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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
|
pubmed:dateCreated |
1990-1-10
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pubmed:abstractText |
In order to clarify the mechanisms involved in the occurrence of lytic bone lesions (BL) in multiple myeloma (MM), we have compared the presenting myeloma-induced histological bone changes of 14 previously untreated MM patients with lytic BL with those of seven MM patients lacking lytic BL at presentation despite similar myeloma cell mass. A major unbalanced bone remodeling (increased bone resorption with normal to low bone formation) was the characteristic feature of patients presenting lytic BL. Furthermore, this unbalanced process was associated with a significant reduction of bone mass. Unexpectedly, a balanced bone remodeling (increase of both bone resorption and bone formation, without bone mass reduction) rather than a true lack of an excessive bone resorption was the usual feature of patients lacking lytic BL. Our current work clearly shows that a majority (72%) of patients with MM present an important unbalanced bone remodeling at diagnosis, leading to bone mass reduction and bone destruction (unbalanced MM). Some patients (20%) retain a balanced bone remodeling with initial absence of bone destruction (balanced MM). Few (8%) patients have pure osteoblastic MM without bone destruction.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0732-183X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
7
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
1909-14
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading | |
pubmed:year |
1989
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pubmed:articleTitle |
Mechanisms of bone destruction in multiple myeloma: the importance of an unbalanced process in determining the severity of lytic bone disease.
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pubmed:affiliation |
Department of Immunorhumatologie, Centre Gui-de-Chauliac, Hôpital Saint-Eloi, Montpellier, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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