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. 2024 Apr 27;14(5):565.
doi: 10.3390/life14050565.

Calcitonin Gene-Related Peptide Level in Cystic Fibrosis Patients

Affiliations

Calcitonin Gene-Related Peptide Level in Cystic Fibrosis Patients

Sabina Galiniak et al. Life (Basel). .

Abstract

Calcitonin gene-related peptide (CGRP) has long been implicated in both the physiology and pathophysiology of the respiratory tract. The objective of our study was to determine the serum concentration of alpha CGRP (αCGRP) in cystic fibrosis (CF) that arises from mutations in the gene responsible for encoding the cystic fibrosis transmembrane conductance regulator (CFTR) protein. Currently, there are not many data in the literature about the role of CGRP in CF. The serum level of αCGRP was estimated using the enzyme-linked immunosorbent assay among 64 patients with CF and 31 healthy controls. The αCGRP concentration in the CF group was 62.51 ± 15.45 pg/mL, while in the control group it was 47.43 ± 8.06 pg/mL (p < 0.001). We also compared the level of αCGRP in CF patients according to the type of CFTR mutation. Homozygotes for ΔF508 had higher αCGRP levels than heterozygotes (67.9 ± 10.2 vs. 54.5 ± 18.3 pg/mL, p < 0.01). The level of this neuropeptide was statistically higher in patients with severe disease than in those with mild CF (p = 0.003) when patients were divided into three groups by spirometry results. αCGRP concentration was not correlated with age, sex, clinical parameters, and pulmonary function test results in the study participants. The results of our study suggest a significant increase in the concentration of αCGRP in the serum of patients with CF compared to the control group. This observation opens interesting possibilities for understanding the role of αCGRP in the context of CF pathophysiology.

Keywords: CFTR mutation; calcitonin gene-related peptide; cystic fibrosis.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Level of CGRP in patients with CF compared to healthy participants (differences between means were analyzed using Mann–Whitney U tests).
Figure 2
Figure 2
CGRP level by the type of CFTR mutations (differences between means were analyzed using Kruskal–Wallis U tests).

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