Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1999-6-24
pubmed:abstractText
Marked parathyroid hyperplasia of heterogeneous degrees is often seen in chronic dialysis patients with severe secondary hyperparathyroidism. In uremia, parathyroid cell proliferation is initially stimulated by decreased concentration of calcium ions and calcitriol and also by direct effect of phosphate accumulation, leading to diffuse hyperplasia of the parathyroid. Then, small nodules caused by monoclonal cell proliferation form within diffuse hyperplasia, which progress to form nodular hyperplasia. Cells in nodular hyperplasia have a lower density of calcitriol receptor and calcium-sensing receptor than diffuse hyperplasia and are thus more resistant to medical therapy, including calcitriol pulse therapy. One of these nodules may grow more vigorously than the others and may finally occupy a large part of the enlarged gland. Genetic mutations and rearrangements of these cells in nodular hyperplasia remain to be fully elucidated in the near future to establish an effective method for the prevention of parathyroid hyperplasia in uremia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0002-9629
pubmed:author
pubmed:issnType
Print
pubmed:volume
317
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
377-82
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Cell biology of parathyroid hyperplasia in uremia.
pubmed:affiliation
Division of Nephrology, Tokyo Teishin Hospital and University of Tokyo School of Medicine, Japan. fukagawa-tky@umin.ac.jp
pubmed:publicationType
Journal Article, Review