Keratinocyte growth factor and hepatocyte growth factor in bronchoalveolarlavage fluid in acute respiratory distress syndrome patients

Citation
Jb. Stern et al., Keratinocyte growth factor and hepatocyte growth factor in bronchoalveolarlavage fluid in acute respiratory distress syndrome patients, CRIT CARE M, 28(7), 2000, pp. 2326-2333
Citations number
35
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
CRITICAL CARE MEDICINE
ISSN journal
00903493 → ACNP
Volume
28
Issue
7
Year of publication
2000
Pages
2326 - 2333
Database
ISI
SICI code
0090-3493(200007)28:7<2326:KGFAHG>2.0.ZU;2-3
Abstract
Objectives: To determine bronchoalveolar lavage (BAL) fluid concentrations of keratinocyte growth factor (KGF) and hepatocyte growth factor (HGF), two potent growth factors for alveolar type II epithelial cells, in patients w ith acute respiratory distress syndrome (ARDS). Design: Prospective study. Setting: An adult trauma/surgical intensive care unit in an urban teaching hospital. Patients: A total of 32 ventilated patients with pulmonary infiltrates pros pectively identified with ARDS (n = 17) or without ARDS (n = 15), including eight patients with hydrostatic edema (HE), and ten nonventilated patients serving as controls. Interventions: None. Measurements and Main Results: BAL was performed 2.88 days +/- 2.4, 3.5 day s +/- 2.4, and 2.3 days +/- 2.2 after the lung insult in ARDS, HE, and othe r non-ARDS patients respectively (p = .32). KGF was detected in BAL fluid i n 13 of the 17 ARDS patients (median, 31.6 pg/mL), in one patient with HE, and in none of other non-ARDS patients. In ARDS patients, detection of KGF in BAL was associated in BAL fluid with the detection of type III procollag en peptide (PIIIP), a biological marker of fibroproliferation. In ARDS pati ents, detection of KGF in BAL was associated with death (p = .02). HGF was detected in 15 ARDS patients (median, 855 pg/mL), in seven patients with HE (median, 294 pg/mL; p = .05 for the comparison with ARDS group), in six of other non-ARDS patients (median, 849 pg/mL; p = .32 with ARDS group). HGF concentrations were higher in nonsurvivors than in survivors (p = .01). Non e of the ten BAL of controls contained either KGF or HGF. Conclusion: KGF was detected almost exclusively in BAL fluid from ARDS pati ents and correlated with a poor prognosis in this group. In contrast, HGF w as detected in the BAL fluid from a majority of patients with or without AR DS. Elevated HGF concentrations were associated with a poor prognosis in th e overall group.