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Epidemiology and outcomes
The association between diet and glucocorticoid treatment in patients with SLE
  1. Cecilia Lourdudoss1,
  2. Ingiäld Hafström2,
  3. Johan Frostegård3 and
  4. Ronald van Vollenhoven1
  1. 1Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden
  2. 2Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden
  3. 3Department of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
  1. Correspondence to Ms Cecilia Lourdudoss; cecilia.lourdudoss{at}ki.se

Abstract

Background Some studies suggest that the risk for and severity of systemic lupus erythematosus (SLE) can be modified by certain nutrients. The aim of this study was to investigate the association between diet and glucocorticoid (GC) treatment, as a proxy for disease activity, in patients with SLE.

Methods We included 111 patients with SLE from the SLE Vascular Impact Cohort (SLEVIC). Dietary data were linked with data on GC treatment during a 2-year period. The association between diet and GC treatment was analysed with logistic regression. GC treatment and unchanged/increased doses were considered a proxy for active SLE.

Results During the 2-year period, 54 patients (48.6%) had continued GC treatment. Dietary vitamin D was associated with GC treatment (OR=2.70–2.85 (95% CI 1.00 to 8.11)), whereas alcohol was inversely associated with GC treatment (OR=0.28–0.39 (95% CI 0.10 to 98)). Beta-carotene, fatty acid C18:2 and vitamin B6 were inversely associated with unchanged/increased GC dose (OR=0.29–0.30 (95% CI 0.10 to 0.90)). Finally, total energy intake was associated with GC doses >5.0 mg/day and >7.5 mg/day, explaining a direct association between 35 nutrients and higher GC dose levels (OR=2.98–23.82 (95% CI 1.01 to 203.88)).

Discussion Dietary vitamin D did not protect against lupus activity. Beta-carotene, fatty acid C18:2 and vitamin B6 may protect against increased GC dose. The inverse association between alcohol intake and GC treatment/lupus activity may provide a partial explanation for the link between moderate alcohol intake and reduced risk of SLE. The association between higher dietary intake and higher GC dose levels indicated GC's influence on increasing appetite.

  • Systemic Lupus Erythematosus
  • Corticosteroids
  • Disease Activity

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

https://doi.org/10.1136/lupus-2015-000135

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    Key messages

    • Vitamin D did not protect against lupus activity.

    • Beta-carotene, fatty acid C18:2 and vitamin B6 may protect against increases in GC dose.

    • Higher GC dose levels indicated increased appetite.

    Introduction

    Glucocorticoids (GCs) are very effective in treating inflammation, but long-term GC treatment is associated with several side effects.1 ,2 GC treatment may reflect disease activity in patients with systemic lupus erythematosus (SLE) with regard to GC treatment dose change over time and/or dose levels. Patients with higher disease activity might be more dependent on GCs than those with lower disease activity. In addition, higher GC doses may be seen in patients with higher disease activity.3 ,4

    Little is known regarding the dietary habits in SLE. A few studies have reported that patients with SLE might have a poor nutritional status compared with the general population, showing low consumption of fruits and vegetables as well as inadequate dietary intake of fibre, vitamin B6, calcium and polyunsaturated fatty acids, especially omega-3 fatty acids.5–7 Elkan et al8 have, in the present cohort, specifically found decreased dietary intake of polyunsaturated fatty acids (including omega-3 and omega-6) and fibre compared with healthy controls. Previous findings suggest that vitamin D and moderate alcohol intake are beneficial for patients with SLE. Vitamin D deficiency has been linked with higher disease activity in patients with SLE9–12 and moderate alcohol consumption has shown to be associated with reduced risk of SLE.13–15 However, there is a lack of studies on the link between diet and treatment results in SLE. Since GCs are frequently used to control active SLE, our interest was to focus on the association between diet and GC treatment. The aim of this study was to investigate whether diet influences GC treatment in patients with SLE.

    Methods

    Study participants

    This study included patients with SLE, fulfilling the 1982 revised criteria of the American College of Rheumatology (ACR) for SLE, from the SLE Vascular Impact Cohort (SLEVIC), Karolinska University Hospital, Stockholm, Sweden. Recruitment and inclusion for SLEVIC have been previously described in detail by Anania et al.16 The inclusion criterion was all patients who completed Food Frequency Questionnaire (FFQ) at inclusion.

