Evidence map›Paper›PMID 39543951›Full record

ReviewTherapeutic advances in respiratory disease

Modulator-refractory cystic fibrosis: Defining the scope and challenges of an emerging at-risk population.

Lindsay Somerville, Larry Borish, Imre Noth, Dana Albon

Abstract readReview
In one paragraph

Review in Therapeutic advances in respiratory disease. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

  1. Trial
  2. Nucleic acid-based therapies for people with cystic fibrosis.The Cochrane database of systematic reviews · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Modulation of host inflammatory pathways byFrontiers in immunology · 2026
    Article
  7. Review
  8. Review
  9. Journal of fungi (Basel, Switzerland) · 2025
    Review
  10. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Lindsay SomervilleUniversity of Virginia, 1215 Lee Street, Charlottesville, VA 2908, USA.ORCID 0000-0001-7052-0640
Larry BorishUniversity of Virginia, Charlottesville, VA, USA.
Imre NothUniversity of Virginia, Charlottesville, VA, USA.
Dana AlbonUniversity of Virginia, Charlottesville, VA, USA.ORCID 0000-0001-9055-3247

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cystic fibrosis (CF) causes life-shortening respiratory and systemic disease due to dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel. Highly effective modulator therapies (HEMT) improve the lives of many people with cystic fibrosis (PwCF) by correcting the structure and function of the defective CFTR channel at the molecular level. Despite these advancements, a subset of patients-termed modulator-refractory CF-continues to experience two or more pulmonary exacerbations per year requiring hospitalization or intravenous antibiotics, regardless of other modulator benefits. This underrecognized group represents an emerging challenge within the CF community. We discuss the benefits and limitations of current CFTR modulator therapies and the urgent need to investigate this emerging at-risk population. While HEMT improves lung function, decreases exacerbations, reduces the need for lung transplantation, and lowers mortality, increasing evidence shows that not all patients benefit equally. At the University of Virginia, nearly 6% of adults with CF exhibit the modulator-refractory phenotype. The driving factors of modulator-refractory CF are likely multifactorial, including genetic variations, variable immune responses, preexisting bronchiectasis, microbiological colonization, preexisting comorbid conditions, and environmental and socioeconomic factors. This perspective review recognizes and defines modulator-refractory CF as a distinct emerging clinical phenotype in the post-modulator era. Understanding this phenotype is crucial for reducing morbidity and mortality, and for improving the quality of life for PwCF. Raising awareness of modulator-refractory CF will help the community address this population and perform further research to identify causes. The emergence of modulator-refractory CF highlights a significant gap in our current treatment landscape and provides an opportunity to develop innovative therapeutic strategies that may benefit the entire CF community, ensuring that no person with CF is left behind.

Indexed as

Cystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorAdultAnti-Bacterial AgentsDisease ProgressionDrug ResistanceHumansLungLung TransplantationPhenotypeRisk FactorsTreatment OutcomeAnti-Bacterial AgentsCFTR protein, humanCystic Fibrosis Transmembrane Conductance Regulatorcystic fibrosishighly-effective modulator therapymodulat0r-refractory cystic fibrosis

Identifiers

PMID39543951
PMCPMC11565698

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.