AN EPIDEMIC OF THYROTOXICOSIS

AN EPIDEMIC OF THYROTOXICOSIS

617 its present members. Therefore, after long discussion, a third course (and the one favoured all along by the council) was accepted. This was to fo...

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617 its present members. Therefore, after long discussion, a third course (and the one favoured all along by the council) was accepted. This was to form a parallel organisation-in appearance not unlike that of the Independence Fund and its trustees—which will be known as the British Medical Guild. The guild is to have no membership. It will in effect be but a board of trustees. The trustees will consist of any or all of the members for the time being of the central council of the B.M.A., who have individually given their assent to serve. The guild will, when so required, endeavour to rouse support and organise action in favour of the association’s policy as then current. To finance the guild’s activities, and to provide resources from which it could indemnify doctors who suffer loss or hardship through participation in collective action, there will have to be substantial funds. These funds it is hoped will be raised within reasonable time by voluntary subscription from the profession. Time alone will show how powerfully and successfully such an organisation can act. Meanwhile the association is fortified by -learned legal opinion that the proposed guild could carry out its intended functions of organising and financing collective action by the profession, and of providing financial compensation to practitioners suffering financial hardship through participation in such collective action, without in any way endangering the life or position of the association itself. AN EPIDEMIC OF THYROTOXICOSIS

BETWEEN 1942 and 1945 a remarkable increase in the incidence of thyrotoxicosis was recorded in Denmark. The rise, and subsequent fall, in the number of cases was abrupt enough to justify the use of the term " epidemic," though without implying that any infectious agent was concerned. The facts have been recorded with admirable thoroughness by Iversen in a monograph published in 1948, and now summarised elsewhere.2 Iversen’s detailed - figures relate to all cases in Copenhagen entering hospital for the first time with the diagnosis of thyrotoxicosis ; and he found that the incidence in the whole country ran parallel to that in the capital. His figures show that there was a slow increase in incidence from 1938 to 1941. In 1942 there was a rapid rise, with a further slight increase until the peak was reached in 1944. After that there was a sharp fall, till- in 1947 the incidence was the same as in 1940. Iversen feels confident that his records include virtually all cases of thyrotoxicosis in Copenhagen, and he is able to state actual figures for the incidence of the disease. Thus, in 1938 there were 0-19 cases per 1000 inhabitants ; in 1944, 0-83 ; in 1947, 0-21. The chances of an inhabitant of Copenhagen developing thyrotoxicosis were about four times as great at the height of the epidemic as before or since. The increase was, he believes, real, and not simply the result of better diagnosis. It cannot have been due simply to the psychological effects of the German occupation, for it started during 1941, when the behaviour of the invaders was comparatively mild, and it showed only a slight further rise in 1944, when the Germans "got tough." Moreover, during the same period the incidence and severity of thyrotoxicosis in Belgium In Holland also tended, if anything, to decrease.3 there seems to have been a fall,4 while in Norway a small increase in incidence in the early stages of the German occupation was followed by a fall.5 Two other factors may have played some part-weather and diet. Iversen points out that the winters of 1940, 1.

Iversen, K. Temporary Rise in the Frequency of Thyrotoxicosis in Denmark, 1941-45. Copenhagen, 1948. 2. Iversen, K. Amer. J. med. Sci. -1949, 217, 121. 3. Bastenie, P. A. Lancet, 1947, i, 789. 4. Schweitzer, P. M. J. Acta. med. scand. 1944, 119, 306. 5. Grelland, R. Ibid, 1946, 125, 108.

were unusually severe, and there is that exposure to cold stimulates evidence experimental It is not perhaps very likely that the the thyroid. hard winter of 1942 would still be causing fresh cases of thyrotoxicosis in 1944, but this possibility cannot be excluded, since Iversen’s cases are grouped by the date, not of onset, but of entry into hospital. During the German occupation the diet of the Danish people varied comparatively little, and was never grossly deficient as in Belgium and Holland. Iversen’s suggestion in this connexion is ingenious, if rather far-fetched. Before the war large quantities of soya-bean oil were imported as cattle-feed ; these imports ceased in 1941. Soya bean is well known to contain an antithyroid factor, and this factor might be contained in the cattle-feed and subsequently in the cow’s milk (though this has never been proved) ; cutting off the supply of this factor might unleash a series of fresh cases. If we review the events in Belgium, Holland, Norway, and Denmark as a whole, the least unacceptable theory seems to be that the invasion of these countries by the Germans did increase the tendency of the inhabitants to develop thyrotoxicosis, but that this tendency was masked in the case of Belgium and Holland by the highly abnormal diet. The masking effect of the diet might be due to lack of calories or of protein, or to excess of vegetables containing antithyroid factors. This theory gets its chief support from the experience of Norway. There the diet remained adequate during the first year or so of the German occupation but became deficient later; and an initial increase in thyrotoxicosis was followed by a decrease at about the time when the diet deteriorated. It. is tempting to suppose that .the increase was caused by the psychological effects of invasion, and the decrease by the poor diet ; but there is no certain proof.

1941, and 1942

TRANSMISSION OF LIGHT THROUGH SKIN

DURING the last years of the German occupation and " in the course of evening hours," Dr. Hansen1 investi-’ gated the transmission of light through the skin. After preliminary experiments he chose to work with a Philips super high-pressure mercury arc-lamp (capable, of emitting a constant supply of ultraviolet rays giving " a quasi-continuous spectrum ") and a photo-electric cell for estimating the intensity of the transmitted He compared transmission through skin excised from the mouse immediately after death or during anaesthesia, skin stored in an ice-chest, skin from pedicle grafts, skin obtained at necropsy, and skin removed at operation He found that all except the stored or after blistering. skin gave almost identical and constant curves. Transmission through stored skin was greater, but the curves were similar. He concludes that within the wave-lengths 500 mµ and 300 mµ the course of the transmission curve is the same for live mouse skin, for skin excised shortly after death, and for frozen sections of both types of skin, decreasing uniformly with the wave-length from 500 to 300 mµ, with a minimum at 415 mµ, attributed mainly to haemoglobin absorption. The various layers of skin are not characteristic in their absorption of radiation, and there is nothing in the results to indicate that there is any wave-length region to which a specific biological effect on skin tissue can be ascribed. The only uncertainty left by these careful experiments is whether the current from the photo-electric cell is proportional to the intensity of the light falling on it. Hansen says he investigated this point at four wavelengths (313-450 mµ) and found that it was proportional, but he admits that this is contrary to accepted opinion and offers the explanation that the light intensities he ‘

light.

1. On the Transmission through Skin of Visible and Ultraviolet Radiation. By K. G. HANSEN. Acta radiol., Stockh. 1948, suppl. 77. Pp. 106. Sw. Kr. 8.

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