Naltrexone is a long acting competitive antagonist at opioid receptors which blocks the subjective and objective responses produced by intravenous opioid challenge. It is suitable for oral administration, and has been studied as an adjunct for use in opioid addiction management programmes. In non-comparative clinical trials involving detoxified patients, oral naltrexone reduced heroin craving and between 23 and 62% of patients remained in treatment after 3 to 4 weeks. However, in two studies 32 to 58% of patients who continued in treatment were opioid-free between 6 and 12 months after stopping naltrexone. As might be expected studies involving highly motivated patients have shown this type of patient group to achieve greater treatment success rates during naltrexone therapy, and remain opioid-free longer than other groups of apparently less motivated patients. In addition, when naltrexone is combined with family support, psychotherapy and counselling, patients are more likely to remain opioid-free. Naltrexone produces a low incidence of side effects, with gastrointestinal effects being the most commonly reported symptoms. Thus, despite the overall high attrition rates from trials, in selected patient groups and in combination with appropriate support mechanisms and psychotherapy, naltrexone represents a useful adjunct for the maintenance of abstinence in the detoxified opioid addict.

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1 Nociceptive tail flick latencies (TFL) were recorded in response to noxious thermal stimuli applied to lightly anaesthetized rats. The effects of intrathecally administered dopamine receptor agonists alone and combined with dopamine receptor antagonists were examined upon the TFL. Experiments were repeated on animals made supersensitive to dopamine following withdrawal from 28 day administration of haloperidol. 2 In untreated animals the D2-receptor agonist LY 171555 and apomorphine produced an increase in TFL. In contrast, the D1-receptor agonist SKF38393 had no significant effect on TEL. 3 Following haloperidol-induced dopamine-supersensitivity, SKF 38393 produced an increase in TFL. In contrast, LY 171555 and apomorphine had minimal effects on TFL in this preparation. 4 In animals not treated with haloperidol, the dopamine receptor antagonists SCH 23390 and (± )-sulpiride both blocked the increase in TFL produced by the D2-agonists. 5 SCH23390 and (±)-sulpiride also blocked the increase in TFL produced by SKF38393 in haloperidol-supersensitized animals. 6 The antinociceptive action of intrathecally administered dopamine agonists appears to be mediated via D2-receptors. Whether the antinociception produced by SKF 38393 is exclusively contingent upon the activation of D1-receptors in the dopamine-supersensitive animal is as yet unresolved.

Tenoxicam is a new non-steroidal anti-inflammatory and analgesic agent of the oxicam class, and therefore closely related to piroxicam. It possesses a long half-life which enables it to be administered once daily. Clinical trials in patients with rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, gout and non-articular rheumatism suggest that tenoxicam 20mg daily is an equally effective anti-inflammatory and analgesic agent compared with piroxicam 20mg daily, and that it is at least as well tolerated. Additionally, a few small studies in rheumatoid arthritis and osteoarthritis suggest that tenoxicam 20mg daily is as effective and as well tolerated as usual therapeutic dosages of diclofenac, ibuprofen, indomethacin and naproxen. Transient mild or moderate gastrointestinal symptoms, in 8% of patients at a dosage of 20mg daily, are the most frequently reported side effects. If further studies confirm the initially favourable efficacy and tolerability findings, particularly the relatively low incidence of adverse effects, tenoxicam can be considered a useful new agent for the symptomatic treatment of rheumatic and inflammatory diseases, and a worthwhile alternative to other non-steroidal anti-inflammatory drugs.

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