Individual Sensitivity for Interstitial Lung Diseases

Interstitial Lung Diseases Clinical Trial

Official title:

Individual Sensitivity for Interstitial Lung Diseases

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT00741572
• Other study ID #: MEC 08.3.048
• Status: Completed
• Phase: N/A
• First received: August 25, 2008
• Last updated: February 22, 2017
• Start date: August 2008
• Est. completion date: September 2009

Study information

• Verified date: September 2009
• Source: Maastricht University Medical Center
• Contact: n/a
• Is FDA regulated: No
• Study type: Observational

Clinical Trial Summary

Interstitial lung diseases (ILD) is a collective noun for various chronic lung diseases, including sarcoidosis and idiopathic lung fibrosis (IPF). Sarcoidosis is a multi-systemic disease that includes damage to the lungs in 90% of the patients. Generally, the disease can be described as a systemic, granulomatous and antigen-driven disorder. IPF is a disease of only the lungs, in which an unknown cause induces a strong inflammation reaction leading to acute lung damage that ultimately results in the formation of scar tissue and stiffness of the lungs.

Unfortunately, the exact cause of ILD is still unknown. It is suggested that environmental and work-related exposure to various triggers can exert an effect on the course of the diseases. Examples of such triggers include bacteria, organic agents such as pollen and cotton dust and inorganic agents like metals and talc. Due to this unknown cause, it is difficult to treat ILD. Consequently, the current guideline is no medication or anti-inflammatory agents in severe cases. Unfortunately, this therapy is not completely effective.

Triggers that are suggested to cause ILD can exert their effects via various mechanisms. On the one hand, they can induce an inflammatory reaction as we recently demonstrated for various triggers including instillation material and sicila. During such an inflammatory reaction, cytokines are released that can induce oxidative stress, i.e. an imbalance between the formation of and the protection against reactive oxygen species (ROS). On the other hand, ILD-inducing triggers may directly cause an increased ROS production that subsequently can evoke an inflammatory reaction.

The objective of the current study is to investigate the individual sensitivity for the development of ILD after exposure to various triggers. Main focus will be the differences in the formation of and the protection against ROS as well as the occurring inflammatory reaction after exposure to such triggers.

Furthermore, a simple blood test will be developed to study and eventually even predict the individual reaction of subjects to various triggers.

Finally, to fully characterize the development of ILD after exposure to various triggers, the exhaled air of patients will be studied in order to identify specific markers of oxidative stress and damage.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 100
• Est. completion date: September 2009
• Est. primary completion date: June 2009
• Accepts healthy volunteers: No
• Gender: All
• Age group: 18 Years and older

Eligibility

Inclusion Criteria:

• ILD diagnosis confirmed by lung biopsy, X ray or BALF analysis

Exclusion Criteria:

• smoking

• pregnancy or lactation

• use of vitamins or nutritional supplements

Related Conditions & MeSH terms

• Hypersensitivity
• Interstitial Lung Diseases
• Lung Diseases
• Lung Diseases, Interstitial

Locations

Country	Name	City	State
Netherlands	Maastricht University	Maastricht

Sponsors (1)

Lead Sponsor	Collaborator
Maastricht University Medical Center

Country where clinical trial is conducted

Netherlands, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	differences in the production of and the protection against ROS		6 hours
Primary	differences in the occurring inflammatory reaction		6 hours
Secondary	differences in the presence of so-called volatile organic compounds (VOCs) in the exhaled air		0 hour

External Links

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