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)

Thirty-three patients with intractable pain caused by diffuse osteoblastic metastases from carcinoma of the prostate were treated with phosphorus-32 (32P) therapy either androgen priming, parathormone rebound, or a combination of both priming methods. Significant response to pain was achieved in 12 of 19 patients receiving testosterone-potentiated therapy, 0 of 5 patients treated with parathormone alone, and 6 of 9 patients receiving a combination of both priming modalities. It is concluded that androgen priming alone is the simplest and most effective method to be used when 32P therapy is being considered for palliative control of pain in patients with carcinoma of prostate.
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PMID:Phosphorus-32 for intractable pain in carcinoma of prostate. Analysis of androgen priming, parathormone rebound, and combination therapy. 6 16

Functioning tumors of the pancreatic islets are now recognized as the source of clinical syndromes affecting the gastrointestinal tract which have a wide variety of catastrophic symptoms. Experiences with thirty-six cases suggest at least four separate diagnostic categories in the ulcerogenic tumor syndrome. These include: a typical history, gastric analysis, and roentgenographic findings with boderline fasting serum gastrin levels; ulcerogenic tumor with evidence of hyperparathyroidism; iatrogenic ulcerogenic syndrome associated with failure of a previous operation for duodenal ulcer; and the classic ulcerogenic syndrome associated with a fulminating ulcer diathesis or diarrhea and high serum gastrin levels. The problems presented at operation include: decisions to be make in the presence of a negative exploration; the finding of a solitary tumor in the wall of the duodenum; solitary pancreatic tumors particularly in the body and tail; ulcerogenic tumors in the very young; liver metastases in the elderly; and the wisdom of removing gross metastases in combination with total gastrectomy. The long-term survival in the ulcerogenic tumor syndrome approximated 50 per cent, with 40 per cent of those having proved malignancy living five years. Evidence of hyperparathyroidism is relatively common in association with both the ulcerogenic and the diarrheogenic tumor syndromes. The association may by a result of a congenital abnormality, metabolic alkalosis, or a direct effect of the islet cell tumor. Parathyroidectomy may be indicated when both the serum calcium and parathormone levels are elevated in the presence of borderline fasting gastrin levels. The latter may return to normal after parathyroidectomy. The evidence of hyperparathyroidism closely parallels the episodes of diarrhea in the diarrheogenic syndrome, and hyperparathyroidism may regress spontaneously after total removal of the pancreatic tumor. Just as routine calcium determinations made the diagnosis of hyperparathyroidism more commonplace, it is suggested that the gastrointestinal syndromes associated with islet cell tumor would receive wider recognition if radioimmunoassays for gastrin as well as secretin, and the other secretin-like polypeptides, were carried out routinely.
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PMID:Islet cell tumors of the pancreas and the alimentary tract. 16 36

Carcinoma of the bronchus can produce several polypeptide hormones and therefore has the capacity to cause most syndromes of endocrine hyperfunction. All pituitary hormones can be synthesized ectopically; furthermore, the production of hormones from the hypothalamus (CRF), the placenta (HCG, HPL) and the C-cells of the thyroid (calcitonin), as well as parathormone and prostaglandins has been described. The paraneoplastic syndrome may often be more dangerous for the patient than the tumor growth itself, and can lead to early death. On the other hand, it may allow the early detection of an unsuspected tumor. The ectopic hormones and other nonendocrine proteins and peptides can be used as tumor markers, and can demonstrate the effect of treatment and early recurrence or metastases. An ideal tumor marker should have the following characteristics: 1. production exclusively by neoplastic tissue, 2. direct correlation with tumor size, 3. substances common to all tumor types ("large spectrum tumor marker") although specific tumor markers for special tumors should be available, 4. the assays must be easy and automation should be possible. At present no tumor marker satisfies all these conditions. The measurement of several tumor markers and the use of discriminant analysis may extend their diagnostic value and open the way for biochemical detection of cancer in the future.
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PMID:[Ectopic hormone formation and tumor markers in bronchial neoplasms]. 22 36

The relations of calcitonin concentrations to the presence of bone marrow metastases and to the concentrations of calcium, parathormone and gastrin in serum were investigated in 74 untreated patients with small cell carcinoma of the lung. Calcitonin concentrations were enhanced in two thirds of the patients, while serum calcium concentrations were normal in all. In 19 of 57 patients parathormone concentrations were slightly above the normal range, but the concentrations of parathormone and calcitonin were not correlated. Bone marrow metastases had no influence on the concentration of serum calcitonin. Finally, a small inverse correlation between the concentrations of gastrin and calcitonin in serum was observed. The results resemble those of the calcitonin-producing medullary carcinoma of the thyroid, supporting the suggestion of an ectopic source of hypercalcitoninemia in small cell carcinoma of the lung.
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PMID:Small cell carcinoma of the lung: relation of calcitonin to bone marrow metastases, parathormone and gastrin. 22 33

An unusual finding of systemic calcinosis in a patient with a nonparathyroid malignant neoplasm stimulated us to do a sclinicopathologic review of similar cases at our institution in the past seven years. Of 3,268 autopsies performed from 1968 to 1975, a total of 17 cases of calcinosis were found, 11 with solid tumors and 6 with hematopoietic neoplasms. Calcinosis was most prominent in the lung, kidney, heart, and stomach and was rarely discovered prior to death. Eighty-two percent of the patients had hypercalcemia and 53% had associated bony metastatic disease. Corticosteroid or phosphate treatment for the hypercalcemia may have contributed to the tissue deposition of calcium. Significant hepatic, renal, metabolic, and pulmonary dysfunctions were also associated with this disorder. Thirty-six percent of the patients had hypercalcemia without skeletal involvement; tumor-produced parathormone-like substances may be responsible for these calcium abnormalities. Calcinosis was a significant complication of neoplastic disease in these patients and contributed to morbidity and mortality.
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PMID:Calcinosis in nonparathyroid malignant disease: an unusual case report and clinicopathologic review of 17 cases. 62 63

