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ticlopidine hydrochloride tablet, coated
TICLOPIDINE HYDROCHLORIDE TABLETS
|* Comparison of ticlopidine plus aspirin to aspirin alone.|
+ Aspirin N=546
|Primary Endpoint||3 (0.5%)||20 (3.6%)||15 (2.7%)||0.15 (0.03, 0.51)||<0.001|
|Deaths||0 (0%)||1 (0.2%)||0 (0%)||-||-|
|Q-Wave MI (Recurrent and Procedure Related)||1 (0.2%)||12 (2.2%)||8 (1.5%)||0.08 (0.002, 0.57)||0.004|
|Angiographically Evident Thrombosis||3 (0.5%)||16 (2.9%)||15 (2.7%)||0.19 (0.03, 0.66)||0.005|
The use of ticlopidine plus aspirin did not affect the rate of non-Q-wave MIs when compared with aspirin alone or aspirin plus anticoagulants in STARS.
The use of ticlopidine plus aspirin was associated with a lower rate of recurrent cardiovascular events when compared with aspirin alone or aspirin plus anticoagulants in the other four randomized trials.
The rate of serious bleeding complications and neutropenia in STARS are shown in the table below. There were no cases of thrombotic thrombocytopenic purpura (TTP) or aplastic anemia reported in 1346 patients who received ticlopidine plus aspirin in the five randomized trials.
|Hemorrhagic Complications||30 (5.5%)||10 (1.8%)||34 (6.2%)|
|Cerebrovascular Accident||0 (0%)||2 (0.4%)||1 (0.2%)|
|Neutropenia (≤1200/mm3)||3 (0.5%)||0 (0%)||1 (0.2%)|
Ticlopidine hydrochloride tablets are indicated:
The use of ticlopidine hydrochloride is contraindicated in the following conditions:
Neutropenia may occur suddenly. Bone-marrow examination typically shows a reduction in white blood cell precursors. After withdrawal of ticlopidine, the neutrophil count usually rises to > 1200/mm3 within 1 to 3 weeks.
TTP is characterized by thrombocytopenia, microangiopathic hemolytic anemia (schistocytes [fragmented RBCs] seen on peripheral smear), neurological findings, renal dysfunction, and fever. The signs and symptoms can occur in any order; in particular, clinical symptoms may precede laboratory findings by hours or days. With prompt treatment (often including plasmapheresis), 70% to 80% of patients will survive with minimal or no sequelae. Because platelet transfusions may accelerate thrombosis in patients with TTP on ticlopidine, they should, if possible, be avoided.
Aplastic anemia is characterized by anemia, thrombocytopenia and neutropenia together with a bone marrow examination that shows decreases in the precursor cells for red blood cells, white blood cells, and platelets. Patients may present with signs or symptoms suggestive of infection, in association with low white blood cell and platelet counts. Prompt treatment, which may include the use of drugs to stimulate the bone marrow, can minimize the mortality associated with aplastic anemia.
Starting just before initiating treatment and continuing through the third month of therapy, patients receiving ticlopidine hydrochloride must be monitored every 2 weeks. Because of ticlopidine’s long plasma half-life, patients who discontinue ticlopidine during this 3-month period should continue to be monitored for 2 weeks after discontinuation. More frequent monitoring, and monitoring after the first 3 months of therapy, is necessary only in patients with clinical signs (e.g., signs or symptoms suggestive of infection) or laboratory signs (e.g., neutrophil count less than 70% of the baseline count, decrease in hematocrit or platelet count) that suggest incipient hematological adverse reactions.
Clinically, fever might suggest neutropenia, TTP or aplastic anemia; TTP might also be suggested by weakness, pallor, petechiae or purpura, dark urine (due to blood, bile pigments, or hemoglobin) or jaundice, or neurological changes. Patients should be told to discontinue ticlopidine hydrochloride and to contact the physician immediately upon the occurrence of any of these findings. Laboratory monitoring should include a complete blood count, with special attention to the absolute neutrophil count (WBC x % neutrophils), platelet count, and the appearance of the peripheral smear. Ticlopidine is occasionally associated with thrombocytopenia unrelated to TTP or aplastic anemia. Any acute, unexplained reduction in hemoglobin or platelet count should prompt further investigation for a diagnosis of TTP, and the appearance of schistocytes (fragmented RBCs) on the smear should be treated as presumptive evidence of TTP. A simultaneous decrease in platelet count and WBC count should prompt further investigation for a diagnosis of aplastic anemia. If there are laboratory signs of TTP or aplastic anemia, or if the neutrophil count is confirmed to be < 1200/mm3, then ticlopidine hydrochloride should be discontinued immediately.
