延长释放纳尔特克松对人类的芬太尼尔阻断作用:三例病例报告
1Retired Addiction Physician and Psychiatrist, London SE1, United Kingdom. ORCID: https://orcid.org/0000-0002-5035-5833.
Journal of opioid management
|September 5, 2025
概括
延长释放的纳尔特 (ER-NTX) 有效地阻断了高剂量芬太尼导致的致命呼吸抑制. 这项研究提供了人类ER-NTX的第一个证据.
科学领域:
- 药理学和毒理学
- 药物成
- 临床研究
背景情况:
- 芬太尼在持续的阿片类药物过量流行中所扮演的角色是一个关键的公共卫生问题.
- 呼吸抑制是像芬太尼这样的μ-agonist阿片类药物的危及生命的副作用.
- 关于延长释放纳尔特克森 (ER-NTX) 阻断芬太尼的呼吸作用的有效性,人类的数据有限.
研究的目的:
- 研究延长释放纳尔特克森 (ER-NTX) 对抗芬太尼诱导的呼吸抑制的能力.
- 在ER-NTX治疗期间接受阿片类药物挑战的患者的临床病史.
- 提供ER-NTX对致命芬太尼剂量有效性的第一个人类证据.
主要方法:
- 在ER-NTX植入物患者中展示了三种涉及临床上指定的阿片类药物挑战的病史.
- 对纳尔特和芬太尼相互作用的现有稀疏文献的审查.
- 对抗剂的血液度的评估及其与阻断μ-激动剂作用的相关性.
主要成果:
- ER-NTX制剂达到足够的血液度,完全阻断至少1000微克静脉注射芬太尼的致命作用.
- 在接受ER-NTX的患者中,病例记录显示了阿片类药物挑战的成功管理.
- 这项研究提供了初步的人类证据,支持ER-NTX对严重芬太尼毒性的保护能力.
结论:
- 延长释放的纳尔特克松有效地阻断高剂量芬太尼引起的危及生命的呼吸抑制.
- 在阿片类药物使用障碍患者中,ER-NTX是减轻过量使用风险的有希望的治疗选择.
- 需要进一步研究以确定ER-NTX在阿片类药物过量预防中的最佳剂量和临床方案.
更多相关视频
07:50A Method for Evaluating the Reinforcing Properties of Ethanol in Rats without Water Deprivation, Saccharin Fading or Extended Access Training
Published on: January 29, 2017
9.8K
10:35A Procedure to Study the Effect of Prolonged Food Restriction on Heroin Seeking in Abstinent Rats
Published on: November 11, 2013
11.2K
相关概念视频
Opioid Analgesics: Synthetic and Semisynthetic Opioids
461
Synthetic and semisynthetic opioids are pivotal in pain management and tackling opioid addiction. Semisynthetic opioids, including morphinans (morphine derivatives), oxycodone, oxymorphone, hydrocodone, and hydromorphone, have improved pharmacokinetic profiles compared to morphine. Additionally, heroin and 6-MAM (6-Monoacetylmorphine) show better CNS penetration than morphine due to heightened lipid solubility. Hydromorphone, a potent opioid, undergoes hepatic metabolism to form the active...
461
Analgesia and Pain Management
849
Pain is critical to various clinical pathologies, provoking an urgent need for effective management. Pain, whether acute or chronic, is a complex neurochemical process. Its alleviation depends on the type, with nonopioid analgesics effective for mild to moderate pain, such as musculoskeletal or inflammatory pain, while neuropathic pain responds best to anticonvulsants, tricyclic antidepressants, or serotonin/norepinephrine reuptake inhibitors. For severe acute or chronic pain, opioids may be...
849
Opioid Receptors: Overview
2.1K
Opioid receptors, including the mu (μ, MOR), delta (δ, DOR), and kappa (κ, KOR) types, belong to the rhodopsin family of G protein-coupled receptors. These receptors are located throughout the central and peripheral nervous systems and in non-neuronal tissues such as macrophages and astrocytes. Opioid receptor ligands can be categorized into agonists or antagonists. Highly selective agonists include [d-Ala2, MePhe4, Gly(ol)5]-enkephalin or DAMGO for MOR, [D-Pen2,...
2.1K
Opioid Analgesics: Morphine and Other Natural Cogeners
401
Opioids are a class of drugs that mimic endogenous opioid peptides and act on opioid receptors, and help in pain relief. These compounds are classified as natural, synthetic, or semi-synthetic. Natural opioids, like morphine, codeine, and thebaine, are derived from the opium poppy plant (Papaver somniferum or Papaver album) and are termed opiates. Synthetic opioids are artificial, while semi-synthetic opioids combine natural and synthetic compounds. Morphine, a prototypical opioid, possesses a...
401
CNS Depressants: Alcohol and Nicotine
384
Ethanol, a clear colorless alcohol, has been consumed by humans for millennia, but its effects on the body are far from benign. At lower doses, it induces decreased inhibitions and loquaciousness, leading to its social appeal. However, it can cause severe consequences at higher doses, such as coma and respiratory depression, due to its zero-order elimination kinetics. Chronic ethanol abuse wreaks havoc on multiple organ systems, particularly the CNS and the liver. Abrupt cessation of ethanol...
384
Desensitization and Tachyphylaxis
2.3K
Tachyphylaxis is described as a rapid decrease in response to a drug after repeated or continuous administration of the same drug dose. It is a phenomenon where the body becomes less responsive to a particular substance or intervention over time, requiring higher doses or stronger interventions to achieve the same effect. It results from adaptive changes in the body's receptors, signaling pathways, or physiological processes that occur in response to prolonged exposure to a stimulus.
2.3K
