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Antiplatelet drugs

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Anti-platelet agents

Site of action



- irreversibly acetylates and inactivates cyclo-oxygenase: enzyme responsible for conversion of membrane arachidonic acid to prostaglandin endoperoxides and thromboxane A2
- platelets lack nuclear machinery to replenish enzyme so platelets are affected for their lifespan
- platelet release inhibited and platelet aggregation impaired
- clinically translates into a prolonged bleeding time and potential for bleeding during surgical procedures for up to 8 days after last dose of aspirin. In most bleeding tendency mild and causes no problems during surgical procedures however in some patients, particularly those with mild associated haemostatic problems, bleeding can be pronounced and troublesome


  • Thioenopyridine platelet inhibitor
  • Prodrug. Requires activation by cytochrome P450 in liver
  • Irreversibly modifies platelet ADP receptor and thus blocks pro-aggregatory effects of ADP


  • Administration: PO. Almost completely absorbed
  • Platelet inhibition reaches a maximum after 5-8 days of repeated doses
  • 50-60% of oral dose eliminated in urine, remainder in faeces

Clinical uses

Unclear. Appears to be more effective than aspirin in preventing stroke in patients who have already had a stroke or a TIA. However aspirin remain treatment of choice because of ticlopidine’s bone marrow suppressant effects.

Ticlopidine plus aspirin is more effective than aspirin alone or aspirin plus anticoagulants in preventing thromboembolic complications related to coronary stenting, but it is not licensed for this use.

Adverse effects

  • Neutropaenia in 2.4%, severe in 0.8%
  • TTP in 0.02%
  • Nausea, diarrhoea.
  • Rashes
  • Abnormal liver function tests rarely. Cholestatic jaundice has been reported
  • Rashes and diarrhoea are more common than with aspirin but other GI effects, including peptic ulceration are less common.


  • history of leucopaenia, thrombocytopaenia or agranulocytosis
  • blood diseases that prolong bleeding time
  • lesions likely to bleed (eg active peptic ulcer, acute haemorrhagic stroke)
  • caution in patients with impaired liver function. Should be discontinued if hepatitis or jaundice develops. There is little experience of its use in patients with renal impairment


Similar to ticlopidine in that it is also a thioenopyridine platelet inhibitor and requires activation by cyctochrome P450. Same mode of action


  • Administration: PO. After repeated oral doses >50% is absorbed.
  • Inhibition of platelet function reaches a maximum after 3-7 days
  • Elimination: 50% of a single oral dose is excreted in the urine and 46% in faeces

Clinical uses

Unclear. Appears to offer little or no worthwhile advantage over aspirin. Little data to support its use in combination with aspirin instead of ticlopidine combined with aspirin.

Adverse effects

  • rash (severe rash more common than with aspirin)
  • GI haemorrhage (severe haemorrhage less common than with aspirin)
  • diarrhoea, upper GI symptoms, neutropaenia, intracranial haemorrhage (similar incidence to aspirin)


  • Severe liver impairment
  • Active bleeding
  • Breast feeding women
  • In first few days following acute myocardial infarction
  • Manufacturer does not recommend its use in unstable angina, in those undergoing PTCA or CABG.
  • Should be used with caution in patients who may be at risk of increased bleeding and should be stopped 7 days prior to surgery if anti-platelet effect is not desired.
  • Use with caution in patients with renal or hepatic impairment.

Further reading

Clopidogrel and ticlopidine – improvements on aspirin? Drugs and Therapeutics Bulletin, 1999, 37:59-61


©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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