Lung DiseasesNCT00005317
Idiopathic Pulmonary Fibrosis--Pathogenesis and Staging - SCOR in Occupational and Immunological Lung Diseases
An observational study of Lung Diseases and Pulmonary Fibrosis, run by National Heart, Lung, and Blood Institute (NHLBI).
Trial summary
To conduct cross-sectional and longitudinal studies of patients with idiopathic pulmonary fibrosis (IPF) and patients with progressive systemic sclerosis (PSS), with and without associated lung disease. Read more about this study
- Who is it for?
- Ages Up to 100 years, men only
- Conditions the study is for
- Lung Diseases, Pulmonary Fibrosis, Lung Diseases, Interstitial
- How many people
- Not given
- Where
- No sites listed yet
- Study dates
- Dec 1986to Nov 1996
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages Up to 100 years
- Men only
- No healthy volunteers
- Child, Adult, Older adult
No eligibility criteria
About this study
To conduct cross-sectional and longitudinal studies of patients with idiopathic pulmonary fibrosis (IPF) and patients with progressive systemic sclerosis (PSS), with and without associated lung disease.
Read the detailed description
BACKGROUND:
Idiopathic pulmonary fibrosis (IPF) is a disease of unknown etiology characterized pathologically by a chronic inflammatory process (alveolitis) that precedes and likely controls the alterations in connective tissue matrix that eventually destroys the normal lung architecture. The mechanisms involved in this process are not known. A complex cell-cell interactive sequence, involving principally neutrophils, lymphocytes, macrophages, fibroblast, and epithelial cells is believed to be responsible.
The SCOR in Occupational and Immunological Lung Diseases was first awarded in December, 1981. The subproject on idiopathic pulmonary fibrosis was first awarded in December, 1986.
DESIGN NARRATIVE:
The cross-sectional comparison examined bronchoalveolar lavage, high resolution, thin-section computer tomography (HRCT), neutrophil or monocyte labeled scintigraphy). The serial, longitudinal evaluation monitored the progression of disease. The study of PSS patients, without disease or with subclinical disease, was particularly useful because it allowed examination of the early events in the pathogenesis of IPF. The long-term goal of the project was to determine what alterations in cellular composition, function and trafficking occurred in the lung parenchyma of patients with IPF and to relate these alterations to the disease stage, prognosis, and therapeutic responsiveness.
The major objectives of the study were: (1) to continue the prospective, longitudinal study of carefully defined cases of IPF; (2) to initiate a study of patients with PSS, a disease that provided a useful paradigm for studying the early events of the disease; (3) to determine the role of the lymphocyte in IPF, by defining the subset of T lymphocytes responsible for modulating macrophage function; (4) to establish the role of non-invasive techniques (bronchoalveolar lavage (BAL), HRCT scanning and scintigraphy -- neutrophil and monocyte labelled cells) in assessing the activity of inflammation in carefully evaluated patients; (5) to determine the relationship of these results to the -- carefully defined and serially obtained -- clinical, radiographical, and physiological findings and to the histopathologic abnormalities (in patients that underwent lung biopsy, predominantly IPF cases). (6) to perform studies utilizing blood, BAL fluid and lung tissue in an effort to understand the pathogenic mechanisms that underlied the inflammatory/immune cellular injury and fibrosis that characterize this disease.
The study completion date listed in this record was obtained from the "Completed Date" entered in the Query View Report System (QVR).
- Medical subject headings
- Lung Diseases, Pulmonary Fibrosis, Lung Diseases, Interstitial, Scleroderma, Systemic
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted26 May 2000 (estimated)
- Study startDec 1986
- Study completionNov 1996
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (34)Papers the sponsor has linked to this study.
- Other trials for Lung DiseasesStudies of the same condition, open and under way.
- More trials run by National Heart, Lung, and Blood Institute (NHLBI)The sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
Sponsor and investigators
- Sponsor type
- US National Institutes of Health
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00005317
- Sponsor's protocol ID
- 4090
- Status last verified
- May 2000
- First submitted
- 25 May 2000
- Last updated
- 12 Jul 2016
- Results posted
- No
Publications
Janson RW, Hance KR, King TE Jr. Human alveolar macrophages produce predominantly the 35-kD pro-forms of interleukin-1 alpha and interleukin-1 beta when stimulated with lipopolysaccharide. Am J Respir Crit Care Med. 1995 May;151(5):1613-20. doi: 10.1164/ajrccm.151.5.7735621.
