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from the red blood-cells. The investigators wereable to produce it in vitro by incubating solutions ofoxyhsemoglobin, methaemoglobin, or sulphsemoglobinat 40° C. for 24 hours or longer in the presence ofsterile plasma. They believe that it is in no waypeculiar to blackwater fever, but will probably befound in the serum in any condition in which thereis sudden severe hsemolysis, such as cold haemo-

globinuria, possibly acute hsemolytic anaemias,and in incompatible blood transfusions. It does not

appear in the urine. Methaemoglobinuria is commonin blackwater fever, but the methaemoglobin is derivedfrom oxyhsemoglobin after it has traversed the

glomeruli and does not result from methaemoglo-binsemia. It is known that the presence of largeamounts of oxyhsemoglobin in the plasma leads toserious renal damage with injury of the renaltubules due to precipitated pigment and consequentanuria and often death. Fairley and Bromfield

suggest therefore that the conversion of free oxy haemo-globin into pseudo-methsemoglobin is to be regardedas a conservative action on the part of the body,since pseudo-meth2emoglobin does not itself passthrough the kidneys and in its formation reducesthe amount of oxyhsemoglobin available to damagethese organs. This reaction, they suggest, is thefirst stage in a hitherto unrecognised mechanism bywhich the body disposes of circulating extracorpuscularblood pigment. Why the cells in blackwater feverare haemolysed is still not known. What propertyor factor in the plasma induces the formation of

pseudo-methsemoglobin remains to be discovered.

Why in some patients oxyhaemoglobin is not con-verted into the less dangerous pseudo-methaemoglobinin sufficient quantity or with sufficient speed to

prevent renal damage is also not ’known. As Fairleyhimself suggested, the recognition of this mechanismopens up the possibility that a drug may be foundthat will convert oxyhaemoglobin into the more

harmless pigment when the body’s own processesfail.

Many must have felt as they listened to Dr. Fairleythat he and Dr. Bromfield with a company of haema-tologists should pack their bags at once for Macedoniato try to answer some of the questions their work hasraised.

COMPATIBLES IN THE MENU

FEw doctors in this country can have escaped beingasked at some time or another what they think of theHay diet. The questioner is more often an acquaint-ance than a patient, and the question casual ratherthan serious ; for the person who intends to followdirections given in his newspaper does not want tohear his regular medical adviser say that these areunreasonable. Dr. W. H. Hay and his businessassociates have shown, if nothing else, that there area great many people who can readily be persuadedto follow such directions ; with suitable assistanceone simple idea can be made to go a very long way.Dr. Hay’s idea-or, as some call it,l bugaboo-is thatcarbohydrates and proteins should not be eaten atthe same meal, because protein (he says) increasesthe gastric secretion of acid and so hinders the

digestion of starch by the saliva. The delayeddigestion of carbohydrate is supposed to allowfermentation to take place and the acids (of secretionand fermentation) are absorbed into the circulation,causing almost every known ailment and eventuallydeath. This month Dr. Eugene Foldes 2 of New Yorkhas demonstrated how completely experience and

1 Hygeia, August, 1936, p. 683.2 Rev. Gastroenterol. June, 1937, p. 125.

experiment contradict this theory. The amount ofhydrochloric acid secreted after taking carbohydratesis not very different from the amount secreted after

taking proteins. Even if there were a significantdifference an increased amount of hydrochloric acidin the stomach would not wholly interrupt starchdigestion ; and even if it did so, fermentation in thestomach would not follow. If there were anyfermentation it would be in the intestines rather thanthe stomach, and it would not lead to the productionof significant quantities of acid ; nor is there anyreason to believe that the body would be unableto cope with such acids even if they formed in largerquantities. So far then there is no evidence tosubstantiate the theory. Against it are the intimatemixture of protein and carbohydrate in many naturalfoods, the fact that contents of the stomach fermentonly where there is achlorhydria, and the comparativeharmlessness of " acids " in a ketogenic diet exceptin one or two well-defined conditions like diabeticcoma. The chief danger run by followers of the

Hay diet is that they may reduce the protein in theirdaily ration unsuitably.

