Effects Of Low-dose Glucocorticoids Research Articles

Low-dose glucocorticoid increase the risk of fracture in postmenopausal women with low bone mass: a retrospective cohort study.

The effect of low-dose glucocorticoid (GC) therapy on the fracture risk in postmenopausal women with low bone mass was investigated. 119,790 66-year-old postmenopausal women with low bone mass based on bone mineral density (BMD) results were included. GC group consisted of patients who had been prescribed oral GCs within 6months of BMD testing. In GC group, GCs dosage was calculated by a defined daily dose (DDD), and divided into five groups according to GC usage (Group 1[G1]; < 11.25 DDDs, G2; ≥ 11.25, < 22.5 DDDs, G3; ≥ 22.5, < 45 DDDs, G4; ≥ 45, < 90 DDDs, G5; ≥ 90 DDDs). The risk of major osteoporotic fractures (MOF) and non-MOF was analyzed and compared with that of the control group during the 1-year follow-up. The risk of total fracture was higher in G3-G5 than in the control group (G3, hazard ratio (HR) 1.25, 95% confidence interval [CI] 1.07-1.46; G4, 1.37 [1.13-1.66]; G5 1.45 [1.08-1.94]). The risk of MOF was higher in all groups except G2 than in the control group (G1, 1.23 [1.05-1.45]; G3, 1.37 [1.11-1.68]; G4, 1.41 [1.09-1.83]; G5, 1.66 [1.14-2.42]). The risk of spine fracture was significantly higher in all GC groups except G2 than in the control group. The risk of non-MOF was higher only in G4 than in the control group (G4, 1.48 [1.13-1.94]). Low-dose GC therapy can increase the risk of osteoporotic fractures, particularly spine fractures, in postmenopausal women with low bone mass.

Effect of low-dose glucocorticoid on corticosteroid insufficient patients with acute exacerbation of chronic obstructive pulmonary disease.

This study aimed to investigate the prevalence rate of critical illness-related corticosteroid insufficiency (CIRCI) and the effect of low-dose glucocorticoid on prognosis of CIRCI in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Since January 2010 to December 2012, 385 patients, who met the criteria of AECOPD, were enrolled in the Intensive Care Unit (ICU) of the First People's Hospital and Municipal Central Hospital of Xiangtan City. The AECOPD patients complicated with CIRCI screened by an adrenalcorticotrophic hormone test within 12 hours after admission to ICU were divided into a treatment group (n=32) and a control group (n=31) for a prospective, randomized and controlled clinical trial. Hydrocortisone (150 mg/d) or normal saline was injected intravenously for 7 days. The patients were followed up for 28 days after injection. The endpoint included 28-day survival time, non-shock time, ICU stay and the period of non-mechanical ventilation. The markers of inflammation C-reactive protein, tumor necrosis factor-α, interleukin 6 and procalcitonin were measured at baseline and 7 days after treatment. The variables were analyzed by Student's t test, the non-parametric statistical test, the Chi-square test or the Kaplan-Meier method with SPSS18.0 statistic software. A P value <0.05 was considered statistically significant. Totally 63 patients were diagnosed with CIRCI by an adrenalcorticotrophic hormone test and the prevalence rate was 16.4%. The shock rate of the AECOPD patients complicated with CIRCI was higher than that of the AECOPD patients without CIRCI (23.8% vs. 8.7%, P<0.01). Kaplan-Meier analysis revealed that the 28-day survival time of the treatment group was obviously longer than that of the control group (P<0.05). Compared with the control group, shock-free days within 28 days was longer in the treatment group (18.2±9.5 vs. 25.8±4.1, P<0.05). Treatment with low-dose glucocorticoid obviously decreased the markers of infection and inflammation (P<0.01), such as C-reactive protein (13.2±5.5 mg/L vs. 8.3±3.1 mg/L for the control group; 13.5±5.9 mg/L vs. 5.1±2.3 mg/L for the treatment group), tumor necrosis factor-α (26.1±16.2 μg/L vs. 17.5±11.7 μg/L for the control group; 25.0±14.8 μg/L vs. 10.4±7.8 μg/L for the treatment group) and procalcitonin (3.88 μg/L vs. 2.03 μg/L for the control group; 3.77 μg/L vs. 1.26 μg/L for the treatment group). Furthermore, the markers in the treatment group decreased more obviously than those in the control group (P<0.01). The prevalence rate of CIRCI was higher in the patients with AECOPD in the department of critical medicine, and low-dose glucocorticoid treatment for one week reduced the 28-day mortality, shock time and markers of infection and inflammation.

Effect of low-dose glucocorticoid on corticosteroid insufficient patients with acute exacerbation of chronic obstructive pulmonary disease

