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Suplementos de ácidos grasos omega‐3 para la fibrosis quística

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Referencias

Referencias de los estudios incluidos en esta revisión

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Hanssens 2016 {published and unpublished data}

Hanssens L, Thiebault I, Lefevre N, Malfroot A, Gaspar V, Knoop C, et al. Benefits of long‐term supplementation with omega‐3 polyunsaturated fatty acids in cystic fibrosis. Journal of Cystic Fibrosis: Official Journal of the European Cystic Fibrosis Society. 2015; Vol. 14 Suppl 1:S52. [Abstract no.: ePS05.9; CENTRAL: 1081482; CFGD Register: GN247a; CRS: 5500135000001304]CENTRAL
Hanssens L, Thiebaut I, Lefevre N, Malfroot A, Knoop C, Duchateau J, et al. The clinical benefits of long‐term supplementation with omega‐3 fatty acids in cystic fibrosis patients ‐ a pilot study. Prostaglandins, Leukotrienes, and Essential Fatty Acids 2016;108:45‐50. [CFGD Register: GN247b; DOI: 10.1016/j.plefa.2016.03.014]CENTRAL

Henderson 1994 {published data only}

Henderson WR. Omega‐3 supplementation in cystic fibrosis. Pediatric Pulmonology 1992;14(S8):S21.2. [CFGD Register: GN45a]CENTRAL
Henderson WR, Astley SJ, McCready MM, Kushmerick P, Becker JU, Ramsey B. Absorption of omega (w) ‐3 fatty acids in CF patients. Pediatric Pulmonology 1992;14(S8):311. [CFGD Register: GN45b]CENTRAL
Henderson WR, Astley SJ, McCready MT, Kushmerick P, Casey S, Becker JW, et al. Oral absorption of omega‐3 fatty acids in patients with cystic fibrosis who have pancreatic sufficiency and in healthy control subjects. Journal of Pediatrics 1994;124(3):400‐8. [CFGD Register: GN45c]CENTRAL

Keen 2010 {published data only}

Keen C, Olin A, Eriksson S, Ekman A, Lindblad A, Basu S, et al. Supplementation with fatty acids influences the airway nitric oxide and inflammatory markers in patients with cystic fibrosis. Journal of Pediatric Gastroenterology and Nutrition 2010;50(5):537‐44. [CFGD Register: GN129b]CENTRAL
Keen C, Olin A, Eriksson S, Lindblad A, Ekman A, Basu S, et al. Supplementation with polyunsaturated fatty acids influences the inflammatory response and airway nitric oxide in patients with cystic fibrosis. European Respiratory Society Annual Congress. 2008:541s. [CFGD Register: GN129a]CENTRAL

Lawrence 1993 {published data only}

Lawrence R, Sorrell T. Eicosapentaenoic acid in cystic fibrosis: evidence of a pathogenetic role for leukotriene B4. Lancet 1993;342(8869):465‐9. [CFGD Register: GN44a]CENTRAL
Lawrence R, Sorrell T. Modulation of abnormal neutrophil response to leukotriene B4 in the chronic pseudomonal lung infection of cystic fibrosis. Australian and New Zealand Journal of Medicine 1993;23:442. [CFGD Register: GN44b]CENTRAL

Panchaud 2006 {published data only}

Panchaud A, Sauty A, Kernan Y, Decosterd LA, Buclin T, Boulat O, et al. Biological effects of a dietary omega‐3 polyunsaturated fatty acids supplementation in cystic fibrosis patients: A randomised, crossover placebo‐controlled trial. Clinical Nutrition 2006;25(3):418‐27. [CFGD Register: GN109b]CENTRAL
Panchaud A, Sauty A, Kernan Y, Decosterd LA, Buclin T, Roule M. Dietary Supplementation with omega 3 in cystic fibrosis (CF) patients. Journal of Cystic Fibrosis 2005;4 Supplement 1:S88. [CFGD Register: GN109a]CENTRAL

Referencias de los estudios excluidos de esta revisión

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Alicandro 2013 {published data only (unpublished sought but not used)}

Alicandro G, Faelli N, Gagliardini R, Santini B, Magazzu G, Biffi A, et al. A randomized placebo‐controlled study on high‐dose oral algal docosahexaenoic acid supplementation in children with cystic fibrosis. Prostaglandins, Leukotrienes and Essential Fatty Acids 2013;88(2):163‐9. [CFGD Register: GN118d; ]CENTRAL
Alicandro G, Gagliardini R, Rise P, Santini B, Biffi A, Tirelli S, et al. Oral DHA supplementation in children with CF: a randomized placebo‐controlled study. Pediatric Pulmonology 2011;46 Suppl 34:394. [Abstract no.: 499; CFGD Register: GN118c; ]CENTRAL
Alicandro G, Gagliardini R, Santini B, Rise P, Biffi A, Tirelli AS, et al. Oral DHA supplementation in children with cystic fibrosis: a randomized placebo‐controlled study. Journal of Cystic Fibrosis 2011;10 Suppl 1:S74. [Abstract no.: 290; CFGD Register: GN118b; ]CENTRAL
Colombo C, Dacco V, Santini B, Garliardini R, Loi S, Casartelli M, et al. DHA supplementation in children affected by cystic fibrosis: an Italian, multicentre clinical trial. Pediatric Pulmonology 2008;43 Suppl 31:427. [CFGD Register: GN118a]CENTRAL

Christophe 1992 {published data only}

Christophe A, Robberecht E, Franckx H. Effects of two different dietary supplements on eicosanoid precursor fatty acids in cystic fibrosis. 11th International Cystic Fibrosis Congress, Dublin, Ireland. 1992:MP76. [CFGD Register: GN54]CENTRAL

