SiR,—Dr Amess and colleagues (Aug. 12, p. 339) illustrate the value of the deoxyuridine-suppression test in assessing the probable cause or causes of the acute marrow failure that occurs in patients under intensive care. It seems unlikely, however, that interference with vitamin-B12 function by nitrous oxide will prove to be the explanation for most instances of this
complication. Although nitrous
oxide may be used
cedures, the risk of bonemarrow failure with long-term
more important consideration. Further, there is long-standing legal right of the Press at stake here. Until 1953 coroners had discretion on admitting the public. Working within a system makes criticism of it difficult, but comparison with practice in other countries can help. In many other countries, including Scotland, suicide is not a news item.
sioned is the
NITROUS OXIDE AND THE BONE-MARROW
Psychiatry Unit, Graylingwell Hospital, Chichester, Sussex PO19 4PQ.
known,’ so it is not often used for this purpose, and was used postoperatively in the patient we reported.2 Furthermore its use in patients receiving intensive care has declined as better and less toxic methods of sedation and analgesia have become available. When this complication of intensive care happens it usually does so some 10-14 days after surgery. Most of these patients have some primary alteration in folate metabolism. In two such patients we have demonstrated folate deficiency in bonemarrow cells using the dU-suppression test, and one of these has been reported.2 Furthermore Wardrop et a1.3 have shown that megaloblastic marrow failure in this situation could be prevented by folic acid alone. These haematological changes can be corrected by folic acid .4 The rapidity and completeness of the responses suggest that these patients had a primary folate deficiency and not a deficiency secondary to a defect in vitamin-B12 metabolism. This explanation is supported by our dU-suppression test results. It seems more likely that the usual cause of megaloblastic marrow failure in patients under intensive care is due to a primary disturbance of folate metabolism.
DEXAMETHASONE TEST IN ALCOHOLICS
Hæmatology Department, Christchurch Hospital, Christchurch. New Zealand
B. M. BARRACLOUGH D. M. SHEPHERD
M. E. J. BEARD J. W. HAMER
SIR,-Smals and Kloppenberg’ reported that hypercorticalism in alcoholics is not the consequence of impaired hydrocortisone metabolism by the liver. They suggested that alcoholmediated pituitary secretion of corticotrophin might contribute to the raised plasma-cortisol concentration found in alcoholics.2 Dr I. Prakhje, Dr T. Rybakova, Dr Yu. Fridlend and I have evaluated hypothalamo-pituitary-adrenal (H.P.A.) activity in alcoholics using a dexamethasone test. 11-hydroxycorticosteroid (11-OHc.s.) concentration in plasma was measured spectrofluorimetrically at 9 A.M. for 3 consecutive days. At 11 P.M. on the first day the subjects took 1 mg dexamethasone (’Dexason’, Galenica, Beograd). In all of five healthy volunteers administration of dexamethasone was followed by a striking fall in plasma-11-HOc.s., the concentration on the first day of the investigation being 10-02+2-08 f1.g/dl (mean±s.s.ht.) falling significantly to 3-32+0.94 and 3-9±0-65 f1.g/dl on the second and third days, respectively