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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of ticlopidine are reviewed. Ticlopidine appears to inhibit platelet aggregation induced by adenosine diphosphate. Ticlopidine hydrochloride is rapidly absorbed after oral administration, and maximum antiplatelet effects occur one to three hours after the dose. In multicenter, randomized, double-blind trials, ticlopidine was more effective than aspirin or placebo in preventing stroke, myocardial infarction, or death caused by vascular events. Ticlopidine was more effective than aspirin in preventing recurrent transient ischemic attacks after six months of therapy. Ticlopidine has also been used to prevent occlusion and improve patency of aortocoronary bypass grafts, to prevent ischemic ulcers in patients with chronic arterial occlusive disease, and to slow the progression of diabetic microangiopathy. The most serious adverse effect, neutropenia, occurred in about 1% of patients. The most frequently reported adverse effects are diarrhea, nausea, vomiting, and abdominal cramps. Ticlopidine is indicated for reducing the risk of thrombotic stroke in patients who have experienced a minor stroke, transient ischemic attack, or completed thrombotic stroke. The recommended dosage is 500 mg/day in two divided doses taken with food. Ticlopidine is an alternative agent for the primary and secondary prevention of stroke. Because of the risk of neutropenia and agranulocytosis and the high cost of therapy, ticlopidine should be reserved for patients who are intolerant of or lack benefit from aspirin.
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PMID:Ticlopidine: a new platelet aggregation inhibitor. 161 11

Approximately 1000 patients who have suffered a well-documented thromboembolic stroke within two weeks to four months of study entry will be enrolled in this double-blind, randomized, placebo controlled, parallel group trial. Five Canadian and five United States study centers will participate. The enrollment period will be two and one half years, and follow-up will run for an additional six months to a common termination point at three years. Ticlopidine hydrochloride, administered as two 125 mg tablets b.i.d. (500 mg/day total dose) will be compared with placebo for efficacy in the prevention of recurrent stroke, myocardial infarction, cardiovascular death, and overall mortality. Inclusion and exclusion criteria will be the minimum necessary to provide safety and scientific validity. After a screening visit, qualifying patients will be randomly assigned to ticlopidine or placebo. Follow-up laboratory studies for monitoring complete blood and platelet counts will be made at weeks 2, 4, 6, 8, 10 and 12, and then months 4, 5, 6, 8 and then every 4 months thereafter. Follow-up clinic visits will be made at 1 month, 4 months, and then every four months thereafter for clinical evaluation and for dispensing test medication. Study outcome events will be appropriately documented on case report forms. The statistical analysis will evaluate the initial comparability of the two treatment groups, and the principal outcomes of the two groups will be compared by using the Mantel-Haenszel life table analysis.
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PMID:Canadian American ticlopidine study (cats) in thromboembolic stroke. 638 53

Ticlopidine hydrochloride is an antiplatelet agent of proven antithrombotic efficacy that in December 1991 became available for general clinical use in the United States. The relative value of ticlopidine compared with aspirin, also an effective antiplatelet agent, has become a key clinical issue. Whereas ticlopidine is somewhat more effective than aspirin for preventing stroke in certain populations, it is also more expensive and potentially toxic. We recommend its use for patients with threatened stroke who are intolerant of aspirin and for patients who have cerebral ischemic symptoms despite aspirin therapy. Patients surviving major ischemic stroke make up a third group for whom ticlopidine use may be recommended in preference to aspirin. The use of ticlopidine rather than aspirin in patients with other cerebrovascular conditions is not strongly supported by existing data. The risk-benefit-cost equation involving ticlopidine versus other antithrombotic therapies is complex, rendering a wide range of acceptable management practices. If reliable laboratory monitoring for neutropenia during the first 3 months of therapy is not feasible, ticlopidine should not be used.
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PMID:Ticlopidine hydrochloride use and threatened stroke. 812 1

Ticlopidine hydrochloride, an inhibitor of platelet aggregation that has been approved for use in the United States for secondary stroke prevention, may be more effective than aspirin for the secondary prevention of stroke, but this advantage decreases greatly over time. The pharmacology, adverse effects, efficacy, drug interactions, and indications for ticlopidine are discussed here with summaries of various clinical trials. The drug is more costly than aspirin, and patients must have complete blood counts during the first 3 months of therapy. It is recommended for those who cannot take aspirin and may be more effective in certain groups--nonwhites, diabetics, and women and those with vertebrobasilar ischemia, intermittent claudication, unstable angina, and nonproliferative retinopathy.
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PMID:Ticlopidine: a new antiplatelet agent for the secondary prevention of stroke. 814 56

Ticlopidine hydrochloride (Ticlid) has been increasingly used as an antiplatelet agent. Some studies showed that it has higher efficacy in reducing stroke recurrence when compared to conventional aspirin. Side effects like gastrointestinal disturbances and blood dyscrasias are common but ticlopidine-induced cholestatic jaundice has been reported only rarely. We present a case report on a patient who has ticlopidine-induced cholestatic jaundice.
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PMID:Ticlopidine induced cholestatic jaundice. 926 84

Clopidogrel (Plavix-Sanofi Winthrop/Bristol-Myers Squibb) and [symbol: see text] ticlopidine (Ticlid-Sanofi Winthrop) are inhibitors of platelet function and are promoted as potential alternatives to aspirin. Clopidogrel is licensed for the secondary prevention of vascular events in patients with established atherosclerotic disease. The manufacturer claims that clopidogrel is "significantly more effective at reducing myocardial infarction, stroke and vascular death" compared to aspirin. Ticlopidine is licensed as an alternative to aspirin for secondary prevention of stroke and coronary complications in patients with intermittent claudication. However, in the UK, ticlopidine is more commonly used with aspirin to prevent complications following insertion of coronary stents during angioplasty. We consider whether the claims for clopidogrel and the current use of ticlopidine are justified.
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PMID:Clopidogrel and [symbol: see text] ticlopidine--improvements on aspirin? 1069 86