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)

Back pain is one of the chief complaints of the elderly. It may be either a chronic deep skeletal muscular pain or an acute circumscribed pain arising from nerve-root irritation. The main causes of back pain in older people are: 1) degenerative changes (spondylosis, osteoarthritis, ankylosing hyperostosis); 2) malignancy (multiple myeloma, metastases from carcinoma or lymphoma); and 3) metabolic disorders (osteoporosis, osteomalacia, chondrocalcinosis, Paget's disease). Mechanisms and variations are discussed in detail.
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PMID:Back pain: osteoarthritis. 13 24

The dosage of calcium ionized serum using a selective electrode, was performed in a series of controls and patients with osteo-articular diseases. Normal values were 43 mg/l between 20 and 50 years of age, and 41 mg/l after 60 years. The level of ionized calcium, when given as a percentage of total blood calcium, did not decrease with age (normal value : 44%). It was increased in hyper-parathyroidism, rhumatoid polyarthritis and lytic bone metastasis. It did not vary in Paget's disease, osteoporosis, osteomalacia, condensing metastasis, Kahler's disease and spasmophilia. The ionized calcium in definitely diminished in hypoparathyroidism.
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PMID:[Dosage of ionized calcium in osteo-articular pathology]. 68 54

Obviously, the relentless decrease in bone mass that accompanies aging will continue the long sought "elixir of youth" is discovered. Individuals, because of race, sex, environmental, dietary, genetic or activity differences, will be more or less predisposed to symptomatic osteoporosis with increasing age. The careful and knowledgeable physician should, however, make every attempt to rule out potentially remediable, subtle forms of demineralizing disorders, such as apathetic or T3-thyrotoxicosis, hyperparathyroidism, malabsorption and osteomalacia or multiple myeloma. Not only do these diseases result in an accelerated loss of bone mass and an increased incidence of skeletal fractures but they mimic postmenopausal or senile osteoporosis radiologically. Once the metabolic or malignant disorders of bone metabolism have been effectively considered and ruled out, the senescent or postmenopausal osteoporotic patient should be treated judiciously with short-term estrogen therapy, a diet sufficient in vitamin D and calcium content and continued attempts to insure adequate skeletal mobilization. The addition of sodium fluoride and/or calcitonin to this regimen should not be attempted without extreme caution until the potentially harmful systemic effects of prolonged therapeutic trials have been appropriately assessed.
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PMID:Senile and postmenopausal osteoporosis. 76 91

Osteocalcin, also called bone gla-protein, is a bone matrix protein synthetized specifically by osteoblasts. It circulates in blood where it can be assayed by the radioimmune method. We measured osteocalcin serum levels in 169 adult controls and 161 patients with different disseminated or localized bone diseases. The normal concentration of 6.2 +/- 0.2 ng/ml increases significantly with age. Serum osteocalcin levels are considerably increased in renal osteodystrophy (114 +/- 23 ng/ml) and to a lesser degree in primary hyperparathyroidism (15.9 +/- 2.8 ng/ml) and Paget's disease (11.4 +/- 0.9 ng/ml), all diseases characterized by increased bone turnover. High levels are also encountered in osteomalacia (9.7 +/- 0.9 ng/ml). Conversely, serum osteocalcin levels are significantly decreased in patients under long-term corticosteroid therapy (4.3 +/- 0.5 ng/ml); they remain normal in patients with bone myeloma and bone metastases under treatment. Finally, osteocalcin is normal in patients with osteoporosis, but its level reflects that of bone turnover as evaluated by iliac bone biopsy. The circulating osteocalcin therefore is the first specific and sensitive marker for bone turnover. Serum osteocalcin measurements make it possible to evaluate the osteoblastic bone formation without biopsy and should provide information on the effectiveness of drugs acting on the bone-forming process.
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PMID:[Osteocalcin (or bone gla-protein), a new biological marker for studying bone pathology]. 293 33

Two patients, one with myeloma (Patient 1) and the other with probable chronic lymphocytic leukemia (Patient 2), had reduced renal tubular phosphate reabsorption in the absence of hyperparathyroidism together with other features of the Fanconi syndrome, as consequences of the nephropathy associated with light-chain proteinuria. Both patients had hypophosphatemic osteomalacia, demonstrated for the first time in this condition by iliac bone histomorphometry after in vivo double tetracycline labeling, despite absence of bone pain or Looser zones. Neither patient was vitamin D-depleted, but plasma calcitriol level was normal in Patient 1 and low in Patient 2; only the latter patient had severe muscle weakness. Complete histologic correction of osteomalacia was achieved by treatment in accordance with the biochemical defects--oral phosphate therapy alone in Patient 1 and combined with calcitriol in Patient 2. Both patients are now symptom-free, five and three years after the initial diagnosis of bone disease and hematogenous malignancy. Thirteen previous instances of the same form of osteomalacia were reviewed; in most cases, the Fanconi syndrome developed before its probable cause became apparent. The Fanconi syndrome has also been reported in two cases of osteomalacia due to mesenchymal tumor, but not in osteomalacia associated with prostatic carcinoma. Light-chain nephropathy and consequent renal tubular dysfunction appears to be a third form of oncogenous osteomalacia.
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PMID:Hypophosphatemic osteomalacia and adult Fanconi syndrome due to light-chain nephropathy. Another form of oncogenous osteomalacia. 310 97

