Signs and Symptoms of Chest Diseases |

Differentiation of IPF From NSIP by Cytokine Profiling FREE TO VIEW

Anthony Loria*, BS; Lei Wang, MS; Mary Smith, BS; Anne Brown, MD; Oksana Shlobin, MD; Steven Nathan, MD
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Inova Advanced Lung Disease and Transplant Program, Department of Medicine, Inova Fairfax Hospital, Falls Church, VA

Chest. 2012;142(4_MeetingAbstracts):957A. doi:10.1378/chest.1390055
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SESSION TYPE: New Insights into Idiopathic Pulmonary Fibrosis

PRESENTED ON: Sunday, October 21, 2012 at 01:15 PM - 02:45 PM

PURPOSE: The differentiation of NSIP from IPF often requires a surgical lung biopsy. Cytokines, characteristic of fibrosis and inflammation, have been identified as potential markers of disease progression in both IPF and NSIP. Here we aimed to determine the viability of using cytokine profiles in differentiating the diagnosis of NSIP from IPF.

METHODS: Patients with IPF or NSIP seen and diagnosed by standard criteria within an Advanced Lung Diseases Clinic were identified. Fasting blood was collected to measure levels of 20 cytokines via Bio-Plex Suspension Array System (Bio-Rad Laboratories, Inc., Hercules, CA). Mann-Whitney U test was performed to determine statistically different levels of cytokines between disease groups. Based on this, variables were selected for logistic regression and ROC curve generation.

RESULTS: Data from 35 patients were obtained and analyzed. Of these, 20 had IPF and 15 NSIP. There were 12 females and the mean age of the group was 62 ± 9 years. Significant differences in levels between IPF and NSIP patients were noted for: TGF-b1 (Z -2.37, p=.018) and IP-10 (Z -2.33, p=.019), while TNF-a trended toward significance (Z-1.82, p=.069). Aforementioned variables were incorporated in a logistic forward conditional regression model to predict NSIP. The significant predictors of diagnosis were TGF-b1 and TNF-a [AUC=0.78 (95% CI=0.63- 0.94), p=.003].

CONCLUSIONS: Despite being preliminary, our promising results suggest that mathematical modeling exploiting different pathogenic pathways or consequences of these diseases may prove to be a viable diagnostic approach.

CLINICAL IMPLICATIONS: Recognition and determination of different cytokine patterns of expression may enable the non-invasive differentiation of NSIP from IPF.

DISCLOSURE: The following authors have nothing to disclose: Anthony Loria, Lei Wang, Mary Smith, Anne Brown, Oksana Shlobin, Steven Nathan

No Product/Research Disclosure Information

Inova Advanced Lung Disease and Transplant Program, Department of Medicine, Inova Fairfax Hospital, Falls Church, VA




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