TROPHOBLAST AND ITS TUMOURS

TROPHOBLAST AND ITS TUMOURS

113 PYELOGRAPHY IN URINARY INFECTION This not yet justified ..." in Dr. James’ article (Dec. 5) prompts me to ask again: when is pyelography justifie...

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113 PYELOGRAPHY IN URINARY INFECTION

This not yet justified ..." in Dr. James’ article (Dec. 5) prompts me to ask again: when is pyelography justified in renal-tract infections ? While R.M.O. at General Infirmary I included intravenous recently, pyelography as a routine all in acute renal-tract infections amongst the investigation The total number of such cases was quite nursing staff. low but, to my surprise, three pyelograms revealed evidence suggestive of obstruction: in two there was persistent unilateral ureteric kinking and in a third a double ureter was shown on one side. As these were all first infections in otherwise healthy young girls surgical intervention was not sought. I am still wondering whether this was the correct attitude or not. There is a wealth 12 of experimental and presumptive clinical evidence showing a correlation between obstruction and renal-tract infection. Of the possible permanent sequelse to such infection we are only too well aware. That obstruction was a possible factor in the pathophysiology of these cases I had little doubt. Yet I am sure most surgeons would be loathe to intervene in the absence of more positive evidence, such as persistent or recurring infections, or calyceal distortion. Logic teaches that this is obviously too late and that many cases of occult persistent infection will be missed. Nevertheless until we are prepared to investigate and treat actively all cases of " minor " anatomical disturbance I see little point in routine pyelography. I wonder does Dr. Tames think likewise ?

SIR,-" Pyelography

statement

Salisbury

St. Vincent’s Hospital, Dublin.

JAMES G. DEVLIN.

TROPHOBLAST AND ITS TUMOURS

SIR,-If the trophoblast is a homograft, the full implications do not appear to be yet realised. Surely if tolerance to a homograft can be induced in a fcetus or newborn animal, but not an adult animal, by injection of donor cells it is an unjustified extrapolation to suggest that a similar mechanism occurs in the human adult pregnant female host. This topic is not new; in your columns I pointed out ten years ago3 in detail the inconsistencies that the present hypothesis leads to and suggested an alternative. The alternative is that the trophoblast is an autograft, at least the syncytial portion of it, and derived from the granulosa cells that cover the ovum when it leaves the follicle. Unorthodox as this suggestion is it at least makes sense, which the present orthodoxy does not. I suggest that the main function of the syncytium is to protect the foetus from the homograft reaction of the mother, and perhaps vice versa to protect the mother from the foetus. Remember that however separate the foetus may be from the mother the syncytium is as intimately involved in the maternal circulation as any cells can be. Public Health Offices, Ilford.

ISRAEL GORDON Medical Officer of Health.

MATERNAL INFLUENZA AND CONGENITAL DEFORMITIES SiR,ŇThe article by Dr. Coffey and Professor Jessop (Nov. 28) merits further comment, especially in view of two contradictory reports on this subject. In all likelihood, these reports were not available to Dr. Coffey and Professor Jessop when they completed their study. 1. Lancet, 1959, i, 614. 2. ibid. p. 1265. 3. Gordon, I. Lancet, 1949,

i, 807.

Wilson and his co-workers as a result of their investigation1 concluded that " No significant teratogenic effect of Asian influenza was demonstrated ..." It is to be noted that the presence or absence of influenza in the patients they studied was confirmed by hsemagglutinationŇinhibition titre determinations. Walker and McKee2 have concluded that " there was no apparent alteration in the number of anomalies in the infants of mothers who had Asian influenza during their pregnancy". In this study serological tests for influenza similar to those employed in Wilson’s investigation were also carried out.

On the basis of the findings of Walker and Wilson one might well question the implications of the Dublin study. Moreover, the methodology of selecting patients for inclusion in the study on the basis of self-diagnosis is vulnerable to criticism. This is so, not so much (in this instance of a disease with a high attack-rate) because those replying in the affirmative may not have had the disease, but, as Walker’s study points out, because those replying in the negative may very well have had the

disease. Seaside Memorial Hospital of Long Beach, Long Beach, California.

GEORGE X. TRIMBLE Director of Medical Education.

FORMATION OF RENAL CALCULI

SIR,-I was very interested indeed to read your annotation of Oct. 24. I have been carrying out a small experiment to try to confirm or refute the claim that the administration of salicylates prevents the formation of urinary calculi. Medo-Chemicals Ltd. have very kindly supplied me with a stock of theirSalimed ’ tablets and also some pseudo-salimed tablets, and I have been administering these to an unselected group of patients who have had recurrent urinary calculi, but in whom there is no local predisposing cause to recurrence, such as chronic infection or stasis. This is obviously a very long-term type of investigation and as yet it is not possible to draw any conclusions. I know that claims have been made in America, both for and against its administration, but I feel that both these investigations were not sufficiently selective or continued for a sufficient length of time to justify the conclusions. I hope in a few years’ time that I shall be able to give some results which may help to decide whether there is any value in the administration of salicylates, or salicylate-containing substances, to patients with recurrent calculi.

S. H. C. CLARKE.

Hove, Sussex.

ÆTIOLOGY OF LEUKÆMIA

leading article3 on the xtiology of leukasmia are intriguing. However, some results of our studies on human leukxmic leukocytes in vitro are in disagreement, not only with the concept of chronic leukaemia as a conditioned neoplasm resulting from deficiency of a blood-borne growth inhibitor but also with the thesis that autonomy of leukxmic cells (i.e., in acute leukxmia) might be specifically indicated by an SIR,-The theories discussed in

your

abnormal chromosomal pattern. We failed to find any chromosomal abnormality in the three cases of acute granulocytic leukxmia reported some time agoand more recently we have found a small, but definite, abnormality, a minute replacing one of the 46 normal chromosomes, in the 2 cases of chronic granulocytic leukaemia investigated.5 Wilson, M. G., Heins, H. L., Imagawa, D. T., Adams, J. M. J. Amer. med. Ass. 1959, 171, 638. Walker, W. M., McKee, A. P. Obstet. Gynec. 1959, 13, 394. Lancet, 1959, ii, 447. Nowell, P., Hungerford, D., Brooks, C. Proc. Amer. Ass. Cancer Res. 1958, 2, 331. 5. Nowell, P., Hungerford, D. (to be published). 1.

2. 3. 4.