Determination of olfactory and taste disorders in chronic respiratory diseases

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Created On: 25/02/2026

Cystic fibrosis, Primary ciliary dyskinesia

Cystic fibrosis (CF) is triggered by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), a chloride channel essential for epithelial function.

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Key take away

Cystic fibrosis patients experience salty taste impairment linked to elevated sweat chloride and salivary CFTR dysfunction, whereas smell impairment is primarily observed in primary ciliary dyskinesia.

Background

Cystic fibrosis (CF) is triggered by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), a chloride channel essential for epithelial function. Emerging evidence from animal models suggests that CFTR dysfunction may also hamper sensory nerve cell activity, potentially contributing to taste and smell disorders.

Hence, this prospective cohort study determined whether chemosensory dysfunction in CF is linked to persistent CFTR abnormalities detected by pilocarpine iontophoresis, or whether it is linked with systemic inflammation or reduced pulmonary function.

Method

A total of 65 volunteers (median age 19 years) were enrolled at the University Children’s Hospital Bochum, including patients with CF (n=23), primary ciliary dyskinesia (PCD; n=22), and healthy controls (n=20). Taste perception (salty, sweet, sour, bitter) was assessed via validated “Taste-strips” (score range 0–16; age-adjusted hypogeusia thresholds <8/<9/<9.9/<10).

Olfactory function was measured via the “U-Sniff” odor identification test (score range 0–12; reduced performance defined as <8). Additional assessments included pilocarpine iontophoresis (sweat chloride testing), spirometry for lung function, inflammatory biomarkers such as C-reactive protein (CRP), and patient-reported chemosensory symptoms.

Result

Taste impairment (hypogeusia) was observed exclusively in the CF group (17.4%). Notably, difficulty identifying salty taste was significantly more frequent in CF patients compared with PCD and healthy controls. This finding was particularly pronounced in those with elevated sweat chloride levels (≥60 mmol/L), indicating persistent CFTR dysfunction. Reduced odor identification was considerably more common in those with PCD compared with CF (Table 1).

Importantly, chemosensory abnormalities were not linked with lung function parameters or systemic inflammatory markers.

Conclusion

Taste disorders in CF were predominantly marked by impaired salty taste perception and were strongly associated with elevated sweat chloride levels, suggesting that altered salivary salt composition due to CFTR dysfunction in salivary glands — rather than direct nerve cell impairment — plays a central role.

In contrast, smell impairment remains a prominent concern in PCD. These findings highlight the importance of evaluating chemosensory function in chronic respiratory diseases and yield new insights into the relationship between CFTR dysfunction and sensory abnormalities.