856
Letters to the Editor
of human growth hormone based on body weight, J Clin Endocrinol Metab 44:22, 1977. 2. Moore DC, Tattoni DS, Limbeck GA, Ruvalcaba RHA, Lindner DS, Gareis FJ, A1-Agba S, and Kelley VC: Studies of anabolic steroids V. Effect of prolonged oxandrolone administration on growth in children and adolescents with uncomplicated short stature, Pediatrics 58:412, 1976. 3. Rosenfield RL, and Fang VS: The effects of prolonged physiologic estradiol therapy on the maturation o f hypogonadal teen-agers, J PEDIAXR 85:830, 1974. 4. Brook CGD, M(irset G, Zachman M, and Prader A: Growth in children with 45, XO Turner's syndrome, Arch Dis Child 49:789, 1974. 5. Zangeneh F, and Steiner MM: Oxandrolone therapy in growth retardation of children, Am J Dis Child 113:234, 1967. 6. Bettmann HK, Goldman HS, Abramowicz M, and Sobel EH: Oxandrolone treatment of short stature: Effect on predicted mature height, J PEDIATR 79:1018, 1971.
Racial difference in frequency of ABO hemolytic disease To the Editor: I was very confused in reading Dr. Kirkman's article, "Further evidence for a racial difference in frequency of ABO hemolytic disease," in the May, 1977, issue of THE JOURNAL Or PEDIAXRICS. Among his conclusions is the statement that the black newborn infant with ABO incompatibility should not be discharged too early from the hospital nursery. Although this conclusion is reasonably based on the increased incidence of ABO incompatibility seen in the black population, the results of Dr. Kirkman's own study do not bear this out. In his group of ABO incompatible neonates, jaundice was noted during the first day to a much higher degree in black newborn infants than among white ABO incompatible neonates. Significant elevation o f serum bilirubin occurred in only three black ABO incompatible babies after the second day o f life, whereas five white ABO incompatible neonates had a significant rise in their bilirubin levels after the second day. Dr. Kirkman also states that the incidence of ABO hemolytic disease is several times greater in black infants than in white infants. His studies do not bear this out. He reports 76 black ABO incompatible babies versus 48 white ABO incompatible newborns--48 does not go into 76 several times. Alvin N. Eden, M.D. Director of Pediatrics Wyckoff Heights Hospital 374 Stockholm St Brooklyn, N Y 11237 REFERENCE
1.
Kirkman, HN: Further evidence for racial difference in frequency of ABO hemolytic disease, J PEDIATR 90:717, 1977.
The Journal of Pediatrics November 1977
Reply To the Editor: Our data refer to infants who were observed to develop jaundice for the first time after the second day. The onset of jaundice, after the second day in infants with a positive Coombs reaction, is statistically a very weak criterion for ABO hemolytic disease. This was true for both races, and there was no significant difference between the two groups. My concern is not so much for infants who develop jaundice for the first time after 48 hours of age as for infants (1) who are discharged during the first 48 hours (as is the trend in some centers now) and (2) whose jaundice is either disregarded or not noted. The cited figures of 76 and 48 represent the number of ABO incompatible infants with a positive Coombs reaction. If Dr. Eden wishes to regard a positive Coombs reaction, alone, as a sign o f ABO hemolytic disease, these number correspond to incidences of 6.23 and 3.84% in black and white newborn infants, respectively. These percentages appear on the bottom line of Table IV. In the calculation of these percentages in Table IV, allowance is give for the total number of neonates of each race and for the number of ABO compatible infants with the same finding (a positive Coombs reaction in this instance). The ratio 6.23/3.84 is 1.62. Admittedly, this is not severalfold, but one can consider two other signs: jaundice in the first day and an indirect serum bilirubin level over 10 mg/dl. There are seven possible combinations of these three signs, representing seven possible criteria for ABO disease (Table IV). The ratios then range from 1.62 to 8.81, with a ratio of 3.24 when all three signs were present. The average ratio is 3.91. When something is 3.24 fold or 3.91 fold, it is severalfold. Henry N. Kirkman Jr., M.D. Department of Pediatrics University o f North Carolina School of Medicine Chapel Hill, NC 27514
Management of pubertal gynecomastia To the Editor: It was with great dismay that I read the report of Stepanas and associates. 1 As they have reported, gynecomastia of puberty is a benign condition, occurring in 65% of adolescent males. In addition, as they point out, the condition is usually selflimited. The most disturbing portion o f their study is that of 19 patients, 11 eventually underwent reduction mammoplasties. Of these 11, several patients had the condition for a short period of time, and several had only 1 cm o f breast tissue. It is difficult to imagine how much improvement surgery might have offered to this group.
