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Administración de suplementos de vitamina E en pacientes con fibrosis quística

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References

References to studies included in this review

Harries 1969 {published data only}

Harries JT, Muller DPR. Absorption of water miscible and fat soluble preparations of vitamin E in cystic fibrosis. 5th International Cystic Fibrosis Conference; 1969 Sept. 22‐26; Cambridge, England. 1969:298‐307. [CFGD Register: GN49]

Keljo 2000 {published and unpublished data}

Keljo DJ, Giroir B, Jialal I. Circulating tumor necrosis factor alpha and interleukin‐6 levels in cystic fibrosis, effect of vitamin E therapy [abstract]. Pediatric Pulmonology 2000;30 Suppl 20:326. [CFGD Register: GN87]

Levin 1961 {published data only}

Levin S. Muscular performance and vitamin E in cystic fibrosis [letter]. Archives of Disease in Childhood 1974;49(3):247. [CFGD Register: GN73a; MEDLINE: 74154485]
Levin S, Gordon MH, Nitowsky HM, Goldman C, di Sant'Agnese P, Gordon HH. Studies of tocopherol deficiency in infants and children: VI. Evaluation of muscle strength and effect of tocopherol administration in children with cystic fibrosis. Pediatrics 1961;27:578‐88. [CFGD Register: GN73b; DOI: 10.1136/adc.49.3.247‐a; MEDLINE: 74154485]

Wong 1988 {published data only}

Wong LTK, Halstead C, Davidson AGF, Fang PM. Comparison of the efficacy of water‐miscible and fat soluble vitamin E in the therapy of vitamin E deficiency in cystic fibrosis patients [abstract]. Pediatric Pulmonology 1988;5 Suppl 2:144. [CFGD Register: GN52]

References to studies excluded from this review

Jacquemin 2009 {published data only}

Jacquemin E, Hermeziu B, Kibleur Y, Friteau I, Mathieu D, Le Coz F, et al. Bioavailability of oral vitamin E formulations in adult volunteers and children with chronic cholestasis or cystic fibrosis. Journal of Clinical Pharmacy and Therapeutics 2009;34(5):515‐22. [CFGD Register: GN216; MEDLINE: 96204950]

Kerem 2009 {published data only}

NCT00889434. Efficacy and safety study of EGCG/Tocotrienol in 18 patients with splicing‐mutation‐mediated cystic fibrosis (CF). http://clinicaltrials.gov/show/NCT00889434 (accessed 10 March 2012). [Clinicaltrials.gov: NCT00889434]

Munck 2010 {published data only}

Munck A, Ginies JL, Huet F, Wizla N, Gerardin M, Darviot E, et al. A new water‐soluble oral vitamin E formulation in cystic fibrosis (CF) children [abstract]. Journal of Cystic Fibrosis 2010;9 Suppl 1:S91, Abstract no: 352. [CFGD Register: GN219; MEDLINE: 96204950]

Nasr 1993 {published data only}

Nasr SZ, O'Leary MH, Hillermeier C. Correction of vitamin E deficiency with fat‐soluble versus water‐miscible preparations of vitamin E in patients with cystic fibrosis. Journal of Pediatrics 1993;122(5 Pt 1):810‐2. [CFGD Register: GN42]

Papas 2007 {published data only}

Papas K, Kalbfleisch J, Mohon R. Bioavailability of a novel, water‐soluble vitamin E formulation in malabsorbing patients. Digestive Diseases and Sciences 2007;52(2):347‐52. [CFGD Register: GN114; MEDLINE: 96204950]

Sagel 2011 {published data only}

Sagel SD, Sontag MK, Anthony MM, Emmett P, Papas KA. Safety and efficacy of an antioxidant‐rich multivitamin supplement in cystic fibrosis. Journal of Cystic Fibrosis 2011;10(1):31‐6. [Clincaltrials.gov: NCT01018303]

Thomas 1995 {published data only}

Thomas PS, Bellamy M, Geddes D. Malabsorption of vitamin E in cystic fibrosis improved after ursodeoxycholic acid [letter]. Lancet 1995;346(8984):1230‐1. [CFGD Register: GN77; MEDLINE: 96054866]

