A1 Refereed original research article in a scientific journal
Neuroendocrine cell hyperplasia of infancy: a prospective follow-up of nine children
Authors: Lukkarinen H, Pelkonen A, Lohi J, Malmstrom K, Malmberg LP, Kajosaari M, Lindahl H, Fohr A, Ruuskanen O, Makela MJ
Publisher: BMJ PUBLISHING GROUP
Publishing place: LONDON; BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
Publication year: 2013
Journal: Archives of Disease in Childhood
Journal name in source: Archives of Disease in Childhood
Journal acronym: Arch.Dis.Child.
Number in series: 2
Volume: 98
Issue: 2
First page : 141
Last page: 144
Number of pages: 4
ISSN: 0003-9888
DOI: https://doi.org/10.1136/archdischild-2012-302115(external)
Abstract
Neuroendocrine cell hyperplasia of infancy (NEHI) has recently been described as an obstructive airway disease that affects infants aged 1-24 months, and presents typically with tachypnoea, crackles and hypoxia. The pathogenesis of the disease is unknown. We describe the clinical course of nine infants with radiologically and histologically confirmed NEHI. Host or environmental factors were not associated with the disease development. All infants with lung function tests demonstrated findings consistent with severe irreversible peripheral airway obstruction, assessed with whole body plethysmography (6/6) or the rapid thoracoabdominal compression technique (5/5). While the symptoms abated in all infants, six infants developed a non-atopic asthma during the follow-up. Systemic or inhaled corticosteroid treatment did not affect the duration of the symptoms. NEHI may mimic severe asthma and thus this entity should be taken into account when evaluating infants with chronic respiratory symptoms.
Neuroendocrine cell hyperplasia of infancy (NEHI) has recently been described as an obstructive airway disease that affects infants aged 1-24 months, and presents typically with tachypnoea, crackles and hypoxia. The pathogenesis of the disease is unknown. We describe the clinical course of nine infants with radiologically and histologically confirmed NEHI. Host or environmental factors were not associated with the disease development. All infants with lung function tests demonstrated findings consistent with severe irreversible peripheral airway obstruction, assessed with whole body plethysmography (6/6) or the rapid thoracoabdominal compression technique (5/5). While the symptoms abated in all infants, six infants developed a non-atopic asthma during the follow-up. Systemic or inhaled corticosteroid treatment did not affect the duration of the symptoms. NEHI may mimic severe asthma and thus this entity should be taken into account when evaluating infants with chronic respiratory symptoms.
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