90

staffing the sanatoria, but as valuable training for thestaffs of the general hospitals (which have their owncases of tuberculosis) and for individual nurses. TheLondon teaching hospitals, by transferring 200-300nurses to sanatoria for periods of two to three monthsevery year, and by training at least as many in their owntuberculosis wards, are ensuring that their new genera-tion of nurses will be well informed about this trouble-some and interesting disease; and some of these nurses will

certainly be drawn to make their careers among tuber-culous- patients. If all the general hospitals in the

country made this provision the problem of staffingtuberculosis beds would be very largely solved, and thespread of information about tuberculosis would be muchmore rapid. Nurses are good public-health teachers inprivate life, and by their informed attitude to thedisease they could help to educate the public in methodsfor its control.

1. Gray, I. R. Brit. Heart J. 1951, 13, 387.2. Josserand, E., Gallavardin, L. Arch. gén. Méd. 1901, 188, 513.3. Boikan. W. S. Virchows Arch. 1931, 282, 46.4. Loeffler, W. Schweiz. med. Wschr. 1936, 17, 817.5. Levy, R. L., Rousselot, L. M. Amer. Heart J. 1933, 9, 178.6. Toreson, W. E. Arch. intern. Med. 1944. 73, 375.7. Ware, E. R., Chapman, B. M. Amer. Heard J. 1947. 33, 530.8. Bedford, D. E., Konstam, G. L. S. Brit. Heart J. 1946, 8, 236.9. Davies. J. N. P. E. Afr. med. J. 1948, 25, 10.

10. Edge, J. R. Lancet, 1946, ii, 675.

ENDOCARDIAL FIBROSIS

CARDIAC enlargement, it is now clear, is not inevitablyassociated with some readily defined cause, such as

rheumatism, syphilis, acute or subacute endocarditis,hypertension, coronary disease, or congenital morbuscordis. Gray 1 has lately reviewed an interesting groupof cases of congestive heart-failure of insidious onsetin young adults in which the main features were cardiac

enlargement, low blood-pressure, and usually sinusrhythm ; the electrocardiogram showed low-voltagecurves with inversion or flattening of the T wave ;embolic phenomena were common. Pathologically, thestriking feature was a thickened and opaque endo-cardium, with fibrous tissue extending into the sub-endocardial myocardium. Mural thrombosis was almost

always present over the affected endocardium, which wascommonly most involved in the apical portion of theventricles.

I According to Gray, this sydrome of endocardialfibrosis was first described in 1901 by Josserand -andGallavardin,2 who termed it " primary subacute myo-carditis." Isolated cases were later recorded under suchtitles as

"

myocarditis perniciosa," " " endocarditis

parietalis fibroplastica with eosinophilia," 4 " cardiac

hypertrophy of unhnown etiology in young adults," 5" diffuse isolated myocarditis," 6 and " chronic fibro-

plastic myocarditis." 7 In 1946 an entirely new light wasthrown on this disorder by Bedford and Konstam,8in an account of 40 cases of " unexplained heart failurein African troops, mostly from West Africa, serving in theMiddle East." Necropsy in the 17 fatal cases revealedhealthy coronary arteries, no significant valvular disease,and subendocardial fibrosis with organised antemortemclots in the ventricles. Davies 9 has since reported 36instances of this disorder in 3759 necropsies at Kampala.Of 229 Africans dying of congestive heart-failure, nearly10% were found to have endocardial fibrosis ; most ofthe deaths occurred in adolescence or early adult life.

Edge 10 described a further case in a European whoseillness began while he was receiving antisyphiliticarsenical treatment *in West Africa ; and Gray himselfadds 2 new cases, in white men, aged 40 and 36, whodeveloped congestive failure in Nigeria.This association with tropical Africa suggests that

either nutritional factors or parasitic infestation may beinvolved in the setiology. A nutritional cause seems

unlikely. The disease has been found in the tropicsamong white men, who were presumably living on a

satisfactory diet and who, as in Gray’s cases, showed no

evidence of malnutrition ; and Bedford and Konstampoint out that their patients were all well nourished.

Similarly, no case has been reported to respond tovitamin Bi ; indeed clinically and pathologically thesyndrome is quite different from beriberi. In favour of a

parasitic aetiology is the quite common finding of aneosinophilia. In one of Gray’s cases, for instance, therewas an eosinophilia of 51%, and in the other of 18%;both patients had been suspected of having had loa loa.Bedford and Konstam also remafrk on an eosinophiliain several of their cases. It would appear, therefore, thatparasitic infection is the most likely cause, and the

question arises whether the condition is a direct outcomeof such infection or is due to a resulting allergic reaction;the common eosinophilia fits in with this secondpossibility Gray, impressed by the resemblance of thelesions to those of scleroderma and disseminated lupuserythematosus, suggests that endocardial fibrosis maybelong to 11 the ill-defined category of the collagendiseases." A further possible clue in the aetiologicaltangle is Davies’s 9 observation that in three of hiscases the adrenals were unusually large.The next step, perhaps, is to observe the effect of

A.C.T.H. or cortisone on these cases. Finally-a practicalpoint of some importance-several of the reported caseshave been submitted to paracentesis pericardii on theassumption that the cardiac enlargement was due to apericardial effusion.

11. Mumme, C. Z. klin. Med. 1940, 138, 22.12. Marshall, J., Zoutendyk, A., Gear, J. S. Afr. med. J. 1951, 25,

764.13. Benacerraf, B., Rabat, E. A. J. Immunol. 1950, 64, 1.14. Storck, H. Dermatologica, 1948, 96, 177.15. Cormia, F. E., Esplin, B. M. Arch. Derm. Syph., Chicago, 1950,

61, 931.16. Moncorps, C. Arch. Derm. Syph., Wien, 190, 180, 56.

AUTOSENSITISATION IN SKIN DISEASES

IN developing a theory of autosensitisation in skindiseases, three South African workers 12 suggest thattissues may become auto-antigenic " following alterationof the cells by toxins, chemical or physical agents or byintracellular parasites." By means of the Coombs testthey have found sensitised red cells in three cases ofacute disseminated lupus erythematosus and two casesof chronic discoid lupus erythematosus, and in cases ofdermatomyositis, scleroderma, and Raynaud’s phenome-non. They suggest that the sensitised red cells may becaused to agglutinate in vivo, with resulting disturbanceof the capillary circulation. (It seems more probable,however, that the in-vivo effect of interaction of antigenand antibody on the surface of the red cell would be

haemolysis.) These workers also postulate a similarsensitisation of other mesenchymal cells. They do notstate what kind of allergic reaction they picture as takingplace in the tissues, but presumably it is of the Arthustype. This reaction is unlikely to be mediated byincomplete antigens 13 such as they have demonstrated.From the clinician’s point of view, it is perhaps unfor-

tunate that this study was not carried out on diseasesof more blatantly allergic origin than lupus erythema-tosus, in which moreover the detection of possible sites of"

auto-antigen " formation is often beyond normal clinical

ability. It has already been shown that material derivedfrom " foci of infection " is antigenic on intradermalinoculation. If we are to believe Storck,14 the skin itselfmay harbour sensitising organisms, and a filtrate fromcultures of these organisms causes eczematous reactionson patch-testing the patients from whom they werederived. Others have found that damaged epidermisproduces an antigenic substance, which, it is thought, maybe carried in the leucocytes to distant sites.15 The

possibility of an indirect effect is suggested by the workof Moncorps,16 who showed that the threshold to contactsensitisers was lower in people with focal infection thanin normals ; and in 60% of cases in which the foci weresuccessfully treated the threshold rose to the control