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YY SYNDROME IN AN AMERICAN NEGRO
281 release of A.D.P. from platelets are not affected " (see figure, site B). Dr. O’Brien’s suggestion, based on site A, that thrombin clumping is not due to free A.D.P. is contrary to the demonstration (on platelets not exposed to aspirin) that free A.D.P. is essential for such clumping.6 I have therefore looked to see whether A.D.P.-like activity is released by thrombin from platelets which have been exposed to aspirin and have found that it is. Slade Hospital, Headington, Oxford.
D. C. MACMILLAN.
YY SYNDROME IN AN AMERICAN NEGRO
SIR,-The possibility of a racial difference in the incidence of the YY syndrome was raised by Dr. Telfer and her colleagues1 in describing what they believed to be the first such case in a Negro. We reported on a 7-year-old 47, XYY Negro male at the Midwest Society for Pediatric Research (Oct. 26, 1967).2 The first case was apparently described by Migeon in a 12-month-old Negro male who also had G1 trisomy.3 We believe it is too early to assess any racial difference in the incidence of this sex-chromosome aberration; the apparent low incidence of XYY in the American Negro may be a reflection of the availability and high cost of karyotypic analysis. Further details of this
SUSPECTED INTERACTION BETWEEN PHENINDIONE AND ETHYLŒSTRENOL SIR,-It has recently been shown that phenformin and ethylaestrenol provide an effective means to increase the in-vitro fibrinolytic activity of human blood.Naturally, many patients for whom such treatment is considered will have received oral anticoagulant drugs. One of us (D. W. V.) recently decided to convert such a patient from oral anticoagulant treatment to fibrinolytic therapy. Because the patient, a 59-year-old man, had had three major vascular occlusions in his legs it was thought dangerous to leave him without treatment of some kind even for a short interval. The fibrinolytic treatment was therefore started while phenindione was being gradually discontinued. The later events, which included heavy subcutane-
haemorrhage and a succeeding superficial venous thrombosis, as shown in the accompanying figure, seem to us to show
ous
clear interaction between the two treatments. Though it is be certain about the mechanism it seems reasonable to suspect an interaction between the 17-alkyl-substituted androgen and phenindione analogous to that described for warfarin.Fibrinolytic drugs alone do not seem to cause bleeding, since one of us (G. R. F.) has given phenformin plus ethyloestrenol to over 300 patients without mishap in this respect. It has been suggested that fibrinolytic therapy should be submitted to controlled trial.9Clearly interactions of the kind which we describe must be fully considered in the design. Department of Pharmacology and Therapeutics, The London Hospital Medical College, D. W. VERE. London E.1. a
impossible to
Gloucestershire Royal Hospital. 6. 7.
8. 9.
G. R. FEARNLEY.
Haslam, R. J. Nature, Lond. 1964, 202, 765. Fearnley, G. R., Chakrabarti, R., Hocking, E. D., Evans, J. Lancet, 1967, ii, 1008. Pyorālā, K., Kekki, M. Scand. J. clin. Lab. Invest. 1963, 15, 367. Lancet, 1968, i, 1017.
case are
in
preparation.
Section on Medical Genetics and Evaluation Center, Department of Pediatrics, Michael Reese Hospital and Medical Center, Chicago, Illinois 60616.
EUGENE PERGAMENT HIDEO SATO STANLEY BERLOW RICHARD MINTZER.
VESICO-URETERIC REFLUX
SIR,-Like Dr. Edwards and his colleagues,4 vesico-ureteric reflux in about
a
we have found third of children with urinary
infection. In the last 10,000 children admitted to this hospital (which has 350 beds and admits children up to seven years of age) we have found 98 cases of reflux, or about 1 % of all the children admitted. In statistical check-ups, made every six months for the past two years, this percentage has remained very constant. Of all the children with vesico-ureteric reflux about a third have congenital obstructive abnormalities of the lower urinary tract, a third have neurogenic bladders, and a third have the congenital variety of reflux with no obstructive or neurogenic lesions to account for it. The obstructive type of reflux was found almost exclusively in boys, and it was diagnosed within the first year of life in 85% of our cases. The incidence of neurogenic type of reflux was roughly equal in boys and girls, and was found very early in life in this group. The congenital, essential type of reflux occurred most often in girls (72% of our cases), and was diagnosed after the second year of life in most of our cases. Whether to operate upon these children or to manage them conservatively is the major question that arises. We feel that it is essential to establish the cause of the reflux and our decision is based on this. We always operate on children with the obstructive type of reflux. The results have been good in 91-9% of cases. By good results we mean disappearance of the reflux and X-ray improvement of the upper urinary tract. Recurrent urinary infection has been prevented in 68% of these children. Surgical methods of treating reflux in children with the neurogenic type have had poor results. They have corrected the reflux, but in the long-term recurrence of urinary infection and progressive impairment of renal function have been disappointing. In several cases we have had to resort to urinary diversion, and we feel that this may be inevitable. In children with congenital reflux we treated conservatively those in whom the reflux appeared at high intravesical pressure; we have had 80% of good results, with control of urinary infection, in our 5 patients treated by long-term antibacterial drugs and periodic voidings. On the contrary, we recommended operation for those in whom the reflux appears at low intravesical pressure, because it is indicative of irreversible anatomical changes. In these children, even if conservative management, which is hardly possible permanently, could prevent recurrence of infection, the mechanical effect of the reflux has to be considered as slowly endangering renal function in the long term (i.e., beyond the four-year period of follow-up). Thus xtiological classification of reflux, plus determination of the intravesical pressure at which it occurs, should be the Telfer, M. A., Baker, D., Longlin, L. Lancet, 1968, i, 95. Mintzer, R., Pergament, E., Berlow, S., Sato, H. J. Pediat. 1968, 72, 572. 3. Migeon, B. R., Hum. Chromos. Newsl. 1965, no. 17, p. 18. 4. Edwards, D., Normand, I. C. S., Smellie, J. M. Lancet, 1968, i, 1376. 1. 2.
