A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Neuroendocrine cell hyperplasia of infancy: a prospective follow-up of nine children
Tekijät: Lukkarinen H, Pelkonen A, Lohi J, Malmstrom K, Malmberg LP, Kajosaari M, Lindahl H, Fohr A, Ruuskanen O, Makela MJ
Kustantaja: BMJ PUBLISHING GROUP
Kustannuspaikka: LONDON; BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
Julkaisuvuosi: 2013
Journal: Archives of Disease in Childhood
Tietokannassa oleva lehden nimi: Archives of Disease in Childhood
Lehden akronyymi: Arch.Dis.Child.
Numero sarjassa: 2
Vuosikerta: 98
Numero: 2
Aloitussivu: 141
Lopetussivu: 144
Sivujen määrä: 4
ISSN: 0003-9888
DOI: https://doi.org/10.1136/archdischild-2012-302115
Tiivistelmä
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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