{"id":{"repo_id":"ghent","oai_identifier":"oai:archive.ugent.be:468659"},"canonical_url":"https://search.dev.ndltd.org/etd/ghent/oai:archive.ugent.be:468659","repository":{"repo_id":"ghent","name":"Ghent University","base_url":"https://biblio.ugent.be/oai"},"display":{"title":"Zinc and essential fatty acid status and supplementation in cystic fibrosis patients","abstract":"Cystic fibrosis is a multi-organ disease in which maintaining a good nutritional status is crucial for its outcome. An overview of the disease is given in chapter 1. In cystic fibrosis, the maldigestion is a factor not only influencing the nutrient but also the micronutrient absorption. The obvious deficiencies in fat soluble vitamins led to a standard monitored supplement for pancreatic insufficient patients. There are other micronutrients which could theoretically influence the course of the disease, where the benefit for the patient is not yet known. Zinc and essential fatty acids mutually influence each other and are important in inflammation and immunity. Chapter 2 summarises the research objectives. In chapter 3 we focus on the zinc status, first by means of the serum zinc concentration. The normal serum zinc concentration in our region is significantly lower than reported in literature (chapter 3.2). This makes our population more sensible for zinc deficiency, especially when malabsorption syndromes are present. Further on, an age dependency was observed with significantly lower serum zinc concentrations in infants. Serum zinc concentrations did not significantly change after the age of 4 years. There was no influence of the type of infant feeding. There is an association of zinc with vitamin A. Since in literature a zinc deficiency was observed in cystic fibrosis infants detected with neonatal cystic fibrosis screening, we performed a study where serum zinc was evaluated at diagnosis and one year later (chapter 3.3). The serum zinc concentration at diagnosis was very low indeed and increased significantly without zinc supplements after 1 year of standard cystic fibrosis treatment. However, there were no significant differences when compared to age matched healthy controls. There was a significant association of zinc with vitamin A and E. In older cystic fibrosis children the same low serum zinc concentrations were observed as in the healthy local control group. There is an association of serum zinc with serum albumin and serum vitamin A. The association with albumin is not surprising since 70% of serum zinc is bound to albumin. Further, multiple aspects of the vitamin A status as absorption, metabolism, release, transport and utilisation are influenced by zinc. There was no relation with nutritional status, growth, inflammation parameters or colonisation with Pseudomonas Aeruginosa. However, a positive association with the forced vital capacity was observed. Serum zinc lacks sensitivity and specificity for the evaluation of the zinc status since only 0.2% circulates in plasma associated with albumin and α-2 macroglobulin. It is kept within a narrow range and only prolonged zinc deficiency will reflect in the serum zinc concentration. Another more complex way to evaluate zinc-deficiency is to look at zinc dependent enzymes. However, there is no consensus in literature on which enzymes are the best in reflecting the zinc status. The earlier studies we performed on intestinal biopsies of newly diagnosed cystic fibrosis patients showed a decreased intestinal alkaline phosphatase activity (chapter 3.4). This was the case in the normal and the damaged mucosa. Alkaline phosphatase is a known metalloprotein, containing zinc or magnesium necessary for the catalytic function. Furthermore intestinal alkaline phosphatase gene expression is activated by a zinc binding protein. Finally, the enzyme has shown to be very sensitive for oxygen free radicals. Zinc deficiency will therefore result in a decreased intestinal alkaline phosphatase activity due to absence of zinc in its catalytic site and increased inactivation as a result of increased presence of oxygen free radicals but also in a decreased concentration as a consequence of the decreased transcription. Chapter 4 deals with the essential fatty acid status of cystic fibrosis patients. The disturbances of the phospholipid essential fatty acid distribution described in literature were also present in the patients we studied. They have significantly lower docosahexaenoic acid (22:6n-3) and linoleic acid (18:2n-6) and higher dihomogammalinolenic acid (18:3n-6), oleic acid (18:1n-9) and Mead acid (20:3n-9), the latter being a sign of essential fatty acid deficiency. This resulted in increased ratios of arachidonic acid/docosahexaenoic acid, Mead acid/arachidonic acid and oleic acid/linoleic acid. There was no relation of serum fatty acid composition with nutritional status, caloric intake, pancreatic function, gender, pulmonary