Rare cases of agranulocytosis, pancytopenia or leukemia have been reported in postmarketing experience, some of which have been fatal. All forms of hematological adverse reactions are potentially fatal.
Ticlopidine hydrochloride therapy causes increased serum cholesterol and triglycerides. Serum total cholesterol levels are increased 8% to 10% within 1 month of therapy and persist at that level. The ratios of the lipoprotein subfractions are unchanged.
The tolerance and safety of coadministration of ticlopidine hydrochloride with heparin, oral anticoagulants, or fibrinolytic agents have not been established. If a patient is switched from an anticoagulant or fibrinolytic drug to ticlopidine hydrochloride, the former drug should be discontinued prior to ticlopidine hydrochloride administration.
Ticlopidine hydrochloride should be used with caution in patients who may be at risk of increased bleeding from trauma, surgery or pathological conditions. If it is desired to eliminate the antiplatelet effects of ticlopidine hydrochloride prior to elective surgery, the drug should be discontinued 10 to 14 days prior to surgery. Several controlled clinical studies have found increased surgical blood loss in patients undergoing surgery during treatment with ticlopidine. In TASS and CATS it was recommended that patients have ticlopidine discontinued prior to elective surgery. Several hundred patients underwent surgery during the trials, and no excessive surgical bleeding was reported.
Prolonged bleeding time is normalized within 2 hours after administration of 20 mg methylprednisolone IV. Platelet transfusions may also be used to reverse the effect of ticlopidine hydrochloride on bleeding. Because platelet transfusions may accelerate thrombosis in patients with TTP on ticlopidine, they should, if possible, be avoided.
Ticlopidine hydrochloride prolongs template bleeding time. The drug should be used with caution in patients who have lesions with a propensity to bleed (such as ulcers). Drugs that might induce such lesions should be used with caution in patients on ticlopidine hydrochloride (See CONTRAINDICATIONS).
Since ticlopidine is metabolized by the liver, dosing of ticlopidine hydrochloride or other drugs metabolized in the liver may require adjustment upon starting or stopping concomitant therapy. Because of limited experience in patients with severe hepatic disease, who may have bleeding diatheses, the use of ticlopidine hydrochloride is not recommended in this population (See CLINICAL PHARMACOLOGY and CONTRAINDICATIONS).
There is limited experience in patients with renal impairment. Decreased plasma clearance, increased AUC values, and prolonged bleeding times can occur in renally impaired patients. In controlled clinical trials, no unexpected problems have been encountered in patients having mild renal impairment, and there is no experience with dosage adjustment in patients with greater degrees of renal impairment. Nevertheless, for renally impaired patients, it may be necessary to reduce the dosage of ticlopidine or discontinue it altogether, if hemorrhagic or hematopoietic problems are encountered (See CLINICAL PHARMACOLOGY).
Patients should be told that a decrease in the number of white blood cells (neutropenia) or platelets (thrombocytopenia) can occur with ticlopidine hydrochloride, especially during the first 3 months of treatment and that neutropenia, if it is severe, can result in an increased risk of infection. They should be told it is critically important to obtain the scheduled blood tests to detect neutropenia or thrombocytopenia. Patients should also be reminded to contact their physicians if they experience any indication of infection such as fever, chills, or sore throat, any of which might be a consequence of neutropenia. Thrombocytopenia may be part of a syndrome called TTP. Symptoms and signs of TTP, such as fever, weakness, difficulty speaking, seizures, yellowing of skin or eyes, dark or bloody urine, pallor or petechiae (pinpoint hemorrhagic spots on the skin), should be reported immediately.
All patients should be told that it may take them longer than usual to stop bleeding when they take ticlopidine hydrochloride and that they should report any unusual bleeding to their physician. Patients should tell physicians and dentists that they are taking ticlopidine hydrochloride before any surgery is scheduled and before any new drug is prescribed.
Patients should be told to promptly report side effects of ticlopidine hydrochloride such as severe or persistent diarrhea, skin rashes, or subcutaneous bleeding or any signs of cholestasis, such as yellow skin or sclera, dark urine, or light-colored stools.
