Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifteen patients (8 male and 7 female) with multiple myeloma, who were admitted to our hospital between July 1986 and August 1988 and suffering from pain and hypercalcemia, were treated with synthetic calcitonin derivative (elcatonin: ECT). ECT was administered intravenously at a dose of 10-640 units twice daily. Seven patients were treated with ECT (ECT group), and eight patients received combination treatment with ECT and other form of chemotherapy (combination group). With regard to the pain score (PS), significant analgesic effects in both groups were observed during 1-4 week treatments (p less than 0.05). There were no significant differences in PS between two groups. Serum calcium levels in the combination group at 1 and 4 weeks were significantly lower than the initial value (p less than 0.05). Hypocalcemia was not seen in any of the patients. Urinary excretion of calcium at 1 week in ECT group was higher than the initial value (p less than 0.05). The observed toxicities of ECT were slight nausea and vomiting in only 2 patients. These findings suggest that ECT is an useful agent for the treatment of pain and hypercalcemia accompanied with multiple myeloma.
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PMID:[Effectiveness of synthetic calcitonin derivative (elcatonin) on the bone pain and serum calcium concentration in multiple myeloma]. 233 72

The signification of serum bone Gla protein (serum BGP, osteocalcin) has been investigated in multiple myeloma. As a first step, quantitative iliac crest bone biopsies were performed in 19 patients; the serum BGP levels strongly correlated with histologic parameters of bone formation (r = 0.72-0.84, P less than 0.001) but not with those of bone resorption (r = 0.10). These results confirm that serum BGP is a marker of bone formation in multiple myeloma, as previously described in many other bone disorders. As a second step, serum BGP was measured in 117 patients with multiple myeloma as a systemic indicator of the degree of bone formation. Twenty-one percent of the patients had abnormal serum BGP levels (25 cases). The 14 patients with increased values (mean, 13.2 +/- 2.7 ng/ml) and thus increased bone formation belonged to a subgroup characterized by a lower osteolytic potential and a more indolent disease. On the other hand, the 11 patients with decreased values (mean, 1 +/- 0.3 ng/ml) and thus reduced bone formation had an advanced disease, extensive lytic bone lesions, a hypercalcemia frequently and a poor survival (mean, 4 months; range, 1-12). The biochemical investigations of the whole patient population, including serial studies in individual patients, have shown a large scatter of serum BGP levels, suggesting major differences in the bone formation rates. However, an overall inverse correlation was found between serum BGP and osteolytic potential. These results have confirmed the important role of the inhibition of bone formation in the occurrence of bone lesions in multiple myeloma and the interest of serum BGP to select a myeloma patient subgroup with low osteolytic potential and characterized by abnormally increased levels of this marker.
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PMID:Abnormal serum bone Gla protein levels in multiple myeloma. Crucial role of bone formation and prognostic implications. 235 3

We evaluated the serum osteocalcin and alkaline phosphatase levels and the urinary hydroxyproline excretion in patients with blastic, lithic or mixed metastases, humoral malignant hypercalcemia (HMH) and myeloma. In patients with metastasis of any type osteocalcin did not reach a significant increase although in blastic metastases an increase approaching signification was observed. However, the sensitivities of alkaline phosphatase or hydroxyproline were much higher. In HMH hydroxyproline increased to levels similar to those found in primary hyperparathyroidism. By contrast, although osteocalcin had a significant increase, its values were much lower than in parathyroid disease. The changes in alkaline phosphatase were nonevaluable. In myeloma none of the three markers changed. The major conclusion of the present study is that osteocalcin has little practical usefulness for the investigation of neoplastic patients.
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PMID:[Bone turnover markers in tumor pathology with bone involvement]. 235 62

It has been assumed, but not documented, that hypercalcemia induces an appreciable reduction in the serum anion gap (AG) because it represents an increase in the level of unmeasured cations. To test this question, we retrospectively compared the data of 59 hypercalcemic patients with malignancy [group 1, serum Ca 13.3 +/- SE 0.3 mg/dl] with those of 108 patients whose hypercalcemia was of parathyroid origin (group 2, serum Ca 12.1 +/- 0.1 mg/dl), and those of 51 control subjects (group 3, serum Ca 9.5 +/- 0.1 mg/dl). The AG of group 2 subjects (8.7 +/- 0.3 mEq/l) was significantly lower than that of the other two groups (p less than 0.001 for both) despite their higher serum albumin and lower serum Ca in comparison to group 1. The AGs of group 1 (11.1 +/- 0.4 mEq/l) and group 3 (11.1 +/- 0.3 mEq/l) were identical. There was no statistically significant correlation between the AG and serum Ca in the hypercalcemic patients. The major finding that the association of hypercalcemia with reduced AG is seen in hyperparathyroidism, but not in malignancy-related hypercalcemia, is not explained by differences in serum albumin, renal function, or acid-base status. Overlap of values between groups limits the diagnostic usefulness of the AG in an individual patient. Nevertheless, in the absence of multiple myeloma, the finding of an AG of 5 mEq/l or less in a hypercalcemic patient may be a helpful clue suggesting that malignancy is not the etiology.
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PMID:Effect of hypercalcemia on the anion gap. 236 30