D. C. MACMILLAN.
YY SYNDROME IN AN AMERICAN NEGRO
SIR,-The possibility of a racial difference in the incidence of the YY syndrome was raised by Dr. Telfer and her colleagues1 in describing what they believed to be the first such case in a Negro. We reported on a 7-year-old 47, XYY Negro male at the Midwest Society for Pediatric Research (Oct. 26, 1967).2 The first case was apparently described by Migeon in a 12-month-old Negro male who also had G1 trisomy.3 We believe it is too early to assess any racial difference in the incidence of this sex-chromosome aberration; the apparent low incidence of XYY in the American Negro may be a reflection of the availability and high cost of karyotypic analysis. Further details of this
SUSPECTED INTERACTION BETWEEN PHENINDIONE AND ETHYLŒSTRENOL SIR,-It has recently been shown that phenformin and ethylaestrenol provide an effective means to increase the in-vitro fibrinolytic activity of human blood.Naturally, many patients for whom such treatment is considered will have received oral anticoagulant drugs. One of us (D. W. V.) recently decided to convert such a patient from oral anticoagulant treatment to fibrinolytic therapy. Because the patient, a 59-year-old man, had had three major vascular occlusions in his legs it was thought dangerous to leave him without treatment of some kind even for a short interval. The fibrinolytic treatment was therefore started while phenindione was being gradually discontinued. The later events, which included heavy subcutane-
haemorrhage and a succeeding superficial venous thrombosis, as shown in the accompanying figure, seem to us to show
ous
clear interaction between the two treatments. Though it is be certain about the mechanism it seems reasonable to suspect an interaction between the 17-alkyl-substituted androgen and phenindione analogous to that described for warfarin.Fibrinolytic drugs alone do not seem to cause bleeding, since one of us (G. R. F.) has given phenformin plus ethyloestrenol to over 300 patients without mishap in this respect. It has been suggested that fibrinolytic therapy should be submitted to controlled trial.9Clearly interactions of the kind which we describe must be fully considered in the design. Department of Pharmacology and Therapeutics, The London Hospital Medical College, D. W. VERE. London E.1. a
impossible to
Gloucestershire Royal Hospital. 6. 7.
8. 9.
G. R. FEARNLEY.
Haslam, R. J. Nature, Lond. 1964, 202, 765. Fearnley, G. R., Chakrabarti, R., Hocking, E. D., Evans, J. Lancet, 1967, ii, 1008. Pyorālā, K., Kekki, M. Scand. J. clin. Lab. Invest. 1963, 15, 367. Lancet, 1968, i, 1017.
case are
in
preparation.
Section on Medical Genetics and Evaluation Center, Department of Pediatrics, Michael Reese Hospital and Medical Center, Chicago, Illinois 60616.
EUGENE PERGAMENT HIDEO SATO STANLEY BERLOW RICHARD MINTZER.
VESICO-URETERIC REFLUX
SIR,-Like Dr. Edwards and his colleagues,4 vesico-ureteric reflux in about
a
we have found third of children with urinary
infection. In the last 10,000 children admitted to this hospital (which has 350 beds and admits children up to seven years of age) we have found 98 cases of reflux, or about 1 % of all the children admitted. In statistical check-ups, made every six months for the past two years, this percentage has remained very constant. Of all the children with vesico-ureteric reflux about a third have congenital obstructive abnormalities of the lower urinary tract, a third have neurogenic bladders, and a third have the congenital variety of reflux with no obstructive or neurogenic lesions to account for it. The obstructive type of reflux was found almost exclusively in boys, and it was diagnosed within the first year of life in 85% of our cases. The incidence of neurogenic type of reflux was roughly equal in boys and girls, and was found very early in life in this group. The congenital, essential type of reflux occurred most often in girls (72% of our cases), and was diagnosed after the second year of life in most of our cases. Whether to operate upon these children or to manage them conservatively is the major question that arises. We feel that it is essential to establish the cause of the reflux and our decision is based on this. We always operate on children with the obstructive type of reflux. The results have been good in 91-9% of cases. By good results we mean disappearance of the reflux and X-ray improvement of the upper urinary tract. Recurrent urinary infection has been prevented in 68% of these children. Surgical methods of treating reflux in children with the neurogenic type have had poor results. They have corrected the reflux, but in the long-term recurrence of urinary infection and progressive impairment of renal function have been disappointing. In several cases we have had to resort to urinary diversion, and we feel that this may be inevitable. In children with congenital reflux we treated conservatively those in whom the reflux appeared at high intravesical pressure; we have had 80% of good results, with control of urinary infection, in our 5 patients treated by long-term antibacterial drugs and periodic voidings. On the contrary, we recommended operation for those in whom the reflux appears at low intravesical pressure, because it is indicative of irreversible anatomical changes. In these children, even if conservative management, which is hardly possible permanently, could prevent recurrence of infection, the mechanical effect of the reflux has to be considered as slowly endangering renal function in the long term (i.e., beyond the four-year period of follow-up). Thus xtiological classification of reflux, plus determination of the intravesical pressure at which it occurs, should be the Telfer, M. A., Baker, D., Longlin, L. Lancet, 1968, i, 95. Mintzer, R., Pergament, E., Berlow, S., Sato, H. J. Pediat. 1968, 72, 572. 3. Migeon, B. R., Hum. Chromos. Newsl. 1965, no. 17, p. 18. 4. Edwards, D., Normand, I. C. S., Smellie, J. M. Lancet, 1968, i, 1376. 1. 2.