P324 Essential fatty acid deficiency in children and young adults with cystic fibrosis – micronutrient assessment is still an actual topic

Data on essential fatty acid deficiency (EFAD) and assessment of lipids and fatty acids (FAs) in CF is largely unknown. However, given the favorable effect of changing nutritional interventions aimed to meet each individual’s unique nutritional needs, the real threat of overweight or obesity and the long-term clinical impact of CFTR modulators on nutrition status over time, dyslipidemia has emerged issues in patients with CF. To evaluate FAs profiles in CF in association with nutritional status and inflammatory activity prior to the use of CFTR modulators. A total of 47 CF subjects on symptomatic therapy (30 children with mean age 9.74 y; 17 adults with mean age 25.47 y) and 50 age, gender and nutritionally matched controls were enrolled. The most significant changes were found in plasma phospholipid fatty acids. PUFAn-6: We demonstrated a significantly lower content of linoleic acid (children p < 0.001, adults p < 0.05) and arachidonic acid (children p < 0.001, adults p < 0.005). FAs abnormalities are related to food intake and subsequent metabolism to arachidonic acid (a precursor of inflammatory mediators). PUFAn-3: We proved a significantly lower content of docosahexaenoic acid (children p < 0.005, adults p < 0.005). MUFA: We found a higher content of palmitoleic acid (children p < 0.001, adults p < 0.05) indicating a higher lipogenesis. The results suggest a higher risk of EFAD in CF and a pro-inflammatory PUFA profile that is an important part of sterile inflammation in CF. As new, routine examination and a personalized nutritional approach including dietary supplementation of PUFAn-3 FAs or their mediators could be a useful non-pharmacological intervention. Lipid profile changes on CFTR modulators present new challenges and opportunities for interdisciplinary partnership in optimizing nutrition for patients, in consideration of FAs potential effects on inflammation and immune response.