EUCTR2006‐004155038‐BE {published data only}

EUCTR2006‐004155‐38‐BE. Biochemical effects of a long‐term supplementation with omega‐3 polyunsaturated fatty acids in cystic fibrosis ‐ omega 3 study. apps.who.int/trialsearch/Trial2.aspx?TrialID=EUCTR2006‐004155‐38‐BE (first received 23 September 2008). CENTRAL

Katz 1996 {published data only}

Katz DP, Manner T, Furst P, Askanazi J. The use of an intravenous fish oil emulsion enriched with omega‐3 fatty acids in patients with cystic fibrosis. Nutrition 1996;12(5):334‐9. [CFGD Register: GN66a]CENTRAL
Manner T, Guida L, Katz DP, Askanazi J, Schlotzer E, Wiesse S. Parenteral fish oil administration in patients with cystic fibrosis. Clinical Nutrition 1992;11(11):40. [CFGD Register: GN66c]CENTRAL
Manner T, Katz DP, Askanazi J, Schlotzer E, Furst P. Parenteral fish oil administration in patients with cystic fibrosis. 17th Clinical Congress of ASPEN (American Society for Parenteral and Enteral Nutrition). 1993:440. [CFGD Register: GN66b]CENTRAL

Koletzko 2000 {published data only}

Koletzko B, Tuxen‐Mengedoht M, Muller I, Demmelmair H, Stern M, Steffan J. Polyunsaturated fatty acids improve outcome of cystic fibrosis patients. 13th International Cystic Fibrosis Conference; 2000 June 4‐8; Stockholm. 2000:78. [CFGD Register: GN65b]CENTRAL
Tuxen‐Mengedoht M, Koletzko B, Demmelmair H, Knapp V, Stern M. Fish oil therapy in cystic fibrosis (CF): A randomised clinical trial. Clinical Nutrition 1999;18(Suppl 1):54. [CFGD Register: GN65a]CENTRAL
Tuxen‐Mengedoht M, Koletzko B, Muller I, Demmelmair H, Knapp V, Stern M, et al. Fish‐oil therapy in mucoviscidosis: A randomised double‐blind study [Fischol‐Therapie bei Mukiviszidose: Eine randomisierte Doppelblindstudie]. Monatsschrift Fur Kinderheilkunde 1999;147(Suppl 2):107. [CFGD Register: GN65c]CENTRAL

Kurlandsky 1994 {published data only}

Kurlandsky LE, Bennink MR, Webb PM, Ulrich PJ, Baer LJ. The absorption and effect of dietary supplementation with omega‐3 fatty acids on serum leukotriene B4 in patients with cystic fibrosis. Pediatric Pulmonology 1994;18(4):211‐7. [CFGD Register: GN46]CENTRAL

Lloyd‐Still 2006 {published data only}

Lloyd‐Still J, Powers C, Hoffman D, Arterburn L, Benisek D, Lester L. Bioavailability and safety of an algal DHA triglyceride in cystic fibrosis. Pediatric Research 2001;49(4 Suppl):455a. [CFGD Register: GN92d]CENTRAL
Lloyd‐Still J, Powers C, Hoffman D, Boyd‐Trull K, Lester L, Benisek D, et al. A randomised controlled study examining the bioavailability and safety of an algal docosahexaenoic acid (DHA) triacylglycerol in cystic fibrosis patients. Pediatric Pulmonology 2004;38(Suppl 27):331. [CFGD Register: GN92c]CENTRAL
Lloyd‐Still J, Powers C, Hoffman D, Boyd‐Trull K, Lester L, Benisek D, et al. Bioavailability and safety of a high dose of docosahexaenoic acid triacylglycerol of algal origin in cystic fibrosis patients: a randomised controlled study. Nutrition 2006;22(1):36‐46. [CFGD Register: GN92e]CENTRAL
Lloyd‐Still J, Powers C, Hoffman D, Boyd‐trull K, Arterburn L, Benisek D, et al. Blood and tissue essential fatty acids after docosahexaenoic acid supplementation in cystic fibrosis. Pediatric Pulmonology 2001;32(Suppl 22):263. [CFGD Register: GN92b]CENTRAL
Powers CA, Lloyd‐Still J, Hoffman D, Arteburn L, Benisek D, Lester L. Lipid soluble antioxidant status during supplementation with algal docosahexaenoic acid triglyceride in CF. Abstracts of the 24th European Cystic Fibrosis Conference. 2001:P133. [CFGD Register: GN92a]CENTRAL

NCT02518672 {published data only}

NCT02518672. Pro‐resolving effect of MAG‐DHA in cystic fibrosis (PREMDIC). clinicaltrials.gov/ct2/show/NCT02518672 (first received 10 August 2015). CENTRAL

NCT02646995 {published data only}

NCT02646995. Lipid formulation to increase the bioavailabilty of fatty acids in cystic fibrosis (CF) patients. clinicaltrials.gov/ct2/show/NCT02646995 (first received 6 January 2016). CENTRAL

NCT02690857 {published data only}

NCT02690857. Study of docosahexanoic acid in patients with cystic fibrosis (CF) (OMEGAMUCO). clinicaltrials.gov/ct2/show/NCT02690857 (first received 24 Feb 2016). CENTRAL

NCT03045198 {published data only}

NCT03045198. Effect of azithromycin on fatty acids in CF. clinicaltrials.gov/ct2/show/NCT03045198 (first received 07 February 2017). CENTRAL

O'Connor 2016 {published data only}

O'Connor MG, Thomsen K, Brown RF, Laposata M, Seegmiller A. Elevated prostaglandin e metabolites and abnormal plasma fatty acids at baseline in pediatric cystic fibrosis patients: a pilot study. Prostaglandins, Leukotrienes, and Essential Fatty Acids 2016;113:46‐9. [CFGD Register: GN250b]CENTRAL
O'connor MG, Thomsen K, Brown RF, Laposata M, Seegmiller AC. DHA supplementation in pediatric CF patients: a randomized, double‐blind clinical trial.. Pediatric Pulmonology. 2015; Vol. Suppl 34:401. [Abstract no.: 582; CFGD Register: GN250a]CENTRAL

