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Query: UMLS:C0020437 (hypercalcemia)
10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The unusual causes of hypercalcemia have been reviewed. These disorders are rarely derived as the cause of hypercalcemia from the usual tests that one obtains in working up hypercalcemic patients (such as PTH level, phosphorus, urinary calcium). These diagnoses (particularly drug-related hypercalcemia) can be determined only from a careful history. The vast majority of hypercalcemic patients have disease secondary to cancer, hyperparathyroidism, or disorders of vitamin D metabolism. It should be noted that some hypercalcemic patients may have more than one disease. Therefore, before assuming that a hypercalcemic patient with Paget's disease, thiazide ingestion, immobilization, or so forth has hypercalcemia secondary to the primary disorder, hyperparathyroidism and cancer should also be considered. Similarly, serum calcium levels can normalize in some patients with mild hyperparathyroidism or bony metastases with mobilization and/or cessation of thiazide therapy.
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PMID:Unusual causes of hypercalcemia. 267 71

The treatment of patients with Zollinger-Ellison syndrome (ZES) has undergone dramatic evolution during the past decade. Although initially regarded as an incurable tumor, resection of gastrinoma for potential cure has been reported in 30% to 40% of selected patients in recent series. Conversely, although definitive control of acid hypersecretion is achieved by total gastrectomy, histamine (H2)-receptor antagonists and the newly introduced agents omeprazole and somatostatin analogues allow effective medical therapy of gastric acid overproduction. Confirmation of the diagnosis is best achieved with the I.V. secretin stimulation test, and tumor localization techniques are mandatory to identify candidates for operative tumor resection. Intraoperative sonography and careful exploration are required for tumor removal; successful tumor resection is associated with prolonged survival. The majority of patients (60%) are still found to have malignant disease at the time of diagnosis, but 10-year overall survival commonly exceeds 40%. The presence of multiple endocrine neoplasia type I (MEN-I) is seen in 10% to 25% of patients; correction of hypercalcemia alone may have therapeutic benefit in some ZES patients, and while gastrinoma resection is rarely possible, MEN-I patients demonstrate prolonged survival. The choice of medical rather than surgical therapy for acid hypersecretion depends on the suitability of each patient for careful and repeated endoscopic and chemical studies, versus the likelihood of a successful postoperative outcome. Socioeconomic, geographic, and related medical factors in each case may dictate the form of long-term antisecretory therapy. Exploration for possible tumor resection is indicated for virtually all patients who have no documented metastatic disease.
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PMID:Current diagnosis and management of Zollinger-Ellison syndrome. 268 66

The search into the way in which skeletal metastases develops has not only shown that there are several mechanisms for the progressive bone destruction and bone formation that occur simultaneously in the majority of skeletal metastases, but also that an understanding of these basic mechanisms has significant therapeutic implications. Our results have shown that there are two main mechanisms for the bone formation: stromal bone formation and reactive bone formation. The former occurs in tumours which tend to be acellular, with a large fibrous stroma, whereas the latter occurs in virtually all metastases. There is no difference in the basic pathological process of sclerotic or lytic metastases, the radiographic appearance purely indicating the net balance between the different types of bone formation and the simultaneous progressive bone destruction. An understanding of the pathophysiological response to skeletal metastases explains why skeletal scintigraphy can be used to diagnose these lesions and the different mechanisms underlying the 'three-phase scintigram'. The first phase indicates the vascularity of the lesion; the second phase or 'blood-pool' image indicates the concentration in the extracellular fluid and the third phase or 'skeletal or delayed image' indicates the uptake in the reactive new bone. The secretion of an osteoblast inhibiting factor by myeloma indicates why there is no reactive bone produced by the majority of lesions in the absence of a fracture, and why scintigraphy is less reliable than plain radiographs for the detection of the lesions. There are two main mechanisms for the bone destruction, the most important being mediated via osteoclasts. An understanding of the humoral mechanisms stimulating the osteoclast proliferation may lead to more effective treatment of malignant hypercalcaemia and lytic metastases. Early results of use of APD are encouraging, and our results also suggest that clinical trials should be established to evaluate the effect of combination therapy with APD or prostaglandin inhibitor combined with the agents normally used in the management of patients with disseminated mammary carcinoma. The development of treatments to inhibit tumour-induced osteolysis will minimise the complications of pathological fracture, spinal instability, etc., and even if these treatments do not affect the primary tumour, its ability to metastasize, or the patient's survival, such treatment will be a major advance in the management of patients with carcinoma, because of the significant morbidity currently associated with the development of skeletal metastases and their complications.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The development of skeletal metastases. 279 40

Three examples of malignant neoplasms primary to the oral cavity and associated with paraneoplastic syndromes are presented. The first case is a squamous cell carcinoma of the maxilla associated with leukocytosis. The second case is a mandibular squamous cell carcinoma associated with hypercalcemia in the absence of bony metastases. The third case is a squamous cancer of the tongue that metastasized to the lumbar vertebrae and right second rib and was associated with both hypercalcemia and leukocytosis. There was no evidence of acute infection or leukemia that could be expected to account for leukocytosis. Hypercalcemia in the second case was defined as humoral hypercalcemia of malignancy by biochemical and clinical evaluations. To our knowledge, this is the first definitive report of a carcinoma primary to the oral cavity associated with humoral hypercalcemia of malignancy. In each case, the severity of hypercalcemia, leukocytosis, or both very closely correlated with tumor growth. Surgical excision of the tumors or regression of tumor mass due to aggressive anticancer drug administration resulted in decreases in leukocyte number, serum calcium level, or both. In contrast, recurrence or regrowth of tumors induced further development of hypercalcemia, leukocytosis, or both. It is therefore likely that humoral factors released by these oral carcinomas are responsible for the hypercalcemia, leukocytosis, or both.
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PMID:Three cases of oral squamous cancer associated with leukocytosis, hypercalcemia, or both. 281 15