Winklhofer‐Roob 1992 {published data only}

Winklhofer‐Roob BM, Shmerling DH, Schimek MG. Response of vitamin E deficient patients with cystic fibrosis (CF) to oral RRR‐alpha‐tocopherol or all‐rac‐alpha‐tocopheryl acetate [abstract]. Clinical Nutrition 1992;11 Suppl:67. [CFGD Register: GN48b]

Winklhofer‐Roob 1996 {published data only}

Winklhofer Roob BM, van't Hof MA, Shmerling DH. Long‐term oral vitamin E supplementation in cystic fibrosis patients: RRR‐alpha‐tocopherol compared with all‐rac‐alpha‐tocopheryl acetate preparations. American Journal of Clinical Nutrition 1996;63(5):722‐8. [CFGD Register: GN48a; MEDLINE: 96204950]

Wood 2003 {published data only}

Wood LG, Fitzgerald DA, Lee AK, Garg ML. Improved antioxidant and fatty acid status of patients with cystic fibrosis after antioxidant supplementation is linked to improved lung function. American Journal of Clinical Nutrition 2003;77(1):150‐9. [CFGD Register: GN98]

Additional references

Aaron 2004

Aaron SD, Ramotar K, Ferris W, Vandemheen K, Saginur R, Tullis E, et al. Adult cystic fibrosis exacerbations and new strains of Pseudomonas aeruginosa . American Journal of Respiratory and Critical Care Medicine 2004;169:811‐5.

Aparicio 2001

Aparicio JM, Belanger‐Quintana A, Suarez L. Ataxia with isolated vitamin E deficiency: case report and review of the literature. Journal of Pediatric Gastroenterology and Nutrition 2001;33(2):206‐10.

Bell 2002

Bell SC, Shepherd RW. Optimising nutrition in cystic fibrosis. Journal of Cystic Fibrosis 2002;1(2):47‐50. [DOI: 10.1016/S1569‐1993(02)00031‐0]

Biesalski 2009

Biesalski HK. Vitamin E requirements in parenteral nutrition. Gastroenterology 2009;137(5):S92‐S104. [DOI: 10.1053/j.gastro.2009.07.073]

Bines 2005

Bines JE, Truby HD, Armstrong DS, Carzino R, Grimwood R. Vitamin A and E deficiency and lung disease in infants with cystic fibrosis. Journal of Paediatrics and Child Health 2005;41:663‐8.

Brigelius‐Flohé 2009

Brigelius‐Flohé R. Vitamin E: The Shrew Waiting to be Tamed. Free Radical Biology & Medicine 2009;46:543–54.

Ciofu 2014

Ciofu O, Lykkesfeldt J. Antioxidant supplementation for lung disease in cystic fibrosis. Cochrane Database of Systematic Reviews 2014, Issue 8. [DOI: 10.1002/14651858.CD007020.pub3]

Cynamon 1988

Cynamon HA, Milov DE, Valenstein E, Wagner M. Effects of vitamin E deficiency on neurologic function in patients with cystic fibrosis. Pediatrics 1988;113:637‐9.

Dodge 2006

Dodge JA, Turck D. Cystic fibrosis: nutritional consequences and management. Best Practice & Research. Clinical Gastroenterology 2006;20(3):531‐46.

Elbourne 2002

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

Farrell 2008

Farrell PM, Rosenstein BJ, White TB, Accurso FJ, Castellani C, Cutting GR, et al. Guidelines for diagnosis of cystic fibrosis in newborns through older adults: Cystic Fibrosis Foundation consensus report. Journal of Pediatrics 2008;153(2):S4‐S14.

Gee 2000

Gee L, Abbott J, Conway S, Etherington C, Webb A. Development of a disease specific health related quality of life measure for adults and adolescents with cystic fibrosis. Thorax 2000;55(11):946‐54.

Goss 2004

Goss CH, Rosenfeld M. Update on cystic fibrosis epidemiology. Current Opinion in Pulmonary Medicine 2004;10(6):510‐4.

Hakim 2007

Hakim F,  Kerem E,  Rivlin J,  Bentur L,  Stankiewicz H,  Bdolach‐Abram T,  et al. Vitamins A and E and pulmonary exacerbations in patients with cystic fibrosis. Journal of Pediatric Gastroenterology and Nutrition 2007;45(3):347‐53.

