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Researchers reported that sphingomyelin C24:0 measured in exhaled breath condensate distinguished idiopathic pulmonary fibrosis from fibrotic hypersensitivity pneumonitis in a study presented at the CHEST meeting. The result is promising but preliminary: the breath samples came from only 39 patients, and researchers said external validation is needed before clinical use.
Researchers reported that a lipid measured in exhaled breath condensate may help distinguish idiopathic pulmonary fibrosis (IPF) from fibrotic hypersensitivity pneumonitis, two conditions that can be difficult to tell apart in advanced disease. In the study presented at the CHEST meeting in Phoenix, sphingomyelin C24:0 correctly predicted the diagnosis in 80% of fibrotic hypersensitivity pneumonitis cases and 85.7% of IPF cases in the sample analyzed; the findings remain preliminary and need external validation.
The test measured sphingolipids in condensed exhaled breath. For sphingomyelin C24:0, the researchers reported an area under the receiver operating characteristic curve (AUC) of 0.897, a measure of how well a test distinguishes between groups. The reported classification rates were 80% for fibrotic hypersensitivity pneumonitis and 85.7% for IPF. These results describe performance in the study, not established accuracy in routine clinical practice.
The study included 101 people who provided blood samples: 28 healthy controls, 33 patients with IPF and 40 with fibrotic hypersensitivity pneumonitis. Breath condensate was available from a smaller subset: 10 controls, 21 IPF patients and 18 patients with fibrotic hypersensitivity pneumonitis. A blood measure, plasma dihydrosphingosine, had an AUC of 0.737 on its own. Adding it to the breath test changed the AUC to 0.906, a modest increase from the breath test’s 0.897.
Jon Mullholand, MD, of Virginia Commonwealth University, presented the findings at the meeting hosted by the American College of Chest Physicians. He said the two diseases can share clinical, imaging and pathological features in late-stage disease, while differing in management and prognosis. He also said the breath test is not yet a widely accepted laboratory assay, and that an external validation study is needed before its potential clinical role can be established.
A Possible Clue for Treatment Decisions
Distinguishing IPF from fibrotic hypersensitivity pneumonitis can matter because the conditions have different management approaches and prognoses, according to Mullholand. When the diagnosis is uncertain, an additional test could potentially provide clinicians with evidence to weigh alongside a patient’s symptoms, imaging and other test results. The study does not show that using this breath test improves treatment choices or patient outcomes; it identifies a possible diagnostic signal for further study.
A breath-based measure may also offer information from the lungs themselves. Mullholand said breath condensate reflects the local lung environment, while a blood sample can reflect changes across the body. In the study, the breath-condensate pattern differed between the conditions, while the blood marker added little to the breath test’s predictive performance. Whether this difference can reliably guide diagnosis in a broader range of patients is not yet known.
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How the Breath Sample Was Collected
Exhaled breath condensate is collected by breathing into a tube-like device. A refrigerant cools the breath so that water vapor and other compounds condense into a sample for laboratory analysis. Mullholand described the collection as noninvasive, but said it can take 15 to 20 minutes and may be difficult for people with severe lung disease. He also noted that the assay can be technically challenging and is not accepted for analysis by many laboratories in the United States.
Sphingolipids have roles in inflammation and fibrosis, and previous research has found changes in sphingolipids in IPF. The new report examined whether specific sphingolipids in breath and blood could help separate IPF from fibrotic hypersensitivity pneumonitis. The breath test’s promising performance in this study does not mean it is available as a standard diagnostic test; the research team says its findings require confirmation in an independent group.
“There’s a diagnostic challenge when we’re trying to differentiate these [two conditions] at end-stage disease, as they can have overlapping clinical presentations as well as imaging features, even pathologic slides.”
— Jon Mullholand, MD, of Virginia Commonwealth University, speaking at the CHEST meeting
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Validation and Practical Limits
The study’s breath-sample group was small, with 39 patients across the two disease groups and 10 healthy controls. The reported performance may not carry over to other hospitals, patient populations or people whose diagnosis is less clear. The source report does not provide enough information to determine how the test would perform across disease stages or alongside the full range of tests used in clinical assessment.
Researchers have not established a standard, widely available assay for measuring these breath lipids. It is also unclear how collection and laboratory methods could be standardized, how often results might be inconclusive, or whether the test would change clinical decisions. The findings do not establish that sphingolipids cause either condition, and the combined blood-and-breath result was only slightly higher than the breath test’s AUC in this study.
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Independent Testing Comes Next
Mullholand said external validation is needed to check whether the breath-test results hold in a separate group of patients. That work would help establish how consistently the marker distinguishes the conditions beyond the participants included in the current study. Researchers could also examine collection and analysis methods, given the practical challenges and limited laboratory availability described at the meeting.
The study team may investigate whether sphingolipids are part of the biological pathway behind fibrosis or instead change as a consequence of disease. Until those questions are addressed and the test is validated, the findings should be treated as an early research result—not a replacement for current diagnostic assessment or a test ready for routine care.
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Key Questions
What did the researchers measure?
They measured sphingolipids, including sphingomyelin C24:0, in exhaled breath condensate. The study also measured plasma dihydrosphingosine in blood.
How well did the breath marker perform?
The study reported that sphingomyelin C24:0 correctly predicted fibrotic hypersensitivity pneumonitis in 80% of cases and IPF in 85.7% of cases, with an AUC of 0.897. These are study results, not confirmed real-world performance.
Could this test replace existing diagnostic methods?
No evidence in this report shows that it can. The test needs validation in an independent patient group, and researchers have not established it as a standard clinical assay.
Why is distinguishing the conditions important?
According to presenting researcher Jon Mullholand, IPF and fibrotic hypersensitivity pneumonitis can look similar in advanced disease but differ in management and prognosis. The study did not test whether using the breath marker improves outcomes.
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