purpose for the past 25 yr. It uptake in skeletal tumor and in osteoblastic new bone adjacent to tumor can be markedly increased by pharmacologic stimulation using androgenic steroids, or during rebound deposition after a course of parathyroid hormone. Although efficacy in terms of subjective pain relief is high, more objective signs of success are often lacking, and survival, while more confortable, is not prolonged. Marrow depression is the most significant side effect. A beta-emitting, bone-seeking isotope, 89Sr, may have a better therapeutic/toxic ratio, and should receive further trial. Radiation-induced necrosis has also been applied, though more hesitantly, to the proliferative, destructive, but nonmalignant synovium in rheumatoid disease. Here, a number of colloidal preparations, most commonly 198Au, have been employed. Again, relief of symptoms, particularly recurrent joint effusions, is quite high, although the basic disease process is not reversed. The major hazard here appears to be leakage of material to regional lymph nodes, resulting in irradiation of circulating lymphocytes. Although chromosomal damage can be detected when such cells are then cultured, the actual consequences of this, if any, are not presently known. Both shorter-lived (165Dy) and longer-lived (32P) larger-size colloids are being evaluated, which may prove safer in this regard than 198Au.
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PMID:Radioisotope therapy in bone and joint disease. 9 Mar 87

Studies of calcium metabolism in 38 patients with cancer indicated that: 1) intestinal absorption of calcium was reduced in patients with skeletal metastases and in those with hypercalcemia; 2) calcium-47 space (a measurement of bone turnover rate) was high in the patients with skeletal metastases; 3) hypercalcemic patients had higher urinary and endogenous fecal excretion of calcium than those who were normocalcemic; 4) levels of plasma immunoreactive parathyroid hormone were similar in normo- and hypercalcemic patients, but the levels for a given serum calcium in malignant disease were lower than those in primary hyperparathyroidism; and 5) some patients had elevated calcitonin levels. Hypercalcemia complicating malignant disease is therefore not due to hyperabsorption or diminished excretion of calcium, and a low calcium diet is unlikely to benefit these patients. Measurement of 47Ca space could be of use in monitoring therapy of patients with skeletal metastases, and measurement of plasma parathyroid hormone could be useful in the differential diagnosis of hypercalcemia.
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PMID:Calcium metabolism in cancer. Studies using calcium isotopes and immunoassays for parathyroid hormone and calcitonin. 18 80

Refractory hypercalcemia developed suddenly in a patient who had undergone a radical cystectomy for an anaplastic transitional cell carcinoma of the bladder. A normal serum parathyroid hormone (PTH) value was obtained by immunoassay while the patient had hypercalcemia and unimpaired renal function. This normal PTH value in the presence of hypercalcemia was consistent with his hypercalcemia being secondary to excessive amounts of circulating PTH. The finding of increased nephrogenous cyclic AMP, however, provided the definitive diagnosis of hyyperparathyroidism. Since autopsy revealed that there was no residual tumor in the bladder area, only evidence of metastatic disease, and since the parathyroid glands were not hyperplastic or adenomatous, we attributed this patient's hypercalcemia to hyperparathyroidism due to the ectopic production of PTH by a metastasis from the transitional cell carcinoma of the bladder.
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PMID:Fulminating hypercalcemia and markedly increased nephrogenous cyclic AMP in a patient with transitional cell carcinoma of the bladder. 22 Aug 74

A woman with metastatic carcinoma of the breast developed hypercalcemia 39 months after mastectomy. The hypercalcemia remitted after treatment but recurred 12 months later, accompanied by elevated levels of serum immunoreactive parathyroid hormone (PTH). A urea/HC1 extract of hepatic metastases contained immunoreactive PTH, material which stimulated the resorption of fetal rat bone in tissue culture, and material which stimulated chick renal adenylate cyclase activity. These findings strongly suggest that this breast cancer produced a PTH-like substance.
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PMID:Carcinoma of the breast associated with hypercalcemia and the presence of parathyroid hormone-like substances in the tumor. 42 76

A patient with adrenocortical carcinoma had three major endocrine abnormalities attributable directly to the tumor: hypercortisolism (Cushing's syndrome), hyperestrogenism (feminization), and hypercalcemia (pseudohyperparathyroidism). There were higher levels of immunoreactive parathyroid hormone in venous effluent from the tumor or its abdominal metastases compared to that found in the veins draining the parathyroid glands. This, together with the presence of normal parathyroid glands on autopsy, established the diagnosis of pseudohyperparathyroidism as the cause of hypercalcemia in this patient.
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PMID:Feminizing adrenocortical carcinoma with Cushing's syndrome and pseudohyperparathyroidism. 62 58

Over a 25-year period, two carcinomas of the parathyroid were observed in 67 cases of primary hyperparathyroidism. The most important signs and symptoms were bone disease, palpable neck metastases, renal stones, and hypercalceamia with high blood levels of parathyroid hormone. Histology revealed that in principle parathyroid carcinoma can be distinguished from adenoma by a trabecular pattern and thick fibrous bands. The presence of cellular atypia and variation or mitotic figures (regressive polymorphia) was not a useful criteria for carcinoma. Local recurrence occurred in both cases.
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PMID:[Parathyroid neoplasm associated with hyperparathyroidism]. 68 29

