Efficient anticoagulation with warfarin therapy requires optimal dosage. An international programme of standardization of prothrombin time tests has been developed in order to achieve correct dosage and efficient anticoagulation. Many South African laboratories use a more conservative therapeutic range for the prothrombin time than that recommended by international bodies. Consequently, warfarin dosage is often lower in the RSA than in many other countries. The use of a slightly lower therapeutic range in the RSA would improve anticoagulation without increasing the risk of haemorrhage. Practical guidelines for efficient warfarin therapy, including induction and maintenance dosage, therapeutic range, management of overdosage, contraindications and use during pregnancy and lactation, are discussed.

The change to the reporting of haematology laboratory results in the SI is now occuring in South Africa. To facilitate uniformity and standardization, the recommendations of a subcommittee of the Southern African Society for Haematology are presented.

SUMMARY Four Bantu male children belonging to 2 families and suffering from an unusual haemorrhagic disorder are described. The laboratory findings are given and it is suggested that the results are consistent with, though not diagnostic of, factor XI defi­ ciency. This condition does not appear to have been hitherto described in Bantu subjects. Treatment of the disorder is briefly discussed.

British Journal of HaematologyVolume 10, Issue 1 p. 50-58 Iron Metabolism in Scurvy with Special Reference to Erythropoiesis* T. H. Bothwell, Corresponding Author T. H. Bothwell Departments of Medicine and Chemical Pathology, University of Witwatersrand Medical School, and Baragwanath Hospital, Johannesburg†Hospital Street, Johannesburg, S. Africa.Search for more papers by this authorB. A. Bradlow, B. A. Bradlow Departments of Medicine and Chemical Pathology, University of Witwatersrand Medical School, and Baragwanath Hospital, JohannesburgSearch for more papers by this authorP. Jacobs, P. Jacobs Departments of Medicine and Chemical Pathology, University of Witwatersrand Medical School, and Baragwanath Hospital, JohannesburgSearch for more papers by this authorK. Keeley, K. Keeley Departments of Medicine and Chemical Pathology, University of Witwatersrand Medical School, and Baragwanath Hospital, JohannesburgSearch for more papers by this authorS. Kramer, S. Kramer Departments of Medicine and Chemical Pathology, University of Witwatersrand Medical School, and Baragwanath Hospital, JohannesburgSearch for more papers by this authorH. Seftel, H. Seftel Departments of Medicine and Chemical Pathology, University of Witwatersrand Medical School, and Baragwanath Hospital, JohannesburgSearch for more papers by this authorS. Zail, S. Zail Departments of Medicine and Chemical Pathology, University of Witwatersrand Medical School, and Baragwanath Hospital, JohannesburgSearch for more papers by this author T. H. Bothwell, Corresponding Author T. H. Bothwell Departments of Medicine and Chemical Pathology, University of Witwatersrand Medical School, and Baragwanath Hospital, Johannesburg†Hospital Street, Johannesburg, S. Africa.Search for more papers by this authorB. A. Bradlow, B. A. Bradlow Departments of Medicine and Chemical Pathology, University of Witwatersrand Medical School, and Baragwanath Hospital, JohannesburgSearch for more papers by this authorP. Jacobs, P. Jacobs Departments of Medicine and Chemical Pathology, University of Witwatersrand Medical School, and Baragwanath Hospital, JohannesburgSearch for more papers by this authorK. Keeley, K. Keeley Departments of Medicine and Chemical Pathology, University of Witwatersrand Medical School, and Baragwanath Hospital, JohannesburgSearch for more papers by this authorS. Kramer, S. Kramer Departments of Medicine and Chemical Pathology, University of Witwatersrand Medical School, and Baragwanath Hospital, JohannesburgSearch for more papers by this authorH. Seftel, H. Seftel Departments of Medicine and Chemical Pathology, University of Witwatersrand Medical School, and Baragwanath Hospital, JohannesburgSearch for more papers by this authorS. Zail, S. Zail Departments of Medicine and Chemical Pathology, University of Witwatersrand Medical School, and Baragwanath Hospital, JohannesburgSearch for more papers by this author First published: January 1964 https://doi.org/10.1111/j.1365-2141.1964.tb00677.xCitations: 35 * This work was supported in part by a grant (AM–04912–02) from the National Institutes of Health, U.S.A., and in part by a grant from the Council for Scientific and Industrial Research, South Africa. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume10, Issue1January 1964Pages 50-58 RelatedInformation

Bundle-branch block dependent upon critical rate is a form of phasic aberrant ventricular conduction (Schamroth and Chesler, 1963). In this arrhythmia, bundle-branch block appears when the rate increases and disappears when it slows. The basis of this arrhythmia, as with all other forms of phasic aberrant ventricular conduction, is the presence of unequal refractory periods of the bundle branches. With relatively slow heart rates (illustrated as RI to R2 in Fig. 1), consecutive impulses find both bundle branches fully recovered and normal intraventricular conduction ensues. With an increase in heart rate (illustrated as RI to R3 in Fig. 1), consecutive impulses find one bundle branch-usually the, right-refractory and the other fully recovered; conduction to the ventricles thus proceeds through one bundle branch only, resulting in an aberrant or bundlebranch block pattern. Examples of this arrhythmia have been reported by Vesell (1941), Shearn and Rytand (1953), and Gardberg and Rosen (1958): in all these cases the transition from the bundle-branch block pattern to normal intraventricular conduction and vice-versa was sudden. We report another example of this arrhythmia where the aberrant pattern was in the form of left bundle-branch block and the transition from normal to aberrant conduction was gradual; this presented a unique opportunity to prove the clinical existence of incomplete left bundle-branch block and to study the various grades of incomplete left bundle-branch block clinically-a procedure that has hitherto been possible only in the experimental animal.

The multiracial population of the African continent provides a unique source of study in regard to environmental, genetic and epidemiological factors in the aetiology of disease in general, and is of particular interest to the cardiologist. The study of geographical pathology in the natural laboratory provided by this vast continent is of particular importance at the present time, because of the rapid development and emergence from the primitive state of the African populace. Nationalism and industrialism have, since the end of the Second World War, created a number of new states, the people of which show an increasing interest in the way of living common to the Western world.

1.1. Racial differences of heart disease in Africa are discussed together with apparent differences in standards of normality of electrocardiograms and serum lipid patterns. 2.2. The high incidence of ischemic heart disease in white South Africans and its virtual absence in the Bantu has been stressed. 3.3. Heart diseases peculiar to Africa, such as idiopathic cardiac hypertrophy and endomyocardial fibrosis, are described. 4.4. The difference in altitude found in two South African cities is shown to result in a different incidence of patent ductus arteriosus and in various differences in blood findings. The possibility of these blood differences causing different incidences of myocardial infarction is discussed. 5.5. The general pattern of heart disease and its relationship to the pattern of other diseases in South Africa receives brief mention.