O'Sullivan 2011 {published data only}

O'Sullivan B, Baker D, Borowitz D, Comeau A, Cleveland R, Freedman S. The effect of formula fortified with docosahexaenoic acid (DHA) on infants with CF. Pediatric Pulmonology 2011;46 Suppl 34:401. [Abstract no.: 519; CFGD Register: GN229; ]CENTRAL

Pastor 2019 {published data only}

Pastor O, Guzman‐Lafuente P, Serna J, Munoz‐Hernandez M, Lopez Neyra A, Garcia‐Rozas P, et al. A comprehensive evaluation of omega‐3 fatty acid supplementation in cystic fibrosis patients using lipidomics. Journal of Nutritional Biochemistry 2019;63:197‐205. [CFGD Register: GN277; DOI: 10.1016/j.jnutbio.2018.09.026]CENTRAL

Romano 1997 {published data only}

Romano L, Gandino M, Fiore P, Shepherd D, Casciaro R, Coccia C, et al. Study on feasibility and results of midterm dietary supplementation in omega‐3 fatty acids. 21st European Cystic Fibrosis Conference; 1997; Davos. 1997:167. [CFGD Register: GN67]CENTRAL

Starling 1988 {published data only}

Starling MB, Elliot RB. EPA and cystic fibrosis. Excerpta Medica, Asia Pacific Congress Series. 10th International Cystic Fibrosis Congress. 1988:74. [CFGD Register: GN59]CENTRAL

van Biervliet 2008 {published data only}

Van Biervliet S, Devos M, Delhaye J, Van Biervliet J, Robberecht E, Christophe A. Oral DHA supplementation in F508 homozygous cystic fibrosis patients. Prostaglandins, Leukotrienes and Essential Fatty Acids 2008;78(2):109‐15. [CFGD Register: GN116]CENTRAL

Vericel 2019 {published data only}

Vericel E, Mazur S, Colas R, Delaup V, Calzada C, Reix P, et al. Moderate intake of docosahexaenoic acid raises plasma and platelet vitamin E. Prostaglandins, Leukotrienes, and Essential Fatty Acids 2016;115:41‐7. [CFGD Register: GN264; DOI: 10.1016/j.plefa.2016.10.008]CENTRAL

Benabdeslam 1998

Benabdeslam H, Garcia I, Bellon G, Gilly R, Revol A. Biochemical assessment of the nutritional status of cystic fibrosis patients treated with pancreatic enzyme extracts. American Journal of Human Nutrition 1998;67(5):912‐8.

CF Trust 2006

Littlewood J, Green M, Stannard W. Finding Out. CF Trust Factsheet2006.

CF Trust 2015

UK CF Trust. CF Trust Factsheet. Steroid treatment in cystic fibrosis. www.cysticfibrosis.org.uk/˜/media/documents/life‐with‐cf/publications/factsheets/factsheet‐steroid‐treatment‐2016.ashx (accessed 10 January 2020).

CF Trust 2016

UK CF Trust. CF Trust Consensus Documents: Nutritional Management of Cystic Fibrosis. September 2016. www.cysticfibrosis.org.uk/˜/media/documents/the‐work‐we‐do/care/consensus‐documents‐with‐old‐address/nutritional‐management‐of‐cystic‐fibrosis‐sep‐16.ashx?la=en (accessed 10 January 2020).

Cheng 1999

Cheng K, Ashby D, Smyth R. Oral steroids for cystic fibrosis. Cochrane Database of Systematic Reviews 1999, Issue 4. [DOI: 10.1002/14651858.CD000407]

Corcoran 1937

Corcoran AC, Rabinowitch IM. A study of the blood lipids and blood proteins in Canadian Eastern Arctic Eskimos. Biochemistry Journal 1937;31:343‐8.

Corey 1998

Corey M, McLaughlin FJ, Williams M, Levison H. A comparison of survival, growth and pulmonary function in patients with cystic fibrosis in Boston and Toronto. Journal of Clinical Epidemiology 1998;41(6):583‐91.

Dodge 1988

Dodge JA. Nutritional requirement in cystic fibrosis: a review. Journal of Pediatric Gastroenterology Nutrition 1988;7(Suppl 1):S8‐11.

Elbourne 2002

Elbourne DR, Altman DG, Higgins JP, Curtin F, Worthington HV, Vail A. Meta‐analyses involving cross‐over trials: methodological issues. International Journal of Epidemiology 2002;31(1):140‐9.

Freedman 1999

Freedman SD, Alvarez JG. Pathogenesis of pancreatic disease in cystic fibrosis. Pediatric Pulmonology 1999;Suppl 19:129.

Gaskin 1982

Gaskin K, Gurwitz D, Durie P, Corey M, Levison H, Forstner G. Improved respiratory prognosis in patients with normal fat absorption. Journal of Pediatrics 1982;100(6):857‐62.

Gaszo 1989

Gazso A, Kaliman J, Horrobin DF, Sinzinger H. Effects of omega‐3 fatty acids on the prostaglandin system in healthy probands. Wiener Klinische Wochenschrift 1989;101(8):283‐8.

Higgins 2003

Higgins JP, Thompson SG, Deeks JJ, Altman DG. Measuring inconsistency in meta‐analyses. BMJ 2003;327(7414):557‐60.

Higgins 2011

Higgins JP, Altman DG, Sterne JA on behalf of the Cochrane Statistical Methods Group and the Cochrane Bias Methods Group. Chapter 8: Assessing risk of bias in included studies. In: Higgins JP, Green S, editor(s). Cochrane Handbook for Systematic Reviews of Interventions Version 5.1.0 (updated March 2011). The Cochrane Collaboration, 2011. Available from handbook.cochrane.org.