function, pseudomonas colonisation or the presence of diabetes mellitus (chapter 4.2). When patients were divided into 2 groups according to genotype (group A: mutation class I, II, or III, group B: mutation class IV, V) the abnormalities were more pronounced in the “severe” genotypes. However, there was no significant difference between the groups for age, pulmonary function, nutritional status and vitamin E concentration. Cystic fibrosis patients can have some concomitant problems known to influence fatty acid composition such as diabetes mellitus and liver disease. Therefore a study was performed to evaluate whether the presence of cystic fibrosis related liver disease influenced the fatty acid status. In the presence of cystic fibrosis related liver disease there is an even more pronounced decrease in docosahexaenoic acid (22:6n-3) and an increase of docosatetraenoic acid (22:4n-6) compared to genotype controls without cystic fibrosis related liver disease. Since in cystic fibrosis transmembrane conductance regulator-/- mice docosahexaenoic acid was capable of reversing the cystic fibrosis symptoms, we performed a double blind placebo controlled study to evaluate the effect of docosahexaenoic acid in humans (chapter 4.3). To eliminate the disturbances due to genotype and liver disease we included only ΔF508 homozygous patients without liver disease. The treatment group had a significant increase in docosahexaenoic acid and eicosapentaenoic acid concentrations. A concomitant decrease of dihomogammalinolenic acid, arachidonic acid, 22:5n-6 and Mead acid was observed. There was no difference between controls and treatment group for weight for height %, caloric intake, forced expiratory volume in 1 second1%, forced vital capacity % at the start and after 1 year of supplements. The laboratory results showed no changes in vitamin E level, liver enzymes, albumin, sedimentation and IgG concentration. Although docosahexaenoic acid -rich oil shifted the serum phospholipid fatty acids to a less pro-inflammatory profile no conclusive clinical improvement could be observed so far.","abstract_html":"Cystic fibrosis is a multi-organ disease in which maintaining a good nutritional status is crucial for its outcome. An overview of the disease is given in chapter 1. In cystic fibrosis, the maldigestion is a factor not only influencing the nutrient but also the micronutrient absorption. The obvious deficiencies in fat soluble vitamins led to a standard monitored supplement for pancreatic insufficient patients. There are other micronutrients which could theoretically influence the course of the disease, where the benefit for the patient is not yet known. Zinc and essential fatty acids mutually influence each other and are important in inflammation and immunity. Chapter 2 summarises the research objectives. In chapter 3 we focus on the zinc status, first by means of the serum zinc concentration. The normal serum zinc concentration in our region is significantly lower than reported in literature (chapter 3.2). This makes our population more sensible for zinc deficiency, especially when malabsorption syndromes are present. Further on, an age dependency was observed with significantly lower serum zinc concentrations in infants. Serum zinc concentrations did not significantly change after the age of 4 years. There was no influence of the type of infant feeding. There is an association of zinc with vitamin A. Since in literature a zinc deficiency was observed in cystic fibrosis infants detected with neonatal cystic fibrosis screening, we performed a study where serum zinc was evaluated at diagnosis and one year later (chapter 3.3). The serum zinc concentration at diagnosis was very low indeed and increased significantly without zinc supplements after 1 year of standard cystic fibrosis treatment. However, there were no significant differences when compared to age matched healthy controls. There was a significant association of zinc with vitamin A and E. In older cystic fibrosis children the same low serum zinc concentrations were observed as in the healthy local control group. There is an association of serum zinc with serum albumin and serum vitamin A. The association with albumin is not surprising since 70% of serum zinc is bound to albumin. Further, multiple aspects of the vitamin A status as absorption, metabolism, release, transport and utilisation are influenced by zinc. There was no relation with nutritional status, growth, inflammation parameters or colonisation with Pseudomonas Aeruginosa. However, a positive association with the forced vital capacity was observed. Serum zinc lacks sensitivity and specificity for the evaluation of the zinc status since only 0.2% circulates in plasma associated with albumin and α-2 macroglobulin. It is kept within a narrow range and only prolonged zinc deficiency will reflect in the serum zinc concentration. Another more complex way to evaluate