PLATELET FUNCTION AND G.-6-P.D. DEFICIENCY

997

crustacean muscle 12-14 and in the frog spinal cord,15 theseas well as our results could point to differences in G.A.B.A.receptor sites in differing animal species. Moreover it isalso possible that several kinds of G.A.B.A. receptors existat different levels of the c.N.s. because bicuculline is a veryweak G.A.B.A. antagonist in the cerebral cortex 3,4 incomparison with its antagonism in the spinal cord.l1 Thiswould not be surprising since the existence of two popula-tions of receptors has also been proposed for glycine,16another inhibitory aminoacid.We believe that the term " specific G.A.B.A. antagonist

should be used for a drug only when the animal speciesand the central or peripheral sites investigated are defined.

A. N. thanks Prof. F. N. Fastier for a sample of tutin. Thiswork was supported in part by a grant from the Governors ofSt. Bartholomew’s Hospital.

Department of Pharmacology,Medical College of St. Bartholomew’s

Hospital,London EC1M 6BQ.

A. NISTRIA. CONSTANTIJ. P. QUILLIAM.

DIPHENYLHYDANTOIN FOR HICCUPS

SIR,-I was interested to read of the use of diphenyl-hydantoin in the treatment of hiccup reported by DrPetroski and Dr Patel (April 20, p. 739). Unfortunately,in a patient with long-established hiccup with whom Ihave recently been concerned, this drug was ineffective.Nevertheless, it should no doubt be added to the list of

preparations to be considered in cases of intractable hiccup.As to the possible inhibitory effect of diphenylhydantoin,

I think it unlikely that this is achieved by modifying theexcitability of the medullary inspiratory centre, as suggestedby Dr Petroski and Dr Patel. Detailed study of theproperties of hiccup indicates that it is a " triggered "phenomenon 17 served by a brainstem mechanism largelydistinct from that generating rhythmic breathing." Intract-able hiccup may be associated with a history of medullarydisease, as in their case, and is most easily explained interms of a lowered central threshold.

Royal Free Hospital,Gray’s Inn Road,

London WC1X 8LF. J. NEWSOM DAVIS.

TRANSLOCATION OF INTRAUTERINECONTRACEPTIVE DEVICES

SIR,-I was very interested in the report by Dr MacKayand Dr Mowat (April 13, p. 652) and I agree wholeheartedlythat an ultrasonic examination in the first instance is thebest available method for detecting the presence or absenceof an I.U.D. and for revealing an early pregnancy withoutsubjecting the pregnant patient to unnecessary ionisingradiation.However, I must take issue with their statement that

the series of patients they describe include the first reportedcases of translocation of the ’ Dalkon Shield ’, particularlysince their only reason for so supposing seems to be thatthey are making an unwarranted assumption-namely, thata uterine perforation at the time of I.U.D. insertion must ofnecessity be painful. I suggest that before one can statecategorically that translocation of an LU.D. has occurred,the following conditions must obtain: (1) there must be

12. Takeuchi, A., Onodera, K. Nature New Biol. 1972, 236, 55.13. Swagel, M. W., Ikeda, K., Roberts, E. ibid. 1973, 244, 180.14. Earl, J., Large, W. A. J. Physiol. Lond. 1974, 236, 113.15. Pixner, D. B. Br. J. Pharmac. 1973, 47, 637P.16. Ryall, R. W., Piercey, M. F., Polosa, C. Brain Res. 1972, 41, 119.17. Newsom Davis, J. New Developments in E.M.G. and Clinical

Neurophysiology (edited by J. E. Desmedt); vol. III, p. 751.

Basle, 1973.18. Newsom Davis, J. Brain, 1970, 93, 851.

no evidence of uterine-wall trauma occurring at the timeof insertion; and (more importantly) (2) there must beclear evidence that the device was wholly in utero at somefinite period after insertion, but before the finding of thedevice in an extrauterine situation.

It is almost certain that in cases 2, 3, and 6 in the reportthe uterine wall was perforated or in some way damagedat the time of insertion or even that the device was insertedwholly or partly through the uterine wall at the time ofinsertion.

A. H. Robins Company, Ltd.,Redkiln Way,

Horsham, Sussex RH13 5QP. J. S. TEMPLETON.

PLATELET FUNCTION AND G.-6-P.D.DEFICIENCY

SiR,—We have reported absence of leucocyte and

erythrocyte glucose-6-phosphate-dehydrogenase (G.-6-P.D.)activity associated with neutrophil dysfunction and haono-lytic anaemia.1 Reduced platelet G.-6-P.D. activity has beenreported in Caucasians with erythrocyte G.-6-P.D. defi-

ciency.2-4 We therefore examined platelet G.-6-P.D.

activity and platelet function in patient 1, who has had

G.-6-P.D. ASSAY AND PLATELET FUNCTION

* Mean d: 1 S.D. No. of determinations in parentheses.

multiple excision biopsies of infected cervical lymph-nodeswithout clinical evidence of defective heemostasis.

Platelet lysates were prepared as described by Chan etal.5 and G.-6-P.D. activity was assayed at 25°C usingA.c.D. blood. The prothrombin-consumption time (P.C.T.)and clot retraction were measured by standard techniques.The bleeding-time was performed according to Harker. 8Platelet function tests were performed on venous blood,mixed with 3-13% NaaC6H607.2H2O (9/1) using plasticequipment. Platelet factor-3 activity was measured by themethod of Hardisty 7 and platelet aggregation 8 was studiedin an aggregometer (Bryston Manufacturing Ltd., Rexdale,Ontario, Canada).

Despite absence of platelet G.-6-P.D. activity, tests of

platelet function were normal (see accompanying table).The platelet-count was 275,000 per 1.; bleeding-time5-5 min.; platelet aggregation with A.D.P., collagen, andadrenaline, normal; and platelet morphology and clotretraction normal. These findings suggest that G.-6-P.D.activity is not essential for in-vitro platelet function.

Departments of Medicine,Pædiatrics, and Pathology,

University of British Columbiaand the Vancouver General

Hospital,Vancouver, Canada V5Z 1M9.

G. R. GRAYS. C. NAIMANG. C. F. ROBINSON.

1. Gray, G. R., Klebanoff, S. J., Stamatoyannopoulos, G., Austin, T.,Naiman, S. C., Yoshida, A., Kliman, M. R., Robinson, G. C. F.Lancet, 1973, ii, 530.

2. Ramot, B., Szeinberg, A., Adam, A., Sheba, C., Gafni, D. J. clin.Invest. 1959, 38, 1659.

3. Doery, J. C. G., Hirsh, J., de Gruchy, G. C. Scand. J. Hœmat.1969, 6, 5.

4. Vuopio, P., Harkonen, M., Johnsson, R., Nuutinen, M. Ann. clin.Res. 1973, 5, 168.

5. Chan, T. K., Todd, D., Wong, C. C. J. Lab. clin. Med. 1965, 66,937.

6. Harker, L. A., Slichter, S. J. New Engl. J. Med. 1972, 287, 155.7. Hardisty, R. M., Hutton, R. A. Br. J. Hœmat. 1965, 11, 258.8. Weiss, H. J., Chervenick, P. A., Zalusky, R., Factor, A. New Engl.

J. Med. 1969, 281, 1264.