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Underlying diseases and clinicopathologic variables of thrombocytopenic dogs with and without platelet-bound antibodies detected by use of a flow cytometric assay: 83 cases (2004–2006)

Brigitte Hedwig DircksSmall Animal Clinic, University of Veterinary Medicine Hannover, 30173 Hannover, Germany.

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Hans-Joachim SchuberthInstitute for Immunology, University of Veterinary Medicine Hannover, 30173 Hannover, Germany.

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Reinhard MischkeSmall Animal Clinic, University of Veterinary Medicine Hannover, 30173 Hannover, Germany.

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Abstract

Objective—To characterize underlying diseases and clinical and clinicopathologic variables of thrombocytopenic dogs with and without platelet-bound antibodies (PBAs) and to evaluate clinicopathologic variables of dogs with primary immune-mediated thrombocytopenia (IMT).

Design—Retrospective case series.

Animals—83 thrombocytopenic dogs.

Procedures—Medical records were reviewed to identify dogs in which PBA tests were performed between 2004 and 2006; PBAs were measured via flow cytometry.

Results—PBAs were detected in 37 of 83 (45%) dogs. Thirteen dogs were suspected of having primary IMT. Median platelet counts were significantly lower in dogs with PBAs, compared with counts in dogs without PBAs. Dogs suspected of having primary IMT had significantly lower median platelet counts, compared with counts for those with secondary IMT. Mean platelet volume (MPV) was increased (> 14.3 fL) significantly more often in dogs without PBAs (19/33 [58%]) than in dogs with PBAs (7/26 [27%]). No dogs suspected of having primary IMT had an increase in MPV. Examination of bone marrow aspirates revealed an increase in megakaryopoiesis in a higher percentage of dogs with PBAs (14/21 [67%]) than in dogs without PBAs (7/18 [39%]). An increase in megakaryopoiesis was detected in all dogs suspected of having primary IMT that had a bone marrow analysis.

Conclusions and Clinical Relevance—Platelet counts, results of bone marrow analysis, and MPV may be helpful in dogs for the differentiation between primary IMT and thrombocytopenia resulting from other diseases. An MPV within or less than the reference range did not rule out an increase in megakaryopoietic activity.

Abstract

Objective—To characterize underlying diseases and clinical and clinicopathologic variables of thrombocytopenic dogs with and without platelet-bound antibodies (PBAs) and to evaluate clinicopathologic variables of dogs with primary immune-mediated thrombocytopenia (IMT).

Design—Retrospective case series.

Animals—83 thrombocytopenic dogs.

Procedures—Medical records were reviewed to identify dogs in which PBA tests were performed between 2004 and 2006; PBAs were measured via flow cytometry.

Results—PBAs were detected in 37 of 83 (45%) dogs. Thirteen dogs were suspected of having primary IMT. Median platelet counts were significantly lower in dogs with PBAs, compared with counts in dogs without PBAs. Dogs suspected of having primary IMT had significantly lower median platelet counts, compared with counts for those with secondary IMT. Mean platelet volume (MPV) was increased (> 14.3 fL) significantly more often in dogs without PBAs (19/33 [58%]) than in dogs with PBAs (7/26 [27%]). No dogs suspected of having primary IMT had an increase in MPV. Examination of bone marrow aspirates revealed an increase in megakaryopoiesis in a higher percentage of dogs with PBAs (14/21 [67%]) than in dogs without PBAs (7/18 [39%]). An increase in megakaryopoiesis was detected in all dogs suspected of having primary IMT that had a bone marrow analysis.

Conclusions and Clinical Relevance—Platelet counts, results of bone marrow analysis, and MPV may be helpful in dogs for the differentiation between primary IMT and thrombocytopenia resulting from other diseases. An MPV within or less than the reference range did not rule out an increase in megakaryopoietic activity.

Contributor Notes

Presented in part at the 17th European College of Veterinary Internal Medicine—Companion Animals Congress, Budapest, September 2007; and the 16th Annual Meeting of the InnLab DVG, Giessen, Germany, February 2008.

Address correspondence to Dr. Mischke (reinhard.mischke@tihohannover.de).