The controversial prognostic significance of serum calcitonin in small-cell lung cancer (SCC) prompted this retrospective study relating serum levels to (1) stage of disease [limited disease (LD) vs. extensive disease (ED)], (2) imaging studies of metastases to bone, liver, and brain, and (3) survival. Of the 127 previously untreated patients with SCC presenting from 1979 to 1984, calcitonin levels could be compared to the stage of the disease in 69 patients (25 LD and 44 ED) and to various staging procedures including 99mTc methylene diphosphonate bone scans (63 patients), 99mTc sulfur colloid liver-spleen scans (64 patients), computed tomography of the head (63 patients) and serum calcium (61 patients). 71% (49/69) of patients had elevated calcitonin of whom 65% (32/49) had ED. 29% (20/69) had normal levels of whom 60% (12/20) had ED. 40% (18/45) of patients with raised calcitonin had liver metastases. 100% (19/19) with normal calcitonin had no liver involvement. Two patients with hypercalcemia and increased calcitonin had extensive bony metastases. The survival experiences of patients with normal and elevated serum calcitonin levels were analyzed. No significant differences were found within each stage or in the group overall. The positive correlation of serum calcitonin to liver metastases was statistically significant. No such relationship could be demonstrated with stage of disease, bone metastases, brain metastases, or survival.
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PMID:Imaging studies and the prognostic value of serum calcitonin in staging small-cell lung cancer. 283 15

A case of severe hypercalcemia due to metastases to bone from a primary breast cancer is presented. The different drugs available for treating hypercalcemia are described, and the rationale for their use is discussed.
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PMID:The treatment of hypercalcemia associated with metastases to bone from primary breast cancer. 284 Jan 53

A case with multiple endocrine neoplasia was reported, including parathyroid adenoma, of the main cells of the gland, multiple small adenomas in the tail of pancreas, (cytologically and electron-microscopically determined as A cellular) and light-cellular adenoma of adrenal. The hyperfunction of parathyroid adenoma was manifested with hypercalcemia (3.75 mmol/l), and morphologically--with the multiple calcium metastases in lungs, kidneys and heart, established at necropsy. The cause for the death was the acutely advanced ischemic disease of myocardium, on the background of chronic pyelonephritis and renal insufficiency. The timely diagnosis of such morbid states is concluded to be important for the clinical practice and could lead to the saving of the patients by operative removal of the tumour.
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PMID:[Multiple endocrine adenomatosis manifested chiefly by hyperparathyroidism]. 287 52

Hypercalcemia associated with metastatic cancer may be due to osteolytic invasion or paraendocrine effects of the neoplasm. A patient with refractory hypercalcemia of long duration underwent cervical parathyroid exploration; three glands were found, but hypercalcemia persisted. After localization studies, a fourth gland was uncovered from the mediastinum. Hypercalcemia persisted, and at operation for kidney stones, squamous cell carcinoma of the renal pelvis was discovered, which progressed to cause the patient's death in hypercalcemia.
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PMID:Hypercalcemia in squamous cell carcinoma of the renal pelvis? Parathyroid or paraendocrine in origin. 287 67

131 patients with osteolytic metastases from breast cancer were randomised to receive long-term oral treatment with aminohydroxy-propylidene-bisphosphonate (APD), 300 mg daily (n = 70), or to act as controls (n = 61) in a multicentre trial. Specific antitumour therapy was at the discretion of the clinician and variable. An interim analysis was made after a median follow-up of 13 months in the APD group and 14 months in the controls. There was a significant reduction in pathological fractures and severe bone pain in the APD group, and hypercalcaemia was prevented. Consequently the necessity for radiotherapy for skeletal complications was more than halved; the number of systemic therapy changes was also reduced. Gastrointestinal side-effects of APD led to a drop-out of 8% of patients. Oral supportive APD therapy is simple and convenient, and significantly reduced skeletal morbidity in advanced breast cancer.
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PMID:Reduced morbidity from skeletal metastases in breast cancer patients during long-term bisphosphonate (APD) treatment. 288 57

Therapy should be individualized on the basis of patient symptoms, severity of hypercalcemia, and prospects for inducing a remission in the underlying malignancy. We have found the most effective approach to be vigorous hydration of the patient, usually intravenously with normal saline at a rate of 300 to 500 mL/h. Intravenous furosemide is given as needed to prevent fluid overload. If the patient is volume replete and if hypercalcemia persists after 24 to 48 hours of intravenous hydration, calcitonin, 200 MRC units subcutaneously every 12 hours plus prednisone, 20 mg orally four times daily, are added. In most cases, a response is seen shortly after institution of this therapy. Meanwhile, attempts to treat the malignancy are initiated, including palliative radiation therapy for bony metastases. If the patient is still hypercalcemic and symptomatic after seven days of this therapy, treatment with plicamycin is given unless the patient's condition is clearly terminal. At present, use of prostaglandin synthetase inhibitors is not recommended, and bisphosphonates are available only for investigational use.
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PMID:Hypercalcemia of malignancy: diagnosis and therapy. 294 51


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