    Dietary assessment

    Patients were asked to complete a semiquantitative FFQ at inclusion. This self-reported FFQ involved frequency of intake of 88 food items and beverages during the previous year from inclusion. Completed FFQs were evaluated and an estimation of daily mean intake of 49 nutrients was calculated, using nutrient composition values based on the Swedish National Food Administration data.

    GC treatment

    Data on GC use and dose levels were extracted from medical records at three time points; at inclusion and at 1 year before and after inclusion. Based on GC use at the three time points, GC dose changes over time, reflecting disease activity, were adjusted for three time periods: previous year to inclusion, following year from inclusion and 1 year before to 1 year after inclusion. GC use over time was categorised into four treatment status groups: ‘none’, ‘discontinued’, ‘started’ and ‘continued’. Dose changes over time were categorised into ‘decreased’, ‘unchanged’ and ‘increased’. GC treatment and higher dose levels (>5.0 mg/day and >7.5 mg/day) were considered a proxy for more active SLE; unchanged or increased GC doses were considered as unfavourable outcomes.

    Statistical analysis

    Statistical analysis was performed with IBM SPSS Statistics V.22. We linked dietary data from FFQ with data on GC treatment from medical records for the year preceding and the year following the FFQ. Associations between diet and GC treatment during the 2-year period were analysed with logistic regression adjusted for age and gender. All nutrient variables were dichotomised into lower and higher intakes with a cut-off at median levels.

    Results

    This study included 111 patients with SLE. Patient characteristics are presented in table 1.

    View this table:
    Table 1

    Patient characteristics at inclusion

    During the 2-year period, the percentage of patients treated with GC ranged between 56.8% and 59.5%. In addition to GC, the most common treatments were hydroxychloroquine (HCQ) and azathioprine (AZA); the percentages of patients treated with HCQ and AZA ranged between 40.5–46.8% and 18.9–25.2%, respectively (table 2). Almost all the patients who were treated with GC at inclusion took also supplementation of calcium+vitamin D (66.7%) or calcium (24.2%) or vitamin D (6.1%) alone.

    View this table:
    Table 2

    Overview of treatment use and doses at −1 year, inclusion and +1 year

    During the 2-year period, 26 patients (23.4%) did not use GC, 4.5% discontinued their GC treatment, 5.4% started GC treatment and 48.6% had continuous GC treatment. 20 patients (18%) had missing data. The distribution of GC treatment statuses over the three time periods is presented in figure 1.

    Figure 1
    Figure 1

    Treatment status of glucocorticoid (GC) from −1 year to inclusion, inclusion to +1 year and –1 year to +1 year.

    Of the 54 patients who had continued treatment over the 2-year period, 31.5% had decreased dose, 35.2% had unchanged dose and 33.3% had increased dose. GC dose changes during the three time periods are presented in table 3.

    View this table:
    Table 3

    GC dose change (decreased/unchanged/increased) from –1 year to inclusion, inclusion to +1 year and –1 year to +1 year

    The association between dietary nutrient intake and GC use is presented in table 4. Vitamin D was associated with GC treatment (OR 2.70–2.85, (95% CI 1.00 to 8.11)), whereas alcohol was inversely associated with GC treatment (OR 0.28–0.39, (95% CI 0.10 to 98)).

    View this table:
    Table 4

    The association between dietary nutrient intake and GC use between −1 year to inclusion, inclusion to +1 year and −1 year to +1 year

    The association between dietary nutrient intake and unchanged/increased GC dose is presented in table 5. Beta-carotene, fatty acid C18:2 and vitamin B6 were inversely associated with unchanged/increased GC dose (OR 0.29–0.30 (95% CI 0.10 to 0.90)), whereas vitamin B12 and calcium were associated with unchanged/increased GC dose (OR 3.20–5.36 (95% CI 1.08 to 17.52)). Omega-3 fatty acids and the ratio between omega-6 and omega-3 fatty acids were not significantly associated with unchanged/increased GC dose.

    View this table:
    Table 5

    The association between dietary nutrient intake and GC dose change (decreased vs unchanged/increased) between –1 year to inclusion, inclusion to +1 year and −1 year to +1 year

    Total energy intake was associated with GC doses >5.0 mg/day and >7.5 mg/day, explaining an association between 35 nutrients and higher GC dose levels (OR 2.98–23.82 (95% CI 1.01 to 203.88)).

    Discussion

    This study focused on the association between diet and GC treatment in patients with SLE. The results were based on data from a Swedish SLE cohort and showed that some dietary nutrients were associated or inversely associated with unfavourable outcomes of GC.

