Boca Raton, FL, June 09, 2013 --(PR.com
)-- Hydromorphone (Dilaudid, Exalgo) is a potent synthetic opioid for relieving moderate to severe pain. As with all other opioids, hydromorphone binds to the opioid µ receptor in the brain for its analgesic effect and is about 7-10 times more potent than morphine. The chemical structure of hydromorphone closely resembles that of morphine. The only difference is that the hydroxyl group in position 6 of the morphine benzyl ring is changed to the keto group in hydromorphone, which makes it easier to penetrate the brain. Hydromorphone is supplied as a tablet, capsule, or solution and can be delivered to the human body by multiple routes. The majority of a hydromorphone dose undergoes glucuronidation and is eliminated through the urinary route as hydromorphone glucuronide. Detection window for hydromorphone in urine is generally within 3 days, though extended-release form may reach 5 days. In oral fluid, hydromorphone remains detectable within 6 hours after last exposure. Urinary hydromorphone concentration, estimated by American Clinical Solutions from 473 patients with prescriptions, averages at 3430 ng/ml. Hydromorphone has great abuse potential and is listed as a Schedule II controlled substance. American Clinical Solutions currently provides test services for hydromorphone and other common opioids in urine and oral fluid.
Interpretation of a hydromorphone test result is not always an easy task. A positive hydromorphone test result without prescription does not necessarily mean Dilaudid abuse, since hydromorphone can be generated through hydrocodone or morphine metabolism. A common question raised by physicians is, "How do you differentiate between hydromorphone formed as a metabolite versus hydromorphone abuse, especially when patients were prescribed morphine?" The key to solving this issue is to look at the ratio of hydromorphone versus morphine.
Morphine can be converted to hydromorphone through a minor metabolic pathway (the predominant pathway for morphine metabolism is through direct glucuronidation), which accounts for less than 2.5% of a morphine dose. Therefore, small amounts of hydromorphone detected in patients with morphine prescriptions should be considered as metabolite formation. Hydromorphone can also be formed by CYP2D6-mediated O-desmethylation of hydrocodone. Unfortunately, the ratio of metabolite formation in this scenario varies dramatically among individuals, depending on human CYP2D6 gene polymorphism and the stage of metabolism. For example, ultrarapid metabolizers would have most of a hydrocodone dose converted to hydromorphone and the ratio would certainly be higher than that of a poor metabolizer, who might only have a small amount of hydromorphone formation. Meanwhile, at the early stage of metabolism, parent compound (hydrocodone) would be the predominant compound detected in urine, since there has not been enough time for hydromorphone formation. On the other hand, at the end stage of metabolism, since most of the hydrocodone dose has been converted to hydromorphone, hydromorphone concentration might surpass that of hydrocodone. However, no matter what is the case, if hydromorphone came from metabolite formation, both compounds should be detected in urine at the same time.
Cheng Fang, MD., PH D., DABT | email@example.com
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