Higgins 2003

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

Higgins 2011a

Higgins JPT, Altman DG. Chapter 8: Assessing risk of bias in included studies. In: Higgins JPT, Green S (editors). Cochrane Handbook of Systematic Reviews of Interventions. Version 5.1.0 [updated March 2011]. Available from www.cochrane‐handbook.org. The Cochrane Collaboration, 2011.

Higgins 2011b

Higgins JPT, Deeks JJ, Altman DG on behalf of the Cochrane Statistical Methods Group (editors). Chapter 16: Special topics in statistics. In: Higgins JPT, Green S (editors). Cochrane Handbook of Systematic Reviews of Interventions. Version 5.1.0 [updated March 2011]. Available from www.cochrane‐handbook.org. The Cochrane Collaboration, 2011.

Higgins 2011c

Deeks JJ, Higgins JPT, Altman DG on behalf of the Cochrane Statistical Methods Group (editors). Chapter 9: Analysing data and undertaking meta‐analysis. In: Higgins JPT, Green S (editors). Cochrane Handbook of Systematic Reviews of Interventions. Version 5.1.0 [updated March 2011]. Available from www.cochrane‐handbook.org. The Cochrane Collaboration, 2011.

Kerem 2005

Kerem E, Conway S, Elborn S, Heijerman H. Standards of care for patients with cystic fibrosis: a European consensus. Journal of Cystic Fibrosis 2005;4:7‐26.

Koscik 2005

Koscik RL, Lai HJ, Laxova A, Zaremba KM, Kosorok MR, Douglas JA, et al. Preventing early, prolonged vitamin E deficiency: an opportunity for better cognitive outcomes via early diagnosis through neonatal screening. Journal of Pediatrics 2005;147(3 Suppl):S51‐S56.

Kozlowska 2008

Kozlowska WJ, Bush A, Wade A, Aurora P, Carr SB, Castle RA, et al. Lung function from infancy to the preschool years after clinical diagnosis of cystic fibrosis. American Journal of Respiratory and Critical Care Medicine 2008;178(1):42‐9.

Linnane 2008

Linnane BM, Hall GL, Nolan G, Brennan S, Stick SM, Sly PD, et al. Lung function in infants with cystic fibrosis diagnosed by newborn screening. American Journal of Respiratory and Critical Care Medicine 2008;178(12):1238‐44.

Mayo Clinic 2009

Mayo Clinic. Vitamin E (oral route). www.mayoclinic.com/health/drug‐information/DR601967/FLUSHCACHE=0&UPDATEAPP=false (accessed 01 March 2011).

Peters 1996

Peters SA, Kelly FJ. Vitamin E supplementation in cystic fibrosis. Journal of Pediatric Gastroenterology and Nutrition 1996;22:341‐5.

Quittner 2009

Quittner AL, Modi AC, Wainwright C, Otto K, Kirihara J, Montgomery AB. Determination of the minimal clinically important difference scores for the Cystic Fibrosis Questionnaire‐Revised respiratory symptom scale in two populations of patients with cystic fibrosis and chronic Pseudomonas aeruginosa airway infection. Chest 2009;135(6):1610‐8.

RevMan 2011 [Computer program]

The Nordic Cochrane Centre, The Cochrane Collaboration. Review Manager (RevMan). Version 5.1. Copenhagen: The Nordic Cochrane Centre, The Cochrane Collaboration, 2011.

Sinaasappel 2002

Sinaasappel M, Stern M, Littlewood J, Wolfe S, Steinkampd G, Heijerman HG, et al. Nutrition in patients with cystic fibrosis: a European Consensus. Journal of Cystic Fibrosis 2002;1(2):51‐75. [PUBMED: 15463811]

Suskind 2009

Suskind DL. Nutritional Deficiencies During Normal Growth. Pediatric Clinics of North America 2009;56(5):1035‐53.

Swann 1998

Swann IL, Kendra JR. Anaemia, vitamin E deficiency and failure to thrive in an infant. Clinical and Laboratory Haematology 1998;20(1):61‐3.

Taylor 2010

Taylor C, Connolly S. Gastrointestinal disease and nutrition. In: Horsley A, Cunningham S, Innes JA editor(s). Cystic Fibrosis. Oxford: Oxford University Press, 2010:81‐93.