    Diet and GC treatment

    Several previous studies have shown that low vitamin D levels in serum are associated with disease activity in SLE.12 ,17–20 Vitamin D supplementation has also been suggested to improve disease activity and fatigue scores in SLE.21 ,22 Based on these and other studies, it has been suggested that vitamin D is protective against lupus activity. However, in this study, dietary vitamin D was positively associated with GC treatment, not suggesting a protective effect, but this association was not significant after adjusting for supplement use of calcium/vitamin D supplementation. Patients included in this study might have been aware of the existing evidence of the beneficial effect of vitamin D, explaining an increased vitamin D intake in patients with GC treatment/higher disease activity. Nevertheless, these results were based on dietary intake and not supplement intake of vitamin D. The results on the association between dietary vitamin D and GC were affected by calcium/vitamin D supplementation. However, if an adequate vitamin D intake is obtained (either through diet or supplementation), it is not necessarily followed by adequate vitamin D levels in blood, since GC reduces absorption of vitamin D.23

    Alcohol was inversely associated with GC treatment, reflecting older findings on the link between moderate alcohol intake and reduced risk of rheumatic diseases,24 ,25 and even specifically of SLE.13–15

    Diet and unchanged/increased GC dose

    Fatty acid C18:2 (linoleic acid) was inversely associated with unchanged/increased GC dose (unfavourable outcome). Fatty acid C18:2 belongs to the omega-6 family and is known to have proinflammatory properties. However, the omega-3 fatty acids (anti-inflammatory) should be considered when looking at the omega-6 intake since the ratio between these two must be well balanced. The omega-6 to omega-3 fatty acid ratio did not show any association with unchanged/increased GC dose. Though, a review has gathered evidence on health benefits of conjugated linoleic acids26 that may be linked with the inverse association between dietary linoleic acid and unchanged/increased GC dose.

    An inverse association was found between beta-carotene and unchanged/increased GC dose. Beta-carotene is an antioxidant and patients with SLE have been found to have lower dietary beta-carotene intake compared with controls.27 Increased antioxidant intake could be beneficial due to the damage of free oxygen radicals that play a role in SLE.28 ,29 Beta-carotene may be linked to protective effect against unchanged/increased GC dose.

    Vitamin B6 was inversely associated with unchanged/increased GC dose. Higher intake of vitamin B6 and dietary fibre may prevent the occurrence of active disease in patients with SLE.6 Pyridoxal 5′-phosphate (PLP) is the active coenzyme form of vitamin B6 and its concentration in plasma is the most common measure of vitamin B6 status.30 ,31 Decreased plasma PLP levels have shown to be associated with chronic or acute disease and increased plasma PLP levels with lower C reactive protein.32–34 Increased dietary vitamin B6 intake may play a role in lupus activity.

    Diet and GC dose

    Energy intake was associated with higher GC dose levels, explaining the association between almost all the nutrients and higher GC dose levels. Contradictory results exist on the effects of GC therapy on energy intake, appetite and body weight in humans.35 GC has shown to be associated with increased appetite and/or body weight.36 Increased appetite during or after GC treatment has been self-reported as one of the major adverse events in several studies.37–39 This study confirms the existing evidence of GC's influence on increasing appetite.

    Limitations

    Patients included in this study had various disease and treatment durations at inclusion. GC treatment may not have fully reflected lupus activity during the 2-year period. Some micronutrients, when consumed together, interfere with each other in the physiological environment; however, interactions between nutrients as well as nutrient bioavailability were not taken into account. Dietary data from FFQ were based on estimated dietary consumption. Recall bias and under-reporting and over-reporting may have occurred when completing the FFQ. Also, dietary patterns were assumed to be the same throughout the 2-year period. Clinical manifestations, treatment history and side effects of GC throughout the disease course from diagnosis were not considered in this study.

    Conclusions

    These data did not support the hypothesis that dietary vitamin D protects against lupus activity. Beta-carotene (antioxidant), fatty acid C18:2 (omega-6) and vitamin B6 may protect against unfavourable outcomes (need for increases in GC dose). The inverse association between alcohol intake and GC treatment/lupus activity may provide a partial explanation for the link between moderate alcohol intake and improved cardiovascular health in rheumatic diseases. The association between dietary intake and higher GC dose levels indicated GC's influence on increasing appetite.