PubMed 7735621Cherniack RM, Colby TV, Flint A, Thurlbeck WM, Waldron JA Jr, Ackerson L, Schwarz MI, King TE Jr. Correlation of structure and function in idiopathic pulmonary fibrosis. Am J Respir Crit Care Med. 1995 Apr;151(4):1180-8. doi: 10.1164/ajrccm/151.4.1180.
PubMed 7697250Willcox M, Kervitsky A, Watters LC, King TE Jr. Quantification of cells recovered by bronchoalveolar lavage. Comparison of cytocentrifuge preparations with the filter method. Am Rev Respir Dis. 1988 Jul;138(1):74-80. doi: 10.1164/ajrccm/138.1.74.
PubMed 3059868Salvatore M, Seeber AC, Nacmias B, Petraroli R, Sorbi S, Pocchiari M. Alpha1 antichymotrypsin signal peptide polymorphism in sporadic Creutzfeldt-Jakob disease. Neurosci Lett. 1997 May 16;227(2):140-2. doi: 10.1016/s0304-3940(97)00308-x.
PubMed 9180223Savici D, Campbell PA, King TE Jr. Bronchoalveolar macrophages from patients with idiopathic pulmonary fibrosis are unable to kill facultative intracellular bacteria. Am Rev Respir Dis. 1989 Jan;139(1):22-7. doi: 10.1164/ajrccm/139.1.22.
PubMed 2492173Kuhn C 3rd, Boldt J, King TE Jr, Crouch E, Vartio T, McDonald JA. An immunohistochemical study of architectural remodeling and connective tissue synthesis in pulmonary fibrosis. Am Rev Respir Dis. 1989 Dec;140(6):1693-703. doi: 10.1164/ajrccm/140.6.1693.
PubMed 2604297Hyde DM, King TE Jr, McDermott T, Waldron JA Jr, Colby TV, Thurlbeck WM, Flint WM, Ackerson L, Cherniack RM. Idiopathic pulmonary fibrosis. Quantitative assessment of lung pathology. Comparison of a semiquantitative and a morphometric histopathologic scoring system. Am Rev Respir Dis. 1992 Oct;146(4):1042-7. doi: 10.1164/ajrccm/146.4.1042.
PubMed 1416394Buschman DL, Gamsu G, Waldron JA Jr, Klein JS, King TE Jr. Chronic hypersensitivity pneumonitis: use of CT in diagnosis. AJR Am J Roentgenol. 1992 Nov;159(5):957-60. doi: 10.2214/ajr.159.5.1414806.
PubMed 1414806Aguayo SM, Miller YE, Waldron JA Jr, Bogin RM, Sunday ME, Staton GW Jr, Beam WR, King TE Jr. Brief report: idiopathic diffuse hyperplasia of pulmonary neuroendocrine cells and airways disease. N Engl J Med. 1992 Oct 29;327(18):1285-8. doi: 10.1056/NEJM199210293271806. No abstract available.
PubMed 1406819Low RB, Giancola MS, King TE Jr, Chapitis J, Vacek P, Davis GS. Serum and bronchoalveolar lavage of N-terminal type III procollagen peptides in idiopathic pulmonary fibrosis. Am Rev Respir Dis. 1992 Sep;146(3):701-6. doi: 10.1164/ajrccm/146.3.701.
PubMed 1519851Lynch DA, Rose CS, Way D, King TE Jr. Hypersensitivity pneumonitis: sensitivity of high-resolution CT in a population-based study. AJR Am J Roentgenol. 1992 Sep;159(3):469-72. doi: 10.2214/ajr.159.3.1503007.
PubMed 1503007King TE Jr, Mortenson RL. Bronchoalveolar lavage in patients with connective tissue disease. J Thorac Imaging. 1992 Jun;7(3):26-48. doi: 10.1097/00005382-199206000-00005.
PubMed 1501266King TE Jr, Mortenson RL. Cryptogenic organizing pneumonitis. The North American experience. Chest. 1992 Jul;102(1 Suppl):8S-13S.