Patients should be told to take ticlopidine hydrochloride with food or just after eating in order to minimize gastrointestinal discomfort.
Ticlopidine hydrochloride therapy has been associated with elevations of alkaline phosphatase, bilirubin and transaminases, which generally occurred within 1 to 4 months of therapy initiation. In controlled clinical trials, the incidence of elevated alkaline phosphatase (greater than two times upper limit of normal) was 7.6% in ticlopidine patients, 6% in placebo patients and 2.5% in aspirin patients. The incidence of elevated AST (SGOT) (greater than two times upper limit of normal) was 3.1% in ticlopidine patients, 4% in placebo patients and 2.1% in aspirin patients. No progressive increases were observed in closely monitored clinical trials (e.g. no transaminase greater than 10 times the upper limit of normal was seen), but most patients with these abnormalities had therapy discontinued. Occasionally patients had developed minor elevations in bilirubin.
Post-marketing experience includes rare individuals with elevations in their transaminases and bilirubin to >10x above the upper limits of normal. Based on postmarketing and clinical trial experience, liver function testing, including ALT, AST, and GGT, should be considered whenever liver dysfunction is suspected, particularly during the first 4 months of treatment.
Therapeutic doses of ticlopidine hydrochloride caused a 30% increase in the plasma half-life of antipyrine and may cause analogous effects on similarly metabolized drugs. Therefore, the dose of drugs metabolized by hepatic microsomal enzymes with low therapeutic ratios or being given to patients with hepatic impairment may require adjustment to maintain optimal therapeutic blood levels when starting or stopping concomitant therapy with ticlopidine. Studies of specific drug interactions yielded the following results:
Ticlopidine potentiates the effect of aspirin or other NSAIDs on platelet aggregation. The safety of concomitant use of ticlopidine with aspirin or other NSAIDs has not been established. The safety of concomitant use of ticlopidine and aspirin beyond 30 days has not been established (See CLINICAL TRIALS: Stent Patients). Aspirin did not modify the ticlopidine-mediated inhibition of ADP-induced platelet aggregation, but ticlopidine potentiated the effect of aspirin on collagen-induced platelet aggregation. Caution should be exercised in patients who have lesions with a propensity to bleed, such as ulcers. Long-term concomitant use of aspirin and ticlopidine is not recommended (See PRECAUTIONS - GI Bleeding).
Administration of ticlopidine hydrochloride after antacids resulted in an 18% decrease in plasma levels of ticlopidine.
Chronic administration of cimetidine reduced the clearance of a single dose of ticlopidine hydrochloride by 50%.
Co-administration of ticlopidine hydrochloride with digoxin resulted in a slight decrease (approximately 15%) in digoxin plasma levels. Little or no change in therapeutic efficacy of digoxin would be expected.
In normal volunteers, concomitant administration of ticlopidine hydrochloride resulted in a significant increase in the theophylline elimination half-life from 8.6 to 12.2 hours and a comparable reduction in total plasma clearance of theophylline.
In 6 normal volunteers, the inhibitory effects of ticlopidine hydrochloride on platelet aggregation were not altered by chronic administration of phenobarbital.
In vitro studies demonstrated that ticlopidine does not alter the plasma protein binding of phenytoin. However, the protein binding interactions of ticlopidine and its metabolites have not been studied in vivo. Several cases of elevated phenytoin plasma levels with associated somnolence and lethargy have been reported following coadministration with ticlopidine hydrochloride. Caution should be exercised in coadministering this drug with ticlopidine hydrochloride, and it may be useful to remeasure phenytoin blood concentrations.
In vitro studies demonstrated that ticlopidine does not alter the plasma protein binding of propranolol. However, the protein binding interactions of ticlopidine and its metabolites have not been studied in vivo. Caution should be exercised in coadministering this drug with ticlopidine hydrochloride.
The oral bioavailability of ticlopidine is increased by 20% when taken after a meal. Administration of ticlopidine hydrochloride with food is recommended to maximize gastrointestinal tolerance. In controlled trials in stroke patients, ticlopidine hydrochloride was taken with meals.
In a 2-year oral carcinogenicity study in rats, ticlopidine at daily doses of up to 100 mg/kg (610 mg/m2) was not tumorigenic. For a 70 kg person (1.73 m2 body surface area), the dose represents 14 times the recommended clinical dose on a mg/kg basis and two times the clinical dose on body surface area basis. In a 78-week oral carcinogenicity study in mice, ticlopidine at daily doses up to 275 mg/kg (1180 mg/m2) was not tumorigenic. The dose represents 40 times the recommended clinical dose on a mg/kg basis and four times the clinical dose on body surface area basis.
