repeated after one week. Four of the patients were postmenopausal; the other six were studied during the same phase of the menstrual cycle on both occasions. Basal plasma prolactin levels were normal in all patients before and during treatment with diazepam. Metoclopramide produced a marked increase in plasma prolactin levels maximal 30 min after injection. An analysis of variance of the log transforms of the plasma prolactin levels showed no significant difference before and during diazepam treatment. The overall trend was also constant at each time before and during diazepam treatment. It is therefore concluded that diazepam does not affect basal prolactin levels or the release of prolactin in response to the dopamine antagonist metoclopramide. This finding compares with earlier reports, which showed that growth hormone production, pituitary-adrenal function,5 and thyroid function6 are unaffected by diazepam.

The figure summarises results for the Arabs and Africans.' For all results (t=407; DF=30; P<0001), and also when the perfusion segment was proximal (t=272; DF=22; P<002), the difference was significant (Student's t test). Mean net water absorption rate in the Arabs was 4 49 (2 30-7-44) ml/30 cm of jejunum/min and in the Africans 1-88 (-1-15-4-72) ml/30 cm of jejunum/min; this difference was significant (t=4 99; DF=30; P<0O001).

24 mmol of magnesium sulphate intramuscularly over the next 24 hours. Then 115 mmol daily of effervescent potassium chloride was given orally for the next two days. Muscle power returned to normal within 12 hours, and it was then found that the patient had been eating about 1-8 kg of liquorice sweets per week. Three months after stopping liquorice she remained well, and all laboratory values were normal. CommentLiquorice has long been known to cause sodium retention with oedema and hypertension, and more recently it has been shown to cause clinically significant hypokalaemia. Sometimes the hypokalaemia is very severe and associated with muscle weakness, raised muscle enzyme levels in the blood, and myoglobinuria.'The aldosterone-like effects of liquorice are due to its glycyrrhizinic acid fraction,2 and liquorice consumption in normal people will cause sodium retention, potassium loss, and suppression of aldosterone levels in the blood.:Our patient had the now well-described syndrome of hypokalaemia and myopathy,4 though without myoglobinuria. She also suffered a cardiac arrest, an event which has not been described in previous reports of liquorice toxicity.

No abstract