PubMed 1623812Cherniack RM, Colby TV, Flint A, Thurlbeck WM, Waldron J, Ackerson L, King TE Jr. Quantitative assessment of lung pathology in idiopathic pulmonary fibrosis. The BAL Cooperative Group Steering Committee. Am Rev Respir Dis. 1991 Oct;144(4):892-900. doi: 10.1164/ajrccm/144.4.892.
PubMed 1718192Carre PC, Mortenson RL, King TE Jr, Noble PW, Sable CL, Riches DW. Increased expression of the interleukin-8 gene by alveolar macrophages in idiopathic pulmonary fibrosis. A potential mechanism for the recruitment and activation of neutrophils in lung fibrosis. J Clin Invest. 1991 Dec;88(6):1802-10. doi: 10.1172/JCI115501.
PubMed 1752942
Study at a glance
From the registry record, last updated by the sponsor on 12 Jul 2016. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Idiopathic Pulmonary Fibrosis--Pathogenesis and Staging - SCOR in Occupational and Immunological Lung Diseases
- ClinicalTrials.gov ID
- NCT00005317
- Acronym / sponsor ID
- 4090
- Study type
- Observational
- Recruitment status
- Completed
- Lead sponsor
- National Heart, Lung, and Blood Institute (NHLBI)US National Institutes of Health
- Study start
- Dec 1986
- Study completion
- Nov 1996 (actual)
- First posted
- 26 May 2000 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
To conduct cross-sectional and longitudinal studies of patients with idiopathic pulmonary fibrosis (IPF) and patients with progressive systemic sclerosis (PSS), with and without associated lung disease.
Detailed description
BACKGROUND:
Idiopathic pulmonary fibrosis (IPF) is a disease of unknown etiology characterized pathologically by a chronic inflammatory process (alveolitis) that precedes and likely controls the alterations in connective tissue matrix that eventually destroys the normal lung architecture. The mechanisms involved in this process are not known. A complex cell-cell interactive sequence, involving principally neutrophils, lymphocytes, macrophages, fibroblast, and epithelial cells is believed to be responsible.
The SCOR in Occupational and Immunological Lung Diseases was first awarded in December, 1981. The subproject on idiopathic pulmonary fibrosis was first awarded in December, 1986.
DESIGN NARRATIVE:
The cross-sectional comparison examined bronchoalveolar lavage, high resolution, thin-section computer tomography (HRCT), neutrophil or monocyte labeled scintigraphy). The serial, longitudinal evaluation monitored the progression of disease. The study of PSS patients, without disease or with subclinical disease, was particularly useful because it allowed examination of the early events in the pathogenesis of IPF. The long-term goal of the project was to determine what alterations in cellular composition, function and trafficking occurred in the lung parenchyma of patients with IPF and to relate these alterations to the disease stage, prognosis, and therapeutic responsiveness.
The major objectives of the study were: (1) to continue the prospective, longitudinal study of carefully defined cases of IPF; (2) to initiate a study of patients with PSS, a disease that provided a useful paradigm for studying the early events of the disease; (3) to determine the role of the lymphocyte in IPF, by defining the subset of T lymphocytes responsible for modulating macrophage function; (4) to establish the role of non-invasive techniques (bronchoalveolar lavage (BAL), HRCT scanning and scintigraphy -- neutrophil and monocyte labelled cells) in assessing the activity of inflammation in carefully evaluated patients; (5) to determine the relationship of these results to the -- carefully defined and serially obtained -- clinical, radiographical, and physiological findings and to the histopathologic abnormalities (in patients that underwent lung biopsy, predominantly IPF cases). (6) to perform studies utilizing blood, BAL fluid and lung tissue in an effort to understand the pathogenic mechanisms that underlied the inflammatory/immune cellular injury and fibrosis that characterize this disease.
The study completion date listed in this record was obtained from the "Completed Date" entered in the Query View Report System (QVR).
Study design
Who may qualify
- Ages
- Up to 100 years
- Sex
- Male only
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult, Older adult
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Not reported in the source record.
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 12 Jul 2016.
- Background: PubMed 7735621Janson RW, Hance KR, King TE Jr. Human alveolar macrophages produce predominantly the 35-kD pro-forms of interleukin-1 alpha and interleukin-1 beta when stimulated with lipopolysaccharide. Am J Respir Crit Care Med. 1995 May;151(5):1613-20. doi: 10.1164/ajrccm.151.5.7735621.