Ticlopidine was not mutagenic in vitro in the Ames test, the rat hepatocyte DNA-repair assay, or the Chinese-hamster fibroblast chromosomal aberration test; or in vivo in the mouse spermatozoid morphology test, the Chinese-hamster micronucleus test, or the Chinese-hamster bone-marrow-cell sister-chromatid exchange test. Ticlopidine was found to have no effect on fertility of male and female rats at oral doses up to 400 mg/kg/day.
Teratology studies have been conducted in mice (doses up to 200 mg/kg/day), rats (doses up to 400 mg/kg/day) and rabbits (doses up to 200 mg/kg/day). Doses of 400 mg/kg in rats, 200 mg/kg/day in mice, and 100 mg/kg in rabbits produced maternal toxicity as well as fetal toxicity, but there was no evidence of a teratogenic potential of ticlopidine. There are, however, no adequate and well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of a human response, this drug should be used during pregnancy only if clearly needed.
Studies in rats have shown ticlopidine is excreted in the milk. It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from ticlopidine, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.
Clearance of ticlopidine is somewhat lower in elderly patients and trough levels are increased. The major clinical trials with ticlopidine in stroke patients were conducted in an elderly population with an average age of 64 years. Of the total number of patients in the therapeutic trials, 45% of patients were over 65 years old and 12% were over 75 years old. No overall differences in effectiveness or safety were observed between these patients and younger patients, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out.
Adverse reactions were relatively frequent, with over 50% of patients reporting at least one. Most (30% to 40%) involved the gastrointestinal tract. Most adverse effects are mild, but 21% of patients discontinued therapy because of an adverse event, principally diarrhea, rash, nausea, vomiting, Gl pain, and neutropenia. Most adverse effects occur early in the course of treatment, but a new onset of adverse effects can occur after several months.
The incidence rates of adverse events listed in the following table were derived from multicenter, controlled clinical trials in stroke patients described above comparing ticlopidine hydrochloride, placebo, and aspirin over study periods of up to 5.8 years. Adverse events considered by the investigator to be probably drug-related that occurred in at least 1% of patients treated with ticlopidine hydrochloride are shown in the following table:
|Incidence of discontinuation, regardless of relationship to therapy, is shown in parentheses.|
|Percent of Patients with Adverse Events in Controlled Studies (TASS and CATS)|
|Event||Ticlopidine hydrochloride (n=2048) Incidence||Aspirin (n=1527) Incidence||Placebo (n=536) Incidence|
|Any Events||60.0 (20.9)||53.2 (14.5)||34.3 (6.1)|
|Diarrhea||12.5 (6.3)||5.2 (1.8)||4.5 (1.7)|
|Nausea||7.0 (2.6)||6.2 (1.9)||1.7 (0.9)|
|Dyspepsia||7.0 (1.1)||9.0 (2.0)||0.9 (0.2)|
|Rash||5.1 (3.4)||1.5 (0.8)||0.6 (0.9)|
|Gl Pain||3.7 (1.9)||5.6 (2.7)||1.3 (0.4)|
|Neutropenia||2.4 (1.3)||0.8 (0.1)||1.1 (0.4)|
|Purpura||2.2 (0.2)||1.6 (0.1)||0.0 (0.0)|
|Vomiting||1.9 (1.4)||1.4 (0.9)||0.9 (0.4)|
|Flatulence||1.5 (0.1)||1.4 (0.3)||0.0 (0.0)|
|Pruritus||1.3 (0.8)||0.3 (0.1)||0.0 (0.0)|
|Dizziness||1.1 (0.4)||0.5 (0.4)||0.0 (0.0)|
|Anorexia||1.0 (0.4)||0.5 (0.3)||0.0 (0.0)|
|Abnormal Liver Function test||1.0 (0.7)||0.3 (0.3)||0.0 (0.0)|
Neutropenia/thrombocytopenia, TTP, aplastic anemia (see BOXED WARNING and WARNINGS), leukemia, agranulocytosis, eosinophilia, pancytopenia, thrombocytosis, and bone marrow depression have been reported.