zinc-deficiency is to look at zinc dependent enzymes. However, there is no consensus in literature on which enzymes are the best in reflecting the zinc status. The earlier studies we performed on intestinal biopsies of newly diagnosed cystic fibrosis patients showed a decreased intestinal alkaline phosphatase activity (chapter 3.4). This was the case in the normal and the damaged mucosa. Alkaline phosphatase is a known metalloprotein, containing zinc or magnesium necessary for the catalytic function. Furthermore intestinal alkaline phosphatase gene expression is activated by a zinc binding protein. Finally, the enzyme has shown to be very sensitive for oxygen free radicals. Zinc deficiency will therefore result in a decreased intestinal alkaline phosphatase activity due to absence of zinc in its catalytic site and increased inactivation as a result of increased presence of oxygen free radicals but also in a decreased concentration as a consequence of the decreased transcription. Chapter 4 deals with the essential fatty acid status of cystic fibrosis patients. The disturbances of the phospholipid essential fatty acid distribution described in literature were also present in the patients we studied. They have significantly lower docosahexaenoic acid (22:6n-3) and linoleic acid (18:2n-6) and higher dihomogammalinolenic acid (18:3n-6), oleic acid (18:1n-9) and Mead acid (20:3n-9), the latter being a sign of essential fatty acid deficiency. This resulted in increased ratios of arachidonic acid/docosahexaenoic acid, Mead acid/arachidonic acid and oleic acid/linoleic acid. There was no relation of serum fatty acid composition with nutritional status, caloric intake, pancreatic function, gender, pulmonary function, pseudomonas colonisation or the presence of diabetes mellitus (chapter 4.2). When patients were divided into 2 groups according to genotype (group A: mutation class I, II, or III, group B: mutation class IV, V) the abnormalities were more pronounced in the “severe” genotypes. However, there was no significant difference between the groups for age, pulmonary function, nutritional status and vitamin E concentration. Cystic fibrosis patients can have some concomitant problems known to influence fatty acid composition such as diabetes mellitus and liver disease. Therefore a study was performed to evaluate whether the presence of cystic fibrosis related liver disease influenced the fatty acid status. In the presence of cystic fibrosis related liver disease there is an even more pronounced decrease in docosahexaenoic acid (22:6n-3) and an increase of docosatetraenoic acid (22:4n-6) compared to genotype controls without cystic fibrosis related liver disease. Since in cystic fibrosis transmembrane conductance regulator-/- mice docosahexaenoic acid was capable of reversing the cystic fibrosis symptoms, we performed a double blind placebo controlled study to evaluate the effect of docosahexaenoic acid in humans (chapter 4.3). To eliminate the disturbances due to genotype and liver disease we included only ΔF508 homozygous patients without liver disease. The treatment group had a significant increase in docosahexaenoic acid and eicosapentaenoic acid concentrations. A concomitant decrease of dihomogammalinolenic acid, arachidonic acid, 22:5n-6 and Mead acid was observed. There was no difference between controls and treatment group for weight for height %, caloric intake, forced expiratory volume in 1 second1%, forced vital capacity % at the start and after 1 year of supplements. The laboratory results showed no changes in vitamin E level, liver enzymes, albumin, sedimentation and IgG concentration. Although docosahexaenoic acid -rich oil shifted the serum phospholipid fatty acids to a less pro-inflammatory profile no conclusive clinical improvement could be observed so far.","abstract_has_math":false,"creators":["Van Biervliet, Stephanie"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Robberecht, E"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2008,"date_issued":"2008","date_published":"2008","updated_at":"2026-07-24T02:22:55Z","subjects":[],"languages":["und"],"rights":["info:eu-repo/semantics/openAccess"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://biblio.ugent.be/publication/468659","http://doi.org/1854/11738","https://biblio.ugent.be/publication/468659/file/4334729"],"render_values":[{"text":"https://biblio.ugent.be/publication/468659","href":"https://biblio.ugent.be/publication/468659","code":true},{"text":"http://doi.org/1854/11738","href":"http://doi.org/1854/11738","code":true},{"text":"https://biblio.ugent.be/publication/468659/file/4334729","href":"https://biblio.ugent.be/publication/468659/file/4334729","code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/1854/LU-468659","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Robberecht, E"]},{"key":"dc:creator","label":"Author","values":["Van