    References

    1. ↵
      1. Schacke H,
      2. Docke WD,
      3. Asadullah K
      . Mechanisms involved in the side effects of glucocorticoids. Pharmacol Therapeut 2002;96:23–43. doi:10.1016/S0163-7258(02)00297-8
      OpenUrlCrossRefPubMedWeb of Science
    2. ↵
      1. Seguro LP,
      2. Rosario C,
      3. Shoenfeld Y
      . Long-term complications of past glucocorticoid use. Autoimmun Rev 2013;12:629–32. doi:10.1016/j.autrev.2012.12.002
      OpenUrlCrossRefPubMed
    3. ↵
      1. Pego-Reigosa JM,
      2. Rúa-Figueroa Í,
      3. López-Longo FJ, et al
      . Analysis of disease activity and response to treatment in a large Spanish cohort of patients with systemic lupus erythematosus. Lupus 2015;24:720–9. doi:10.1177/0961203314563818
      OpenUrlAbstract/FREE Full Text
    4. ↵
      1. Mosca M,
      2. Tani C,
      3. Carli L, et al
      . Glucocorticoids in systemic lupus erythematosus. Clin Exp Rheumatol 2011;29(5 Suppl 68):S126–9.
      OpenUrlPubMed
    5. ↵
      1. Borges MC,
      2. dos Santos FDM,
      3. Telles RW, et al
      . Nutritional status and food intake in patients with systemic lupus erythematosus. Nutrition 2012;28:1098–103. doi:10.1016/j.nut.2012.01.015
      OpenUrlCrossRefPubMedWeb of Science
    6. ↵
      1. Minami Y,
      2. Hirabayashi Y,
      3. Nagata C, et al
      . Intakes of vitamin B6 and dietary fiber and clinical course of systemic lupus erythematosus: a prospective study of Japanese female patients. J Epidemiol 2011;21:246–54. doi:10.2188/jea.JE20100157
      OpenUrlCrossRefPubMed
    7. ↵
      1. Pestka JJ
      . n-3 polyunsaturated fatty acids and autoimmune-mediated glomerulonephritis. Prostaglandins Leukot Essent Fatty Acids 2010;82:251–8. doi:10.1016/j.plefa.2010.02.013
      OpenUrlCrossRefPubMed
    8. ↵
      1. Elkan AC,
      2. Anania C,
      3. Gustafsson T, et al
      . Diet and fatty acid pattern among patients with SLE: associations with disease activity, blood lipids and atherosclerosis. Lupus 2012;21:1405–11. doi:10.1177/0961203312458471
      OpenUrlAbstract/FREE Full Text
    9. ↵
      1. Yap KS,
      2. Northcott M,
      3. Hoi AB, et al
      . Association of low vitamin D with high disease activity in an Australian systemic lupus erythematosus cohort. Lupus Sci Med 2015;2:e000064. doi:10.1136/lupus-2014-000064
      OpenUrlAbstract/FREE Full Text
    10. ↵
      1. Kamen DL,
      2. Cooper GS,
      3. Bouali H, et al
      . Vitamin D deficiency in systemic lupus erythematosus. Autoimmun Rev 2006;5:114–17. doi:10.1016/j.autrev.2005.05.009
      OpenUrlCrossRefPubMedWeb of Science
    11. ↵
      1. Bonakdar ZS,
      2. Jahanshahifar L,
      3. Jahanshahifar F, et al
      . Vitamin D deficiency and its association with disease activity in new cases of systemic lupus erythematosus. Lupus 2011;20:1155–60. doi:10.1177/0961203311405703
      OpenUrlAbstract/FREE Full Text
    12. ↵
      1. Schoindre Y,
      2. Jallouli M,
      3. Tanguy ML, et al
      . Lower vitamin D levels are associated with higher systemic lupus erythematosus activity, but not predictive of disease flare-up. Lupus Sci Med 2014;1:e000027. doi:10.1136/lupus-2014-000027
      OpenUrlAbstract/FREE Full Text
    13. ↵
      1. Kiyohara C,
      2. Washio M,
      3. Horiuchi T, et al
      . Cigarette smoking, alcohol consumption, and risk of systemic lupus erythematosus: a case-control study in a Japanese population. J Rheumatol 2012;39:1363–70. doi:10.3899/jrheum.111609
      OpenUrlAbstract/FREE Full Text
    14. ↵
      1. Hardy CJ,
      2. Palmer BP,
      3. Muir KR, et al
      . Smoking history, alcohol consumption, and systemic lupus erythematosus: a case-control study. Ann Rheum Dis 1998;57:451–5. doi:10.1136/ard.57.8.451
      OpenUrlAbstract/FREE Full Text
    15. ↵
      1. Bengtsson AA,