In 82 patients, a preoperative diagnosis of primary hyperparathyroidism has been established by means of transfemoral neck vein catheterization and measurement of serum immunoreactive parathyroid hormone (iPTH). Twenty-five of these patients have had cancer in other parts of the body but with no evidence of recurrence or metastasis. One patient had carcinoma of the colon with metastases, and four were members of families with multiple endocrine adenomatosis (MEA, Types I and II). In six other hypercalcemic patients, high levels of iPTH were found also in the effluent blood from cancer sites other than the parathyroid gland, secondary to ectopic hormone production or pseudohyperparathyroidism. In addition, a high serum level of iPTH was found in the superior vena cava of a seventh patient who had carcinoma of the breast but no clinical or radiological signs of recurrence or metastasis with the exception of an enlarged liver. This iPTH finding was interpreted as being, probably, the result of parathyroid adenoma in either the neck or the mediastinum. At the time of operation, a transcervical mediastinal search was made. Four normal cervical parathyroid glands were found; three were removed. Hypercalcemia persisted after operation, and the patient died. At postmortem examination, microscopic study revealed that the disease had metastasized to lungs and hilar lymph nodes. There was massive metastasis in the liver; the liver contained a large amount of iPTH. The results of these investigations suggest that (1) venous catheterization of the neck veins and the effluent blood from extraparathyroid tumors aid in identifying and localizing iPTH production; (2) primary benign hyperparathyroidism is not uncommon in patients with cancer, and its co-existence must be recognized; (3) high serum iPTH level in the superior vena cava may be found in patients with metastatic or primary cancer of the thoracic cavity; and (4) hyperparathyroidism may be the first hint of a familial multiple endocrine syndrome.
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PMID:Hypercalcemia in patients with known malignent disease. 96 5

Circulating levels of immunoreactive (i) PGE, calcium and parathyroid hormone (iPTH) were examined in 21 patients with neoplasia and 3 patients with primary hyperparathyroidism. Plasma iPGE was elevated in 4 of 11 hypercalcemic cancer patients; all extracts of liver metastases obtained from 3 of these 4 patients had elevated iPGE levels (metastases = 19.43 +/- 3.43, n = 11; normal liver = 2.04 +/- 0.23; ng/g tissue, x +/- SE, P less than .001). In contrast, only one of 10 normocalcemic cancer patients and none of 3 hyperparathyroid patients had elevated plasma iPGE. There were no apparent relationships between the presence of metastases and either hypercalcemia or elevations of plasma iPGE. Serum iPTH levels were undetectable or below the mean of the normal range in 19 of 21 cancer patients; only the three hyperparathyroid patients had elevated levels. Seven hypercalcemic patients were treated with indomethacin; plasma iPGE decreased in 6 (-34 +/- 10% decrement, n = 6, P less than .01). Decreases in serum calcium occurred only in those patients (2 of 6) who had abnormally elevated plasma iPGE prior to the therapy. It is concluded that plasma iPGE elevations are found in some cancer patients, especially those with hypercalcemia, and that this marker may identify those patients who will respond to indomethacin treatment.
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PMID:Plasma prostaglandin E in patients with cancer with and without hypercalcemia. 100 18

A fifty-three-year-old man with epidermoid carcinoma of the penis metastatic to the right inguinal lymph nodes and adjacent areas was found to have persistent hypercalcemia. Associated with this biochemical abnormality was an elevated parathormone activity in the absence of any bony metastases. Other than a transient response to furosemide-inducded diuresis he was refractory to treatment with oral inorganic phosphates and mithramycin. Ablation of the primary tumor did not affect his hypercalcemia. However, when therapy using external irradiation and parenteral bleomycin was directed to the metastases, his serum calcium stabilized and became normal and remained so until further progression of his humor. We postulate that the penile cancer metastases were elaborating parathyroid hormone-like substances responsible for the hypercalcemia and suppression of normal parathyroid activity.
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PMID:Metastatic carcinoma of penis complicated by hypercalcemia. 112 68

Seminomas are germ cell tumors that are rarely associated with hypercalcemia. In this report, four cases of seminoma with concomitant hypercalcemia are presented and another three from the literature are reviewed. All seven patients exhibited hypercalcemia with a normal serum concentration of inorganic phosphorus and no evidence of skeletal metastases. The peripheral venous level of parathyroid hormone (PTH) was normal in four of the five patients in whom it was measured. The serum concentration of calcitriol was elevated in the two patients in whom it was measured. After systemic chemotherapy, the serum "corrected" total calcium concentration returned to normal and remained normal; the decrease in the levels temporally paralleled the decrease in tumor volume. Both patients with elevated calcitriol levels remained eucalcemic after treatment of the malignancy, suggesting that the increased serum calcitriol level was linked to the development of hypercalcemia as this humoral agent was inappropriately elevated by patients with this syndrome. In contrast to many forms of malignancy, the development of hypercalcemia did not adversely affect the prognosis of the patients with seminoma, since all seven patients entered complete remission. Hypercalcemia appears to be heretofore unrecognized paraneoplastic syndrome associated with seminoma.
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PMID:Humoral hypercalcemia in seminomas. 137 70


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