Biervliet, Stephanie"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2008"]},{"key":"dc:type","label":"Dc Type","values":["dissertation","info:eu-repo/semantics/doctoralThesis","info:eu-repo/semantics/publishedVersion"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["und"]},{"key":"dc:rights","label":"Dc Rights","values":["info:eu-repo/semantics/openAccess"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://biblio.ugent.be/publication/468659","http://hdl.handle.net/1854/LU-468659","http://doi.org/1854/11738","https://biblio.ugent.be/publication/468659/file/4334729"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Cystic fibrosis is a multi-organ disease in which maintaining a good nutritional status is crucial for its outcome. An overview of the disease is given in chapter 1. In cystic fibrosis, the maldigestion is a factor not only influencing the nutrient but also the micronutrient absorption. The obvious deficiencies in fat soluble vitamins led to a standard monitored supplement for pancreatic insufficient patients. There are other micronutrients which could theoretically influence the course of the disease, where the benefit for the patient is not yet known. Zinc and essential fatty acids mutually influence each other and are important in inflammation and immunity. Chapter 2 summarises the research objectives. In chapter 3 we focus on the zinc status, first by means of the serum zinc concentration. The normal serum zinc concentration in our region is significantly lower than reported in literature (chapter 3.2). This makes our population more sensible for zinc deficiency, especially when malabsorption syndromes are present. Further on, an age dependency was observed with significantly lower serum zinc concentrations in infants. Serum zinc concentrations did not significantly change after the age of 4 years. There was no influence of the type of infant feeding. There is an association of zinc with vitamin A. Since in literature a zinc deficiency was observed in cystic fibrosis infants detected with neonatal cystic fibrosis screening, we performed a study where serum zinc was evaluated at diagnosis and one year later (chapter 3.3). The serum zinc concentration at diagnosis was very low indeed and increased significantly without zinc supplements after 1 year of standard cystic fibrosis treatment. However, there were no significant differences when compared to age matched healthy controls. There was a significant association of zinc with vitamin A and E. In older cystic fibrosis children the same low serum zinc concentrations were observed as in the healthy local control group. There is an association of serum zinc with serum albumin and serum vitamin A. The association with albumin is not surprising since 70% of serum zinc is bound to albumin. Further, multiple aspects of the vitamin A status as absorption, metabolism, release, transport and utilisation are influenced by zinc. There was no relation with nutritional status, growth, inflammation parameters or colonisation with Pseudomonas Aeruginosa. However, a positive association with the forced vital capacity was observed. Serum zinc lacks sensitivity and specificity for the evaluation of the zinc status since only 0.2% circulates in plasma associated with albumin and α-2 macroglobulin. It is kept within a narrow range and only prolonged zinc deficiency will reflect in the serum zinc concentration. Another more complex way to evaluate zinc-deficiency is to look at zinc dependent enzymes. However, there is no consensus in literature on which enzymes are the best in reflecting the zinc status. The earlier studies we performed on intestinal biopsies of newly diagnosed cystic fibrosis patients showed a decreased intestinal alkaline phosphatase activity (chapter 3.4). This was the case in the normal and the damaged mucosa. Alkaline phosphatase is a known metalloprotein, containing zinc or magnesium necessary for the catalytic function. Furthermore intestinal alkaline phosphatase gene expression is activated by a zinc binding protein. Finally, the enzyme has shown to be very sensitive for oxygen free radicals. Zinc deficiency will therefore result in a decreased intestinal alkaline phosphatase activity due to absence of zinc in its catalytic site and increased inactivation as a result of increased presence of oxygen free radicals but also in a decreased concentration as a consequence of the decreased transcription. Chapter 4 deals with the essential fatty acid status of cystic fibrosis patients. The disturbances of the phospholipid essential fatty acid distribution described in literature were also present in the patients we studied. They have significantly lower docosahexaenoic acid (22:6n-3) and linoleic acid (18:2n-6) and higher dihomogammalinolenic acid (18:3n-6), oleic acid (18:1n-9) and Mead acid (20:3n-9), the latter being a sign of essential fatty acid deficiency. This resulted in increased ratios of arachidonic