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Strokan

COMPOSITION

Each tablet contains Ticlopidine Hydrochloride 250 mg

DESCRIPTION

STROKAN TABLET is a 9mm round tablet with marking "d/d" and pink in colour

ACTION AND MODE OR MECHANISMS OF ACTION

Ticlopidine HCI is an inhibitor of platelet aggregation. When taken orally it causes a time and dosedependent inhibition of platelet aggregation and release of platelet factors, as well as a prolongation of bleeding time. The drug has no significant in vitro activity. The exact mechanism of action is not fully characterised, but does not involve inhibition of the prostacyclin/thromboxane pathways. Platelet cyclic AMP does not seem to play a role in the mechanism of action of Ticlopidine HCI. Ticlopidine HCI interferes with platelet membrane function by inhibiting ADP induced platelet-fibrinogen binding and subsequent platelet-platelet interactions. The effect of Ticlopidine HCI on platelet function is irreversible as shown both by inhibition of fibrinogen binding after washing and by inhibition of platelet aggregation after resuspension of platelets in buffered medium. Although it is unclear how ticlopidine brings about these changes, a suggested mechanism is that it inhibits ADP-induced exposure of the fibrinogen binding site of the glycoprotein IIb-IIIa complex.

PHARMACOLOGY

Inhibition of platelet aggregation is detected within 4 days of administration of a dosage regimen of 250 mg twice daily. Maximum platelet aggregation inhibition (60 to 70%) is achieved 8 to 11 days following dosing with 250 mg twice daily. At the therapeutic dose. ADP-induced platelet aggregation is inhibited by 50 to 70%. Lower total daily doses of 375 mg and 250 mg result in 30 to 60% and 25 to 50% inhibition of platelet aggregation respectively. Template bleeding time is usually prolonged by two to five-fold of baseline values with the therapeutic dose of Ticlopidine HCI. Upon discontinuation of Ticlopidine HCI dosing, bleeding time and other platelet function tests return to normal within two weeks in the majority of patients. At the recommended therapeutic doses, Ticlopidine HCI has no known significant pharmacological actions in man other than inhibition of platelet function.

PHARMACOKINETICS

After oral administration of the therapeutic dose of Ticlopidine HCI, rapid absorption occurs, with peak plasma levels occurring at approximately 2 hours after dosing. Absorption is at least 80% in plasma. Administration of Ticlopidine HCI after meals results in an increased (20%) level of ticlopidine in plasma. Ticlopidine hydrochloride displays non-linear pharmacokinetics and clearance decreases markedly on repeated dosing. In older volunteers the apparent half-life of ticlopidine after a single 250 mg dose is about 12.6 hours, with repeat dosing at 250 mg twice daily, the terminal elimination half-life rises to 4 to 5 days and steady state levels of ticlopidine hydrochloride in plasma are obtained after approximately 14 to 21 days. Ticlopidine binds reversibly (98%) to plasma proteins, mainly to serum albumins and lipoproteins. The binding to albumin and lipoproteins is non-saturable over a wide concentration range. Ticlopidine also binds in a saturable manner to alpha-1 acid glycoprotein At concentrations attained with the recommended dose, only 15% or less ticlopidine is detected in the urine. Following an oral dose of radioactive ticlopidine hydrochloride administered in solution, 60% of the radioactivity was recovered in the urine and 23% in the faeces. Unmetabolised ticlopidine is a minor component in plasma after a single dose, but at steady state, ticlopidine is the major component. Approximately 40 to 50% of the radioactive metabolites circulating in plasma are covalently bound to plasma proteins. Clearance of ticlopidine decreases with age. Steady state trough values in elderly patients (mean age 70 years) are about twice those in young volunteer populations.

 

Hepatically impaired patients: Ticlopidine HCI has been studied in patients with varying degrees of liver function abnormalities Impaired hepatic function resulted in higher than normal levels of unchanged ticlopidine following single or multiple doses.


Renally Impaired patients: Patients with mildly (Ccr to to 80 mL/min) or moderately (Ccr 20 to 50 mL/min) impaired renal function were compared to normal subjects (Ccr 80 to 150 mL/min) in a study of the pharmacokinetic and platelet pharmacodymic effects of Ticlopidine HCI (250 mg twice daily) for 11 days. Concentrations of unchanged Ticlopidine HCI were, measured after a single 250 mg dose and after the final 250 mg dose on Day 11. AUC values of Ticlopidine increased by 28 and 60% in mild and moderately impaired patients respectively and plasma clearance decreased by 37 and 52% respectively, but there were no statistically significant differences in ADP-induced platelet aggregation. In this small study (26 patients) bleeding times showed significant prolongation only in the moderately impaired patients.