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

A young male had an assumed dentigerous cyst marsupialized and later a recurrent ameloblastoma resected. Eleven years later he was admitted with renal stones and hypercalcemia and metastases of the ameloblastoma in the left lung were discovered. Death occurred as a result of spinal and hepatic spread of his tumor and thrombosis of the renal veins. Renal calcification was demonstrated. The possible causes of the hypercalcaemia which was not associated with a raised serum parathormone or affected by parathyroidectomy is discussed.
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PMID:A metastasising ameloblastoma associated with renal calculi and hypercalcaemia. 120 77

Patients suffering from malignant disease will probably develop some metabolic abnormality of electrolytes. Hypernatremia is defined as an elevation of serum natrium over 150 mEq/l and caused by decrease of water intake, low level of ADH secretion and impaired response of kidney to ADH. Hyponatremia below 135 mEq/l of serum natrium is caused by SI-DAH, sick cell syndrome and increased loss of natrium from the kidney. On the other hand, hyperkalemia is defined as an elevation of serum kalium over 5.0 mEq/l and caused by acute tumor cell lysis syndrome, adrenal and renal insufficiency. Hypokalemia is caused by kalium loss from kidney and hypersecretion of mineral corticoid. Hypercalcemia is found in the high frequency among patients with malignant disease. Hypercalcemia is defined as an elevation of serum calcium over 11.0 mg/dl, although the most important aspect is the level of ionized calcium. The excess calcium causes defective urinary concentration with polydipsia, nausea and vomiting leading to volume depletion. At serum calcium levels about 13.8 mg/dl, there may be rapid deterioration or renal function, dehydration, coma and cardiac arrhythmias. Hypercalcemia is rarely the first manifestation of cancer. There are three principle pathogenic causes of malignant hypercalcemia, 1) hypercalcemia is a feature of several hematological cancers, including Burkitt's lymphoma, T cell leukemia, but most commonly with myeloma. The hypercalcemia in these myeloma patients is due to the secretion of an osteoclast activator, a lymphokine by the myeloma cells. 2) all patients with bony metastases have biochemical evidence of increased bone resorption. However, not all patients with bony metastases develop hypercalcemia. Probably the hypercalcemia is due partially to increased renal tubular reabsorption of calcium, mediated by a humoral factor, with activity similar to that of parathormone. 3) hypercalcemia in the patients without bony metastases is due to increased bone resorption caused by the ectopic secretion by the tumor. Mildly symptomatic patients will benefit from modest salt loading. They are dehydrated and replacement of the extracellular fluid is the first line of treatment. This may require 4-10 l normal saline/24 h. In addition, frusemide will increase calcium excretion. Calcitonin may be given subcutaneously or intravenously to refuse the mobilisation of calcium from bone. Glucocorticoids are unhelpful, but will prolong the effect of calcitonin. A diphosphonate is also useful.
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PMID:[Palliative therapy in cancer. 4. Palliation of the symptoms from a malignant tumor. (2)]. 169 56

A case of fatal hepato-renal failure occurring during mithramycin treatment is reported. A 64 year-old female patient was admitted to hospital in a state of acute renal failure. She also presented with hypercalcaemia and bilateral pulmonary metastases. She had been operated on 10 years previously of a parathyroid cancer. Despite treatment with mithramycin (total dose 8.25 mg) and haemodialysis, the hypercalcaemia returned; it was then decided to remove the secretory lung metastases (parathormone 420 micrograms X ml-1). 48 hours before surgery, the patient was again given 1.25 mg mithramycin. Immediately after surgery, she developed hepatic failure with massive cell destruction and anuria. The patient died 48 h after the operation. The hepatic and renal complications of mithramycin are discussed.
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PMID:[Acute fatal hepatorenal failure during treatment with mithramycin]. 316 Feb 68

A 41-year-old woman was operated on for severe hyperparathyroid syndrome. At surgery a parathyroid tumor with the histopathologic pattern of carcinoma was found. After surgery serum calcium settled within normal limits (10.5 mg/dl, N.V. 8.5-10.8), whereas parathormone and calcitonin reached progressively high levels, respectively 400 ng/dl (N.V. up to 250) and 500 pg/ml (N.V. up to 100 ng/ml). Serum ultrafiltration analysis for parathormone and calcitonin showed many peaks of immunoreactivity with high molecular weight of both hormones. One year after surgery, metastases developed in the lymph nodes of the neck and the mediastinal, pleural and pancreatic regions. After death for tumor wasting, immunohistochemical study of the tumoral tissue with the peroxidase-antiperoxidase technique showed a relatively high density of calcitonin-containing cells. The findings in this case suggest that: several cells in this parathyroid cancer could secrete both parathormone and calcitonin; the hormonal secretion was impaired as suggested by the high molecular weight of both hormones found at gel-filtration analysis; the macromolecular profile of parathormone could explain the apparent function of the parathyroid cancer.
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PMID:Apparently nonfunctioning metastases of parathyroid carcinoma. 357 16


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