Osteopenia in the elderly is responsible for 1.3 million fractures per year in the United States. The acute care costs associated with this disorder are between $6 and $10 billion dollars annually. Although much has been learned over the last few years of the factors that predispose patients to osteoporosis and how these factors may be avoided, the precise pathophysiologic mechanisms for bone loss remain obscure. Significant technological advances have been made in the 1980s in the development of noninvasive methods for measuring bone mineral density that give indirect assessments of bone mass. However, these methods are very controversial, are not suitable for mass screening for detecting subjects potentially at risk, and have a limited place in routine clinical care. Osteoporosis is characterized by thinning and fragmentation of trabecular bone, which is probably irreversible when it is far advanced. The most reasonable therapeutic approach may be prevention, which can be achieved in many patients by estrogen therapy in the perimenopausal years and insuring an adequate dietary calcium intake, particularly in adolescents and in the elderly. Physical activity throughout life is also likely to be important in maintaining adequate bone mass. It is important to differentiate osteoporosis from other causes of osteopenia, for example, osteomalacia, primary hyperparathyroidism, and malignant diseases such as myeloma, since these bone diseases have a different natural history, pathophysiology, and treatment.
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PMID:Osteopenia. 331 29

Results are presented of measurements of skeletal blood flow made in 80 patients with painful benign or malignant diseases of the skeleton, excluding patients with Paget's disease. In crush fracture osteoporosis, total bone blood flow was slightly lower than normal although skeletal perfusion was normal. High values of bone blood flow were seen in 14/20 patients with osteomalacia and 3/12 patients with primary hyperparathyroidism. Very high values, comparable to those seen in the most severely affected patients with Paget's disease, were seen in polyostotic fibrous dysplasia, 2 out of 4 cases of Engelmann's disease and 1 out of 3 cases of renal osteodystrophy. Results were less elevated in myositis ossificans, secondary skeletal involvement with breast and prostatic carcinomata, myelomatosis and sympathetic osteodystrophy.
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PMID:Skeletal blood flow in metabolic disorders of the skeleton. 342 88

Diphosphonates were administered intravenously to 4 patients with myeloma-induced hypercalcaemia. All patients received EHDP 4.3 mg/kg/day for 3 to 8 days. One of them, whose hypercalcaemia recurred, was later treated with Cl 2 MDP 5 mg/kg i.v. for 8 days. In 2 patients EHDP infusions were followed by EHDP administered orally (5 mg/kg/d) for 3 weeks, after which transiliac bone biopsy was performed. In all patients calcemia fell from 130 +/- 14 to 99 +/- 4 mg/l at the end of the intravenous treatment, with parallel decrease in calciuria. Histomorphometric analysis of the bone biopsies showed few osteoclasts but massive infiltration with plasmocytes. In one case, EHDP probably induced a deficit in mineralization. Intravenous diphosphonates therefore proved to be rapidly effective in the treatment of hypercalcaemia due to malignancy. However prolonged administration of EHDP in high doses is not recommended, as it may result in osteomalacia.
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PMID:[Treatment of hypercalcemia of myelomatous origin with intravenous diphosphonates]. 622 88

The authors undertake a general review of the association between hypophosphoraemia and connective tissue tumour, based upon three personal cases and 27 cases of benign connective tissue tumours, as well as cases of hypophosphoraemia related to malignant tumours or to diffuse dysplasia of connective tissue origin, collected from the literature. This syndrome is distinguished from hypophosphoraemia induced by other tumours (myeloma, carcinoma of the prostate) which are based upon different mechanisms. Hypophosphoraemia, associated with a fall in plasma levels of 1-25 (OH)2 D3 by inhibition of renal 1 alpha hydroxylase, suggests the existence of a complex tubular deficit. Removal of the tumour, most often vascular and intra- or para-osseous, results in rapid normalisation of laboratory then radiological and clinical abnormalities. The physiopathology of the syndrome remains very mysterious. It may be likened to certain tubulotoxic syndromes due to cadmium and in particular to maleic acid. However no precise data yet exists regarding any possible abnormal tumour secretion. In practice, any case of hypophosphoraemic osteomalacia requires investigation to locate a possible tumour of connective tissue, and this all the more so when it is accompanied by very low plasma levels of 1-25(OH)2 D2.
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PMID:[Hypophosphoremic osteomalacia of connective tissue tumors]. 628 21

The case here reported of 72 year-old female with osteomalacia in whom an adult's Fanconi's syndrome with distal tubular involvement and a monoclonal IgG-lambda paraprotein were discovered. There was urinary excretion of lambda light chains without evidence of myeloma or amyloidosis. Such apparently unrelated entities might be subject to an unitary pathophysiological approach: the nephrotoxicity of light chains could cause a Fanconi's syndrome, which in turn would give rise to osteomalacia through phosphate depletion. It is noteworthy that in this patient the urinary excretion of light chains was of the lambda type, in contrast to similar cases described in the literature which presented mostly kappa chains. The likelihood of this patient developing myeloma or amyloidosis at a later stage is discussed.
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PMID:[Monoclonal IgG lambda paraprotein, Fanconi's syndrome of the adult, and osteomalacia (author's transl)]. 678 49


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