Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3-4
pubmed:dateCreated
1986-1-10
pubmed:abstractText
Based on findings in 2 fluoride-toxic patients, it was suspected that hyperkalemia played a clinically important role in the etiology of sudden death from fluoride poisoning. Using fluoridated human erythrocytes as an in vitro model, it was confirmed that fluoride produced a marked potassium efflux from intact cells. Further, neither glucose and insulin in pharmacologic doses, nor various buffers could halt the efflux by shifting the potassium intracellularly. If these results can be extrapolated to the clinical situation, removal of potassium and fluoride via exchange resins or dialysis remains the only reasonable approach to this life threatening problem. Aside from sudden hyperkalemia and hypocalcemia, no serologic marker for fluoride toxicity has been identified. A high degree of clinical suspicion is therefore essential to the diagnosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0300-483X
pubmed:author
pubmed:issnType
Print
pubmed:volume
37
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
233-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1985
pubmed:articleTitle
The manipulation of potassium efflux during fluoride intoxication: implications for therapy.
pubmed:publicationType
Journal Article, In Vitro