Antiplatelet drugs adverse effects

Aspirin inhibits cyclooxygenase, thus impairing platelet aggregation, This may be additive to other drugs with a similar effect and to those which affect other aspects of blood clotting. The risk of interactions and adverse effects is reduced by using a lower dose (e.g. 75mg) fortunately, a full antiplatelet effect is seen at this dose,... 

Numerous investigators have reported and reviewed the chnical application of monoclonal antibodies in various areas, including organ transplantation, neoplastic diseases, severe sepsis, and chronic inflammatory diseases. Collectively, these antibodies generally did not produce major adverse effects. The rapid development of antibodies against murine monoclonal antibodies is one of the most important clinical hmitations to their therapeutic use, but the development of humanized (chimeric human/ murine) monoclonal antibodies has improved their safety. Monoclonal antibodies have also been used in non-immune mediated diseases, such as cancer, septic shock, reperfusion, and as antiplatelet drugs. Treatment of neoplastic diseases with monoclonal antibodies is theoretically attractive. Unfortunately none of the monoclonal antibodies available at present has been demonstrated to be strictly tumor-specific, and binding of antibody to normal cells has been shown to be the major unknown factor for toxicity (6). 

Thrombocytopenia is a rare adverse effect of vancomycin and may be associated with the presence of vancomycin-dependent antiplatelet IgG antibodies. Reports of drug-induced thrombocytopenia have been systematically reviewed (51). Among the 98 different drugs described in 561 articles the following antibiotics were found with level I (definite) evidence co-trimoxazole, rifampicin, vancomycin, sulfisoxazole, cefalothin, piperacillin, methicillin, novobiocin. Drugs with level II (probable) evidence were oxytetracycline and ampicillin. 

Ginkgo biloba has been associated with platelet, bleeding and clotting disorders and there are isolated reports of serious adverse reactions after its concurrent use with antiplatelet drugs such as aspirin, clopidogrel and ticlopidine. An animal study su ests that Kangen-Katyu may also enhance the antiplatelet and antithrombotic effects of ticlopidine. 

Celecoxib is currently indicated for the relief of signs and symptoms of osteoarthritis and rheumatoid arthritis and to reduce the number of adenomatous colorectal polyps in familial adenomatous polyposis as an adjunct to usual care. Celecoxib is at least as effective as naproxen in the symptomatic management of osteoarthritis and at least as effective as naproxen and diclofenac in the symptomatic treatment of rheumatoid arthritis, and it is less likely to cause adverse Gl effects. Celecoxib appears to be effective in the management of pain associated with both of these arthritic conditions, but effectiveness in acute or chronic pain has not been fully demonstrated. Unlike aspirin, celecoxib does not exhibit antiplatelet activity. Concomitant administration of aspirin and celecoxib may increase the incidence of Gl side effects. Another notable potential drug interaction with celecoxib is its ability, like other NSAIDs, to reduce the blood pressure response to angiotensin-converting enzyme inhibitors. A more detailed discussion of the chemical, pharmacological, pharmacokinetic, and clinical aspects of celecoxib is available (81). 

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