Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urinary adenosine -3' ,5' - cyclic monophosphate was measured in 14 patients with hypercalcaemia not caused by primary hyperparathyroidism. Increased levels were found in patients with malignant disease without bone metastases and believed to be examples of paraendocrine syndrome. Decreased levels were found in patients with metastatic carcinoma involving bone, and in patients with multiple myeloma, lymphoma and immobilisation after fracture. Results obtained during treatment for hypercalaemia are described in three patients. In two hypercalcaemic patients (one with hyperthyroidism and one with breast cancer with bone metastases) normal levels were found. This measurement is a useful substitute for assay of serum parathyroid hormone and is of value in the diagnosis of hypercalcaemia, in monitoring effects of treatment and in revealing underlying mechanisms.
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PMID:Urinary cyclic AMP in diagnosis and management of hypercalcaemia: studies of patients without primary hyperparathyroidism. 16 77

An assessment of free and total calcium measurements was made in 691 patients with suspected hypercalcemia or disorders often associated with hypercalcemia. In 18.9% of the 1049 specimens analyzed from nine different patient groups, a different impression of hypercalcemia was obtained depending on whether the free or total calcium was considered. Analysis of the ratio of free to total calcium indicated that there are two main factors which influence the distribution of calcium in the serum of hypercalcemic patients: the concentrations of albumin and parathyroid hormone. A lowered albumin concentration accounted for the altered distribution of calcium in patients with malignancies and partially accounted for the altered distribution in patients postrenal transplantation. In patients with confirmed primary hyperparathyroidism a higher ratio of free to total calcium was found, which could not be explained by alterations in protein, albumin, pH, or CO2 content but was related to parathyroid hormone concentration. Free calcium appears to be a slightly better indicator of elevated calcium states than total calcium. Measurements of free calcium should be particularly useful in patients with altered albumin concentration, with multiple myeloma in whom a calcium-binding protein could be present, after renal transplantation, and with suspected hyperparathyroidism and normal or slightly elevated total calcium values.
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PMID:Relationship of free and total calcium in hypercalcemic conditions. 42 92

PRAD1 (parathyroid adenoma 1) gene at chromosome 11q13 has been cloned from parathyroid adenomas as a putative oncogene, activated by translocation with the parathyroid hormone gene. 4.5 kb and 1.7 kb mRNA are transcribed and both have the same open reading frame of 885 bp encoding 34 kd protein of a cyclin gene family, cyclin D1. Recently, overexpression of PRAD1 gene has been reported to be correlated closely with the rearrangement of bcl-1 locus, particularly in centrocytic lymphoma. In our study, overexpression of PRAD1 gene was shown in five B cell lines with t(11;14)(q13;q32) including one centrocytic lymphoma line and 4 myeloma lines, when compared with other hematopoietic cell lines without translocation. One of the cell lines, SP-49, demonstrated a truncated mRNA of 3.4 kb, in addition to 1.7 kb of normal size. Southern blot analysis demonstrated a rearrangement with PRAD1 cDNA probe, suggesting that the gene is altered in this particular cell line. By cloning analysis, we confirmed that 1.8 kb deletion in 3' region of PRAD1 gene eliminating the destabilizing signal of PRAD1 mRNA, gave rise to the aberrant mRNA of 3.4 kb. These findings suggest that PRAD1 gene is most likely the candidate oncogene for bcl-1 activated by t(11; 14)(q13;q32) translocation. The gene alteration found in one cell line, SP-49, might also play an important role for deregulation of the gene.
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PMID:[Overexpression of PRAD1 gene in B-cell malignancy with t(11;14)(q13;q32) translocation]. 151 59

Circulating monomeric human calcitonin (hCT-M), parathyroid hormone, osteocalcin, alkaline phosphatase, urinary hydroxyproline, corrected serum calcium and inorganic phosphate were measured in 49 multiple myeloma patients and 49 matched controls. In patients with Durie-Salmon stage III disease hCT-M levels (16.9 +/- 5.8 ng/l, mean +/- SD) were significantly higher than controls and stage I patients (P less than 0.01), and correlated directly with corrected serum calcium (r = 0.74; P less than 0.001). In the same subgroup 14 of 15 patients had plasma hCT-M concentrations higher than the mean + 2SD of the controls. The calcium infusion test induced an increase of hCT-M in normocalcemic patients which was significantly greater in patients with advanced disease than in either controls or stage I patients. These findings suggest that hCT-M may be a biochemical index of bone resorption and disease activity in myeloma patients with osteolysis. In fact, its plasma concentrations were elevated in a large proportion (93%) of patients with severe bone involvement, and correlated directly with serum calcium. Moreover, our findings suggest the presence of a calcitonin-dependent calcium homeostatic mechanism, that protects against hypercalcemia due to tumor osteolysis.
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PMID:Plasma monomeric calcitonin as a marker of disease activity in multiple myeloma patients with osteolysis. 163 26

