677

the thirty or so villages exclusively affected are situated northand south of the Iron Gates of the Danube, in a somewhatrectangular area of nearly 150 km. wide, in the adjoiningparts of Bulgaria, Rumania, and Yugoslavia. The nameDanubian endemic familial nephropathy (D.E.F.N.) mightbetter reflect actual knowledge and suggest further inquiries inother countries and continents.’ 7

We thank Dr. Janet Niven (National Institute for MedicalResearch) and Prof. A. C. Lendrum (Queens College, Dundee) forvaluable information and practical suggestions.

V. Babes Institute of Pathology,Bucharest 35, Rumania.

E. C. CRACIUNS. NICOLESCOC. RAUE. TOMESCU.

POSTOPERATIVE DEEP-VEIN THROMBOSIS

SIR,-I read with interest the paper on postoperative deep-vein thrombosis by Mr. Flanc and his colleagues (March 8,p. 477), particularly their demonstration that the incidence ofthis complication in elderly patients undergoing major opera-tions is 61 %, and their remark that the thrombus often startsduring the operation-I share this belief.

They kindly referred to my joint work on this subject, butI should be obliged if you would let me correct a mistake theyhave made with regard to it. They say we showed that venousstasis during anaesthesia was prevented by elevation of the legs.In 1964, in a carefully planned trial using one of the patients’legs as a control to the other, we demonstrated that during amajor operation the venous return often slowed as much as itdoes when the patient is confined to bed for two weeks, and thatthis stasis could be eliminated by electrically stimulating the calfmuscles. We did not test elevation. Then in 1967, in a properlyconstructed clinical trial on 200 patients undergoing majoroperations, we proved mathematically that the incidence ofdeep-vein thrombosis in the control limb, which just lay flat onthe table, was much greater than it was in the limb which waselectrically stimulated. Moreover, both the fatal emboli in thatseries came from the unstimulated leg.Kidderminster General Hospital, Worcs. F. S. A. DORAN.

DIPLOMA IN THE HISTORY OF MEDICINE

SIR,-Dr. Clarke (March 15, p. 572) rightly draws attentionto the sub-department of the history of medicine at UniversityCollege London where he has been developing teaching andresearch in the subject since it was established in October,1966. The phrase which he quotes from my letter was usedin the context of the resolution of the International Society ofthe History of Medicine that a course in the history ofmedicine should be a regular part of the medical under-graduate’s training. I was present at the discussion of thisresolution and I took it to mean a course more closely inte-grated with the curriculum than the type of lecture coursewhich Dr. Clarke mentions, such as has been given at otherschools, including the Middlesex and King’s College.

All who are interested in the subject are anxious to supportand develop the initiative of the Wellcome Trustees in helpingto establish academic departments. Far from competing inany way with this, the Apothecaries’ plans should make itpossible for more medical students and others, in London andelsewhere, to learn something of the subject and so provideinterested recruits for the sub-department at UniversityCollege London and for any others which may be establishedin the coming years.

W. S. C. COPEMANChairman, Faculty of theHistory of Medicine and

Pharmacy.

The Worshipful Society ofApothecaries of London,

London E.C.4.

7. Lancet, 1966, i, 304.

FIBRINOLYSIS IN CHILDREN WITH CONGENITALHEART-DISEASE

Sir have read with interest the report of Dr. Johnson andher colleagues, who found no coagulation abnormalities inchildren with cyanotic congenital heart-disease.

In 31 children with cyanotic congenital heart-disease(haematocrit 48-88%, arterial oxygen saturation 60-80%),I have studied the spontaneous fibrinolytic activity of plasma,plasminogen activity, and antiplasmin activity (all by Marbet’s

TABLE I-SPONTANEOUS PLASMALYSIS IN 35 HEALTHY CHILDREN AND31 CHILDREN WITH CYANOTIC CONGENITAL HEART-DISEASE (C.H.D.)

TABLE II-VALUES FOR PLASMINOGEN, PLASMINOGEN PROACTIVATOR,AND ANTIPLASMIN ACTIVITY IN 35 NORMAL CHILDREN AND 31CHILDREN WITH CYANOTIC C.H.D.

method 3), and the activity of plasminogen proactivator (Blix’smethod 4) . The results are shown in tables i and 11. Com-

pared with the healthy control group, I found increasedfibrinolytic activity in the diseased children. Plasminogenactivity and the activity of plasminogen proactivator alsoincreased significantly. The antiplasmin titre was withinnormal limits. I did not find correlation between eitherha:matocrit value and enzyme activity, or systemic arterialoxygen saturation and enzyme activity.2nd Department of Pædiatrics,

University of Budapest. B. GOLDSCHMIDT.

FÆCAL BLOOD-LOSS AFTER SODIUM

ACETYLSALICYLATE TAKEN WITH ALCOHOI

SIR,-I feel some rebuttal is required of the rejoinder byDr. Bouchier and Mr. Williams to Dr. Dobbing’s letter

(March 8, p. 528). The points below deserve consideration.(i) Dr. Dobbing’s mean difference can hardly be challenged

by citing an experimental error for individual observations ofsimilar magnitude; the influence of the latter on 18 sets ofdifferences of means from 6 sets of observations would be verymuch smaller.

(ii) The inclusion or exclusion of subject 22 critically affectsthe results of any statistical evaluation; that the cause for theblood-loss was unknown does not mean that it was necessarilyattributable to the drugs administered some days earlier, andDr. Dobbing’s exclusion of this case seems to be the wisestcourse to follow.

(iii) Since a mean daily loss is calculated by dividing the totalloss by the number of days, the validity of restoring the mean1. Johnson, C. A., Abildgaard, C. F., Schulman, I. Lancet, 1968, ii, 660.2. Goldschmidt, B. Mschr.Kinderheilk. 1968, 116, 140.3. Jurgens, J. Klinische Methoden der Blutgerinungsanalyse; p. 242.

Stuttgart, 1959.4. Blix, S. Acta med. scand. 1964. 176. 649.