ABSTRACT. Babies with chronic bronchopulmonary dysplasia (BPD) can sometimes develop pallor, systemic and pulmonary edema, oliguria, and hyponatremia not attributable to cardiopulmonary or renal impairment. These signs and symptoms might, however, be explained by inappropriate control of vasopressin secretion. To test this hypothesis, we measured plasma vasopressin and osmolality, serum sodium and potassium concentrations, urine output and osmolality, and free water clearance in 26 normoxic infants with BPD aged 1-4 months. All of these infants required supplemental oxygen (FiOz 0.41 2 0.03, mean -C 1 S E ) to maintain O 2 saturation of >88%, and six infants also required mechanical ventilation. As controls, 1 0 infants of similar age but without B P D were also studied. None of the infants had been discharged from the nursery and was receiving any medications, and all were clinically stable when studied. Compared to control infants, infants with BPD had significantly elevated plasma vasopressin concentrations (control 5.2 2 0.9 pg/ml; BPD 42.4 k 5.1; mean k SE, p < 0.05). Moreover, infants with B P D had hyponatremia and hypotonic plasma, and both urine output and free water clearance were significantly reduced. These data suggest that some infants with chronic BPD have elevated vasopressin levels that are functionally significant. W e speculate that excessive stimulation of vasopressin secretion may explain some of the pulmonary and nonpulmonary signs and symptoms in infants with chronic BPD. (Pediatr Res 23: 86-88,1988) Abbreviations BPD, bronchopulmonary dysplasia ADH, antidiuretic hormone CPAP, continuous positive airway pressure FiOz, inspired oxygen concentration PaC02, arterial P C 0 2 tension Babies with chronic BPD can sometimes develop systemic and pulmonary edema, oliguria, hyponatremia, and hypertension that cannot be attributed to chronic congestive heart failure or to renal disease. In some infants with BPD, treatment with diuretics has resulted in improvement in lung function and in systemic edema (1, 2). Some of these signs and symptoms are

A literature review failed to support tl1e suggestion tl1at adolescent female athletes routinely should take iron supplements. ft1ereforc, female t1igh school track athletes were compared to non-athlete controls from tl1c same scl1ools. Medical and nutrition history, anthropometrics, hemoglobin (Hgb), hematocrit (tlct), mean corpusct1lar volume, transferrin satl1ration, and serum fcrritin (Sf) level were obtained. All participants were menstruating regularly.Recent or current illness, recent transfusion, excessive menstrl1a1 or otl1er bleeding, and current medication or iron supplement use were reasons fc>r Resl1lts sl1owed that 2 of JJ subjects (6%) and l of 37 controls (3/) were anemic (Le., low llgb.). 14 of 33 subjects (40%) and 9 of 37 controls (30%J had low SF's. There was no difference bctwt;cn the two groups on any of these measures hy X2 analysis and, for SF, hy use of Wilcoxon's Rank Sums Test. An unexpected finding showed significantly more black girls (subjects and controls) had low SF's than white !;irls (p=0.005) even though there was no in the number who were anemic or in the mean llgbs. of tl1c two grot1ps. We conclude tt1at female l1igh school athletes arc in no more need of iron supplementation tl1an are non-atl1letes.Screc11ing for iron status should be done by using SF as well as Hgb. or Hct. We did not address whether low iron stores withol1t anemia adversely affect atl1letic performance. Black girls may he at greater risk for iron deficiency, tl1ough we did not rule out the importance of socioeconomic factors.