      2. Rylander L,
      3. Hagmar L, et al
      . Risk factors for developing systemic lupus erythematosus: a case-control study in southern Sweden. Rheumatology 2002;41:563–71. doi:10.1093/rheumatology/41.5.563
      OpenUrlAbstract/FREE Full Text
    16. ↵
      1. Anania C,
      2. Gustafsson T,
      3. Hua X, et al
      . Increased prevalence of vulnerable atherosclerotic plaques and low levels of natural IgM antibodies against phosphorylcholine in patients with systemic lupus erythematosus. Arthritis Res Ther 2010;12:R214. doi:10.1186/ar3193
      OpenUrlCrossRefPubMed
    17. ↵
      1. Roman MJ,
      2. Crow MK,
      3. Lockshin MD, et al
      . Rate and determinants of progression of atherosclerosis in systemic lupus erythematosus. Arthritis Rheum 2007;56:3412–19. doi:10.1002/art.22924
      OpenUrlCrossRefPubMedWeb of Science
    18. ↵
      1. Petri M,
      2. Bello KJ,
      3. Fang H, et al
      . Vitamin D in systemic lupus erythematosus modest association with disease activity and the urine protein-to-creatinine ratio. Arthritis Rheum 2013;65:1865–71. doi:10.1002/art.37953
      OpenUrlCrossRefPubMedWeb of Science
    19. ↵
      1. Mok CC,
      2. Birmingham DJ,
      3. Ho LY, et al
      . Vitamin D deficiency as marker for disease activity and damage in systemic lupus erythematosus: a comparison with anti-dsDNA and anti-C1q. Lupus 2012;21:36–42. doi:10.1177/0961203311422094
      OpenUrlAbstract/FREE Full Text
    20. ↵
      1. Chaiamnuay S,
      2. Chailurkit LO,
      3. Narongroeknawin P, et al
      . Current daily glucocorticoid use and serum creatinine levels are associated with lower 25(OH) vitamin D levels in Thai patients with systemic lupus erythematosus. J Clin Rheumatol 2013;19:121–5. doi:10.1097/RHU.0b013e318289bd16
      OpenUrlCrossRefPubMed
    21. ↵
      1. Lima GL,
      2. Paupitz J,
      3. Aikawa NE, et al
      . A randomized double-blind placebo-controlled trial of vitamin D supplementation in adolescents and young adults with Juvenile-onset SLE: improvement in disease activity and fatigue scores. Arthritis Care Res (Hoboken) 2015. doi:10.1002/acr.22621
    22. ↵
      1. Abou-Raya A,
      2. Abou-Raya S,
      3. Helmii M
      . The effect of vitamin D supplementation on inflammatory and hemostatic markers and disease activity in patients with systemic lupus erythematosus: a randomized placebo-controlled trial. J Rheumatol 2013;40:265–72. doi:10.3899/jrheum.111594
      OpenUrlAbstract/FREE Full Text
    23. ↵
      1. Godschalk M,
      2. Levy JR,
      3. Downs RW
      . Glucocorticoids decrease vitamin-D receptor number and gene-expression in human osteosarcoma cells. J Bone Miner Res 1992;7:21–7. doi:10.1002/jbmr.5650070105
      OpenUrlPubMed
    24. ↵
      1. Sofat N,
      2. Keat A
      . Alcohol intake in rheumatic disease: good or bad? Rheumatology 2002;41:125–8. doi:10.1093/rheumatology/41.2.125
      OpenUrlFREE Full Text
    25. ↵
      1. Lu B,
      2. Solomon DH,
      3. Costenbader KH, et al
      . Alcohol consumption and risk of incident rheumatoid arthritis in women: a prospective study. Rheumatology (Oxford) 2014;66:1998–2005. doi:10.1002/art.38634
      OpenUrl
    26. ↵
      1. Benjamin S,
      2. Spener F
      . Conjugated linoleic acids as functional food: an insight into their health benefits. Nutr Metab 2009;6:36. doi:10.1186/1743-7075-6-36
      OpenUrlCrossRef
    27. ↵
      1. Bae SC,
      2. Kim SJ,
      3. Sung MK
      . Impaired antioxidant status and decreased dietary intake of antioxidants in patients with systemic lupus erythematosus. Rheumatol Int 2002;22:238–43. doi:10.1007/s00296-002-0241-8
      OpenUrlCrossRefPubMedWeb of Science
    28. ↵
      1. Comstock GW,
      2. Burke AE,
      3. Hoffman SC, et al