Objective To investigate the effect of low-dose glucocorticoid on prognosis of critical illness-related corticosteroid insufficient (CIRCI) patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD).Methods A total of 385 eligible patients met the criteria of AECOPD were admitted from January 2010 to December 2012.The AECOPD patients co-morbid with CIRCI screened by an adrenal corticotrophic hormone test within 12 hours after admission were randomly divided into treatment group (n =32) and control group (n =31) for prospective,randomized (random number) and controlled clinical study.Hydrocortison (150mg/d) for treatment group or normal saline instead for control group was injected intravenously for 7 days.The 28-day mortality,shock-free days,length of ICU stay within 28 days and ventilator-free days were evaluated.And the markers of inflammation C-reactive protein,tumor necrosis factor-α,interleukin 6 and procalcitonin were measured before and 7 days after treatment.The variables were analyzed by Student' s t-test,non-parametric statistical test,Chi-square test or KaplanMeier test with SPSS 18.0 statistic software.P ＜ 0.05 was considered statistically significant.Results A cohort of 385 patients with AECOPD was screened,and the prevalence rate of CIRCI was 16.4％.The shock rate was higher in the AECOPD patients co-morbid with CIRCI than that in the AECOPD patients without CIRCI (23.8％ vs 8.7％,P ＜0.01).Compared with the control group,the 28-day mortality was significantly lower in treatment group (2/32 vs 8/31,P ＜ 0.05),and shock-free days within 28 days longer in the treatment group (18.2 ± 9.5 vs 25.8 ± 4.1,P ＜ 0.05).However,there was no difference in the shock rate,days of ICU stay and ventilator-free days between the two groups.After treatment,the levels of infection markers were decreased and obviously lower than those in control group (P ＜ 0.01),such as Creactive protein (13.2 ± 5.5 mg/L vs 8.3 ± 3.1 mg/L for control group; 13.5 ± 5.9 mg/L vs 5.1 ± 2.3mg/L for treatment group),tumor necrosis factor-α (26.1 ± 16.2 μg/L vs 17.5 ± 11.7 μg/L for control group ; 25.0 ± 14.8 μg/L vs 10.4 ± 7.8 μg/L for treatment group) and procalcitonin [3.88 (0.25,8.5) μg/L vs 2.03 (0.15,5.1) μg/L for control group; 3.77 (0.21,8.0) μg/L vs 1.26 (0.10,3.2) μg/L for treatment group],furthermore,the levels of infection markers were decrease more obviously in the treatment group than those in the control group (P ＜ 0.01).Conclusions There was high prevalence rate of CIRCI in the patients with AECOPD in the department of critical medicine,and low-dose glucocorticoid reduced 28-day mortality,shock days and markers of infection and inflammation. Key words: Chronic obstructive pulmonary disease; Acute exacerbation glucocorticoid; Critical illness ; Corticosteroid insufficiency; Prevalence rate; Prognosis ; Inflammation

Lessons for the use of non-biologic anchor treatments for rheumatoid arthritis in the era of biologic therapies

Optimizing the use of key non-biologic drugs (MTX, prednisone) may prolong disease control, thereby delaying the need for costly biologic therapies. A number of lessons about the optimal use of therapy emerge from clinical studies. Clinical outcomes with non-biologic treatments, given early in the course of the disease, are as good as with biologic treatments. Combinations of treatments are usually required to achieve rapid and sustained remission. MTX remains an important anchor drug for RA therapy and should be given as soon as the diagnosis is made. As early disease control is important, the dose of MTX should be escalated rapidly to adequate levels. Tolerability of MTX is generally good relative to that of other alternative treatments. MTX (s.c.) may be considered if the response to oral MTX is inadequate or MTX is poorly tolerated. In addition to suppressing signs and symptoms of RA, glucocorticoids appear to have disease-modifying effects, at least in early RA. The disease-modifying effects of glucocorticoids probably persist after discontinuation of therapy. The risk of adverse effects of low-dose glucocorticoids is often overestimated. Administration of low-dose glucocorticoids in accordance with physiological circadian rhythms may bring efficacy and safety benefits. As a case in point, the CAMERA (Computer Assisted Management in Early Rheumatoid Arthritis) II study applied these lessons and has clearly shown the benefits of optimizing MTX and prednisone therapy.

Adverse effects of low-dose glucocorticoids and DMARD therapy in patients with RA—a complex relationship?

Although low-dose glucocorticoids, in conjunction with DMARDs, are known to halt or severely retard the erosive destruction of joints in patients with early rheumatoid arthritis (RA), the potential adverse effects of low-dose glucocorticoids and the benefit:risk ratio of treatment are a concern for many clinicians. Malysheva and colleagues undertook a retrospective, open-label review of the incidence and severity of adverse effects associated with DMARD treatment with or without glucocorticoids in patients with RA. Their results suggest that low-dose glucocorticoids actually help to postpone the occurrence of adverse effects caused by most standard DMARDs, which, if translated into a delay before biologic agents were required, would provide a substantial cost saving. Unfortunately, an increased incidence of adverse reactions was noted for glucocorticoid-treated patients compared with those patients on monotherapy; however, the undesirable effects were mostly mild in nature. This study sheds new light on the relative risks and benefits of low-dose glucocorticoid therapy in RA and adds further weight to the arguments for its appropriate use in early disease.

The use of low- dose glucocorticoids for the treatment of early rheumatoid arthritis: What can we learn about bone effects of glucocorticoids from randomized controlled trials?

Introduction: The use of low-dose glucocorticoids for the treatment of rheumatoid arthritis (RA) has been debated for many years. Glucocorticoids were first introduced as RA treatment in 1950 and Hench and Kendall received the Nobel Prize in Medicine for their efforts in discovering this novel treatment [1]. Over the subsequent years, adverse effects of glucocorticoids began to restrict their use to lower doses. Indeed, newer data on their apparent disease modifying properties have further rejuvenated their use and it is now estimated that at least 40% of RA patients in the United States receive glucocorticoids at some point during their disease course [2]. Despite their widespread use, the one glucocorticoid adverse event that has continued to generate the greatest discussion is osteoporosis. An observational study suggested that patients taking a mean of only 8.6 mg daily of prednisone had a 34% chance of experiencing a fracture after 5 years of follow-up [3]. Data of this type have reasonable generalizability, but suffer from selection biases inherent in therapeutic observational studies. The randomized, controlled trials (RCTs) recently have suggested mixed, but generally only modest effects of low-dose glucocorticoids on the bone [4–7]. Two recent studies have examined the use of low-dose prednisolone in combination with disease-modifying antirheumatic drugs (DMARDs) in early RA during a 2-year period. Both of these RCTs also have included data on the adverse effects of glucocorticoids—in particular, their effects on bone.