Ticlopidine hydrochloride therapy has been associated with a variety of gastrointestinal complaints including diarrhea and nausea. The majority of cases are mild, but about 13% of patients discontinued therapy because of these. They usually occur within 3 months of initiation of therapy and typically are resolved within 1 to 2 weeks without discontinuation of therapy. If the effect is severe or persistent, therapy should be discontinued. In some cases of severe or bloody diarrhea, colitis was later diagnosed.
Ticlopidine hydrochloride has been associated with increased bleeding, spontaneous post-traumatic bleeding, and perioperative bleeding including, but not limited to, gastrointestinal bleeding. It has also been associated with a number of bleeding complications such as ecchymosis, epistaxis, hematuria, and conjunctival hemorrhage.
Intracerebral bleeding was rare in clinical trials with ticlopidine hydrochloride, with an incidence no greater than that seen with comparator agents (ticlopidine 0.5%, aspirin 0.6%, placebo 0.75%). It has also been reported postmarketing.
Ticlopidine has been associated with a maculopapular or urticarial rash (often with pruritus). Rash usually occurs within 3 months of initiation of therapy, with a mean onset time of 11 days. If drug is discontinued, recovery occurs within several days. Many rashes do not recur on drug rechallenge. There have been rare reports of severe rashes, including Stevens-Johnson syndrome, erythema multiforme, and exfoliative dermatitis.
Clinical adverse experiences occurring in 0.5% to 1.0% of patients in the controlled trials include:
• Digestive System: Gl fullness
• Body as a Whole: asthenia, pain
• Skin and Appendages: urticaria
• Hemostatic System: epistaxis
• Nervous System: headache
• Special Senses: tinnitus
In addition, rarer, relatively serious and potentially fatal events associated with the use of ticlopidine hydrochloride have also been reported from postmarketing experience: Hemolytic anemia with reticulocytosis, immune thrombocytopenia, hepatitis, hepatocellular jaundice, cholestatic jaundice, hepatic necrosis, hepatic failure, peptic ulcer, renal failure, nephrotic syndrome, hyponatremia, vasculitis, sepsis, allergic reactions (including angioedema, allergic pneumonitis, and anaphylaxis), systemic lupus (positive ANA), peripheral neuropathy, serum sickness, arthropathy, and myositis.
One case of deliberate overdosage with ticlopidine hydrochloride has been reported by a foreign postmarketing surveillance program. A 38 year old male took a single 6000 mg dose of ticlopidine hydrochloride (equivalent to 24 standard 250 mg tablets). The only abnormalities reported were increased bleeding time and increased SGPT. No special therapy was instituted and the patient recovered without sequelae.
Single oral doses of ticlopidine at 1600 mg/kg and 500 mg/kg were lethal to rats and mice, respectively. Symptoms of acute toxicity were Gl hemorrhage, convulsions, hypothermia, dyspnea, loss of equilibrium and abnormal gait.
The recommended dose of ticlopidine hydrochloride tablets is 250 mg bid taken with food. Other doses have not been studied in controlled trials for these indications.
Ticlopidine hydrochloride is available in white to off-white, oval, biconvex, unscored, film-coated 250 mg tablets, debossed with “G” on one side and "T250" on the other. They are provided:
- in unit of use bottles of 30 tablets (NDC 55567-054-13)
- in bottles of 100 tablets (NDC 55567-054-18)
- in bottles of 500 tablets (NDC 55567-054-25)
- in cartons of 98 blister packed tablets (NDC 55567-054-07).
Store at 15° to 30°C (59° to 86°F). Dispense in a tight light-resistant container. A Patient Package Insert should be dispensed with each prescription.
The information in this leaflet is intended to help you use ticlopidine hydrochloride safely. Please read the leaflet carefully. Although it does not contain all the detailed medical information that is provided to your doctor, it provides facts about ticlopidine hydrochloride that are important for you to know. If you still have questions after reading this leaflet or if you have questions at any time during your treatment with ticlopidine hydrochloride, check with your doctor.
Ticlopidine hydrochloride is recommended to help reduce your risk of having a stroke, but only for patients who have had a stroke or early warning symptoms while on aspirin, or for those who have these symptoms but are intolerant or allergic to aspirin.
Ticlopidine hydrochloride is recommended with aspirin for up to 30 days in patients who have had a stent implanted in their coronary arteries to reduce the risk of blood clots forming inside the stent.
