877 between patients in whom calcification of the aortic valve cusps produced stenosis and those patients with aortic sclerosis could be identified. Roberts12 has suggested that minor inequalities in cusp size could explain why some patients with senile AVC have stenosis in a tricuspid aortic valve. In a patient with unequally sized valve cusps, stress on the valve cusps will not be equally distributed and may lead to premature ageing changes and calcification which eventually progress to stenosis. Inequalities in aortic valve cusp size are common,24 and may explain why some dialysis patients have more severe calcification, and hence stenosis, than patients with a similar duration of uraemia and increase of C x P product. An association between MAC and AVC has been reported in patients with3 and without end-stage renal disease.14,25 Pathologically AVC and MAC are similar, suggesting that there may be a common pathogenesis. We have confirmed that there is an increased incidence of MAC in dialysis patients,1,4 and that premature MAC is related to abnormal calcium and phosphate metabolism.3,7 Both AVC and MAC may produce significant valve stenosis, although this appears to be more frequent with AVC. We and others15 have found that the clinical diagnosis of aortic stenosis can be difficult in dialysis patients. Systolic murmurs are commonly attributed to "flow murmurs" and the other signs of aortic stenosis may be masked by hypertension and increased cardiac output. For this reason, 2D- echocardiography and doppler ultrasound is indicated in patients on long-term haemodialysis, particularly if cardiovascular symptoms develop, and may be especially helpful in distinguishing haemodynamically significant valve lesions. We thank Dr K. MacRae and Dr R. Bond for statistical advice. E. R. M. was supported by the North West Thames Regional Health Authority. Correspondence should be addressed to E. R. M., Department of Nephrology, Royal Free Hospital, Pond Street, Hampstead, London NW3 2QG. REFERENCES 1. Schott CR, Kotler MN, Parry WR, Segal BL Mitral anular calcification: Clinical and echocardiographic correlations. Arch Intern Med 1977; 137: 1143-50. 2 Fulkerson PK, Beaver BM, Auseon JC, Graber HL. Calcification of the mitral annulus. Am J Med 1979; 66: 967-77. 3. Forman MB, Virmani R, Robertson RM, Stone WJ. Mitral annular calcification in chronic renal failure. Chest 1984; 85: 367-71. 4. Nesser HJ, Baumgaertner G, Danzer E, Davogg E, Watschinger B. Mitralring- verkalkung bei dialysepatienten. Dtsch Med Wochenschr 1984; 109: 170-74. 5. Hammer WJ, Roberts WC, deLeon AC. "Mitral stenosis" secondary to combined "massive" mitral anular calcific deposits and small, hypertrophied left ventricles. Am J Med 1978; 64: 371-76. 6 Depace NL, Rohrer AH, Kotler MN, Brezin JH, Parry WR. Rapidly progressing, massive mitral annular calcification. Arch Intern Med 1981; 141: 1663-65. 7. Nestico PF, Depace NL, Kotler MN, et al. Calcium phosphorus metabolism in patients with and without mitral anular calcium. Am J Cardiol 1983; 51: 497-500. 8 Davidson RC, Pendras JP. Calcium-related cardiorespiratory death in chronic hemodialysis. Trans Am Soc Artif Intern Organs 1967; 13: 36-40 9 Maher ER, Curtis JR. Calcific aortic stenosis in chronic renal failure. Lancet 1985; ii 1007 10 Maher ER, Pazianas M, Curtis JR. Calcific aortic stenosis: a complication of chronic uraemia. Nephron 1987; 47: 119-22. 11. Memmos DE, Williams GB, Eastwood JB, et al. The role of parathyroidectomy in the management of hyperparathyroidism in patients on maintenance haemodialysis and after renal transplantation Nephron 1981; 30: 143-48. 12. Roberts WC. The structure of the aortic valve in clinically isolated aortic stenosis: an autopsy study of 162 patients over 15 years of age. Circulation 1970; 42: 91-97. 13 Pomerance A. Pathogenesis of aortic stenosis and relation to age. Br Heart J 1972; 34: 569-74. 