1070
Editorial correspondence
with white infants of similar birth weight and socioeconomic status. During a recent study,' we found that specific airway conductance during nose breathing (Sgaw = conductance/thoracic gas volume) was significantly higher in black infants than in their white counterparts, and postulated that this might reflect anatomic differences in nasal structure, resulting in a lower nasal resistance in black infants. A further study of 43 different infants, in whom nasal resistance (Rn) was measured, confirmed this hypothesis.' In this latter study, the percentage contribution of Rn to total airways resistance during nose breathing (Raw [nJ) was significantly higher in white infants (49.2% ± 7.5 SD) than in black infants (31.1% ± 6.8 SD). In absolute terms, the Rn of a typical white preterm infant of 1.5 kg was 22.4 em H,OII/sec, whereas that of a black infant of the same weight was only 10.5 em H,O/llsec. Furthermore, the presence of any upper respiratory tract infection or nasogastric tube caused a far greater increase in Rn in white preterm infants than in their black counterparts. Neonates are obligate nose breathers and cannot therefore bypass any nasal obstruction by switching to mouth breathing. It seems possible that one of the reasons for the higher mortality rates among low-birth-weight white infants may be related to the fact that they are more likely to be severely compromised by any form of nasal obstruction which will increase the work of breathing and may lead to 'fatal apneic attacks. Janet Stocks Simon Godfrey Departments of Pediatrics and Neonatal Medicine Hammersmith Hospital Du Cane Road London WI20H8 England
REFERENCES
The Journal of Pediatrics December 1978
Our data also confirm that ferritin values and transferrin saturations correlate with the amount of transfused blood, as reported by Cohen and Schwartz.' In addition, our data on patients having a wide range of values for transferrin saturation, total iron-binding capacity (TIBC), serum iron, and serum ferritin demonstrate the following correlations: (1) Serum ferritin correlates with transferrin saturation (P < 0.0001). (2) Serum ferritin correlates inversely with the TIBC (P < 0.0001). (3) Serum ferritin correlates with the serum iron (P < 0.0 1). Although these three correlations were not reported by O'Brien' or by Cohen and Schwartz,' we have performed the calculations on their data. The values presen~ed separately in both studies for transferrin saturation, TIBC, and seru m iron cover narrow and different ranges. When the data for each report are evaluated separately. some but not all of the correlations are significant. If we combine the data presented in both papers, they show similar correlations to those presented above. In 1972Jacobs et al" demonstrated a correlation among normal females between the transferrin saturation and serum ferritin concentration. Our data confirm a similar correlation among patients with sickle cell anemia. Among our 20 patients, the correlation is more significant among females (P < 0.00 I) than among males (P < 0.05). Lipschitz et aI' reported an inverse correlation between the mean values for TIRC and serum ferritin in normal subjects and in patients with iron deficiency. renal disease, inflammation. liver disease. and iron overload. This is similar to our findings in patients with sickle cell anemia. These data suggest that the relationship between values of serum ferritin and of TIBe. transferrin saturation. and serum iron demonstrates similar patterns in patients with sickle cell anemia as those described in patients with a variety of other clinical disorders which vary from iron deficiency to iron overload. Barry S. Mahony, B.A. Daniel R. Ambruso, M.D. John H. Githens, M.D. Department of Pediatrics Box C220 University of Colorado School of Medicine 4200 East Ninth Ave. Denver, CO 80262
\,
North AF Jr., MacDonald HM: Why are neonatal mortality rates lower in small black infants than in white infants in similar birth weight? J PEDIATR 90:809, 1977. 2. Stocks J, and Godfrey S: Specific airway conductance in relation to postconceptional age during infancy, J Appl Physiol 43:144, 1977. 3. Stocks J, and Godfrey S: Nasal resistance during infancy, Respir Physiol (in press.) REFERENCES
Iron studies in sickle cell anemia To the Editor:
Much data of interest were presented recently by O'Brien i and by Cohen and Schwartz' regarding iron studies of patients with sickle cell anemia. We have collected similar data on 20 patients with sickle cell anemia followed by the Colorado Sickle Cell Treatment and Research Center at the University of Colorado. Our data agree with and confirm the correlation, as reported by O'Brien,' between serum ferritin values and the patient's age.
1. O'Brien RT: Iron burden in sickle cell anemia, J PEDIATR 92:579, 1978. 2. Cohen A, and Schwartz E: Excretion of iron in response to deferoxamine in sickle cell anemia, J PWIATR 92:659, 1978. 3. Jacobs A, Miller F, WOTWood M. Beamish MR. and Wardrop CA: Ferritin in the serum of normal subjects and patients with iron deficiency and iron overload. Br Med J 4:206. 1972. 4. Lipschitz DA. Cook JD, and Finch CA: A clinical evaluation of serum ferritin as an index of iron stores, N Engl J Med 290:1213.1974.