Hunt 1985

Hunt B, Geddes DM. Newly diagnosed cystic fibrosis in middle and later life. Thorax 1985;40(1):23‐6.

Imrie 1975

Imrie J, Fagan D, Sturgess J. Quantitative evaluation of the development of the exocrine pancreas in cystic fibrosis and controlled subjects. American Journal Pathology 1975;95(3):697‐708.

Jüni 2001

Jüni P, Douglas G, Altman G, Egger M. Assessing the quality of controlled clinical trials. BMJ 2001;323(7303):42‐6.

Konstan 1996

Konstan MW. Treatment of airway inflammation in cystic fibrosis. Current Opinion in Pulmonary Medicine 1996;2(6):452‐6.

Lands 2007

Lands LC, Stanojevic S. Oral non‐steroidal anti‐inflammatory drug therapy for lung disease in cystic fibrosis. Cochrane Database of Systematic Reviews 2007, Issue 4. [DOI: 10.1002/14651858.CD001505.pub2]

Lloyd‐Still 1996

Lloyd‐Still JD, Bibus DM, Powers CA, Johnson SB, Holman RT. Essential fatty acid deficiency and predisposition to lung disease in cystic fibrosis. Acta Paediatrica 1996;85(12):1426‐32.

Osterud 1995

Osterud B, Elvevoll E, Barstad H, Brox J, Halvorsen H, Lia K, et al. Effect of marine oils supplementation on coagulation and cellular activation in whole blood. Lipids 1995;30(12):1111‐8.

Schünemann 2011a

Schünemann HJ, Oxman AD, Vist GE, Higgins JPT, Deeks JJ, Glasziou P, Guyatt GH on behalf of the Cochrane Applicability and Recommendations Methods Group. Chapter 12: Interpreting results and drawing conclusions. In: Higgins JP, Green S, editor(s). Cochrane Handbook for Systematic Reviews of Interventions Version 5.1.0 (updated March 2011). The Cochrane Collaboration, 2011. Available from handbook.cochrane.org.

Shwachman 1958

Shwachman H, Kulczycki LL. Long term study of 105 patients with cystic fibrosis. American Journal of Diseases of Children 1958;96(1):6‐10.

UK CF Registry 2018

UK CF Trust. UK Cystic Fibrosis Registry Annual Data Report 2018. www.cysticfibrosis.org.uk2019.

Wilmott 2000

Wilmott RW, Khurana‐Hershui G, Stark JM. Current concepts on pulmonary host defence mechanisms in children. Current Opinion in Pediatrics 2000;12(3):187‐93.

Referencias de otras versiones publicadas de esta revisión

Ir a:

Beckles‐Willson 2002

Beckles‐Willson NNR, Elliott T, Everard MML. Omega‐3 fatty acids (from fish oils) for cystic fibrosis. Cochrane Database of Systematic Reviews 2002, Issue 3. [DOI: 10.1002/14651858.CD002201.pub2]

Oliver 2010

Oliver C, Everard M, N'Diaye T. Omega‐3 fatty acids (from fish oils) for cystic fibrosis. Cochrane Database of Systematic Reviews 2010, Issue 1. [DOI: 10.1002/14651858.CD002201.pub2]

Oliver 2011

Oliver C, Jahnke N. Omega‐3 fatty acids for cystic fibrosis. Cochrane Database of Systematic Reviews 2011, Issue 8. [DOI: 10.1002/14651858.CD002201.pub3]

Oliver 2013

Oliver C, Watson H. Omega‐3 fatty acids for cystic fibrosis. Cochrane Database of Systematic Reviews 2013, Issue 11. [DOI: 10.1002/14651858.CD002201.pub4]

Oliver 2016

Oliver C, Watson H. Omega‐3 fatty acids for cystic fibrosis. Cochrane Database of Systematic Reviews 2016, Issue 1. [DOI: 10.1002/14651858.CD002201.pub5]

Characteristics of studies

Characteristics of included studies [ordered by study ID]

Ir a:

Hanssens 2016

Methods

RCT (double‐blind placebo‐controlled).

Design: parallel.

Duration: 12 months.

Location: multicentre (2 centres) in Belgium.

Participants

15 people with CF, homozygous Del508, PI and over 5 years of age.

Age, mean: intervention group 14 years (5.2 ‐ 26.0 years); placebo group 17.5 years (4.6 ‐ 30.4 years).

Gender (M:F): intervention group (4:3); placebo group (7:1).

Participants all established on azithromycin treatment for at least 3 months.

Interventions

Intervention group (n = 7): oral supplement of omega‐3, 60 mg/kg.

Control group (n = 8): identical placebo.

Outcomes

Clinical and nutritional status; lung function, changes in erythrocyte levels of EPA and DHA.

Notes

N = 13 completed, 6 intervention, 7 placebo. Supplement well‐tolerated.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

Low risk

Block stratification, pre‐defined block list, stratified by pharmacist. 4‐digit sequence generation to individualise participants.

Allocation concealment (selection bias)

Unclear risk

No mention of concealment allocation. Stratified by participant weight which could enable recruiter to identify allocation.

Blinding (performance bias and detection bias)
All outcomes

Unclear risk

Identical capsules, blinded to person responsible for care, participant and outcome assessor, no description of placebo capsules and 1 dropout was due to fishy taste of capsules.

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Attrition rate very simply, clearly explained and justified. 15 participants were recruited, 13 participants completed the study. Study was not analysed as ITT, authors stated they would only analyse ITT if participant attended for first 3‐month follow‐up visit. The 2 participants dropped out prior to this 3‐month follow‐up.