THE BLOOD AT HIGH ALTITUDES

Krupski and Almasy have been studying theinfluence of high altitude on the physiology of theblood. The material of their research consisted oftwo men aged 45 and 33, two women both aged 25,a bull-calf aged 4 months, and a goat aged 6 years.These spent 83 days at Zurich, 19 days on the

Jungfraujoch (11,200 feet), and 27 days again atZurich. Like other workers, Krupski and Almasyfound that the rise in altitude brought an increasein the red blood-cells, not excteding 15 per cent.The maximum increase for the four volunteers andthe goat was in the second and third week ; for thecalf it was in the first week. The human beingsalso showed individual differences. On going downinto the valley the red cell counts returned to normal.The reticulocyte count increased during the firstweek’s residence at high altitude and diminishedduring the second week. An important fact wasthat the maximum amount of haemoglobin in allfour persons was reached during the second weekthey remained at a height-that is, at a time whenthe reticulocyte count had already decreased. In thecalf and the goat no reticulocytes were observed inany of the three periods, but this is not interpretedas meaning that there was no increase in bone-marrowactivity. The number of leucocytes was hardly changedat a high altitude, but a decrease of lymphocytes wasnoteworthy and all investigators are agreed on anincrease of neutrophils, such as Hartmann discoveredat over 10,000 feet in the Himalayas. The Jung-fraujoch counts showed neutrophil-lymphocyte ratiosdifferent from those described by Hartmann at thesame altitude. At the high altitude the calf and thegoat had no diminution of lymphocytes, but a relativeincrease of neutrophils. (A high lymphocyte count isnormal in goats and cattle.) A slight increase of

monocytes was noticed in three of the human beingsand the two animals. During the residence on theJungfraujoch hardly any deviation from the normalwas apparent in eosinophils and basophils. This

corresponds with Hartmann’s observations. Serumof both the animals showed a negative bilirubinreaction (Ehrlich-Proscher) not only in the valleybut also at a height and even after considerablereduction of the erythrocyte count in the third period

1 Krupski, A., and Almasy, F., Helv. med. Acta, February,1937, p. 94.

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at Zurich. Determination of the dry substance of theplasma showed that the changes in the red blood-cellcount are seldom due to loss of water from the plasma.The comparison of oxygen capacity with carbon

monoxide capacity of normal blood, used for thedetermination of hsemoglobin, showed agreement.The oxygen capacity is normally proportionate tothe red blood-cell count, any deviation from thisbeing expressed in the average oxygen capacity

, per erythrocyte (SKE=Sauerstoffkapazitat pro Ery-throzyt). In the valley when the red blood-cellcount was raised SKE diminished and vice versa ;on the Jungfraujoch when the red cells rose SKErose too. The influence of intensive walking exerciseat medium and at high altitudes was investigatedon three occasions in one individual. The number of

leucocytes was much increased on two of the expe-ditions and on the third remained unaltered. It isto be noted that there was a decrease of lymphocytesand an increase of neutrophils. On the thirdexpedition, after 14 days at high altitude and fivehours’ strenuous exercise, there was no definiteincrease of reticulocytes.

Authorities do not agree about the effects of thealtitude on the oxyhsemoglobin absorption bands seenin spectroscopy of the blood, but during residence onthe Jungfraujoch the oxyheamoglobin absorptionbands almost always showed an increase, both inhumans and in animals.

MEDICAL PROTECTION

THERE should be no need to harp upon the advisa-bility of joining a professional defence society. Mem-bership has become particularly important since thepassing of the Law Reform (Miscellaneous Provisions)Act of 1934, whereby the estate of a deceased personmay now be made liable to claims based on some actor fault during his life-time. Whether or not the

sponsors of this so-called law reform intended merelyto give a remedy to the victims of fatal accidents in" running down " actions, the recent case of Rubra v.Connolly has shown that the widow of a doctor maybe adjudged liable to pay heavy damages out of hisestate for some alleged default by her dead husbandin the course of his practice. The medical defencesocieties have consequently been extending theirbenefits so as to give the personal representativesof a deceased member all such privileges as wouldhave been available if the member were still alive.The report’ of the London and Counties Medical

