Anti-streptolysin O titre in rheumatic carditis.

The definition of rheumatic fever has been broadened of recent years and many people take it to include not only articular and skin manifestations but also all those signs that are commonly regarded as evidence of an active carditis. While this conception may be pathologically correct and at times convenient in use, it is clear that there are many cases of rheumatic fever where there is no proof of cardiac involvement and equally others where rheumatic involvement of the heart is evident without the other features of the rheumatic state. The commonly held view that rheumatic fever is the sequel of a streptococcal infection led to the investigation of immune bodies produced by these streptococci amongst which are to be numbered the anti-streptolysins, anti-fibrolysin, and anti-hyaluronidase. In spite of modern diagnostic aids, recognition of the presence of rheumatic activity, especially in the heart, remains a problem of great difficulty. It seemed to us, therefore, that it was important to reassess the various criteria by which rheumatism and rheumatic carditis are at present judged. Although most of our observations have embraced clinical, electrocardiographic, radiological, biochemical, and bacteriological investigations, the present report is devoted to the anti-streptolysin 0 titre (A.S.O.). Our series differs from those of most hitherto published work in the length of observations made in the individual patient. The clinical and certain other observations have continued over several years. The anti-streptolysin studies extend over a period of many months and sometimes more than a year. Estimations were made fortnightly with an average of 12 for each patient. Amongprevious studies oftheanti-streptolysinOtitre there is considerable variation in what should be accepted as normal. Rantz et al. (1952) gave figures of 150 for children between the ages of five and seven, and of 184 for those between eight and twelve. Faver (1953) regarded the level as normal below 200 and thought that when there was a rise above this level it was due to previous streptococcal infection. Denny et al. (1950) recorded a higher titre in those cases that developed rheumatic fever, while Rantz et al. (1948) found the titre lower in those who develop carditis than in those with joint pains. More recently Stollerman et al. (1956) accepted 200 as the upper limit of normal. A great variation is also found in the type of the curve, which generally rose in one to two weeks and was maximal in four weeks (McCarty, …