- Background: PubMed 7697250Cherniack RM, Colby TV, Flint A, Thurlbeck WM, Waldron JA Jr, Ackerson L, Schwarz MI, King TE Jr. Correlation of structure and function in idiopathic pulmonary fibrosis. Am J Respir Crit Care Med. 1995 Apr;151(4):1180-8. doi: 10.1164/ajrccm/151.4.1180.
- Background: PubMed 3059868Willcox M, Kervitsky A, Watters LC, King TE Jr. Quantification of cells recovered by bronchoalveolar lavage. Comparison of cytocentrifuge preparations with the filter method. Am Rev Respir Dis. 1988 Jul;138(1):74-80. doi: 10.1164/ajrccm/138.1.74.
- Background: PubMed 9180223Salvatore M, Seeber AC, Nacmias B, Petraroli R, Sorbi S, Pocchiari M. Alpha1 antichymotrypsin signal peptide polymorphism in sporadic Creutzfeldt-Jakob disease. Neurosci Lett. 1997 May 16;227(2):140-2. doi: 10.1016/s0304-3940(97)00308-x.
- Background: PubMed 2492173Savici D, Campbell PA, King TE Jr. Bronchoalveolar macrophages from patients with idiopathic pulmonary fibrosis are unable to kill facultative intracellular bacteria. Am Rev Respir Dis. 1989 Jan;139(1):22-7. doi: 10.1164/ajrccm/139.1.22.
- Background: PubMed 2604297Kuhn C 3rd, Boldt J, King TE Jr, Crouch E, Vartio T, McDonald JA. An immunohistochemical study of architectural remodeling and connective tissue synthesis in pulmonary fibrosis. Am Rev Respir Dis. 1989 Dec;140(6):1693-703. doi: 10.1164/ajrccm/140.6.1693.
- Background: PubMed 1416394Hyde DM, King TE Jr, McDermott T, Waldron JA Jr, Colby TV, Thurlbeck WM, Flint WM, Ackerson L, Cherniack RM. Idiopathic pulmonary fibrosis. Quantitative assessment of lung pathology. Comparison of a semiquantitative and a morphometric histopathologic scoring system. Am Rev Respir Dis. 1992 Oct;146(4):1042-7. doi: 10.1164/ajrccm/146.4.1042.
- Background: PubMed 1414806Buschman DL, Gamsu G, Waldron JA Jr, Klein JS, King TE Jr. Chronic hypersensitivity pneumonitis: use of CT in diagnosis. AJR Am J Roentgenol. 1992 Nov;159(5):957-60. doi: 10.2214/ajr.159.5.1414806.
- Background: PubMed 1406819Aguayo SM, Miller YE, Waldron JA Jr, Bogin RM, Sunday ME, Staton GW Jr, Beam WR, King TE Jr. Brief report: idiopathic diffuse hyperplasia of pulmonary neuroendocrine cells and airways disease. N Engl J Med. 1992 Oct 29;327(18):1285-8. doi: 10.1056/NEJM199210293271806. No abstract available.
- Background: PubMed 1519851Low RB, Giancola MS, King TE Jr, Chapitis J, Vacek P, Davis GS. Serum and bronchoalveolar lavage of N-terminal type III procollagen peptides in idiopathic pulmonary fibrosis. Am Rev Respir Dis. 1992 Sep;146(3):701-6. doi: 10.1164/ajrccm/146.3.701.
- Background: PubMed 1503007Lynch DA, Rose CS, Way D, King TE Jr. Hypersensitivity pneumonitis: sensitivity of high-resolution CT in a population-based study. AJR Am J Roentgenol. 1992 Sep;159(3):469-72. doi: 10.2214/ajr.159.3.1503007.
- Background: PubMed 1501266King TE Jr, Mortenson RL. Bronchoalveolar lavage in patients with connective tissue disease. J Thorac Imaging. 1992 Jun;7(3):26-48. doi: 10.1097/00005382-199206000-00005.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
The record lists no contact. Use the official record to reach the sponsor.
Questions about this trial
What is this clinical trial studying?
An observational study of Lung Diseases and Pulmonary Fibrosis, run by National Heart, Lung, and Blood Institute (NHLBI).
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 12 Jul 2016. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT00005317, which also lists 34 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 12 Jul 2016.