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Iron deficiency in adolescence
THE JOURNAL OF PEDIATRICS • www.jpeds.com
Iron deficiency in adolescence — William S. Ferguson, MD
How mild is the outcome of mild neonatal encephalopathy? — Paul G. Fisher, MD
2
T
he prevalence of iron deficiency anemia is estimated at 2-5% among reproductive age women, with perhaps 3 times that number having deficient iron stores that may contribute to fatigue, cognitive deficits, and other symptoms even in the absence of overt anemia. The combination of rapid growth, menstrual blood loss, and often inadequate dietary intake of iron places adolescent females at particular risk. Although general recommendations in favor of routine screening for iron deficiency have been made by the Centers for Disease Control and Prevention, the current US Preventive Services Task Force guidelines state that there is insufficient evidence to recommend universal laboratory screening for iron deficiency in nonpregnant women. In older women, dietary iron intake and menstrual blood loss have been shown to correlate with iron deficiency, and questions targeting those areas are included in the American Academy of Pediatrics’ Bright Futures adolescent previsit questionnaire. However, these screening questions have not been validated in adolescent females, whose risk factors for iron deficiency differ from older women. In this volume of The Journal, Sekhar et al report on a cross-sectional study of 96 adolescent females in whom laboratory evaluation of iron status was compared to the results of the 4 questions from the Bright Futures questionnaire, as well as an expanded model that also incorporated body mass index along with self-reported measures of depression, attention, food insecurity, and daytime sleepiness. Disappointingly, neither model proved predictive of iron status or anemia; indeed, most cases of anemia were missed by the questionnaires, while most patients identified at risk for anemia had normal iron studies. These results lend support to the Centers for Disease Control and Prevention’s recommendation for routine laboratory evaluation of iron status in adolescent women, although the optimal methodology and frequency of testing are still to be defined. Article page 194 ▶
O
ver 4 decades ago, Sarnat defined stage I, or mild, neonatal encephalopathy following fetal distress as a postanoxic state characterized by a hyperalert level of consciousness with normal muscle tone on exam, no clinical seizures, and a normal EEG (Arch Neurol 1976;33:696-705). In that report of just 21 patients >36 weeks’ gestation with fetal distress and investigator-defined stage I mild to stage III severe encephalopathy, those neonates with <5 days in stage II moderate encephalopathy and a predominance of stage I findings were all developmentally normal subsequently at age 12 months. The derivative conclusion was that newborns with mild neonatal encephalopathy are largely developmentally normal months later. Since then, many changes in neonatal care have taken place, including technology to rescue younger and sicker term and preterm babies, use of surfactant for lung immaturity, and implementation of neonatal hypothermia for babies with neonatal encephalopathy, acidosis, and gestational age 34 to 35 weeks. But is mild neonatal encephalopathy truly associated with mildly abnormal or normal outcomes when larger samples of newborns are examined, especially after the application of therapeutic hypothermia for concerns of distress, acidosis, or seizures with decreasing gestational age? In this volume of The Journal, Walsh et al report a limited, single institution, historical cohort study of 89 neonates >34 weeks’ gestation with neonatal encephalopathy and pH <7.1, all treated with hypothermia. The investigators sought to determine whether magnetic resonance imaging detected brain abnormalities after hypothermia were any different among those with mild, moderate, or severe neonatal encephalopathy, based upon more modern grading criteria. They studied 48 infants with mild encephalopathy, with 35 moderate, yet just 6 with severe neonatal encephalopathy. (Continues on next page)
Volume 187
Iron deficiency in adolescence — William S. Ferguson, MD
How mild is the outcome of mild neonatal encephalopathy? — Paul G. Fisher, MD
2
T
he prevalence of iron deficiency anemia is estimated at 2-5% among reproductive age women, with perhaps 3 times that number having deficient iron stores that may contribute to fatigue, cognitive deficits, and other symptoms even in the absence of overt anemia. The combination of rapid growth, menstrual blood loss, and often inadequate dietary intake of iron places adolescent females at particular risk. Although general recommendations in favor of routine screening for iron deficiency have been made by the Centers for Disease Control and Prevention, the current US Preventive Services Task Force guidelines state that there is insufficient evidence to recommend universal laboratory screening for iron deficiency in nonpregnant women. In older women, dietary iron intake and menstrual blood loss have been shown to correlate with iron deficiency, and questions targeting those areas are included in the American Academy of Pediatrics’ Bright Futures adolescent previsit questionnaire. However, these screening questions have not been validated in adolescent females, whose risk factors for iron deficiency differ from older women. In this volume of The Journal, Sekhar et al report on a cross-sectional study of 96 adolescent females in whom laboratory evaluation of iron status was compared to the results of the 4 questions from the Bright Futures questionnaire, as well as an expanded model that also incorporated body mass index along with self-reported measures of depression, attention, food insecurity, and daytime sleepiness. Disappointingly, neither model proved predictive of iron status or anemia; indeed, most cases of anemia were missed by the questionnaires, while most patients identified at risk for anemia had normal iron studies. These results lend support to the Centers for Disease Control and Prevention’s recommendation for routine laboratory evaluation of iron status in adolescent women, although the optimal methodology and frequency of testing are still to be defined. Article page 194 ▶
O
ver 4 decades ago, Sarnat defined stage I, or mild, neonatal encephalopathy following fetal distress as a postanoxic state characterized by a hyperalert level of consciousness with normal muscle tone on exam, no clinical seizures, and a normal EEG (Arch Neurol 1976;33:696-705). In that report of just 21 patients >36 weeks’ gestation with fetal distress and investigator-defined stage I mild to stage III severe encephalopathy, those neonates with <5 days in stage II moderate encephalopathy and a predominance of stage I findings were all developmentally normal subsequently at age 12 months. The derivative conclusion was that newborns with mild neonatal encephalopathy are largely developmentally normal months later. Since then, many changes in neonatal care have taken place, including technology to rescue younger and sicker term and preterm babies, use of surfactant for lung immaturity, and implementation of neonatal hypothermia for babies with neonatal encephalopathy, acidosis, and gestational age 34 to 35 weeks. But is mild neonatal encephalopathy truly associated with mildly abnormal or normal outcomes when larger samples of newborns are examined, especially after the application of therapeutic hypothermia for concerns of distress, acidosis, or seizures with decreasing gestational age? In this volume of The Journal, Walsh et al report a limited, single institution, historical cohort study of 89 neonates >34 weeks’ gestation with neonatal encephalopathy and pH <7.1, all treated with hypothermia. The investigators sought to determine whether magnetic resonance imaging detected brain abnormalities after hypothermia were any different among those with mild, moderate, or severe neonatal encephalopathy, based upon more modern grading criteria. They studied 48 infants with mild encephalopathy, with 35 moderate, yet just 6 with severe neonatal encephalopathy. (Continues on next page)
Volume 187