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Query: UMLS:C0278080 (physical dependence)
 1,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alcohol abuse is associated with neurological dysfunction, brain morphological deficits and frank neurotoxicity. Although these disruptions may be a secondary effect due to hepatic encephalopathy, no clear evidence of causality is available. This study examined whether a 72h period of alcohol intoxication known to induce physical dependence, followed by a single withdrawal, was sufficient to induce signs of hepatic encephalopathy in male and female mice. Animals were continuously intoxicated via alcohol vapor inhalation, a procedure previously shown to induce significant neurotoxicity in female mice. At peak synchronized withdrawal (8h following the end of alcohol exposure), blood samples were taken and levels of several liver-regulated markers and brain swelling were characterized. Glutathione levels were also determined in the medial frontal cortex (mFC) and hippocampus. Results revealed elevated levels of cholesterol, albumin, alkaline phosphatase (ALP), alanine aminotransferase (ALT) and decreased levels of blood urea nitrogen and total bilirubin in alcohol-exposed male and female groups compared to controls. Brain water weight was not affected by alcohol exposure, though males tended to have slightly more water weight overall. Alcohol exposure led to reductions in tissue levels of glutathione in both the hippocampus and mFC which may indicate increased oxidative stress. Combined, these results suggest that hepatic encephalopathy does not appear to play a significant role in the neurotoxicity observed following alcohol exposure in this model.
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PMID:A neurotoxic alcohol exposure paradigm does not induce hepatic encephalopathy. 2726 33

Opioid use, misuse, and risky use contribute to a critically important and complex crisis in current healthcare. Consequences of long-term opioid use, including opioid induced hyperalgesia, physical dependence, and opioid use disorder, can be considered iatrogenic, or partially iatrogenic, in cases where therapeutic opioid exposures were contributory. Research investigation and presumptive clinical action are needed to attenuate the iatrogenic component of the opioid crisis; treatment of individuals already suffering from opioid use disorder will not prevent incident cases. This work will be challenged by a remarkably high degree of complexity involving myriad and highly variable factors along the continuum from initial opioid exposure to long-term opioid use. An organized view of this complex problem should accelerate the pace of innovation and facilitate clinical implementation of research findings. Herein, we propose a theoretical framework and modern nomenclature for characterizing therapeutic opioid exposure and the degree to which it contributes iatrogenically to adverse outcomes. In doing so, we separate the role of exposure from other factors contributing to long-term opioid use, clarify the relationship between opioid exposure and outcomes, emphasize that exposure source is an important consideration for health services research and practice in the areas of pain treatment and opioid prevention, and recommend terminology necessary to quantify therapeutic opioid exposure separately from nonmedical exposure.
Am J Drug Alcohol Abuse 2020 Nov 01
PMID:A theoretical framework and nomenclature to characterize the iatrogenic contribution of therapeutic opioid exposure to opioid induced hyperalgesia, physical dependence, and opioid use disorder. 3289 13


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