INDICATIONS

Indicated for the following :- Maintenance of patency of coronary artery by-pass grafts. Maintenance of patency of access sites in patients on chronic haemodialysis. Reducing risk of thrombotic stroke (fatal or non-fatal) in patients who have experienced stroke precursors and in patients who have had a completed stroke.

CONTRAINDICATIONS

Ticlopidine is contraindicated in the following cases :
Hypersensitivity to the drug or its excipients.
Presence of haematopoietic disorders such as neutropenia, agranulocytosis and thrombocytopenia.
Presence of haemostatic disorder or of active pathological bleeding (eg. bleeding peptic ulcer or intracranial bleeding).

Patients with severe liver impairment or cholestatic jaundice. Elderly patients (>65 years) with hepatic impairment.

Patients with renal disease on haemodialysis.

SIDE EFFECTS/ADVERSE REACTIONS

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 were mild, but 21 % of patients discontinued therapy because of an adverse event, principally diarrhoea, rash, nausea, vomiting G.I. 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.


Gastrointestinal: Ticlopidine HCI therapy has been associated with a variety of gastrointestinal complaints including diarrhoea 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.

 

Haemorrhagic: Ticlopidine HCI has been associated with a number of bleeding complications such as ecchymosis, epistaxis, haematuria, conjunctival haemorrhage, gastrointestinal bleeding, and perioperative bleeding. Intracerebral bleeding was rare in clinical trials with Ticlopidine HCI with an incidence no greater than seen with comparator agents. (Ticlopidine 0.5%, aspirin 0.6%, placebo 0.75%).


Rash: Ticlopidine HCI has been associated with a maculopapular 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 should occur within several days Many rashes do not recur on drug rechallenge. There have been rare reports of more severe rashes.


Less frequent adverse reactions (probably related): Clinical adverse experiences occurring in 0.5 to 1.0 percent of patients in the controlled trials include:
Digestive system: G.I. fullness;

Skin and Appendages: urticaria;

Nervous System: headache;

Body as a whole: asthenia, pain;

Haemostatic system: epistaxis;

Special senses: tinnitus.


In addition, rarer, relatively serious events have also been reported, mainly from overseas post marketing experience: Pancytopenia, aplastic anaemia, haemolytic anaemia with reticulocytosis, allergic pneumonitis, systemic lupus (positive ANA), peripheral neuropathy, vasculitis, serum sickness, arthropathy, hepatitis, cholestatic jaundice, angioedema, fever, nephrotic syndrome, myositis, hyponatraemia, immune thrombocytopenia and thrombocytopenic thrombotic purpura (TTP).

PRECAUTIONS /WARNINGS
LABORATORY MONITORING: ALL PATIENTS SHOULD HAVE A BASELINE WHOLE BLOOD COUNT (WBC) WITH WHITE CELL DIFFERENTIAL AND PLATELET COUNTS PERFORMED PRIOR TO THE START OF TREATMENT AND THEN EVERY 2 WEEKS DURING THE FIRST 4 MONTHS OF THERAPY (MORE FREQUENT MONITORING IS NECESSARY FOR PATIENTS WHOSE ABSOLUTE NEUTROPHIL COUNTS HAVE BEEN CONSISTENTLY DECLINING OR ARE 30% LESS THAN THE BASELINE COUNT). THEREAFTER, WBC (INCLUDING PLATELET COUNT) AND WHITE CELL DIFFERENTIAL COUNT NEED ONLY BE REPEATED FOR SYMPTOMS OR SIGNS SUGGESTIVE OF NEUTROPENIA OR THROMBOCYTOPENIA SINCE TICLOPIDINE HAS A LONG PLASMA HALF-LIFE, IT IS RECOMMENDED THAT PATIENTS DISCONTINUING THERAPY FOR ANY REASON DURING THE FIRST FOUR MONTHS SHOULD HAVE A WBC WHITE CELL DIFFERENTIAL AND PLATELET COUNT PERFORMED 2 WEEKS AFTER CESSATION OF THERAPY PERIODIC LIVER FUNCTION TESTS AND MEASUREMENT OF CHOLESTEROL LEVELS SHOULD ALSO BE CONDUCTED DURING THERAPY WITH TICLOPIDINE HCL.
 

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