Naloxone challenge

Krishnan-Sarin, S., Rosen, M.I., O Malley, S.S. Naloxone challenge in smokers. Preliminary evidence of an opioid component in nicotine dependence. Arch. Gen. Psychiatry. 56 663, 1999. 

If there is any question of occult opioid dependence, perform a naloxone challenge... 

Administer a naloxone challenge test (see below). If signs of opioid withdrawal are still observed following challenge, do not treat with naltrexone. The naloxone challenge can be repeated in 24 hours. 

Patients receiving opioid analgesics opioid-dependent patients patients in acute opioid withdrawal failed naloxone challenge positive urine screen for opioids history of sensitivity to naltrexone acute hepatitis or liver failure. 

Naloxone challenge test to determine if patient is opioid dependent IV Alert Expect to perform the naloxone challenge test if there is any question that the patient is opioid dependent. Don t administer naltrexone until the naloxone challenge test is negative. 

Contraindications Acute hepatitis, acute opioid withdrawal, failed naloxone challenge test, hepatic failure, history of hypersensitivity to naltrexone, opioid dependence, positive urine screen for opioids... 

In the tail flick assay -conotoxin GVIA in combination with morphine leads to an additive effect similar to the combination of morphine with SNX-111 in the formalin test. But when -conotoxin GVIA was applied 24 h before morphine, antinociception was greatly reduced. In morphine-dependent rats, w-conotoxin GVIA given i.c.v. 15 min before naloxone challenge (2 mg/kg i.p.), significantly attenuated the withdrawal symptoms (Table 4, Basilico et al., 1992). 

DH Catlin, JC Schaeffer, MB Liewen. 2-Diazomorphine directed antiserum Determination of morphine in brain after naloxone challenge in morphine pellet implanted mice. Life Sci 20 123, 1977. 

Naloxone precipitation, nnlike nicotine-antagonist challenge, fails to decrease DA-activity, yet still precipitates somatic signs (Carboni et al. 2000). Thus the aversiveness of nicotine withdrawal can be dissociated in part from those effects on the mesolimbic-DA reinforcement pathway that have sometimes been proposed to account for the affective aspects of withdrawal (Balfour 2004 Paterson et al. 2007). 

Small open-label pilot studies or challenge studies have been reported for the treatment of tics with various agents such as topiramate (Abuzzahab and Brown, 2001), levodopa (Black and Mink, 2000), low-dose naloxone (van Wattum et ah, 2000), donepezil (Hoopes, 1999), cyproterone (Izmir and Dursun, 1999), and ondansetron (Toren et ah, 1999). The safety and effectiveness of the chronic use of these agents, especially in children, requires more systematic studies. 

This approach also has been employed in the design of naltrexone-derived ligands with mu agonist/delta antagonist properties [75,76]. One such compound, 30 (SoRI 9409), was reported not to induce tolerance in mice and produced fewer withdrawal signs when challenged with naloxone in acute and chronic morphine dependence models [75]. However, discrepancy between the in vivo/in vitro data requires additional investigation in order to better define the mechanism of the improved in vivo profile [76,77]. 

Pierce et al. (1996) used slow release emulsion formulations of methadone to induce dependence in rats. Withdrawal was induced following i.p. challenge with either naloxone or saline, and dependence was assessed in terms of the presence or absence of characteristic withdrawal signs. 

The commercial production of medicinally useful opiate-derived products is faced with two major challenges. The first of these is the introduction of the C14 hydroxy group and the second is the formal exchange of the W-methyl group for another alkyl group such as allyl (naloxone, 9), methylcyclopropyl (naltrexone, 8, buprenorphine, 10) or methylcyclobutyl groups (nalbuphine, 11) as outlined in Scheme 20 [72-77]. 

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