Selective reporting (reporting bias)

High risk

Outcomes both primary and secondary were modified from protocol to study. Authors acknowledged change from inflammatory biomarkers as primary outcome due to lack of facilities to test the outcome. We have concern over conclusions made regarding impact of n3 supplementation on antibiotic duration and frequency, (clinical status) as this outcome was not explicitly defined at the study protocol stage.

The significant decrease in number of respiratory exacerbations is only reported in the supplement group with data not provided for the placebo group.

Other bias

Low risk

No additional bias identified.
Henderson 1994

Methods

RCT.

Design: parallel with 4 arms.

Duration: 6‐weeks.

Location: single centre in the USA (Children's Hospital Medical Center, Seattle).

Participants

12 children and young adults diagnosed with CF on genotype or sweat test, pancreatic insufficiency and able to complete the spirometric tests.

Age, mean (SD): age 12.2 (5.4) years.

Gender: 7 males, 5 females.

Plasma vitamin A and E levels within the normal range.

13 gender and age‐matched people without CF (mean (SD) age 13.4 (6.3) years), 7 males, 6 females.

Interventions

Intervention group: 8 x 1g capsules fish oil (4 capsules twice daily) containing 3.19 g EPA and 2.21 g DHA.

Control: olive oil placebo capsules flavoured to obtain a slight fish taste.

Outcomes

Outcomes included in this review:
number of people experiencing adverse events;
number of deaths;
changes in haematological indices;
changes in plasma and erythrocyte levels of EPA and DHA and EPA/AA ratio.

Notes

Significantly lower plasma n‐6 fatty acids (linoleic acid and AA) noted at baseline in participants with CF compared with the group who did not have CF.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

Low risk

Randomised using a stratified randomised block design.

Allocation concealment (selection bias)

Unclear risk

Not discussed in paper.

Blinding (performance bias and detection bias)
All outcomes

Low risk

Described as double blind ‐ while the capsules were not described as identical, it was stated that the placebo olive oil capsules were flavoured to obtain a slight fish taste which we agreed would be sufficient to blind participants.

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Withdrawals from the study were discussed with explanations (20 out of 25 randomised participants completed the study). Study included all participants in the data analysis, which was performed according to the ITT principle.

Selective reporting (reporting bias)

Unclear risk

Protocol not available for comparison, so unable to definitely eliminate selective reporting.

Other bias

Low risk

No additional bias identified.
Keen 2010

Methods

RCT.

Design: parallel.

Duration: 3 months.

Location: single centre in Sweden (west Sweden CF Centre).

Participants

45 children and adults with "severe" CF mutations randomised; 43 commenced study and 35 participants completed the study. 8 participants discontinued the study and the inclusion parameters of these participants did not differ from those who completed the study.

Age, range: 7 to 41 years.

Gender: 17 males, 18 females.

Disease status: 20 participants were chronically infected with Pseudomonas aeruginosa.

Interventions

Intervention group A: 50 mg/kg per day fatty acid blend capsules containing predominantly EPA and DHA.

Intervention group B: placebo capsules containing predominantly saturated fatty acids.

Intervention group C: 50 mg/kg per day fatty acid blend capsules containing a high proportion of linoleic acid and AA.

Participants increased their pancreatic enzymes by 10% to 20% to maintain normal stools.

Outcomes

Outcomes included in this review:
changes in serum phospholipid essential fatty acid content;
changes in inflammatory markers;
adverse effects;
BMI and weight;
lung function;
medical treatment.

Notes

Actual dose of EPA and DHA administered not described.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

Low risk

Randomised using random number generator.

Allocation concealment (selection bias)

Unclear risk

Not discussed in paper.

Blinding (performance bias and detection bias)
All outcomes

Unclear risk

Described as double‐blind; treatment was assumed to be administered as identical capsules; however, 2 participants complained of fish smell in group A.

Incomplete outcome data (attrition bias)
All outcomes

Unclear risk

45 participants were initially randomised, but 2 were excluded due to acute exacerbations and therefore did not enter the study. Withdrawls from study were described: 35 participants completed the study; 8 discontinued because of low compliance (n = 4), stomach pains (n = 2) and weight gain (n = 2). Study did not include all participants in the data analysis, therefore, data were not analysed as ITT.

Selective reporting (reporting bias)

Unclear risk

Protocol not available for comparison, so unable to definitely eliminate selective reporting.

Other bias

High risk

The lack of information on dosage is a potential risk of bias.
Lawrence 1993

Methods

RCT.

Design: cross‐over study planned. However, significant carry‐over effect of treatment noted at end of study, therefore analysis restricted to the first 6‐week treatment period.

Duration: 6 weeks.

Location: single centre in Australia (Sydney).

Participants

19 adolescents and adults diagnosed with CF on genotype, sweat test, or clinically.

Age, median (range): 17 years (12 years ‐ 26 years).

Gender: 11 males, 5 females.
3 participants excluded due to requiring a course of corticosteroids for asthma attacks.
Disease status: recruited within 4 weeks of hospitalisation for acute respiratory infection and judged to be in optimum condition for disease stage. All were Pseudomonas aeruginosa colonised and produced at least 5 mL sputum daily.

Interventions

Intervention group: capsules with 2.7 g EPA daily.

Control group: identical olive oil placebo capsules.

Outcomes

Outcomes included in this review:
number of people experiencing adverse events;
number of deaths;
changes in haematological and growth indices;
changes in lung function;
changes in in vitro neutrophil chemotaxis.

Notes

Initial randomisation gave groups with comparable baseline characteristics except for age. The treatment group also had significantly greater weight, peripheral blood leucocyte and neutrophil counts.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

Unclear risk

Did not state the randomisation technique.

Allocation concealment (selection bias)

Unclear risk

No details were provided in the primary paper.

Blinding (performance bias and detection bias)
All outcomes

Low risk

Described as double blind, treatment was administered as 'identical olive oil capsules'.