acid/docosahexaenoic acid, Mead acid/arachidonic acid and oleic acid/linoleic acid. There was no relation of serum fatty acid composition with nutritional status, caloric intake, pancreatic function, gender, pulmonary function, pseudomonas colonisation or the presence of diabetes mellitus (chapter 4.2). When patients were divided into 2 groups according to genotype (group A: mutation class I, II, or III, group B: mutation class IV, V) the abnormalities were more pronounced in the “severe” genotypes. However, there was no significant difference between the groups for age, pulmonary function, nutritional status and vitamin E concentration. Cystic fibrosis patients can have some concomitant problems known to influence fatty acid composition such as diabetes mellitus and liver disease. Therefore a study was performed to evaluate whether the presence of cystic fibrosis related liver disease influenced the fatty acid status. In the presence of cystic fibrosis related liver disease there is an even more pronounced decrease in docosahexaenoic acid (22:6n-3) and an increase of docosatetraenoic acid (22:4n-6) compared to genotype controls without cystic fibrosis related liver disease. Since in cystic fibrosis transmembrane conductance regulator-/- mice docosahexaenoic acid was capable of reversing the cystic fibrosis symptoms, we performed a double blind placebo controlled study to evaluate the effect of docosahexaenoic acid in humans (chapter 4.3). To eliminate the disturbances due to genotype and liver disease we included only ΔF508 homozygous patients without liver disease. The treatment group had a significant increase in docosahexaenoic acid and eicosapentaenoic acid concentrations. A concomitant decrease of dihomogammalinolenic acid, arachidonic acid, 22:5n-6 and Mead acid was observed. There was no difference between controls and treatment group for weight for height %, caloric intake, forced expiratory volume in 1 second1%, forced vital capacity % at the start and after 1 year of supplements. The laboratory results showed no changes in vitamin E level, liver enzymes, albumin, sedimentation and IgG concentration. Although docosahexaenoic acid -rich oil shifted the serum phospholipid fatty acids to a less pro-inflammatory profile no conclusive clinical improvement could be observed so far."]},{"key":"dc:format","label":"Dc Format","values":["application/msword"]},{"key":"dc:title","label":"Title","values":["Zinc and essential fatty acid status and supplementation in cystic fibrosis patients"]}]}],"canonical_facts":{"dc:contributor":["Robberecht, E"],"dc:creator":["Van Biervliet, Stephanie"],"dc:date":["2008"],"dc:description":["Cystic fibrosis is a multi-organ disease in which maintaining a good nutritional status is crucial for its outcome. An overview of the disease is given in chapter 1. In cystic fibrosis, the maldigestion is a factor not only influencing the nutrient but also the micronutrient absorption. The obvious deficiencies in fat soluble vitamins led to a standard monitored supplement for pancreatic insufficient patients. There are other micronutrients which could theoretically influence the course of the disease, where the benefit for the patient is not yet known. Zinc and essential fatty acids mutually influence each other and are important in inflammation and immunity. Chapter 2 summarises the research objectives. In chapter 3 we focus on the zinc status, first by means of the serum zinc concentration. The normal serum zinc concentration in our region is significantly lower than reported in literature (chapter 3.2). This makes our population more sensible for zinc deficiency, especially when malabsorption syndromes are present. Further on, an age dependency was observed with significantly lower serum zinc concentrations in infants. Serum zinc concentrations did not significantly change after the age of 4 years. There was no influence of the type of infant feeding. There is an association of zinc with vitamin A. Since in literature a zinc deficiency was observed in cystic fibrosis infants detected with neonatal cystic fibrosis screening, we performed a study where serum zinc was evaluated at diagnosis and one year later (chapter 3.3). The serum zinc concentration at diagnosis was very low indeed and increased significantly without zinc supplements after 1 year of standard cystic fibrosis treatment. However, there were no significant differences when compared to age matched healthy controls. There was a significant association of zinc with vitamin A and E. In older cystic fibrosis children the same low serum zinc concentrations were observed as in the healthy local control group. There is an association of serum zinc with serum albumin and serum vitamin A. The association with albumin is not surprising since 70% of serum zinc is bound to albumin. Further, multiple aspects of the vitamin A status as absorption, metabolism, release, transport