Thurnham 1986

Thurnham DI, Davies JA, Crump BJ, Situnayake RD, Davis M. The use of different lipids to express serum tocopherol: lipid ratios for the measurement of vitamin E status. Annals of Clinical Biochemistry 1986;23(Pt 5):514‐20.

Ueda 2009

Ueda N, Suzuki Y, Rino Y, Takahashi T, Imada T, Takanashi Y, et al. Correlation between neurological dysfunction with vitamin E deficiency and gastrectomy. Journal of the Neurological Sciences 2009;287:216‐20. [DOI: 10.1016/j.jns.2009.07.020]

UK Cystic Fibrosis Trust 2002

UK Cystic Fibrosis Trust Nutrition Working Group. Nutritional Management of Cystic Fibrosis. UK Cystic Fibrosis Trust, April 2002. [ISBN 0‐9540536‐5‐6]

Welsh 2001

Welsh M, Ramsey B, Accurso F, Cutting G. Cystic Fibrosis. In: Scriver CR, Beaudet AL, Sly WS, Valle D editor(s). The Metabolic and Molecular Basis of Inherited Disease. 8th Edition. New York: McGraw‐Hill, 2001:5121‐88.

Wilfond 1994

Wilfond BS, Farrell PM, Laxova A, Mischler E. Severe hemolytic anemia associated with vitamin E deficiency in infants with cystic fibrosis. Implications for neonatal screening. Clinica Pediatrica 1994;33(1):2‐7.

Winbauer 1999

Winbauer AN, Pingree SS, Nuttall KL. Evaluating serum alpha‐tocopherol (vitamin E) in terms of a lipid ratio. Annals Clinical and Laboratory Science 1999;29(3):185‐91.

Characteristics of studies

Characteristics of included studies [ordered by study ID]

Jump to:

Harries 1969

Methods

Randomised controlled study of parallel design with 3 arms.

Single‐centre study in UK.

Duration 1 month.

Participants

30 children with CF on pancreatic enzyme supplementation. Age range 6 months to 14.5 years.

Interventions

Acute supplementation and long‐term supplementation.

Children received either:

  • no supplementation;

  • water‐miscible preparation of vitamin E at a dose of 10 mg/kg;

  • fat‐soluble vitamin E at a dose of 10 mg/kg.

Outcomes

Serum vitamin E levels and serum RBC haemolysis.

Notes

Acute supplementation (called oral load test in the paper) was only done in 2 participants without controls.

The study does not clarify whether the participants were pancreatic sufficient or insufficient.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

Unclear risk

Not clearly specified in the the paper, states "chosen at random and arbitrarily assigned to one of three groups".

Allocation concealment (selection bias)

Unclear risk

Not clearly specified in the the paper.

Blinding of participants and personnel (performance bias)
All outcomes

Low risk

Not clearly specified in the the paper. Very likely not blinded, as 1 of arms was no treatment. Objective outcome is measured so absence of blinding unlikely to increase risk of bias.

Blinding of outcome assessment (detection bias)
All outcomes

Low risk

Not clearly specified in the the paper. Objective outcome is measured so absence of blinding unlikely to increase risk of bias.

Incomplete outcome data (attrition bias)
All outcomes

Low risk

At 1 month reported data for 9 out of 10 participants in fat‐soluble group (i.e. 1 dropout) and for 8 out of 10 participants in water miscible group (i.e. 2 dropouts), no discussions of reasons for dropouts. However, these missing data are unlikely to have a significant impact on the results.

Selective reporting (reporting bias)

Unclear risk

Trial protocol not available, but outcomes stated in 'Methods' section reported in 'Results'.

Other bias

Unclear risk

Limited information the basis of diagnosis of CF, pancreatic sufficiency/insufficiency etc.

Keljo 2000

Methods

Randomised double‐blind placebo‐controlled study of parallel design.

Single centre in the USA.

Participants stratified according to FEV1 (70% ‐ 85% predicted and > 85% predicted) and use of DNAse.

Duration 3 months.

Participants

40 participants with CF and mild lung disease (FEV1 % predicted > 70%). No details of age or gender split. Evenly distributed to treatment and placebo groups.

Interventions

Participants randomised to take vegetable oil placebo or RRR alpha‐tocopherol (participants < 20 kg = 600 IU/Day < 20 kg; participants > 20 kg = 1200 IU/day).

