After intense pressure, Chinese officials allowed international officials to investigate the situation there. This revealed problems plaguing the aging mainland Chinese healthcare system, including increasing decentralization, red tape, and inadequate communication.Many healthcare workers in the affected nations risked their lives and died by treating patients, and trying to contain the infection before ways to prevent infection were known. Spread to other regions
The epidemic reached the public spotlight in February 2003, when an American businessman traveling from China, Johnny Chen, became affected by pneumonia-like symptoms while on a flight to Singapore. The plane stopped in Hanoi, Vietnam, where the patient died in Hanoi French Hospital. Several of the medical staff who treated him soon developed the same disease despite basic hospital procedures. Italian doctor Carlo Urbani identified the threat and communicated it to WHO and the Vietnamese government; he later died from the disease.The severity of the symptoms and the infection among hospital staff alarmed global health authorities, who were fearful of another emergent pneumonia epidemic. On 12 March 2003, the WHO issued a global alert, followed by a health alert by the United States Centers for Disease Control and Prevention (CDC). Local transmission of SARS took place in Toronto, Ottawa, San Francisco, Ulaanbaatar, Manila, Singapore, Taiwan, Hanoi and Hong Kong whereas within China it spread to Guangdong, Jilin, Hebei, Hubei, Shaanxi, Jiangsu, Shanxi, Tianjin, and Inner Mongolia. Hong Kong
The disease spread in Hong Kong from Liu Jianlun, a Guangdong doctor who was treating patients at Sun Yat-Sen Memorial Hospital.
While higher CYP2D6 activity increases the effects of oxycodone (owing to increased conversion into oxymorphone), higher CYP3A4 activity has the opposite effect and decreases the effects of oxycodone (owing to increased metabolism into noroxycodone and noroxymorphone). The dose of oxycodone must be reduced in patients with reduced liver function. Elimination
The clearance of oxycodone is 0.8 L/min. Oxycodone and its metabolites are mainly excreted in urine. Therefore, oxycodone accumulates in patients with kidney impairment. Oxycodone is eliminated in the urine 10% as unchanged oxycodone, 45% ± 21% as N-demethylated metabolites (noroxycodone, noroxymorphone, noroxycodols), 11 ± 6% as O-demethylated metabolites (oxymorphone, oxymorphols), and 8% ± 6% as 6-keto-reduced metabolites (oxycodols). Duration of action
Oxycodone has a half-life of 4.5 hours. It is available as a generic medication. The manufacturer of OxyContin, a controlled-release preparation of oxycodone, Purdue Pharma, claimed in their 1992 patent application that the duration of action of OxyContin is 12 hours in "90% of patients". It has never performed any clinical studies in which OxyContin was given at more frequent intervals. In a separate filing, Purdue claims that controlled-release oxycodone "provides pain relief in said patient for at least 12 hours after administration". However, in 2016 an investigation by the Los Angeles Times found that "the drug weans off hours early in many people", inducing symptoms of opiate withdrawal and intense cravings for OxyContin. One doctor, Lawrence Robbins, told journalists that over 70% of his patients would report that OxyContin would only provide 4–7 hours of relief.