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      Oral steroid-sparing effect of high-dose inhaled corticosteroids in asthma

      , , , ,

      European Respiratory Journal

      European Respiratory Society (ERS)

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          Abstract

          Background

          The proportion of the efficacy of high-dose inhaled corticosteroids (ICS) in oral corticosteroid-dependent asthma that is due to systemic effects is uncertain. This study aimed to estimate the ICS dose–response relationship for oral corticosteroid-sparing effects in oral corticosteroid-dependent asthma, and to determine the proportion of oral corticosteroid-sparing effects due to their systemic effects, based on the comparative dose–response relationship of ICS versus oral corticosteroids on adrenal suppression.

          Methods

          Systematic review and meta-analysis of randomised controlled trials reporting oral corticosteroid-sparing effects of high-dose ICS in oral corticosteroid-dependent asthma. In addition, reports of oral corticosteroid to ICS dose-equivalence in terms of adrenal suppression were retrieved. The primary outcome was the proportion of the oral corticosteroid-sparing effect of ICS that could be attributed to systemic absorption, per 1000 µg increase of ICS, expressed as a ratio. This ratio estimates the oral corticosteroid sparing effect of ICS due to systemic effects.

          Results

          11 studies including 1283 participants reporting oral corticosteroid-sparing effects of ICS were identified. The prednisone dose decrease per 1000 µg increase in ICS varied from 2.1 mg to 4.9 mg, depending on the type of ICS. The ratio of the prednisone-sparing effect due to the systemic effects per 1000 µg of fluticasone propionate was 1.02 (95% CI 0.68–2.08) and for budesonide was 0.93 (95% CI 0.63–1.89).

          Conclusion

          In patients with oral corticosteroid-dependent asthma, the limited available evidence suggests that the majority of the oral corticosteroid-sparing effect of high-dose ICS is likely to be due to systemic effects.

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          Most cited references 33

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          Inhaled corticosteroids and the risks of diabetes onset and progression.

          Systemic corticosteroids are known to increase diabetes risk, but the effects of high-dose inhaled corticosteroids are unknown. We assessed whether the use and dose of inhaled corticosteroids increase the risk of diabetes onset and progression. We formed a new-user cohort of patients treated for respiratory disease during 1990-2005, identified using the Quebec health insurance databases and followed through 2007 or until diabetes onset. The subcohort treated with oral hypoglycemics was followed until diabetes progression. A nested case-control analysis was used to estimate the rate ratios of diabetes onset and progression associated with current inhaled corticosteroid use, adjusted for age, sex, respiratory disease severity, and co-morbidity. The cohort included 388,584 patients, of whom 30,167 had diabetes onset during 5.5 years of follow-up (incidence rate 14.2/1000/year), and 2099 subsequently progressed from oral hypoglycemic treatment to insulin (incidence rate 19.8/1000/year). Current use of inhaled corticosteroids was associated with a 34% increase in the rate of diabetes (rate ratio [RR] 1.34; 95% confidence interval [CI], 1.29-1.39) and in the rate of diabetes progression (RR 1.34; 95% CI, 1.17-1.53). The risk increases were greatest with the highest inhaled corticosteroid doses, equivalent to fluticasone 1000 μg per day or more (RR 1.64; 95% CI, 1.52-1.76 and RR 1.54; 95% CI, 1.18-2.02; respectively). In patients with respiratory disease, inhaled corticosteroid use is associated with modest increases in the risks of diabetes onset and diabetes progression. The risks are more pronounced at the higher doses currently prescribed in the treatment of chronic obstructive pulmonary disease. Copyright © 2010 Elsevier Inc. All rights reserved.
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            Adrenal Insufficiency in Corticosteroids Use: Systematic Review and Meta-Analysis.

            We aimed to estimate pooled percentages of patients with adrenal insufficiency after treatment with corticosteroids for various conditions in a meta-analysis. Secondly, we aimed to stratify the results by route of administration, disease, treatment dose, and duration.
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              A low dose ACTH test to assess the function of the hypothalamic-pituitary-adrenal axis.

              The insulin tolerance test (ITT) has long been used to assess the hypothalamic-pituitary-adrenal axis, but may be hazardous. The standard synthetic ACTH (Synacthen) test has been advocated as a substitute but is sometimes insensitive. In this study the ITT has been compared to a low dose ACTH stimulation test (1 microg) and the standard ACTH stimulation test (250 microg). Twenty-seven subjects were studied, 24 with verified or suspected hypothalamic-pituitary disorders and three on long-term glucocorticoid therapy. Insulin tolerance, low dose ACTH and standard ACTH tests were performed in all patients. The ITT was performed less than 48 hours after the ACTH tests. Synacthen was administered as an intravenous bolus. Serum cortisol values were determined by radioimmunoassay. The peak cortisol value during ITT was compared to the cortisol levels during the ACTH tests. There was a highly significant correlation between peak cortisol values during ITT and cortisol levels after 20-60 minutes in the low dose ACTH test (r(s) = 0.91-0.93; P < 0.0001) and after 30 and 60 minutes in the standard ACTH test (r(s) = 0.85 and 0.89 respectively; P < 0.0001). Four patients showed discrepancies between the three tests. The 1-microg ACTH test follows the ITT more closely and may be more sensitive than the standard ACTH test in detecting more subtle insufficiency of the hypothalamic-pituitary-adrenal axis. The standard ACTH test and the insulin tolerance test may thus be replaced by the 1-microg ACTH test in screening for secondary cortisol insufficiency. We recommend that serum cortisol is measured before and 30 and 40 minutes after the ACTH injection.
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                Author and article information

                Journal
                European Respiratory Journal
                Eur Respir J
                European Respiratory Society (ERS)
                0903-1936
                1399-3003
                January 02 2020
                January 2020
                January 2020
                September 26 2019
                : 55
                : 1
                : 1901147
                Article
                10.1183/13993003.01147-2019
                © 2019

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