14 Lewandowski BJ, Winsberg F. Incidence of aortic cusp and mitral annulus calcification as determined by echocardiography: Significance and interrelationship. Am J Radiol 1982; 138: 829-32 15 Castro L, Hofling B, Hassler R, et al. Progression of coronary and valvular heart disease in patients on dialysis. Trans Am Soc Artif Intern Organs 1985; 31: 647-50. 16 Von Grobmann R, Albert FW. Echokardiographische befunde bei terminal niereninsuffizienten patienten unter chromsch intermittierender dialyse- behandlung. Nieren-und Hochruckkrankheiten 1984; 13: 401-04. 17. Terman DS, Alfrey AC, Hammond WS, Donndelinger T, Ogden DA, Holmes JH. Cardiac calcification in uremia. a clinical biochemical and pathological study. Am J Med 1971; 50: 744-55. 18. Kuzela DC, Huffer WE, Conger JD, Winter SD, Hammond WS Soft tissue calcification in chronic dialysis patients. Am J Pathol 1977; 86: 403-17 19. Roberts WC, Waller BF. Effect of chronic hypercalcemia on the heart: an analysis of 18 necropsy patients. Am J Med 1981; 71: 371-84. 20. Bradley JR, Williams PF, Evans DB. Aortic valve replacement in chronic renal failure. Lancet 1985; ii: 1370 21. Roberts WC. The congenitally bicuspid aortic valve: a study of 85 autopsy cases. Am J Cardiol 1970; 26: 72-83. 22. Sprecher DL, Schaefer EJ, Kent KM, et al. Cardiovascular features of homozygous familial hypercholesterolemia: Analysis of 16 patients. Am J Cardiol 1984; 54: 20-30. 23. Roberts WC. The senile cardiac calcification syndrome. Am J Cardiol 1986; 88: 572-74. 24. Vollebergh EMG, Becker AE. Minor congenital variations in cusp size in tricuspid aortic valves. Br Heart J 1977; 39: 1006-11. 25. Roberts WC. Morphological features of the normal and abnormal mitral valve. Am J Cardiol 1983; 51: 1005-28. PLACEBO-CONTROLLED TRIAL OF RECOMBINANT &agr;2-INTERFERON IN CHINESE HBsAg-CARRIER CHILDREN CHING-LUNG LAI HSIANG-JU LIN ENG-KIONG YEOH ANNA SUK-FONG LOK PUI-CHEE WU CHAP-YUNG YEUNG Departments of Medicine and Paediatrics, University of Hong Kong, Queen Mary Hospital, Hong Kong Summary 24 Chinese children aged 1·5-5 years and positive for hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), hepatitis B virus DNA polymerase (HBV DNAp), and HBV DNA on at least three occasions in the 6 months before the trial were randomised to receive either vitamin B complex or intra- muscular recombinant &agr;2-interferon (r-IFN) (’Roferon’) 10 x 106 IU/m2 thrice weekly for 12 weeks. In all 12 subjects receiving r-IFN, HBV DNAp and HBV DNA levels fell during the course of r-IFN injections. Within 4 weeks of cessation of r-IFN injection, the HBV DNAp and HBV DNA returned to pre-trial levels except in 2 subjects, in whom loss of HBV DNAp and HBV DNA was sustained for up to 18 months from onset of the trial. 1 child lost HBeAg at 18 months. 2 of the 12 children in the placebo group also had a sustained loss of HBV DNAp and HBV DNA during the 18 months, with 1 child losing HBeAg at 18 months. All 24 subjects remained positive for HBsAg. r-IFN produced very slight side-effects except for pyrexia and the "flu" syndrome, both of which showed rapid tachyphylaxis. In the dose given r-IFN was safe but had no long-term beneficial effects on HBsAg carriage in Chinese children. Introduction Asou’r 75 % of the world’s 200 million hepatitis B surface antigen (HBsAg) carriers are Chinese. Most Chinese HBsAg carriers acquire their hepatitis B virus (HBV) infection either perinatally or during early childhood2-5 from the family, especially from HBsAg carrier mothers.6 Of the various antiviral agents prescribed in the hope of decreasing mortality due to liver disease resulting from HBV carriage,’ the most promising agent seems to be interferon?-10 Most of these studies were done in Caucasian adults. In adult Chinese HBsAg-carriers, the results seem to be less promising.’’ Few trials of the effect of interferon on HBsAg carriage in childhood have been published. The first three studies were