Required section · Section 4 of 6
Guided example
LTA is performed on platelet-rich plasma from a properly filled 3.2% buffered sodium-citrate specimen, tested within four hours alongside a parallel normal control. ADP 2 µM, epinephrine 5 µM, and collagen each aggregate within the laboratory's local reference limits. Those three agonists activate platelets and drive fibrinogen-bridged aggregation directly; in this static, cuvette-based method they do not depend on the VWF-GPIb tether, so a normal tracing to all three does not rule in or out a VWF-mediated finding by itself.
Ristocetin at the standard 1.2 mg/mL concentration shows reduced agglutination compared with the parallel normal control. Low-dose ristocetin at 0.5–0.7 mg/mL is a separate step with a different purpose: it looks for agglutination that is exaggerated relative to the normal control, a pattern that would raise concern for platelet hyperreactivity to VWF rather than a tethering defect. In the guided case the low-dose response is not enhanced relative to the parallel control and stays within the laboratory's local acceptance boundary, so this step does not by itself add a subtype-level finding.
The count is normal, the smear has no giant platelets, ADP, epinephrine, and collagen aggregation are within local limits, and ristocetin agglutination is reduced at the standard dose without low-dose enhancement. That combination points toward a VWF-mediated adhesion defect: normal aggregation to agonists that do not require the VWF-GPIb tether makes Glanzmann thrombasthenia less consistent, since that disorder abolishes aggregation to those same agonists while ristocetin-induced agglutination stays preserved. Bernard-Soulier syndrome remains a look-alike at the adhesion step, but it typically has thrombocytopenia with large or giant platelets. These observations narrow a differential; they do not name a VWD subtype.
The defensible next laboratory information is VWF antigen, platelet-dependent VWF activity, and factor VIII activity. A structured bleeding history can support context, but the ISTH Bleeding Assessment Tool measures bleeding phenotype rather than VWF concentration or subtype. CLSI H21 provides general plasma coagulation specimen principles and explicitly excludes platelet-function testing and whole-blood platelet counts from its scope. Separate the assay pattern from the diagnosis and release only the conclusion the evidence supports.
| Agonist | Case observation | Localization use |
|---|---|---|
| ADP 2 µM | Aggregation within local reference limits | Does not require the VWF-GPIb tether; a normal response argues against Glanzmann thrombasthenia but does not by itself confirm or exclude a VWF-mediated finding. |
| Epinephrine 5 µM | Aggregation within local reference limits | Does not require the VWF-GPIb tether; a normal response argues against Glanzmann thrombasthenia but does not by itself confirm or exclude a VWF-mediated finding. |
| Collagen | Aggregation within local reference limits | Does not require the VWF-GPIb tether; a normal response argues against Glanzmann thrombasthenia but does not by itself confirm or exclude a VWF-mediated finding. |
| Ristocetin 1.2 mg/mL (standard dose) | Reduced agglutination compared with the parallel normal control | Directs attention to VWF-GPIb-mediated adhesion. |
| Ristocetin 0.5–0.7 mg/mL (low dose) | Not enhanced relative to the parallel normal control; within the local acceptance boundary | Screens for platelet hyperreactivity to VWF; an unremarkable result here adds no subtype-level finding. |
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