GONADAL DYSGENESIS

GONADAL DYSGENESIS

1019 GONADAL DYSGENESIS SIR,-Dr. Ferguson-Smith (May 3) is to be congratulated on his enterprise in determining the nuclear sex of 325 male patients ...

168KB Sizes 1 Downloads 31 Views

1019 GONADAL DYSGENESIS

SIR,-Dr. Ferguson-Smith (May 3) is to be congratulated on his enterprise in determining the nuclear sex of 325 male patients in a mental-deficiency hospital. He will undoubtedly be followed in his rewarding aetiological foray by a host of chromatographers, endocrinologists, and biochemists. He cannot be equally congratulated on his choice of the words " primary to describe his 4 patients with gonadal microrchidism It is quite true that it is not yet possible to dysgenesis. an exact aetiological description of such cases, but to give microrchidism "-unprodescribe their condition as "

"

nounceable word for the Sassenach-is

to relate no more than our grandfathers knew. The testicular appearances described and the conclusions which Dr. Ferguson-Smith draws from his cases have already reached the textbooks.1 Lawson Wilkins uses the group-term, gonadal dysgenesis, and the two types of testicular disorder described by Dr.

Ferguson-Smith he

names " tubular germinal aplasia " and He recognises that these disorders have a varying pathogenesis. The primitive gonad has a cortex (germinal epithelium), from which the germ cells are derived, and a medulla (mesonephros) from which the tubules and the interstitial cells are developed. He suggests that the defective development of the cortex results in germinal aplasia, while hyaline or fibrotic changes in the tubules may derive either from a defect in development of the medulla or from subsequent "

tubular nbrosis ".

regressive changes. We may wait some time for a more exact knowledge of pathogenesis, but we have already a sensible descriptive nomenclature based on rational aaiological ideas.

other hand it is assumed, as Laurie and Woods have dorie, that the major factor in the production of cerebral thrombosis and haemorrhage is atheromatosis, then the incidence of cerebral catastrophe in my series would rise to about 1% of all necropsy cases, which is comparable with Laurie and Wood’s figure of 31 cases in 2000 autopsies (1-5%). In our last 144 consecutive necropsies on Bantu subjects there were 3 cases of cerebral vascular accident (2%)-a small series but perhaps sufficient to show that the incidence of these lesions in the Bantu lies somewhere between 1 and 2%. Laurie and Woods further state that I " found severe atherosclerosis in 26% of Bantu patients over 45, but only in 0-4% of the whole "series was atherosclerosis the cause of death". They find a significant discrepancy " between these two figures which they cannot explain. My definition of severe lesions at that time was " many lesions, together with complications such as dilatation, deformity, calcification, ulceration and thrombosis ". I detailed 11cases in which I considered the cause of death was due solely and entirely to atheromatosis, and clearly stated that it was difficult to assess how far atheroma contributed to the fatal outcome of disease of the cardiovascular system when it was associated with other cardiovascular diseases. Of 137 cases which were classed as severe atheroma, 35 % died a cardiac death, but many of these The so-called cases had evidence of hypertension as well. discrepancy resolves itself into different points of view.

Finally, I should like to stress that on occasion the Bantu can and does develop just as much atherosclerosis as the European in this country. There is no inherent racial immunity to the disease. I believe that the incidence of serious complications in the Bantu, particularly coronary occlusive disease, is significantly lower. Department of Pathology and Microbiology, University of the Witwatersrand, Johannesburg.

B.

J. P. BECKER.

DOUGLAS HUBBLE. THE DOCTOR’S ATTITUDE TO HIS PATIENT

ATHEROSCLEROSIS AND ITS CEREBRAL COMPLICATIONS IN THE SOUTH AFRICAN BANTU

SIR,-In their stimulating article2 on this subject, Dr. Laurie and Dr. Woods make some statements in connection with my findings in atherosclerosis in the Bantu which, in view of the considerable attention this article has attracted, cannot go unchallenged. They state that " In 3000 consecutive necropsies on Bantu in South Africa, Becker (1946)3 found only 1 cerebral catastrophe, whereas in just under 2000 consecutive necropsies we have found 31 such patients-a prevalence almost fifty times greater than that in Becker’s series ". This is not correct. In my series of 3000 consecutive autopsies, I reported 68 cerebral catastrophes, an overall incidence of 23%.4 The

bosis)

causes were as

of cerebral apoplexy (haemorrhage and thromfollows:

SIR,-From the sidelines I have followed this correspondence with growing interest. My attention was first directed to the subject by Dr. Balint’s two papers in 19541and 1955,2which whetted my appetite for a careful study of his book.3 The papers by Dr. Clyne4 and Dr. Pasmorewere obviously direct results of Dr. Balint’s teaching and showed that a prophet is not necessarily without honour in his own (or adopted) country. Whilst it would be too much to ask for a universal acceptance of psychoanalytic teaching, it had not seemed to me that Balint, Clyne, Hopkins,6 and Pasmore had put forward any particularly controversial views: they had merely stated facts and observations that any practitioner could confirm for himself if he cared to listen to his patients-though he may have to learn to listen. But evidently I was wrong. The subject is extremely controversial-and highly charged-and I have no doubt that Dr. Balint could give a ready interpretation of the resistances shown. Yet it passes all understanding that anyone should put Scanforward-let alone swallow-the proposition of " ner that " the emotional history should not have any direct influence on the doctor’s clinical opinion ". That the clinician may reach that opinion " without the emotional history " is no doubt often true; but to say that he can give just as good advice and get just as good a result without ever hearing it seems to deny many of "

The case ascribed to atheromatosis was one in which it was considered that this condition was the sole cause of the apoplexy; whereas in the cases of hypertensive arteriosclerosis, although atheromatosis was present in 64% of the cases, and in patients over 40 was present in nearly 100%,3 I considered the hypertensive condition more important in the pathogenesis of the cerebral complication than the atheroma. If on the 1.

Wilkins, L. The Diagnosis and Treatment of Endocrine Disorders in Childhood and Adolescence; p. 236, p. 265. 2nd ed. Springfield, Ill. Laurie, I. M., Woods, J. D. Lancet, Feb. 1, 1958, p. 231. 3. Becker, B. J. P. S. Afr. J. med. Sci. 1946, 11, 97. 4. Becker, B. J. P. ibid. p. 1. 2.

"

"

Balint, M. Brit. med. J. 1954, i, 115. Balint, M. Lancet, 1955, i, 684. Balint, M. The Doctor, His Patient, and the Illness. London, 1957. Clyne, M. B. Lancet, Feb. 1, 1958, p. 232. Pasmore, H. S. ibid. March 8, 1958, p. 524. 6. Hopkins, P. ibid. 1956, ii, 455. 7. ibid. April 12, 1958, p. 800.

1. 2. 3. 4. 5.