Clinical Chemistry AACC Online Job Center
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Clinical Chemistry 43: 1072-1076, 1997;
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit an electronic Letter to
the Editor about this paper
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via ISI Web of Science (8)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Osselaer, J.-C.
Right arrow Articles by Scheiff, J.-M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Osselaer, J.-C.
Right arrow Articles by Scheiff, J.-M.
Related Collections
Right arrow Evidence Based Laboratory Medicine and Test Utilization
Right arrow Hematology
(Clinical Chemistry. 1997;43:1072-1076.)
© 1997 American Association for Clinical Chemistry, Inc.

Articles

Platelet distribution width for differential diagnosis of thrombocytosis

Jean-Claude Osselaer1,a, Jacques Jamart2 and Jean-Marie Scheiff3

1 Laboratory of Clinical Biology and
2 Center of Biostatistics and Medical Documentation, Mont-Godinne UCL University Hospital, 5530 Yvoir, Belgium.

3 Laboratory of Hematology, St-Luc–UCL University Hospital, 1200 Brussels, Belgium.
a Author for correspondence. Fax (32) 81 42 32 39.

Differential diagnosis of thrombocytosis is not always obvious. The routine clinical chemistry laboratory classically provides only limited help in distinguishing between reactive thrombocytosis (RT) and autonomous thrombocytosis, where platelet production escapes normal regulatory processes, and which is seen in myeloproliferative diseases (MPD) such as essential thrombocythemia and polycythemia vera. We explored the clinical use of platelet distribution width (PDW) in the differential diagnosis of thrombocytosis. During a 3-month period, 250 patients presenting with a platelet count >500 x 109/L were studied; 174 were classified as having RT, 42 had a diagnosis of MPD, and 34 patients were excluded because they had a hemopathy different from MPD, and either did or did not present a known etiologic factor for RT. First, we determined that in the RT group the value of PDW was closely linked to both mean platelet volume (MPV) and platelet count (PLT) (PDW = 79.5 - 0.005 PLT - 3.5 MPV; r = 0.848, R2 = 0.720). Therefore a new parameter, PDWresidual, was defined (PDWresidual = PDWobserved - PDWexpected). Second, the discrimination between reactive and autonomous thrombocytosis obtained with PDWresidual was compared with that obtained with either PDW, MPV, or PLT. PDWresidual proved much more powerful than each of the other parameters used separately: 76% of MPD patients had a PDWresidual above the 95th percentile value of the RT population and none of the MPD patients had a PDWresidualbelow the 50th percentile. Thus, the combined interpretation of PLT, MPV, and PDW through the use of a PDWresidualappears highly useful in the differential diagnosis of thrombocytosis. Also, through simple modeling, more information can be drawn from parameters such as PDW that hitherto were mostly discarded as being without clinical interest.


Key Words: indexing terms: myeloproliferative disease • platelets






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1997 by the American Association for Clinical Chemistry.