Pruritus is a frequent and troublesome symptom in primary biliary cirrhosis (PBC). Increased plasma endogenous opioids play an important part in its pathogenesis and antagonists such as nalmefene are used in treatment; 1 their use is, however, limited by opioid withdrawal reactions. 2 W e report a 44-year-old woman with severe pruritus due to PBC who responded to codeine. Her total bilirubin was 21 mmol/L, alkaline phosphatase 516 U/L,-glutamyl transpeptidase 256 U/L, aspartate aminotransferase 77 U/L and alanine aminotransferase 120 U/L. Previous treatment with ondansetron, ursodeoxycholic acid, phenobarbital, and rifampicin was unsuccessful. After paroxetine 3 and naltrexone she experienced severe headache, nausea, vomiting, and cold shivers. 2 years previously she had been treated for a severe headache with a subcutaneous morphine injection. The headache did not change, but pruritus disappeared for several hours. Accordingly, we treated her with codeine 20 mg 4 hourly. Pruritus intensity decreased from 10/10 before treatment (on a numeric analogue scale where 0 was no itch and 10 worst possible itch) to 0–1/10 2 weeks later. Pruritus was absent for 2 months until she discontinued codeine because of constipation. Pruritus returned but her pruritus score averaged 5/10 1 month later. Reintroduction of codeine with laxatives had no effect at all. Increased availability of endogenous opioids in PBC may be due to their reduced liver clearance and/or enhanced production. High concentrations may be responsible for increased central opioidergic neuromodulation. 4 In this situation complete inhibition by opioid antagonists may be responsible for withdrawal symptoms. Non-antagonistic opioids like morphine and codeine bind to the receptors but stimulate them less than do endogenous opioids. They may work as competitive inhibitors in comparison with endogenous opioids, without producing withdrawal symptoms. Buprenorphine, a partial-agonist, appeared to have antipruritic effects in two out of five patients with