Anticoagulants adverse effects

The pharmacological and/or adverse effects of a drug can be reversed by co-administration of drugs which compete for the same receptor. For example, an opioid receptor antagonist naloxone is used to reverse the effects of opiates. Drugs acting at the same site with opposite effects also can affect each other, e.g. the reduction in the anticoagulant effect of warfarin by vitamin K. 

Overall no evidence was found to support the claim that anticoagulants offer a net advantage over aspirin in patients with acute ischemic stroke. There was evidence, however, to suggest that combination anticoagulant and aspirin therapy was associated with a small increase in the number of deaths at the end of follow-up, equivalent to 20 more deaths per 1000 patients treated. This adverse effect can probably be attributed partly to the 10 extra sICHs, and the 5 extra major extracranial hemorrhages per 1000 patients treated with combination anticoagulant/ aspirin therapy. 

Heparin-induced thrombocytopenia (HIT) is a very serious adverse effect associated with UFH use. Platelet counts should be monitored every 2 to 3 days dining the course of UFH therapy.5 HIT should be suspected if the platelet count drops by more than 50% from baseline or to below 120,000. In patients with contraindications to anticoagulation therapy, UFH should not be administered (Table 7-7). 

Onset of action is slow at around 30 minutes, which limits spontaneity. In addition, patients and partners may complain of a cold, lifeless, discolored penis that has a hinge-like feel. Painful ejaculation or inability to ejaculate are additional adverse effects. VEDs are contraindicated in persons with sickle cell disease and should be used with caution in patients on oral anticoagulants or who have bleeding disorders due to the increased possibility of priapism. 

Evaluate the patient for adverse effects, including peripheral neuropathy and deep vein thrombosis. Prophylactic anticoagulation therapy should be considered in thalidomide or lenalidomide based therapy. 

Adverse effects include changes in libido and the occurrence of oedema, weight gain and gynecomastia, may occur. Androgens are potentially hepato-toxic, testosterone less than methyltestosterone and fluoxymesterone. Androgens can potentiate anticoagulant action. 

COX-2 specific inhibition good choice for patients with inflammatory conditions who are at high risk of gastrointestinal adverse effects (e.g., older than 60 years history of peptic ulcer disease prolonged, high-dose NSAID therapy concurrent use of corticosteroids or anticoagulants)... 

Rare adverse effects of fibrates include rashes, gastrointestinal symptoms, myopathy, arrhythmias, hypokalemia, and high blood levels of aminotransferases or alkaline phosphatase. A few patients show decreases in white blood count or hematocrit. Both agents potentiate the action of coumarin and indanedione anticoagulants, and doses of these agents should be adjusted. Rhabdomyolysis has occurred rarely. Risk of myopathy increases when fibrates are given with reductase inhibitors. The use of fenofibrate with rosuvastatin appears to minimize this risk. Fibrates should be avoided in patients with hepatic or renal dysfunction. There appears to be a modest increase in the risk of cholesterol gallstones. 

In patients who have preexisting bowel disease or cholestasis, steatorrhea may occur. Malabsorption of vitamin occurs rarely, leading to hypoprothrombinemia. Prothrombin time should be measured frequently in patients who are taking resins and anticoagulants. Malabsorption of folic acid has been reported rarely. Increased formation of gallstones, particularly in obese persons, was an anticipated adverse effect but has rarely occurred in practice. 

The adverse effect profile of thalidomide is extensive. The most important toxicity is teratogenesis. Because of this effect, thalidomide prescription and use is closely regulated by the manufacturer. Other adverse effects of thalidomide include peripheral neuropathy, constipation, rash, fatigue, hypothyroidism, and increased risk of deep vein thrombosis. Thrombosis is sufficiently frequent, particularly in the hematologic malignancy population, that most patients are placed on some type of anticoagulant when thalidomide treatment is initiated. 

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