All participants also took ADEKs® for the duration of the study.

Outcomes

Beginnning and end of study: serum vitamin E levels; TNF‐alpha measurements; and IL‐6 measurements.

End of study only: liver enzyme levels; PT measurements; and PTT measurements.

Adverse effects reported.

Notes

Authors provided full manuscript later, but it did not have much more information.

Vitamin E and placebo capsules donated by Henkel Corporation. ADEKs® vitamins and partial financial support provided by Axcan Scandipharm.

The study does not clarify whether the participants were pancreatic sufficient or insufficient.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

Unclear risk

Described as randomized, but method not stated.

Allocation concealment (selection bias)

Unclear risk

Not stated.

Blinding of participants and personnel (performance bias)
All outcomes

Low risk

Described as double‐blind, but not stated who was blinded. Objective outcome is measured so absence of blinding unlikely to increase risk of bias.

Blinding of outcome assessment (detection bias)
All outcomes

Low risk

Described as double‐blind, but not stated who was blinded. Objective outcome is measured so absence of blinding unlikely to increase risk of bias.

Incomplete outcome data (attrition bias)
All outcomes

Unclear risk

Implies some dropouts as at end of study 20 participants stated as taking DNAse and 15 as not taking DNAse, but not clearly stated.

Selective reporting (reporting bias)

High risk

Protocol later provided by authors but did not provide much more information, no presentation of SD of the effect in the control group.

Other bias

Unclear risk

Limited information on the basis for diagnosis of CF. Not clear if pancreatic sufficient or insufficient.

Levin 1961

Methods

Randomised double‐blind placebo‐controlled study of parallel design.

Single‐centre trial in the USA.

Duration 6 months, planned to see participants every 2 months when possible.

No efforts made to counterbalance groups from which individuals were lost during study.

Participants

49 participants accepted with proven diagnosis of CF and stabilised; 45 children followed for at least 2 months; 37 completed 6 months (18 in treatment group; 19 in placebo group).

Each participant rated independently by 2 observers as to condition at the beginning of study on an arbitrary scale (1 = good condition up to 5 = very severe illness).

Tocopherol Group
20 participants, mean (SD) age 113.1 (65.12) months, 9 males and 11 females, mean (SD) illness severity score 2.22 (1.09), mean (SD) weight 24.3 (9.75) kg.

Placebo Group
25 participants, mean (SD) age 113.5 (63.99) months, 17 males and 8 females, mean (SD) illness severity score 2.10 (0.913), mean (SD) weight 26.8 (12.0) kg.

Interventions

10 mg/kg/day of vitamin E tocopherol (d‐l alpha‐tocopheryl acetate) in water‐miscible solution in 2 or 3 divided doses (n = 20) versus placebo (n = 25).

Outcomes

Weight, muscle power, serum tocopherol, activity of S‐GOT in serum and subjective improvement.

Notes

Reported data at baseline, 2 and 6 months

Tocopherol and placebo provided by U.S. Vitamin Corporation.

Supported in part by grants from the National Institute of Arthritis and Metabolic Diseases, National Institutes of Public Health, Public Health Service and the Muscular Dystrophy Associations of America.

Limited information on the basis for diagnosis of CF.

The study does not clarify whether the participants were pancreatic sufficient or insufficient.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

Low risk

Randomisation was performed as follows: cards labelled 1 or 2 were individually placed in sealed envelopes in groups of 4 (2 for each mixture number). Envelopes were divided into 3 groups, according to age of participants: < 5 years, 5 ‐ 10 years, and ≥ 10 years and over. Each child accepted into the study group was assigned an envelope from the appropriate age group, and the enclosed card indicated the mixture to be given.

Allocation concealment (selection bias)

Low risk

Sealed envelopes with designated randomisation, each child accepted into study was assigned an envelope from the appropriate age group.

Blinding of participants and personnel (performance bias)
All outcomes

Low risk

From the paper in plan of study: "Patients and testers did not know which preparation was taken" (double‐blind method) also stated "Physicians blind to vitamin E results".

Blinding of outcome assessment (detection bias)
All outcomes

Low risk

Outcome assessors blinded.