      . Serum concentrations of alpha tocopherol, beta carotene, and retinol preceding the diagnosis of rheumatoid arthritis and systemic lupus erythematosus. Ann Rheum Dis 1997;56:323–5. doi:10.1136/ard.56.5.323
      OpenUrlAbstract/FREE Full Text
    29. ↵
      1. Suryaprabha P,
      2. Das UN,
      3. Ramesh G, et al
      . Reactive oxygen species, lipid peroxides and essential fatty-acids in patients with rheumatoid-arthritis and systemic lupus-erythematosus. Prostag Leukotr Ess 1991;43:251–5. doi:10.1016/0952-3278(91)90038-7
      OpenUrl
    30. ↵
      1. Lamers Y
      . Indicators and methods for folate, vitamin B-12, and vitamin B-6 status assessment in humans. Curr Opin Clin Nutr Metab Care 2011;14:445–54. doi:10.1097/MCO.0b013e328349f9a7
      OpenUrlCrossRefPubMed
    31. ↵
      1. Leklem JE
      . Vitamin B-6: a status report. J Nutr 1990;120(Suppl 11):1503–7.
      OpenUrlAbstract/FREE Full Text
    32. ↵
      1. Chiang EPI,
      2. Bagley PJ,
      3. Selhub J, et al
      . Abnormal vitamin B-6 status is associated with severity of symptoms in patients with rheumatoid arthritis. Am J Med 2003;114:283–7. doi:10.1016/S0002-9343(02)01528-0
      OpenUrlCrossRefPubMedWeb of Science
    33. ↵
      1. Lotto V,
      2. Choi SW,
      3. Friso S
      . Vitamin B-6: a challenging link between nutrition and inflammation in CVD. Br J Nutr 2011;106:183–95. doi:10.1017/S0007114511000407
      OpenUrlCrossRefPubMed
    34. ↵
      1. Paul L,
      2. Ueland PM,
      3. Selhub J
      . Mechanistic perspective on the relationship between pyridoxal 5′-phosphate and inflammation. Nutr Rev 2013;71:239–44. doi:10.1111/nure.12014
      OpenUrlAbstract/FREE Full Text
    35. ↵
      1. Berthon BS,
      2. MacDonald-Wicks LK,
      3. Wood LG
      . A systematic review of the effect of oral glucocorticoids on energy intake, appetite, and body weight in humans. Nutr Res 2014;34:179–90. doi:10.1016/j.nutres.2013.12.006
      OpenUrlCrossRefPubMed
    36. ↵
      1. Cheskin LJ,
      2. Bartlett SJ,
      3. Zayas R, et al
      . Prescription medications: a modifiable contributor to obesity. South Med J 1999;92:898–904. doi:10.1097/00007611-199909000-00009
      OpenUrlCrossRefPubMedWeb of Science
    37. ↵
      1. Buchbinder R,
      2. Hoving JL,
      3. Green S, et al
      . Short course prednisolone for adhesive capsulitis (frozen shoulder or stiff painful shoulder): a randomised, double blind, placebo controlled trial. Ann Rheum Dis 2004;63:1460–9. doi:10.1136/ard.2003.018218
      OpenUrlAbstract/FREE Full Text
    38. ↵
      1. Aaron SD,
      2. Vandemheen KL,
      3. Hebert P, et al
      . Outpatient oral prednisone after emergency treatment of chronic obstructive pulmonary disease. New Engl J Med 2003; 348:2618–25. doi:10.1056/NEJMoa023161
      OpenUrlCrossRefPubMedWeb of Science
    39. ↵
      1. Halvorsen P,
      2. Raeder J,
      3. White PF, et al
      . The effect of dexamethasone on side effects after coronary revascularization procedures. Anesth Analg 2003;96:1578–83. doi:10.1213/01.ANE.0000063922.90966.3A
      OpenUrlPubMedWeb of Science

    Footnotes

    • Contributors CL collected data on GC treatment from medical records and performed all statistical analyses. JF provided data on dietary intake from SLEVIC master file. RvV played a major role in study design and drafting the manuscript together with CL. JF and IH were instrumental in establishing the SLEVIC registry and contributed to study design and interpretation. All authors approved the final manuscript.

    • Competing interests None declared.

    • Patient consent Obtained.

    • Ethics approval This study was approved by regional ethical review board at Karolinska Institutet, Stockholm, Sweden.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Data sharing statement No additional data are available.