Type of test Blood, urine
Normal findings
Platelet closure time (blood)
- Collagen/adenosine-5′-diphosphate (CADP): 64-120 seconds
- Collagen/epinephrine (CEPI): 89-193 seconds
11-Dehydro-thromboxane B2 (urine)
- Males: 0-1089 pg/mg of creatinine
- Females: 0-1811 pg/mg of creatinine
Bleeding time (blood)
1-9 minutes (Ivy method)
Test explanation and related physiology
Platelet dysfunction may be acquired, inherited, or induced by platelet-inhibiting agents. It is clinically important to assess platelet function as a potential cause of a bleeding diathesis (epistaxis, menorrhagia, postoperative bleeding, or easy bruising). The most common causes of platelet dysfunction are related to uremia, liver disease, von Willebrand disease (vWD), and expo sure to such agents as acetyl salicylic acid (ASA, aspirin). Several tests are used to evaluate platelet function. To measure bleeding time, a small standard superficial incision is made in the forearm, and the time required for the bleeding to stop is recorded. If a larger skin vessel is lacerated during the test, the bleeding time will be artificially prolonged. A repeat test is required. Compared with other alternatives, bleeding time (BT) is a bit more labor intensive, and its accuracy is heavily dependent on operator skills. Furthermore, its results are not easily reproduced and quantified. The platelet aggregation study (p. 700) may also have similar problems. With the development of an automated platelet function analyzer device, clinical laboratories can easily measure plate let closure time (PCT) to quantify platelet function. Furthermore, PCT can differentiate aspirin affects from other causes of platelet dysfunction.
This test can also be used to determine resistance of aspirin’s therapeutic anticoagulation effects on platelets. This is one of several aspirin resistance tests that are performed to determine the effectiveness of aspirin on inhibiting platelet aggregation and thereby protecting the patient from vascular thromboembolic disease (Table 1).
Table1. Platelet closure time
Aspirin resistance can be determined by platelet closure time or by measurement of 11-dehydro-thromboxane B2 (11 dTXB2) in the urine. Thromboxane A2 is produced by the enzyme cyclo-oxygenase-1 (COX1) by activated platelets and still further stimulates platelet activation, platelet aggregation, and vasoconstriction. 11-dTXB2 is the stable, inactive metabolite of thromboxane A2. Urinary 11-dTXB2, therefore is an indication of platelet activation and aggregation. Elevated values are associated with an increased risk of acute ischemic stroke and myocardial infarction. Effective aspirin therapy should reduce the level of this metabolite in the urine. If not, the patient may be aspirin resistant and may be more safely treated with an alternative therapy such as increasing the dos age of aspirin or placing the patient on another antiplatelet medication.
Urinary 11-dTXB2 offers an advantage over blood aspirin resistance tests because it is not subject to interference from in vitro platelet activation caused by local vein trauma or insufficient anticoagulation during blood sample collection.
Interfering factors
• Low hematocrit or platelet count can prolong PCT and BT.
* Aspirin and nonsteroidal antiinflammatory drugs (NSAIDs) can prolong PCT and DT test results or decrease urinary 11-dTXB2 levels.
* Thienopyridines can prolong test PCT.
Procedure and patient care
• See inside front cover for Routine Blood Testing.
• Fasting: no
• Blood tube commonly used: light blue
• Obtain a drug history to determine whether the patient has recently had aspirin or any other medications that may affect test results. Patient should not have taken NSAIDs within 72 hours or aspirin within 2 weeks before collection of a specimen for baseline analysis.
• For urinary 11-dTXB2, randomly collect 10 mL of urine. No preservative is necessary.
Abnormal findings
Prolonged times or increased values
Intrinsic platelet defects
- Some myelodysplastic syndromes
- Some myeloid leukemias
- Some myeloproliferative neoplasms
- Bernard–Soulier syndrome
- Glanzmann thromboasthenia
- Hermansky–Pudlak syndrome
- Hereditary telangiectasia
Platelet–blood vessel interaction defects
- von Willebrand disease
- Cushing syndrome
- Henoch–Schönlein syndrome
- Uremia
Elevated B2 (11-dTXB2) (on aspirin therapy)
- Increased risk of thromboembolic disease