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Of the 19 participants recruited, 3 participants were excluded from the study before analysis due to corticosteroid treatment during the first treatment period.

Selective reporting (reporting bias)

Unclear risk

Protocol not available for comparison, so unable to definitely eliminate selective reporting.

Other bias

Low risk

No additional bias identified.
Panchaud 2006

Methods

RCT.

Design: cross‐over trial with no washout period.

Duration: 1 year (2 x 6‐month periods).

Location: single centre in Switzerland (Lausanne CF Center).

Participants

17 children and young adults with CF and PI; 1 participant discontinued study after 8 months for personal convenience.

Age, mean (SD): 18 (9) years).

Gender: 10 males, 7 females.

Interventions

Intervention Group: liquid dietary supplement containing PUFA mixture (EPA, DHA, GLA and STA).

Control Group: liquid dietary supplement without PUFA mixture.

Volume of supplementation was determined according to participant's weight; intake ranged from 100 mg ‐ 300 mg DHA. and 200 mg ‐ 600 mg EPA per day.

Outcomes

Outcomes included in this review:
number of people experiencing adverse events;
number of deaths;
changes in peripheral blood neutrophil membrane composition;
in vitro neutrophilic response to inflammatory stimuli;
changes in in vitro neutrophil chemotaxis.

Notes

Relatively low daily dose of EPA and DHA compared to previous clinical trials.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

Unclear risk

Did not state the randomisation technique.

Allocation concealment (selection bias)

Unclear risk

No details were provided in the primary paper.

Blinding (performance bias and detection bias)
All outcomes

Low risk

Described as double blind, placebo treatment was not stated to be identical but it was described as the same liquid dietary supplement as the intervention but without the PUFA mixture.

Incomplete outcome data (attrition bias)
All outcomes

Unclear risk

17 participants were randomised; 16 completed the study and one discontinued after 8 months for personal convenience.
Due to technical reasons, data could not be analysed for several participants' samples at baseline (4 participants), after treatment with omega‐3 supplements (1) and after placebo (2).
High possibility of attrition bias since the analysis of the final cohort differed from the original cohort.

Selective reporting (reporting bias)

Unclear risk

Protocol not available for comparison, so unable to definitely eliminate selective reporting.

Other bias

Low risk

No additional bias identified.

AA: arachidonic acid
BMI: body mass index
CF: cystic fibrosis
DHA: docosahexaenoic acid
EPA: eicosapentaenoic acid
GLA: gamma‐linolenic acid
ITT: intention‐to‐treat
PI: pancreatic insufficient
PUFA: polyunsaturated fatty acids
RCT: randomised controlled trial
SD: standard deviation
STA: stearidonic acid

Characteristics of excluded studies [ordered by study ID]

Ir a:

Study

Reason for exclusion

Alicandro 2013

Omega‐3 supplementation compared with large omega‐6 fatty acid source (germ oil) rather than a neutral placebo that contains relatively little omega‐3 or omega‐6 fatty acid (olive oil).

Christophe 1992

Omega‐3 supplementation compared with large omega‐6 fatty acid source (borache oil) rather than a neutral placebo that contains relatively little omega‐3 or omega‐6 fatty acid (olive oil).

EUCTR2006‐004155038‐BE

No published outcome data available.

Katz 1996

Parenteral (via blood stream), not enteral (oral) supplementation with omega‐3 fatty acids.

Koletzko 2000

Eligibility unclear, attempts made to contact author for further information, but no response received.

Kurlandsky 1994

Omega‐3 supplementation compared with large omega‐6 fatty acid source (sunflower oil) rather than a neutral placebo that contains relatively little omega‐3 or omega‐6 fatty acid (olive oil).

Lloyd‐Still 2006

Omega‐3 supplementation compared with large omega‐6 fatty acid source (corn/soy) rather than a neutral placebo that contains relatively little omega‐3 or omega‐6 fatty acid (olive oil).

NCT02518672

Omega‐3 supplementation with large omega‐6 fatty acid source (sunflower oil) rather than a neutral placebo that contains relatively little omega‐3 or omega‐6 fatty acid (olive oil).

NCT02646995

Omega‐3 supplementation not compared to placebo. Fish oil compared to actively modified lipid.

NCT02690857

Omega‐3 supplementation with large omega‐6 fatty acid source (sunflower oil) rather than a neutral placebo that contains relatively little omega‐3 or omega‐6 fatty acid (olive oil).

NCT03045198

Clinical trial currently still in enrolment by invitation.

O'Connor 2016

Omega‐3 supplementation with large omega‐6 fatty acid source (sunflower oil) rather than a neutral placebo that contains relatively little omega‐3 or omega‐6 fatty acid (olive oil).

O'Sullivan 2011

Eligibility unclear. Attempts made to contact the author for further information , but no response received.

Pastor 2019

Study to identify a suitable approach for monitoring the incorporation of omega‐3 fatty acids in nutritional studies, not a comparison of omega‐3 fatty acids with control.

Romano 1997

Eligibility unclear, attempts made to contact author for further information, but no response received.

Starling 1988

Eligibility unclear, attempts made to contact author for further information, but no response received.

van Biervliet 2008

Omega‐3 supplementation compared with large omega‐6 fatty acid source (sunflower oil) rather than a neutral placebo that contains relatively little omega‐3 or omega‐6 fatty acid (olive oil).

Vericel 2019

Omega‐3 supplementation with large omega‐6 fatty acid source (sunflower oil) rather than a neutral placebo that contains relatively little omega‐3 or omega‐6 fatty acid (olive oil).

Data and analyses

Open in table viewer
Comparison 1. Omega‐3 fatty acids versus placebo

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Adverse events Show forest plot

1

Odds Ratio (M‐H, Fixed, 95% CI)

Totals not selected
Analysis 1.1
Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 1 Adverse events.

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 1 Adverse events.

1.1 Diarrhoea and eructation

1

Odds Ratio (M‐H, Fixed, 95% CI)

0.0 [0.0, 0.0]

2 FEV1 % predicted (post‐treatment) Show forest plot

1

Mean Difference (IV, Fixed, 95% CI)

Totals not selected
Analysis 1.2
Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 2 FEV1 % predicted (post‐treatment).

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 2 FEV1 % predicted (post‐treatment).

2.1 At 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

3 FVC % predicted (post treatment) Show forest plot

1

Mean Difference (IV, Fixed, 95% CI)

Totals not selected
Analysis 1.3
Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 3 FVC % predicted (post treatment).

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 3 FVC % predicted (post treatment).

3.1 At 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

4 BMI (SD score) (post treatment) Show forest plot

1

Mean Difference (IV, Fixed, 95% CI)

Totals not selected
Analysis 1.4
Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 4 BMI (SD score) (post treatment).

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 4 BMI (SD score) (post treatment).

4.1 At 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

5 EPA and DHA % content of neutrophil membrane (post treatment) Show forest plot

1

Mean Difference (IV, Fixed, 95% CI)

Totals not selected
Analysis 1.5
Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 5 EPA and DHA % content of neutrophil membrane (post treatment).

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 5 EPA and DHA % content of neutrophil membrane (post treatment).

5.1 EPA at 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

5.2 DHA at 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

6 Leukotriene B4 to leukotriene B5 ratio (post treatment) Show forest plot

1

Mean Difference (IV, Fixed, 95% CI)

Totals not selected
Analysis 1.6
Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 6 Leukotriene B4 to leukotriene B5 ratio (post treatment).

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 6 Leukotriene B4 to leukotriene B5 ratio (post treatment).

6.1 At 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

7 EPA and DHA content of serum phospholipids (change from baseline) Show forest plot

1

Mean Difference (IV, Fixed, 95% CI)

Totals not selected
Analysis 1.7
Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 7 EPA and DHA content of serum phospholipids (change from baseline).

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 7 EPA and DHA content of serum phospholipids (change from baseline).

7.1 EPA At 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

7.2 DHA at 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

8 N6/N3 ratio content of serum phospholipids (change from baseline) Show forest plot

1

Mean Difference (IV, Fixed, 95% CI)

Totals not selected
Analysis 1.8
Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 8 N6/N3 ratio content of serum phospholipids (change from baseline).

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 8 N6/N3 ratio content of serum phospholipids (change from baseline).

8.1 At 3 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

Study flow (PRISMA) diagram
Figuras y tablas -
Figure 1

Study flow (PRISMA) diagram

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Risk of bias summary: review authors' judgements about each risk of bias item for each included study.
Figuras y tablas -
Figure 2

Risk of bias summary: review authors' judgements about each risk of bias item for each included study.

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Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 1 Adverse events.
Figuras y tablas -
Analysis 1.1

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 1 Adverse events.

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Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 2 FEV1 % predicted (post‐treatment).
Figuras y tablas -
Analysis 1.2

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 2 FEV1 % predicted (post‐treatment).

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Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 3 FVC % predicted (post treatment).
Figuras y tablas -
Analysis 1.3

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 3 FVC % predicted (post treatment).

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Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 4 BMI (SD score) (post treatment).
Figuras y tablas -
Analysis 1.4

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 4 BMI (SD score) (post treatment).

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Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 5 EPA and DHA % content of neutrophil membrane (post treatment).
Figuras y tablas -
Analysis 1.5

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 5 EPA and DHA % content of neutrophil membrane (post treatment).

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Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 6 Leukotriene B4 to leukotriene B5 ratio (post treatment).
Figuras y tablas -
Analysis 1.6

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 6 Leukotriene B4 to leukotriene B5 ratio (post treatment).

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Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 7 EPA and DHA content of serum phospholipids (change from baseline).
Figuras y tablas -
Analysis 1.7

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 7 EPA and DHA content of serum phospholipids (change from baseline).

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Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 8 N6/N3 ratio content of serum phospholipids (change from baseline).
Figuras y tablas -
Analysis 1.8

Comparison 1 Omega‐3 fatty acids versus placebo, Outcome 8 N6/N3 ratio content of serum phospholipids (change from baseline).

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Summary of findings for the main comparison. Summary of findings: omega‐3 fatty acid supplementation compared with placebo for cystic fibrosis

Omega‐3 fatty acid supplementation compared with placebo for cystic fibrosis

Patient or population: children and adults with cystic fibrosis

Settings: outpatients

Intervention: oral omega‐3 supplementation (EPA or DHA, or both)

Comparison: placebo

Outcomes

Illustrative comparative risks* (95% CI)

Relative effect
(95% CI)

No of Participants
(studies)

Quality of the evidence
(GRADE)

Comments

Assumed risk

Corresponding risk

Placebo

Omega‐3 supplementation

Number of pulmonary exacerbations (median number of exacerbations during the study)

Follow‐up: 12 months

The number of exacerbations in the placebo group was greater than in the omega‐3 group (3.5 versus 1.7 (range 1 ‐ 3)).

N/A

13
(1)

⊕⊝⊝⊝
very lowa,b

The authors only report the number of exacerbations in the supplemented group compared to the 12 months prior to the trial. Extra data was provided by the study authors to allow a between group comparison.

This outcome was not included in the study protocol.

Adverse events: diarrhoea

Follow‐up: 6 weeks

1 study reported drop out due to diarrhoea. 2 out of 7 participants in the fish oil group dropped out and 2 out of 5 participants in the placebo group, OR 0.6 (0.05 to 6.79).

OR 0.6 (0.05 to 6.79)

12
(1)

⊕⊝⊝⊝
very lowc,d

Other adverse events included stomach pains (5/35 participants) but the intervention arm wasn't specified (Keen 2010).

FEV1 % predicted

Follow‐up: 6 months

The mean FEV1 % predicted was 64% in the control group.

The mean FEV1 % predicted in the intervention group was 2% higher (19.1% lower to 23.11% higher)

MD 2.00 (19.11 to 23.11)

17
(1)

⊕⊝⊝⊝
very lowb,e

A further study (n = 16) reported a significant increase from baseline in the EPA group compared to the control group measured in L compared to the placebo group (P = 0.06) (Lawrence 1993).

Two studies reported no difference in FEV1 % predicted or lung function (measurement not stated) between groups (Hanssens 2016; Keen 2010)

FVC % predicted

Follow‐up: 6 months

The mean FVC % predicted in the control group was 81%.

The mean FVC % predicted in the intervention group was 1% lower (16.65 % lower to 14.65 % higher).

MD ‐1.00 (‐16.65 to 14.65)

17
(1)

⊕⊝⊝⊝
very lowb,e

1 study reported a significant rise in FVC (L) in the EPA group (P = 0.01) (Lawrence 1993).

2 studies reported no difference in FVC between groups, but no data were available for analysis (Hanssens 2016; Keen 2010).

Growth and nutrition: BMI SD score

Follow‐up: 6 months

No significant difference was seen between the PUFA group and the placebo group after 6 months.

MD 0.00 (95 % CI ‐0.64 to 0.64)

29
(1)

⊕⊝⊝⊝
very lowb,e

A further study reported on BMI but reported only that BMI z scores remained stable throughout the study (Hanssens 2016).

Biochemical markers of essential fatty acid status: EPA and DHA % content of neutrophil membrane

Follow‐up: 6 months

1 study reported a higher EPA content of the neutrophil membrane in the omega‐3 PUFA‐supplemented group compared to the placebo group, MD 0.90 (95% CI 0.46 to 1.34).

In the same study, no difference was observed in DHA membrane concentration between groups, MD 0.10 (95% CI ‐0.45 to 0.65)

29
(1)

⊕⊝⊝⊝
very lowb,e

At 6 months, Keen reported a significant increase from baseline in both EPA and DHA content of serum phospholipids in the omega‐3 supplemented group compared to placebo, MD 0.70 (95% CI 0.42 to 0.98) and MD 1.10 (95% CI 0.39 to 1.81), respectively (Keen 2010).

*The basis for the assumed risk (e.g. the median control group risk across studies) is provided in footnotes. The corresponding risk (and its 95% confidence interval) is based on the assumed risk in the comparison group and the relative effect of the intervention (and its 95% CI).
BMI: body mass index; CI: confidence interval; DHA: docosahexaenoic acid; EPA: eicosapentaenoic acid; FEV1 : forced expiratory volume in 1 second; FVC: forced vital capacity; MD: mean difference; OR: odds ratio; PUFA: polyunsaturated fatty acid; SD: standard deviation.

GRADE Working Group grades of evidence
High quality: further research is very unlikely to change our confidence in the estimate of effect.
Moderate quality: further research is likely to have an important impact on our confidence in the estimate of effect and may change the estimate.
Low quality: further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate.
Very low quality: we are very uncertain about the estimate.

aDowngraded twice due to risk of bias within the included study for this outcome. There was uncertainty around allocation concealment and blinding and a high risk of bias due to selective reporting.

bDowngraded once due to imprecision from very low participant numbers and low event rates.

cDowngraded once due to risk of bias within the included study. It was unclear whether allocation was concealed and whether the outcomes were predefined as there was no protocol available.

dDowngraded twice due to very low participant numbers (n = 12) and low event rates.

eDowngraded twice due to risk of bias within the trial. The risk of bias was unclear across several domains including; randomisation, allocation concealment, incomplete outcome assessment and selective reporting.

Figuras y tablas -
Summary of findings for the main comparison. Summary of findings: omega‐3 fatty acid supplementation compared with placebo for cystic fibrosis
Ir a la tabla de la revisión
Comparison 1. Omega‐3 fatty acids versus placebo

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Adverse events Show forest plot

1

Odds Ratio (M‐H, Fixed, 95% CI)

Totals not selected

1.1 Diarrhoea and eructation

1

Odds Ratio (M‐H, Fixed, 95% CI)

0.0 [0.0, 0.0]

2 FEV1 % predicted (post‐treatment) Show forest plot

1

Mean Difference (IV, Fixed, 95% CI)

Totals not selected

2.1 At 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

3 FVC % predicted (post treatment) Show forest plot

1

Mean Difference (IV, Fixed, 95% CI)

Totals not selected

3.1 At 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

4 BMI (SD score) (post treatment) Show forest plot

1

Mean Difference (IV, Fixed, 95% CI)

Totals not selected

4.1 At 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

5 EPA and DHA % content of neutrophil membrane (post treatment) Show forest plot

1

Mean Difference (IV, Fixed, 95% CI)

Totals not selected

5.1 EPA at 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

5.2 DHA at 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

6 Leukotriene B4 to leukotriene B5 ratio (post treatment) Show forest plot

1

Mean Difference (IV, Fixed, 95% CI)

Totals not selected

6.1 At 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

7 EPA and DHA content of serum phospholipids (change from baseline) Show forest plot

1

Mean Difference (IV, Fixed, 95% CI)

Totals not selected

7.1 EPA At 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

7.2 DHA at 6 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]

8 N6/N3 ratio content of serum phospholipids (change from baseline) Show forest plot

1

Mean Difference (IV, Fixed, 95% CI)

Totals not selected

8.1 At 3 months

1

Mean Difference (IV, Fixed, 95% CI)

0.0 [0.0, 0.0]
Figuras y tablas -
Comparison 1. Omega‐3 fatty acids versus placebo
Ir a la tabla de la revisión