|
|
||||||||
Letters to the Editor |
Departments of
1
Laboratory Medicine, and
2 Medicine, University of Washington, School of Medicine, Seattle, WA 98195
aAddress correspondence to this author at: University of Washington, Department of Laboratory Medicine, Box 357110, Seattle, WA 98195-7110. Fax 206-598-6189; e-mail syuan@u.washington.edu.
| The first 20% of the full text of this article appears below. |
To the Editor:
The crystal arthropathies, gout and calcium pyrophosphate dihydrate deposition disease, are caused by deposition of monosodium urate (MSU) or calcium pyrophosphate dihydrate (CPPD) crystals, respectively. A diagnosis of urate gout or calcium pyrophosphate dihydrate deposition disease is based on characteristic clinical findings and the microscopic identification of intracellular crystals in synovial fluid.
Several studies have shown the lack of sensitivity of microscopic examination of synovial fluid for MSU or CPPD crystals [sensitivity, 78% (1) and 79% (2) for MSU and 12% (1) and 67%(2) for CPPD]. Not surprisingly, this leads to a lack of reproducibility of synovial fluid analyses (1)(2). The suboptimal sensitivity, frequently attributed to the low concentrations or the small sizes of the crystals, has been difficult to improve without resorting to clinically impractical methods such as crystal extraction from synovial fluid (3) or electron microscopy(4). Problems with sensitivity have led experts to caution that a negative examination by polarized light microscopy does not exclude the presence of small numbers of crystals (5
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |