TC-99M-LABELED IMMUNOGLOBULIN SCINTIGRAPHY IN ARTHRITIS - AN ANALYSISOF SYNOVIAL-FLUID ACTIVITY

Citation
F. Jamar et al., TC-99M-LABELED IMMUNOGLOBULIN SCINTIGRAPHY IN ARTHRITIS - AN ANALYSISOF SYNOVIAL-FLUID ACTIVITY, Scandinavian journal of clinical & laboratory investigation, 57(7), 1997, pp. 621-628
Citations number
27
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
00365513
Volume
57
Issue
7
Year of publication
1997
Pages
621 - 628
Database
ISI
SICI code
0036-5513(1997)57:7<621:TISIA->2.0.ZU;2-5
Abstract
The distribution of Tc-99m-labelled human polyclonal non-specific immu no-globulin G (HIG) in the synovial fluid was studied in 14 patients w ith rheumatoid and non-rheumatoid arthritides. Analysis included the d etermination of the total activity per mi synovial fluid 6 h post-inje ction (p.i.) of the tracer as well as of the protein-and cell-bound fr actions. At 6h p.i., >60% of the injected dose remained in plasma as p rotein-bound radioactivity. Values in the synovial fluid ranged betwee n 0.001 and 0.009% of the injected dose per mi. Importantly, the synov ial fluid to plasma ratio was consistently <1 (range: 0.09-0.43), whic h is in the range of ratios observed for endogenous proteins in vivo. Similar values were obtained in samples of synovial tissue obtained at surgery in two patients. These data are consistent with the hypothesi s that labelled HIG accumulates in the extracellular fluid (both withi n the synovial tissue and fluid) by non-specific mechanisms (such as i ncreased blood pool and capillary permeability) and does not equilibra te with circulating plasma proteins in accordance with basic knowledge of synovial physiology. In addition, it was found that most of the ac tivity remained bound to the proteins in the fluid and that cell-bindi ng occurred to a very low degree that cannot be considered an importan t mechanism of uptake of this radiolabelled agent in vivo. These resul ts provide the first evidence in an in vivo human setting that radiola belled HIG accumulates mainly by non-specific mechanisms in inflamed j oints.