If you’re like the majority of Americans, you take an aspirin when you have a headache, or possibly as a preventative measure against heart attack or stroke. Aspirin accomplishes the former by inhibiting the release of prostaglandins, which sensitize nerve endings. It achieves the latter by inactivating cyclooxygenase (COX), a membrane-bound enzyme responsible for the oxidation of arachidonic acid to prostaglandin G2. This reaction is a precursor to the formation of thromboxane A2, a potent platelet aggregator. Through this mechanism, aspirin down-regulates platelet aggregation, which causes thrombosis – also known as a blood clot.
But do you ever notice that aspirin doesn’t really get rid of your headache or other aches and pains? Or that you have to take a higher dose than a friend of a similar weight? Approximately eighty million aspirin tablets are consumed in the United States every day, but scientists are discovering that not all aspirin users respond to the same dosages to the same degree. Those who lack a response to aspirin are said to have aspirin resistance. According to one (admittedly imprecise) study, between five and fifty-seven percent of the population has aspirin resistance. With the negative side effects accompanying this ubiquitous drug, including stomach irritation, ringing in the ears, allergic reaction and Reye’s syndrome in children, it is important to avoid taking a higher dosage than necessary, especially if it will only prove ineffective.
Scientists at the Cayman Chemical Company in Ann Arbor, Michigan, and the Corgenix Medical Corporation in Broomfield, CO, have noted the unmet need for a highly specific and reproducible assay that measures aspirin’s effectiveness in reducing platelet aggregation. Their patent, “Methods and kits for detection of thromboxane A2 metabolites,” fills that need such that health care professionals can quickly and accurately quantify aspirin resistance prior to or during a thrombotic event.
The patent discloses a method of identifying aspirin response in a subject by administering a dosage, collecting a urine sample, and measuring the amount of two thromboxane A2 metabolites in the urine sample by using a monoclonal antibody capable of binding to thromboxane B2. The method further teaches normalizing the amount of A2 metabolites to an amount of a standard protein in the subject’s urine to obtain a ratio, and comparing the ratio to a threshold ratio value. A ratio below the threshold value indicates aspirin responsiveness in the subject. The subjects for this test are those who suffer from or are suspected of suffering from thrombotic disease, cardiovascular disease, or cerebrovascular disease.
