st. john's hospital dermatological society
TRANSCRIPT
21
MEDICAL SOCIETIES.
ST. JOHN’S HOSPITAL DERMATOLOGICAL
SOCIETY
ON June 22nd, Prof. Charles Flandin deliveredthe Prosser White oration at 1, Wimpole-street, W.,with Dr. W. N. Goldsmith, the president, in the chair.The subject of the address was
Recent Advances in Leprosywith special reference to the methods adopted fordealing with the problem in France.
Prof. Flandin thought that the time was ripe tobring before British dermatologists the presentposition of leprosy, as summed up at the recent congressof the International Leprosy Association held at
Cairo, and to draw their attention to conditions inFrance, which might have considerable interest forthis country. The recorded amount of leprosy in
any country depended very largely on the effort
expended in ascertainment, but there were certaindisquieting features in the present situation in Europewhich might lead to a reconsideration of our attitudeto the whole problem. Although it was almost alaw that leprosy declines as social and hygienicstandards rise and although the great leprologistsof the last generation had declared that they had neveror hardly ever come across leprosy of indigenousorigin in Western Europe during the whole of theirlives, yet Prof. Flandin had found in the short spaceof three years ten cases in Paris, none of which hadever left France. He referred to the discovery ofindigenous cases in England by Dr. J. M. H. MacLeodand stated that in certain other European countries,notably Rumania, the disease was said to be greatlyon the increase.
In his clinic at the Hôpital Saint Louis he hadbeen able to make some exact observations of theincubation period and had been surprised to find acertain number of cases in which that period wascomparatively short. In soldiers, officials, and otherswho returned from countries in which leprosy wasendemic the disease might appear at an interval offrom six months to twenty years, but in some of theindigenous cases the incubation period was less thansix months, in one case apparently as little as
two months. Moreover he was convinced that thefirst objective sign of leprosy by no means denotedthe beginning of infection. " Leprous fever," a
continued fever with pains especially round the joints,was nearly always noted before the actual develop-ment of the lesions. Such persons had undoubtedlybeen infected and were in a state of allergy, as couldbe shown by a non-specific reaction following the
injection of tuberculin. The intradermal injectionof chaulmoogra oil would attract Hansen’s bacillito the site of the injection and a definite diagnosiscould be obtained by demonstrating them in it afterabout an eight-day interval. The site of electionfrom which to obtain bacilli was undoubtedly thelobule of the ear.As to treatment, he had seen many methods come
and go but he had considerable hopes of a colloidalpreparation of cholesterol and chaulmoogra esterswhich was given intravenously daily in doses of about10 to 15 c.cm. Treatment was recommenced at thefirst sign of a relapse, but he thought that it mightbe better to continue treatment after all signs haddisappeared on the analogy of the arsenical compoundsin the treatment of syphilis.Commenting on administrative methods, he
expressed his conviction that the compulsory notifica-tion in force in France was useless. The leper wouldchange his name and run the risk of prison rather thanexpose himself to the possibility of being shut upin a leprosarium. As in tuberculosis, the examinationof family contacts was essential, but this was impossiblethrough official machinery. The education of thepublic was perhaps the most important need. Theymust be taught that only prolonged and intimatecontact as in family life was dangerous and thatleprosy could be regarded as less contagious thantuberculosis and at least equally amenable to treat-ment. Meanwhile he pleaded for close coordinationbetween the specialists of England and Franceinterested in the subject in order that, first, someascertainment of the real numbers might be made,and secondly that such action as might be neededshould be the result of the experience of bothcountries pooled in a " front commun de la ]6pre."
DEVON AND EXETER MEDICO-
CHIRURGICAL SOCIETY
AT a meeting of this society held on May 26thDr. CRICHTON MACGAFFEY gave an address entitled
Type Reactions of the Kidney to DiseaseThe classification and nomenclature of renal disorders,he said, has been a source of controversy and perplexityever since Bright’s disease was first described. Bright’soriginal description was itself confusing, in that itembraced more than one variety of kidney disease.Volhard and Farr in 1914 did much to clear the issue,and Van Slyke materially advanced our knowledgeby the introduction of his urea-clearance test. Roperin 1926 laid stress on the changes that take place in thealbumin content of the blood where there is muchoedema.
It is now possible to include all the varieties of renaldisease under three type reactions-degenerative,hsemorrhagic, and hypertensive.The degenerative type includes all those cases in
which albuminuria is the prominent feature, such aschronic parenchymatous nephritis or nephrosis.Although the tubules are sometimes severely damaged,there is reason to believe that the kidney is not theprimary focus of disease. There is in fact a prerenaldeviation of salt and water causing their retentionwith resultant cedema, and the albumin found in theurine comes, in the first instance, not from the
kidney but from the blood stream. When albumin inthe blood stream falls from the normal 4-3 percent. to 2-7 per cent., oedema appears. Further
proof of this prerenal deviation is afforded by experi-ment. For example, large draughts of normal salinedo not cause diuresis ; egg albumin, intravenouslyinjected, appears in the urine as such even when thekidneys are normal; intravenous saline causes
diuresis, but not if an artificial acidosis is producedas a result of temporary ischaemia ; indeed all the
symptoms of uraemia follow if the experiment is
pushed to its limits. This explains the perplexingnormal renal function often met with in nephrosisand also the fact that mercurial poisoning, whichprimarily affects the tubules, does not cause oedemauntil the glomeruli are damaged.The haemorrhagic type, both acute and chronic,
is a true nephritis, in that the blood-cells in theurine denote active renal damage, the main brunt ofthe disease falling on the glomeruli. In the acute