Letters to the Editor
of human growth hormone based on body weight, J Clin Endocrinol Metab 44:22, 1977. 2. Moore DC, Tattoni DS, Limbeck GA, Ruvalcaba RHA, Lindner DS, Gareis FJ, A1-Agba S, and Kelley VC: Studies of anabolic steroids V. Effect of prolonged oxandrolone administration on growth in children and adolescents with uncomplicated short stature, Pediatrics 58:412, 1976. 3. Rosenfield RL, and Fang VS: The effects of prolonged physiologic estradiol therapy on the maturation o f hypogonadal teen-agers, J PEDIAXR 85:830, 1974. 4. Brook CGD, M(irset G, Zachman M, and Prader A: Growth in children with 45, XO Turner's syndrome, Arch Dis Child 49:789, 1974. 5. Zangeneh F, and Steiner MM: Oxandrolone therapy in growth retardation of children, Am J Dis Child 113:234, 1967. 6. Bettmann HK, Goldman HS, Abramowicz M, and Sobel EH: Oxandrolone treatment of short stature: Effect on predicted mature height, J PEDIATR 79:1018, 1971.
Racial difference in frequency of ABO hemolytic disease To the Editor: I was very confused in reading Dr. Kirkman's article, "Further evidence for a racial difference in frequency of ABO hemolytic disease," in the May, 1977, issue of THE JOURNAL Or PEDIAXRICS. Among his conclusions is the statement that the black newborn infant with ABO incompatibility should not be discharged too early from the hospital nursery. Although this conclusion is reasonably based on the increased incidence of ABO incompatibility seen in the black population, the results of Dr. Kirkman's own study do not bear this out. In his group of ABO incompatible neonates, jaundice was noted during the first day to a much higher degree in black newborn infants than among white ABO incompatible neonates. Significant elevation o f serum bilirubin occurred in only three black ABO incompatible babies after the second day o f life, whereas five white ABO incompatible neonates had a significant rise in their bilirubin levels after the second day. Dr. Kirkman also states that the incidence of ABO hemolytic disease is several times greater in black infants than in white infants. His studies do not bear this out. He reports 76 black ABO incompatible babies versus 48 white ABO incompatible newborns--48 does not go into 76 several times. Alvin N. Eden, M.D. Director of Pediatrics Wyckoff Heights Hospital 374 Stockholm St Brooklyn, N Y 11237 REFERENCE
1.
Kirkman, HN: Further evidence for racial difference in frequency of ABO hemolytic disease, J PEDIATR 90:717, 1977.
The Journal of Pediatrics November 1977
Reply To the Editor: Our data refer to infants who were observed to develop jaundice for the first time after the second day. The onset of jaundice, after the second day in infants with a positive Coombs reaction, is statistically a very weak criterion for ABO hemolytic disease. This was true for both races, and there was no significant difference between the two groups. My concern is not so much for infants who develop jaundice for the first time after 48 hours of age as for infants (1) who are discharged during the first 48 hours (as is the trend in some centers now) and (2) whose jaundice is either disregarded or not noted. The cited figures of 76 and 48 represent the number of ABO incompatible infants with a positive Coombs reaction. If Dr. Eden wishes to regard a positive Coombs reaction, alone, as a sign o f ABO hemolytic disease, these number correspond to incidences of 6.23 and 3.84% in black and white newborn infants, respectively. These percentages appear on the bottom line of Table IV. In the calculation of these percentages in Table IV, allowance is give for the total number of neonates of each race and for the number of ABO compatible infants with the same finding (a positive Coombs reaction in this instance). The ratio 6.23/3.84 is 1.62. Admittedly, this is not severalfold, but one can consider two other signs: jaundice in the first day and an indirect serum bilirubin level over 10 mg/dl. There are seven possible combinations of these three signs, representing seven possible criteria for ABO disease (Table IV). The ratios then range from 1.62 to 8.81, with a ratio of 3.24 when all three signs were present. The average ratio is 3.91. When something is 3.24 fold or 3.91 fold, it is severalfold. Henry N. Kirkman Jr., M.D. Department of Pediatrics University o f North Carolina School of Medicine Chapel Hill, NC 27514
Management of pubertal gynecomastia To the Editor: It was with great dismay that I read the report of Stepanas and associates. 1 As they have reported, gynecomastia of puberty is a benign condition, occurring in 65% of adolescent males. In addition, as they point out, the condition is usually selflimited. The most disturbing portion o f their study is that of 19 patients, 11 eventually underwent reduction mammoplasties. Of these 11, several patients had the condition for a short period of time, and several had only 1 cm o f breast tissue. It is difficult to imagine how much improvement surgery might have offered to this group.