Protection Society, presented at the annual meetingon June 16th, rightly draws attention to thisnew risk of practice. In addition it repeats muchsalutary advice of a general kind. Members intheir own interests should refer matters imme-

diately to the society before dealing with them inany. other way. Not for the first time the practitioneris urged to secure X ray examination in all cases ofinjury which may have caused fracture or dislocationor to provide proof that X ray examination wasadvised but refused. He should also, tiresome as itmay be, keep accurate records of all work done forindividual patients at the time when treatment iscarried out. This advice applies even to dentalpractitioners who see a casual patient of whom theyhave no knowledge. A defence society can be seriouslyembarrassed in the task of defending a dental memberthrough want of accurate entries in his dental charts.Many a panel doctor would have been saved anxietyif he had made systematic entries on his recordcards, especially entries of visits to patients. It isnot mental anxiety alone that the incalculable risksof litigation inflict. Financial loss is also involved.

Reports of a defence society’s operations, describinglegal action taken to check or defeat some claim

against a professional man, frequently have occasionto record that the claimant was a person withoutmeans and that it was useless to attempt to recoverthe costs. When a society takes up a case, it paysall the costs of its member, whether he be plaintiffor defendant, and whether he succeeds or not. Ifthe society recovers damages for a member, hereceives them without deduction. Societies can offerthese advantages because members’ subscriptionsmake them possible. The bigger the membership,the greater its resources for mutual protection.

ALLERGY AND NEPHRITIS

REFERENCE was made in these columns a year ago 1to the experimental production of a glomerulo-nephritis, histologically similar to Bright’s diseasein man, by the injection of heteronephrotoxins.This work, originally brought into prominence byMatsugi, was confirmed in Edinburgh by Arnott,Kellar, and Matthew using rabbits. The methodthey adopted, in brief, was to subject rabbits to aseries of intravenous injections of duck’s serum, theducks having previously received numerous intra-

peritoneal injections of a suspension of rabbits’

kidneys. The rabbits so treated showed a glomerulo-nephritis closely comparable to human Bright’sdisease. The experimental facts may now be takenas established, but the mechanism of causationremains doubtful. Most observers seem to agreethat the nephritis is an allergic manifestation, butthis statement leaves us in some doubt as to what

actually takes place in the body. Amongst pointsawaiting clarification are the following. First, weneed to know whether the " nephrotoxin " is specificfor the kidney or whether comparable effects canbe produced by sera prepared from other organs.Klinge and Knepper consider that it is only one ofseveral factors required to induce sensitisation andis not specific. Next, it has been suggested thatthe effect on the kidney is due to a hsemolysin evokedby blood included during the preparation of theserum. But Arnott, Kellar, and Matthew perfusedthe kidneys of their rabbits with saline to removeblood ; it therefore appears that a haemolysin canbe excluded in their experimental nephritis. Otherworkers, however, state that when perfused organsare used a tubular degeneration only is induced bythe prepared serum. Lastly, it is claimed by Knepperthat the so-called localisation of allergic responsecan be observed after the use of mechanical, thermal,pharmacological, and hormonal factors.A theory deserving close attention is that advanced

by C. E. Kellett,2 who suggests that the mechanisminvolved in this experimental nephritis is that of" reversed anaphylaxis." By this, as he has explainedin an earlier paper,3 it is understood that the ana-

phylactic reaction ensues when circulating antibodyunites with antigen which is fixed to the cell-incontrast to the usual type of reaction in which theantibody is fixed to the cell and the antigen is inthe circulation. Kellett thinks that the procedureinvolved in the experimental nephritis under con-sideration closely mimics the mechanism of reversed

anaphylaxis. Glomerulonephritis in man, he sug-gests, may result from a reaction between antibodieselaborated by the body in response to an infectionand the toxins resulting from that infection whichhave become fixed to the tissues, more particularly

1 Lancet, 1936, 1, 1078.2 Ibid, 1936, 2, 1262.

3 J. Path. Bact. 1935, 41, 479.