Hyperphosphatemia (HP) is usually seen in patients with hypoparathyroidism, renal failure, and tumor lysis. The authors described a patient with HP due to a phosphate-binding immunoglobulin (Ig). An 86-year-old woman had serum phosphate levels as high as 4.75 mmol/l, (normal, 0.77 to 1.45 mmol/l). Serum ionized calcium, blood urea nitrogen (BUN), creatinine, and N-terminal parathyroid hormone (PTH) levels were normal, but serum 1,25-dihydroxyvitamin D level was subnormal at less than 12 pmol/l (normal, 36 to 146 pmol/l). Serum total protein was elevated at 105 g/l (normal, 60 to 80 g/l), and additional studies confirmed a diagnosis of immunoglobulin G (IgG) multiple myeloma. Results of in vitro studies using anti-human IgG antibodies showed that the IgG of the patient bound inorganic phosphate. Several isolated case reports have documented spurious HP due to interference of the paraprotein in the routine serum phosphate assay. In only one patient, however, has actual binding of phosphate to a myeloma protein been documented. The studies of the authors document phosphate binding by an IgG paraprotein and suggest that in this setting HP may be of physiologic significance as evidenced by depressed serum levels of 1,25-dihydroxyvitamin D.
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PMID:Hyperphosphatemia in multiple myeloma due to a phosphate-binding immunoglobulin. 191 79

Monoclonal antibodies to the biologically active N terminal region of parathyroid hormone (PTH) suitable for use in the measurement of circulating PTH concentrations have proved difficult to produce. In this study, no serum PTH antibody titres could be detected in mice using synthetic human PTH (1-34) (free or coupled to albumin) or PTH (1-10) (coupled to keyhole limpet haemocyanin) as immunogen. A consistent response to PTH (1-34) peptide was obtained in DA rats. We have produced five monoclonal antibodies to PTH (1-34) derived from the fusion of DA rat spleen cells and the mouse myeloma line X63 Ag.8.653. Bulk production of the antibodies was achieved using congenitally athymic mice for ascites production. Antibody assessment studies revealed the antibodies to be sensitive to the oxidation state of the methionine residues in PTH (1-34). Two of the antibodies, 3B3 and 6E3, were shown to be of potential use in measuring circulating PTH (1-84) when used in combination with available antibodies to C terminal PTH. A third antibody, 4G3, which failed to recognise PTH (1-84) when used in combination with 3B3, formed the basis of a specific assay for PTH (1-34).
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PMID:Production and characterisation of monoclonal antibodies to parathyroid hormone (1-34). 201 95

The mechanisms of paraneoplastic hypercalcemic syndromes are heterogeneous. Neoplastic hypercalcemia without bone metastatic disease is caused by parathyroid hormone related protein, whose action is comparable to parathyroid hormone. Growth transforming factors, platelet derived growth factor, tumor necrosis factors and interleukin 1 are also involved in humoral hypercalcemia of malignancy. In addition to these substances, hypercalcemia in bone metastatic disease may be related to PGE. Tumor necrosis factors and interleukin 1 play a major role in multiple myeloma as well as in Adult T cell Leukemia/Lymphoma where overproduction of vit D3 by lymphomatous cells can also be significant.
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PMID:[Hypercalcemia and neoplasms: recent advances in pathogenesis]. 229 Oct 7

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

A 66 year-old woman with multiple myeloma developed hypoparathyroidism during combination chemotherapy with melphalan, prednisolone, and alpha-interferon (INF). Seven weeks after commencement of the therapy, the serum calcium (Ca) level decreased to 7.4 mg/dL, and the phosphorus (P) level increased to 7.2 mg/dL; parathyroid hormone (PTH) was at a critically low level. By 13 weeks after discontinuation of alpha-INF, the levels of Ca, P, and PTH had returned to normal values: 8.6 mg/dL, 4.5 mg/dL, and 310 pg/ml, respectively. These changes suggest a strong correlation between hypoparathyroidism and the administration of alpha-INF. Autoantibodies against the parathyroid gland cell were not present in the serum of this patient by indirect immunofluorescent techniques. The mechanism of hypoparathyroidism by alpha-INF could not be identified, but this is the first case of this condition during alpha-INF therapy.
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PMID:Hypoparathyroidism during alpha-INF therapy in a patient with multiple myeloma. 262 20

Clodronate, an inhibitor of osteoclast function, reduces bone resorption in osteolytic metastases and in multiple myeloma. We have evaluated its ability to decrease bone destruction in patients with multifocal eosinophilic granuloma of the skeleton. Two patients, whose multifocal bone granulomas appeared with a frequency of about 6 months, received 1.6 g day-1 oral clodronate for 6 months. Both patients had a reduction in serum calcium level which was accompanied by a decline in the fasting urinary hydroxyproline/creatinine and calcium/creatinine ratios and a slight increase in parathyroid hormone (PTH) level. Pain relief was observed in both patients. No new bone lesions were seen during the treatment and the old lesions healed. After discontinuing the therapy, however, new painful lesions appeared after 5 years in patient 1 and after 3, 4 and 5 years in patient 2. We suppose that clodronate delayed the appearance of new granulomas.
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PMID:Experiences of clodronate treatment of multifocal eosinophilic granuloma of bone. 291 72


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