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dc.contributor.authorYeh, Kuang-Tingen_US
dc.contributor.authorWu, Wen-Tienen_US
dc.contributor.authorSubeq, Yi-Maunen_US
dc.contributor.authorNiu, Chi-Chienen_US
dc.contributor.authorLiao, Kuang-Wenen_US
dc.contributor.authorChen, Ing-Hoen_US
dc.contributor.authorWang, Jen-Hungen_US
dc.contributor.authorLee, Ru-Pingen_US
dc.date.accessioned2019-04-03T06:35:36Z-
dc.date.available2019-04-03T06:35:36Z-
dc.date.issued2015-10-02en_US
dc.identifier.issn1932-6203en_US
dc.identifier.urihttp://dx.doi.org/10.1371/journal.pone.0137225en_US
dc.identifier.urihttp://hdl.handle.net/11536/128230-
dc.description.abstractIn addition to adequate surgical fixation and an aggressive rehabilitation program, pain relief is one of the most critical factors in the acute stage of fracture treatment. The most common analgesics are nonsteroid anti-inflammatory drugs and Acetaminophen, both of which relieve pain and reduce body temperature. In clinical experiences, they exhibit effective pain control; however, their influence on body temperature remains controversial. This study is aimed at determining the effects of analgesics at the acute stage of traumatic fracture by performing a clinical retrospective study of patients with fractures and a fracture animal model. The retrospective study revealed that, in the acetaminophen group, the mean value of postmedication body temperature (BT) was significantly higher than that of the premedication BT. The change in BT was highly related with the medication rather than other risk factors. Forty eight 12-week-old male Wistar rats were divided into 6 groups: a control group, fracture group, fracture-Acetaminophen group, Acetaminophen group, fracture-Arcoxia group, and Arcoxia group. Fracture rats were prepared by breaking their unilateral tibia and fibula. Their inflammation conditions were evaluated by measuring their serum cytokine level and their physiological status was evaluated by estimating their central temperature, heart rate, and mean blood pressure. The hepatic adverse effects were assessed by measuring the serum levels of aspartate aminotransferase (sGOT) and alanine aminotransferase (sGPT). The central temperature in the fracture-Acetaminophen group exceeded that in the groups fed normal saline water or Arcoxia. Accumulated hepatic injury was presented as steadily ascending curves of sGOT and sGPT. Inflammation-related cytokine levels were not higher in the Acetaminophen fracture group and were significantly lower in the fracture-Arcoxia group. Fever appeared to be aggravated by acetaminophen and more related to the elevation of hepatic enzymes than to the change in the inflammation-related cytokines. We suggest that acetaminophen may aggravate fever at the acute stage of fracture. This response is highly related to the accumulated and exacerbated side effects of hepatitis that are caused by the medication and trauma.en_US
dc.language.isoen_USen_US
dc.titleNon-Steroid Anti-Inflammatory Drugs Are Better than Acetaminophen on Fever Control at Acute Stage of Fractureen_US
dc.typeArticleen_US
dc.identifier.doi10.1371/journal.pone.0137225en_US
dc.identifier.journalPLOS ONEen_US
dc.citation.volume10en_US
dc.citation.issue10en_US
dc.citation.spage0en_US
dc.citation.epage0en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.identifier.wosnumberWOS:000362178700006en_US
dc.citation.woscount0en_US
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