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Out of the initial 49 participants accepted, 37 completed the study but intention‐to‐treat analysis was not carried out. 3 died within 6 months (all in placebo group), 2 declined to continue medication after 2 months, 1 participant removed due to diabetes mellitus and 7 participants studied for less than 6 months. However, we feel the attrition is balanced among the two groups; hence we judged this study to have a low risk of bias.

Planned to measure data at baseline, end of study (6 months) and every 2 months where possible, reported data at baseline, 2 and 6 months.

Selective reporting (reporting bias)

Unclear risk

Protocol not available, but the paper reports data for each outcome measurement listed in the 'Methods' section of the paper.

Other bias

Unclear risk

None identified.

Limited information on the basis for diagnosis of CF and whether pancreatic sufficient or insufficient.

Wong 1988

Methods

Controlled clinical study.

Single centre in Canada.

Duration 10 ‐ 14 days.

Participants

22 CF participants admitted for pulmonary infection.

Interventions

Group A: oral fat‐soluble vitamin E 10 mg/kg/day (n = 8).

Group B: oral water‐miscible vitamin E (Aquasol E) 10 mg/kg/day (n = 5).

Group C: no supplementation (n = 9).

Outcomes

Serum vitamin E levels, alpha‐tocopherol/cholesterol ratio, 3‐day faecal fat excretion.

Notes

All participants also received appropriate intravenous antibiotics, 10% Nutralipid 15 ml/kg/day and usual dosage of enteric‐coated pancreatic enzymes.

The study does not clarify whether the participants were pancreatic sufficient or insufficient.

Abstract only available.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

Unclear risk

Randomisation not stated, abstract states participants divided into 3 groups.

Allocation concealment (selection bias)

Unclear risk

Not stated.

Blinding of participants and personnel (performance bias)
All outcomes

Low risk

Not stated, blinding of no treatment compared to either of treatment arms not possible, but not clear if blinded between treatment arms. Objective outcome is measured so absence of blinding unlikely to increase risk of bias.

Blinding of outcome assessment (detection bias)
All outcomes

Low risk

Blinding of no treatment compared to either of treatment arms not possible, but not clear if blinded between treatment arms. Objective outcome is measured so absence of blinding unlikely to increase risk of bias.

Incomplete outcome data (attrition bias)
All outcomes

Unclear risk

Number of participants recruited and randomized not stated, only numbers of participants for whom results available given.

Selective reporting (reporting bias)

Unclear risk

Protocol not available, abstract only so no 'Methods' section available to compare to 'Results' section.

Other bias

Unclear risk

None identified.

Limited information on the basis for diagnosis of CF and if pancreatic sufficient or insufficient.

CF: cystic fibrosis
DNAse: dornase alfa
IU: international units
PI: pancreatic insufficient
PS: pancreatic sufficient
PT: prothrombin
PTT: partial thromboplastin time
RBC: red blood cell
SD: standard deviation
S‐GOT: glutamic oxalacetic transaminase

Characteristics of excluded studies [ordered by study ID]

Jump to:

Study

Reason for exclusion

Jacquemin 2009

Compares bioavailability of preparations, no placebo or control arm.

Kerem 2009

It is not a study of vitamin E supplementation compared to placebo or control.

Munck 2010

Lack of placebo or control group.

Nasr 1993

Compares two preparations of vitamin E, no control or placebo group.

Papas 2007

Compares bioavailability of preparations, no control group.

Sagel 2011

Not a randomised or quasi‐randomised study.

Thomas 1995

Comparison of vitamin E given with placebo to vitamin E given with ursodeoxycholic acid in a single participant.

Winklhofer‐Roob 1992

No placebo or control group. Compared 3 preparations of vitamin E to baseline status.

Winklhofer‐Roob 1996

Compared levels of vitamin E after supplementation with 3 different preparations of vitamin E and compared to matched controls.

Wood 2003

Compared low‐dose to high‐dose supplements. No placebo or control group.

Data and analyses

Open in table viewer
Comparison 1. Water‐miscible vitamin E supplementation versus control

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Serum vitamin E levels Show forest plot

3

Mean Difference (IV, Fixed, 95% CI)

Subtotals only

Analysis 1.1

Comparison 1 Water‐miscible vitamin E supplementation versus control, Outcome 1 Serum vitamin E levels.