Editorial correspondence
with white infants of similar birth weight and socioeconomic status. During a recent study,' we found that specific airway conductance during nose breathing (Sgaw = conductance/thoracic gas volume) was significantly higher in black infants than in their white counterparts, and postulated that this might reflect anatomic differences in nasal structure, resulting in a lower nasal resistance in black infants. A further study of 43 different infants, in whom nasal resistance (Rn) was measured, confirmed this hypothesis.' In this latter study, the percentage contribution of Rn to total airways resistance during nose breathing (Raw [nJ) was significantly higher in white infants (49.2% ± 7.5 SD) than in black infants (31.1% ± 6.8 SD). In absolute terms, the Rn of a typical white preterm infant of 1.5 kg was 22.4 em H,OII/sec, whereas that of a black infant of the same weight was only 10.5 em H,O/llsec. Furthermore, the presence of any upper respiratory tract infection or nasogastric tube caused a far greater increase in Rn in white preterm infants than in their black counterparts. Neonates are obligate nose breathers and cannot therefore bypass any nasal obstruction by switching to mouth breathing. It seems possible that one of the reasons for the higher mortality rates among low-birth-weight white infants may be related to the fact that they are more likely to be severely compromised by any form of nasal obstruction which will increase the work of breathing and may lead to 'fatal apneic attacks. Janet Stocks Simon Godfrey Departments of Pediatrics and Neonatal Medicine Hammersmith Hospital Du Cane Road London WI20H8 England
REFERENCES
The Journal of Pediatrics December 1978
Our data also confirm that ferritin values and transferrin saturations correlate with the amount of transfused blood, as reported by Cohen and Schwartz.' In addition, our data on patients having a wide range of values for transferrin saturation, total iron-binding capacity (TIBC), serum iron, and serum ferritin demonstrate the following correlations: (1) Serum ferritin correlates with transferrin saturation (P < 0.0001). (2) Serum ferritin correlates inversely with the TIBC (P < 0.0001). (3) Serum ferritin correlates with the serum iron (P < 0.0 1). Although these three correlations were not reported by O'Brien' or by Cohen and Schwartz,' we have performed the calculations on their data. The values presen~ed separately in both studies for transferrin saturation, TIBC, and seru m iron cover narrow and different ranges. When the data for each report are evaluated separately. some but not all of the correlations are significant. If we combine the data presented in both papers, they show similar correlations to those presented above. In 1972Jacobs et al" demonstrated a correlation among normal females between the transferrin saturation and serum ferritin concentration. Our data confirm a similar correlation among patients with sickle cell anemia. Among our 20 patients, the correlation is more significant among females (P < 0.00 I) than among males (P < 0.05). Lipschitz et aI' reported an inverse correlation between the mean values for TIRC and serum ferritin in normal subjects and in patients with iron deficiency. renal disease, inflammation. liver disease. and iron overload. This is similar to our findings in patients with sickle cell anemia. These data suggest that the relationship between values of serum ferritin and of TIBe. transferrin saturation. and serum iron demonstrates similar patterns in patients with sickle cell anemia as those described in patients with a variety of other clinical disorders which vary from iron deficiency to iron overload. Barry S. Mahony, B.A. Daniel R. Ambruso, M.D. John H. Githens, M.D. Department of Pediatrics Box C220 University of Colorado School of Medicine 4200 East Ninth Ave. Denver, CO 80262
\,
North AF Jr., MacDonald HM: Why are neonatal mortality rates lower in small black infants than in white infants in similar birth weight? J PEDIATR 90:809, 1977. 2. Stocks J, and Godfrey S: Specific airway conductance in relation to postconceptional age during infancy, J Appl Physiol 43:144, 1977. 3. Stocks J, and Godfrey S: Nasal resistance during infancy, Respir Physiol (in press.) REFERENCES
Iron studies in sickle cell anemia To the Editor:
Much data of interest were presented recently by O'Brien i and by Cohen and Schwartz' regarding iron studies of patients with sickle cell anemia. We have collected similar data on 20 patients with sickle cell anemia followed by the Colorado Sickle Cell Treatment and Research Center at the University of Colorado. Our data agree with and confirm the correlation, as reported by O'Brien,' between serum ferritin values and the patient's age.
1. O'Brien RT: Iron burden in sickle cell anemia, J PEDIATR 92:579, 1978. 2. Cohen A, and Schwartz E: Excretion of iron in response to deferoxamine in sickle cell anemia, J PWIATR 92:659, 1978. 3. Jacobs A, Miller F, WOTWood M. Beamish MR. and Wardrop CA: Ferritin in the serum of normal subjects and patients with iron deficiency and iron overload. Br Med J 4:206. 1972. 4. Lipschitz DA. Cook JD, and Finch CA: A clinical evaluation of serum ferritin as an index of iron stores, N Engl J Med 290:1213.1974.