and utilisation are influenced by zinc. There was no relation with nutritional status, growth, inflammation parameters or colonisation with Pseudomonas Aeruginosa. However, a positive association with the forced vital capacity was observed. Serum zinc lacks sensitivity and specificity for the evaluation of the zinc status since only 0.2% circulates in plasma associated with albumin and α-2 macroglobulin. It is kept within a narrow range and only prolonged zinc deficiency will reflect in the serum zinc concentration. Another more complex way to evaluate zinc-deficiency is to look at zinc dependent enzymes. However, there is no consensus in literature on which enzymes are the best in reflecting the zinc status. The earlier studies we performed on intestinal biopsies of newly diagnosed cystic fibrosis patients showed a decreased intestinal alkaline phosphatase activity (chapter 3.4). This was the case in the normal and the damaged mucosa. Alkaline phosphatase is a known metalloprotein, containing zinc or magnesium necessary for the catalytic function. Furthermore intestinal alkaline phosphatase gene expression is activated by a zinc binding protein. Finally, the enzyme has shown to be very sensitive for oxygen free radicals. Zinc deficiency will therefore result in a decreased intestinal alkaline phosphatase activity due to absence of zinc in its catalytic site and increased inactivation as a result of increased presence of oxygen free radicals but also in a decreased concentration as a consequence of the decreased transcription. Chapter 4 deals with the essential fatty acid status of cystic fibrosis patients. The disturbances of the phospholipid essential fatty acid distribution described in literature were also present in the patients we studied. They have significantly lower docosahexaenoic acid (22:6n-3) and linoleic acid (18:2n-6) and higher dihomogammalinolenic acid (18:3n-6), oleic acid (18:1n-9) and Mead acid (20:3n-9), the latter being a sign of essential fatty acid deficiency. This resulted in increased ratios of arachidonic acid/docosahexaenoic acid, Mead acid/arachidonic acid and oleic acid/linoleic acid. There was no relation of serum fatty acid composition with nutritional status, caloric intake, pancreatic function, gender, pulmonary function, pseudomonas colonisation or the presence of diabetes mellitus (chapter 4.2). When patients were divided into 2 groups according to genotype (group A: mutation class I, II, or III, group B: mutation class IV, V) the abnormalities were more pronounced in the “severe” genotypes. However, there was no significant difference between the groups for age, pulmonary function, nutritional status and vitamin E concentration. Cystic fibrosis patients can have some concomitant problems known to influence fatty acid composition such as diabetes mellitus and liver disease. Therefore a study was performed to evaluate whether the presence of cystic fibrosis related liver disease influenced the fatty acid status. In the presence of cystic fibrosis related liver disease there is an even more pronounced decrease in docosahexaenoic acid (22:6n-3) and an increase of docosatetraenoic acid (22:4n-6) compared to genotype controls without cystic fibrosis related liver disease. Since in cystic fibrosis transmembrane conductance regulator-/- mice docosahexaenoic acid was capable of reversing the cystic fibrosis symptoms, we performed a double blind placebo controlled study to evaluate the effect of docosahexaenoic acid in humans (chapter 4.3). To eliminate the disturbances due to genotype and liver disease we included only ΔF508 homozygous patients without liver disease. The treatment group had a significant increase in docosahexaenoic acid and eicosapentaenoic acid concentrations. A concomitant decrease of dihomogammalinolenic acid, arachidonic acid, 22:5n-6 and Mead acid was observed. There was no difference between controls and treatment group for weight for height %, caloric intake, forced expiratory volume in 1 second1%, forced vital capacity % at the start and after 1 year of supplements. The laboratory results showed no changes in vitamin E level, liver enzymes, albumin, sedimentation and IgG concentration. Although docosahexaenoic acid -rich oil shifted the serum phospholipid fatty acids to a less pro-inflammatory profile no conclusive clinical improvement could be observed so far."],"dc:format":["application/msword"],"dc:identifier":["https://biblio.ugent.be/publication/468659","http://hdl.handle.net/1854/LU-468659","http://doi.org/1854/11738","https://biblio.ugent.be/publication/468659/file/4334729"],"dc:language":["und"],"dc:rights":["info:eu-repo/semantics/openAccess"],"dc:title":["Zinc and essential fatty acid status and supplementation in cystic fibrosis patients"],"dc:type":["dissertation","info:eu-repo/semantics/doctoralThesis","info:eu-repo/semantics/publishedVersion"]},"updated_at":"2026-07-24T02:22:55Z"}