The pathogenesis, prognosis, and reversibility of renal failure were assessed in 494 consecutive, previously untreated patients with multiple myeloma. For patients with a similar extent of disease, the presence or degree of azotemia did not adversely affect prognosis. Hypercalcemia and/or Bence Jones proteinuria explained the renal failure in 97% of patients. After treatment with a combination of hydration and chemotherapy, normal renal function was achieved in 51% of patients, reversibility usually being rapid and occurring more often in those with slight elevation of serum creatinine. Myeloma control was much more important for survival prolongation than reversal of renal failure, supporting the prompt institution of effective therapy for the underlying malignancy.
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PMID:Renal failure in multiple myeloma. Pathogenesis and prognostic implications. 238 64

Bone remodeling is a constant phenomenon balancing between osteoblastic bone formation and osteoclastic bone resorption in the neighbourhood of a cellular micro-environment including stromal and hemopoietic cells. Numerous local factors and hormones modulate such a mechanism and act synergistically, usually through the indirect production of osteoblastic coupling factors. The majority of the cytokines acting on bone remodeling possess both actions upon activation of mature osteoclasts and differentiation of hemopoietic osteoclast progenitors. Components from bone matrix which include non-collagenous bone proteins and other local factors are major products acting on bone remodeling. The presence of a cancer may determine changes in bone remodeling, directly through tumor-mediated resorption or indirectly through the action of local or systemic factors with or without tumor involvement of bone. Bone remodeling associated with cancer is usually an uncoupled phenomenon with decreased bone formation and increased bone resorption. In B-cell malignancies, abnormal bone remodeling is an early event linked to specific bone involvement. Abnormal osteoclast differentiation (micro- or macro-resorption) represents a major difference between myeloma and other B-cell malignancies. Several synergistic factors produced by tumor cells and micro-environment are usually implicated in the pathogenesis of bone lytic lesions, hypercalcemia or histomorphometric bone changes associated with cancers.
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PMID:[Bone tissue and cancer]. 240 92

A patient with hypercalcemia and newly diagnosed multiple myeloma developed acute pancreatitis. Other etiologic factors for pancreatitis were excluded. Hypercalcemia secondary to hyperparathyroidism is associated with acute pancreatitis. In English literature, only one other case has been published where the hypercalcemia of multiple myeloma may have caused pancreatitis. Pancreatitis should be considered in patients with hypercalcemia and multiple myeloma who develop nausea/vomiting, and abdominal pain.
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PMID:Acute pancreatitis in a case of multiple myeloma with hypercalcemia. 248 50

The major causes of renal insufficiency, present initially in half of the patients with multiple myeloma, are "myeloma kidney" and hypercalcemia. There is no reliable evidence that the isoelectric point (pI) or the type of light chain has an important role in renal failure. Acute renal failure must be treated vigorously with appropriate fluids and electrolytes as well as hemodialysis if necessary. The benefit of plasma exchange has not been proven. Primary systemic amyloidosis or light-chain deposition disease is the usual cause of the nephrotic syndrome in patients with monoclonal gammopathy. The monoclonal gammopathies are a group of disorders that are characterized by the proliferation of plasma cells producing a homogeneous, monoclonal protein (M-protein).
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PMID:Monoclonal gammopathies and the kidney. 249 46

A 73-year-old man was admitted into the hospital because of lumbago in October, 1986. Laboratory examination on admission showed anemia, an IgA-kappa Bence Jones proteinemia. The bone marrow picture disclosed a marked involvement by the neoplastic cells, followed by leukemic conversion 2 weeks later. The leukemic cells displayed a lymphoblastoid appearance on light microscopy, but rather compatible with plasma cells on electron microscopy, showing some strands of rough endoplasmic reticulum and a prominent Golgi apparatus in the cytoplasm. The cells expressed a wide spectrum of surface markers, including those of plasma cell (PCA-1, OKT10), B cell (B1, sIg) and CALLA. Reverse hemolytic plaque assay disclosed the immunoglobulin production of monoclonal kappa chain, but a heavy chain production was recognized only in a small proportion of the cells. Under the diagnosis of multiple myeloma, he was treated with vincristine, cyclophosphamide, and prednisolone. But he died of renal failure complicating hypercalcemia after only three months of the admission in accordance with previous reports that CALLA-positive myeloma was associated with poor prognosis. This case may also represent the clinical, morphological and phenotypic diversity in multiple myeloma.
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PMID:[CALLA-positive leukemic multiple myeloma of IgA-kappa type]. 250 77

A 48-year-old man developed a marked and persistent hypercalcemia 3 months after admission for paraplegia resulting from severe peripheral neuropathy most likely of alcoholic etiology. Serum ionized calcium was elevated, and parathyroid hormone levels were low normal by the two separate radioimmunoassays. Urinary calcium excretion was markedly elevated, and serum 1,25-dihydroxyvitamin D level was decreased. An extensive clinical evaluation for possible occult malignancy, myeloma, and sarcoidosis as a cause of hypercalcemia produced no positive findings. Treatment with calcitonin caused prompt normalization of serum calcium, and its discontinuation resulted in recurrence of hypercalcemia. With improvement of neuropathy, the patient started active physical therapy. We gradually discontinued calcitonin, and the patient's serum calcium remained normal during the following 11 months. We discuss difficulties in both clinical and laboratory diagnosis of hypercalcemia of immobilization in the adult patient because no specific laboratory test is available.
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PMID:Hypercalcemia of immobilization in an adult patient with peripheral neuropathy. 253 19


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