Ticlopidine hydrochloride is not prescribed for those who can take aspirin to reduce the risk of stroke because ticlopidine hydrochloride can cause life-threatening blood problems. Getting your blood tests done and reporting symptoms to your doctor as soon as possible can avoid serious complications.
The white cells of the blood that fight infection may drop to dangerous levels (a condition called neutropenia). This occurs in about 2.4% (1 in 40) of people on ticlopidine. You should be on the lookout for signs of infection such as fever, chills or sore throat. If this problem is caught early, it can almost always be reversed, but if undetected it can be fatal.
Another problem that has occurred in some patients taking ticlopidine is a decrease in cells called platelets (a condition called thrombocytopenia). This may occur as part of a syndrome that includes injury to red blood cells, causing anemia, kidney abnormalities, neurologic changes and fever. This condition is called TTP and can be fatal.
Things you should watch for as possible early signs of TTP are yellow skin or eye colour, pinpoint dots (rash) on the skin, pale colour, fever, weakness on a side of the body, or dark urine. If any of these occur, contact your doctor immediately.
Both complications occur most frequently in the first 90 days after ticlopidine hydrochloride is started. To make sure you don’t develop either of these problems, your doctor will arrange for you to have your blood tested before you start taking ticlopidine hydrochloride, and then every 2 weeks for the first 3 months you are on ticlopidine hydrochloride. If detected, neutropenia and thrombocytopenia can almost always be reversed. It is essential that you keep your appointments for the blood tests and that you call your doctor immediately if you have any indication that you may have TTP or neutropenia. If you stop taking ticlopidine hydrochloride for any reason within the first 3 months, you will still need to have your blood tested for an additional 2 weeks after you have stopped taking ticlopidine hydrochloride.
Rarely, decreases in the white blood cells, red blood cells and platelets can occur together. This condition is called aplastic anemia and can be fatal.
Things you should watch for as possible early signs of aplastic anemia are feelings of excessive weakness and tiredness, paleness, bruising, and bleeding from areas such as your nose or gums. You may also develop signs of infection such as fever. If any of these occur, contact your doctor immediately.
A few people may develop jaundice while being treated with ticlopidine hydrochloride. The signs of jaundice are yellowing of the skin or the whites of the eyes or consistent darkening of the urine or lightening in the colour of the stools. These symptoms should be reported to your physician promptly.
If any of the symptoms described above for neutropenia, TTP, aplastic anemia or jaundice occur, contact your doctor immediately.
Ticlopidine hydrochloride should be used only as directed by your doctor. Do not give ticlopidine hydrochloride to anyone else.
Keep ticlopidine hydrochloride out of reach of children!
Some people may have such side effects as diarrhea, skin rash, stomach or intestinal discomfort. If any of these problems are persistent, or if you are concerned about them, bring them to your doctor’s attention.
It may take longer than usual to stop bleeding when taking ticlopidine hydrochloride. Tell your doctor if you have any more bleeding or bruising than usual, and, if you have emergency surgery, be sure to let your doctor or dentist know that you are taking ticlopidine hydrochloride. Also, tell your doctor well in advance of any planned surgery (including tooth extraction), because he or she may recommend that you stop taking ticlopidine hydrochloride temporarily.
Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.
A stroke occurs when a clot (or thrombus) forms in a blood vessel in the brain or forms in another part of the body and breaks off, then travels to the brain (an embolus). In both cases the blood supply to part of the brain is blocked and that part of the brain is damaged. Ticlopidine hydrochloride works by making the blood less likely to clot, although not so much less that it causes you to become likely to bleed, unless you have a bleeding disorder or some injury (such as a bleeding ulcer of the stomach or intestine) that is especially likely to bleed.
A heart attack or angina (chest pain) can occur when fatty deposits block the arteries that carry oxygen and nutrient-rich blood to your heart. To decrease the chance of fatty deposits building up over time, the doctor may recommend the placement of a coronary stent. Ticlopidine hydrochloride may be given to you with aspirin to make blood clots less likely to form inside the stent so that the artery remains open.
Contact your doctor immediately and do not take ticlopidine hydrochloride if:
Manufactured by: Genpharm ULC, Toronto, ON M8Z 2S6 Canada
Printed in Canada.
003-621 REV.#10 September 2008
ticlopidine hydrochloride tablet, coated
Revised: 10/2008 Genpharm
Reproduced with permission of U.S. National Library of Medicine
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