Comparison 1 Water‐miscible vitamin E supplementation versus control, Outcome 1 Serum vitamin E levels.

1.1 Up to 1 month

2

32

Mean Difference (IV, Fixed, 95% CI)

17.66 [10.59, 24.74]

1.2 Up to 3 months

1

45

Mean Difference (IV, Fixed, 95% CI)

11.61 [4.77, 18.45]

1.3 Up to 6 months

1

45

Mean Difference (IV, Fixed, 95% CI)

19.74 [13.48, 26.00]

2 Weight Show forest plot

1

Mean Difference (IV, Random, 95% CI)

Totals not selected

Analysis 1.2

Comparison 1 Water‐miscible vitamin E supplementation versus control, Outcome 2 Weight.

Comparison 1 Water‐miscible vitamin E supplementation versus control, Outcome 2 Weight.

2.1 Up to 3 months

1

Mean Difference (IV, Random, 95% CI)

0.0 [0.0, 0.0]

2.2 Up to 6 months

1

Mean Difference (IV, Random, 95% CI)

0.0 [0.0, 0.0]

Open in table viewer
Comparison 2. Fat‐soluble vitamin E supplementation versus control

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Serum vitamin E levels Show forest plot

3

Mean Difference (IV, Fixed, 95% CI)

Subtotals only

Analysis 2.1

Comparison 2 Fat‐soluble vitamin E supplementation versus control, Outcome 1 Serum vitamin E levels.

Comparison 2 Fat‐soluble vitamin E supplementation versus control, Outcome 1 Serum vitamin E levels.

1.1 Up to 1 month

2

36

Mean Difference (IV, Fixed, 95% CI)

13.59 [9.52, 17.66]

1.2 Up to 3 months

1

36

Mean Difference (IV, Fixed, 95% CI)

6.40 [‐1.45, 14.25]

Study flow diagram
Figures and Tables -
Figure 1

Study flow diagram

Comparison 1 Water‐miscible vitamin E supplementation versus control, Outcome 1 Serum vitamin E levels.
Figures and Tables -
Analysis 1.1

Comparison 1 Water‐miscible vitamin E supplementation versus control, Outcome 1 Serum vitamin E levels.

Comparison 1 Water‐miscible vitamin E supplementation versus control, Outcome 2 Weight.
Figures and Tables -
Analysis 1.2

Comparison 1 Water‐miscible vitamin E supplementation versus control, Outcome 2 Weight.

Comparison 2 Fat‐soluble vitamin E supplementation versus control, Outcome 1 Serum vitamin E levels.
Figures and Tables -
Analysis 2.1

Comparison 2 Fat‐soluble vitamin E supplementation versus control, Outcome 1 Serum vitamin E levels.

Comparison 1. Water‐miscible vitamin E supplementation versus control

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Serum vitamin E levels Show forest plot

3

Mean Difference (IV, Fixed, 95% CI)

Subtotals only

1.1 Up to 1 month

2

32

Mean Difference (IV, Fixed, 95% CI)

17.66 [10.59, 24.74]

1.2 Up to 3 months

1

45

Mean Difference (IV, Fixed, 95% CI)

11.61 [4.77, 18.45]

1.3 Up to 6 months

1

45

Mean Difference (IV, Fixed, 95% CI)

19.74 [13.48, 26.00]

2 Weight Show forest plot

1

Mean Difference (IV, Random, 95% CI)

Totals not selected

2.1 Up to 3 months

1

Mean Difference (IV, Random, 95% CI)

0.0 [0.0, 0.0]

2.2 Up to 6 months

1

Mean Difference (IV, Random, 95% CI)

0.0 [0.0, 0.0]

Figures and Tables -
Comparison 1. Water‐miscible vitamin E supplementation versus control
Comparison 2. Fat‐soluble vitamin E supplementation versus control

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Serum vitamin E levels Show forest plot

3

Mean Difference (IV, Fixed, 95% CI)

Subtotals only

1.1 Up to 1 month

2

36

Mean Difference (IV, Fixed, 95% CI)

13.59 [9.52, 17.66]

1.2 Up to 3 months

1

36

Mean Difference (IV, Fixed, 95% CI)

6.40 [‐1.45, 14.25]

Figures and Tables -
Comparison 2. Fat‐soluble vitamin E supplementation versus control