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Acute Exacerbation of IPF Is Not Associated with Shorter Telomeres in Patients with IPF
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A7685 - Acute Exacerbation of IPF Is Not Associated with Shorter Telomeres in Patients with IPF
Author Block: W. Shapiro1, G. J. Criner1, N. Marchetti1, A. J. Mamary2, Y. Dotan1, E. Male1, W. Cornwell3, T. J. Rogers4; 1Department of Thoracic Medicine and Surgery, Temple Univ Hosp, Philadelphia, PA, United States, 2Department of Thoracic Medicine and Surgery, Temple University School of Medicine, Philadelphia, PA, United States, 3CILR, Temple University School of Medicine, Philadelphia, PA, United States, 4CILR, Temple University Sch of Med, Philadelphia, PA, United States.
RATIONALE: Patients with idiopathic pulmonary fibrosis (IPF) and shorter telomeres have been shown to have higher mortality than those with longer telomeres. The mechanism of this increased mortality is unknown. IPF has a variable course with up to 30% of the mortality attributable to acute exacerbation of IPF (AEIPF). If acute exacerbation of IPF represents the accelerated phase of a progressive disease then a possible hypothesis is that patients with AEIPF may have shorter telomeres than those with stable disease.
METHODS:68 consecutive patients with IPF (diagnosed by explant histopathology or HRCT) who underwent lung transplantation at our institution who had blood samples available were identified. Genomic DNA was purified from blood samples taken at the time of lung transplantation. Telomere length was measured by quantitative polymerase chain reaction. Telomere length was also measured from seven normal control subjects.
RESULTS:24 patients underwent lung transplantation during an episode of AEIPF. 44 patients underwent lung transplantation during stable disease. Median telomere lengths were similar in the groups with and without AEIPF; relative fold change of 0.668±0.354 in the AEIPF group and 0.76±0.341 in the stable disease group (each compared to healthy controls). 29% of the subjects in the AEIPF group and 20% of the stable IPF group had telomere lengths in shortest quartile of telomere length of our cohort.
CONCLUSIONS:There were no significant differences in telomere lengths of subjects with and without acute exacerbation of IPF. Acute exacerbation of IPF is not significantly associated with shorter telomeres. Limitations include the retrospective nature of this single center study and that the study may be under powered to detect a small difference.
Author Block: W. Shapiro1, G. J. Criner1, N. Marchetti1, A. J. Mamary2, Y. Dotan1, E. Male1, W. Cornwell3, T. J. Rogers4; 1Department of Thoracic Medicine and Surgery, Temple Univ Hosp, Philadelphia, PA, United States, 2Department of Thoracic Medicine and Surgery, Temple University School of Medicine, Philadelphia, PA, United States, 3CILR, Temple University School of Medicine, Philadelphia, PA, United States, 4CILR, Temple University Sch of Med, Philadelphia, PA, United States.
RATIONALE: Patients with idiopathic pulmonary fibrosis (IPF) and shorter telomeres have been shown to have higher mortality than those with longer telomeres. The mechanism of this increased mortality is unknown. IPF has a variable course with up to 30% of the mortality attributable to acute exacerbation of IPF (AEIPF). If acute exacerbation of IPF represents the accelerated phase of a progressive disease then a possible hypothesis is that patients with AEIPF may have shorter telomeres than those with stable disease.
METHODS:68 consecutive patients with IPF (diagnosed by explant histopathology or HRCT) who underwent lung transplantation at our institution who had blood samples available were identified. Genomic DNA was purified from blood samples taken at the time of lung transplantation. Telomere length was measured by quantitative polymerase chain reaction. Telomere length was also measured from seven normal control subjects.
RESULTS:24 patients underwent lung transplantation during an episode of AEIPF. 44 patients underwent lung transplantation during stable disease. Median telomere lengths were similar in the groups with and without AEIPF; relative fold change of 0.668±0.354 in the AEIPF group and 0.76±0.341 in the stable disease group (each compared to healthy controls). 29% of the subjects in the AEIPF group and 20% of the stable IPF group had telomere lengths in shortest quartile of telomere length of our cohort.
CONCLUSIONS:There were no significant differences in telomere lengths of subjects with and without acute exacerbation of IPF. Acute exacerbation of IPF is not significantly associated with shorter telomeres. Limitations include the retrospective nature of this single center study and that the study may be under powered to detect a small difference.
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