TY - GEN
T1 - Lactate dehydrogenase predicts disease progression in patients with IPF
AU - Hoyer, Nils
AU - Andersen, Michael Brun
AU - Collatz, Lene
AU - Åttingsberg, Emilia Kassandra Achilles
AU - Shaker, Saher Burhan
PY - 2023/9/9
Y1 - 2023/9/9
N2 - Introduction: Lactate dehydrogenase (LDH), a widely available biomarker, is associated with disease severity in IPF. However, LDH is unspecific, and these associations could be caused by factors unrelated to lung fibrosis.Ojective: To assess the association between LDH and lung fibrosis on HRCT.Methods: We selected IPF patients with HRCT scans at the time of diagnosis and after two years. The scans were scored by two experienced thoracic radiologists using a standardized form and blinded to patient data, each-others scores and the time of scan. The extent of reticulation, traction bronchiectasis and honeycombing was combined into a composite quantitative fibrosis score.Results: The 66 included patients were divided into a “high LDH” and a “low LDH” group around the baseline median LDH.During the first two years after the IPF diagnosis, the mean fibrosis score increased in the “high LDH” group from 3.08 to 4.57 (p-value for change: 0.0065). No significant change in fibrosis score was observed in the “low LDH” group (2.67 to 2.93, p-value: 0.47). This association was confirmed by multiple linear regression analysis adjusted for age, sex and antifibrotic treatment received during follow-up (p=0.004).Conclusions: LDH, measured at the time of IPF diagnosis, can predict subsequent increase in fibrosis on the HRCT scan. The known association between LDH and disease severity in IPF is therefore likely to be directly related to progression of lung fibrosis.FootnotesCite this article as: European Respiratory Journal 2023; 62: Suppl. 67, PA1143.This abstract was presented at the 2023 ERS International Congress, in session “Inflammatory endotyping: the macrophage across disease areas”.This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).
AB - Introduction: Lactate dehydrogenase (LDH), a widely available biomarker, is associated with disease severity in IPF. However, LDH is unspecific, and these associations could be caused by factors unrelated to lung fibrosis.Ojective: To assess the association between LDH and lung fibrosis on HRCT.Methods: We selected IPF patients with HRCT scans at the time of diagnosis and after two years. The scans were scored by two experienced thoracic radiologists using a standardized form and blinded to patient data, each-others scores and the time of scan. The extent of reticulation, traction bronchiectasis and honeycombing was combined into a composite quantitative fibrosis score.Results: The 66 included patients were divided into a “high LDH” and a “low LDH” group around the baseline median LDH.During the first two years after the IPF diagnosis, the mean fibrosis score increased in the “high LDH” group from 3.08 to 4.57 (p-value for change: 0.0065). No significant change in fibrosis score was observed in the “low LDH” group (2.67 to 2.93, p-value: 0.47). This association was confirmed by multiple linear regression analysis adjusted for age, sex and antifibrotic treatment received during follow-up (p=0.004).Conclusions: LDH, measured at the time of IPF diagnosis, can predict subsequent increase in fibrosis on the HRCT scan. The known association between LDH and disease severity in IPF is therefore likely to be directly related to progression of lung fibrosis.FootnotesCite this article as: European Respiratory Journal 2023; 62: Suppl. 67, PA1143.This abstract was presented at the 2023 ERS International Congress, in session “Inflammatory endotyping: the macrophage across disease areas”.This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).
U2 - 10.1183/13993003.congress-2023.PA1143
DO - 10.1183/13993003.congress-2023.PA1143
M3 - Conference article
SN - 1399-3003
SN - 0904-1850
VL - 62
SP - PA1143
JO - Eur Respir J
JF - Eur Respir J
IS - suppl 67
ER -