Dataset Information

Perspectives of Glucocorticoid Use in Patients with Rheumatoid Arthritis.

ABSTRACT:

Objective

Prednisolone is an effective oral glucocorticoid for managing symptoms of rheumatoid arthritis (RA) but has predictable and common adverse effects. We explored patient perspectives of prednisolone use in RA.

Methods

Patients with RA registered with the Australian Rheumatology Association Database (ARAD) who had completed an ARAD questionnaire in the preceding 12 months were invited to participate in an online survey. Responses were linked to already collected respondent demographics, medication use, and patient-reported outcome measures. The Beliefs about Medicine Questionnaire (BMQ) measured patient beliefs on medication necessity and concerns. Free-text responses outlining reasons for stopping or declining prednisolone underwent thematic analysis using NVivo 12.

Results

The survey response rate was 79.6% (804/1010), including 251 (31.2%) reporting current prednisolone use and 432 (53.7%) reporting previous use. Compared with previous users, current users were older (P = 0.0002) and had worse self-reported pain, disease activity, health-related quality of life, and function (all P < 0.001). Current users had higher BMQ scores for prednisolone-specific necessity (3.6 versus 1.7; P <0.001) and concerns (2.7 versus 2.3; P <0.001). In previous prednisolone users (n = 432), the most frequent themes identified in free-text responses for cessation were adequate disease control (30.3%), adverse effects (25.2%), and predetermined short courses (21.3%). Of respondents citing adverse effects for cessation (n = 131), weight gain (27.5%), osteoporosis (14.7%), and neuropsychiatric issues (13.8%) were most frequent.

Conclusions

In our cohort, patients with RA taking prednisolone believed it was necessary yet remained concerned about its use. Adequate disease control and adverse effects were important considerations for patients using prednisolone.

SUBMITTER: Venter G

PROVIDER: S-EPMC8063143 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:INTRODUCTION: The glucocorticoid receptor (GR) plays an important regulatory role in the immune system. Four polymorphisms in the GR gene are associated with differences in glucocorticoid (GC) sensitivity; the minor alleles of the polymorphisms N363 S and BclI are associated with relative hypersensitivity to GCs, while those of the polymorphisms ER22/23EK and 9? are associated with relative GC resistance. Because differences in GC sensitivity may influence immune effector functions, we examined whether these polymorphisms are associated with the susceptibility to develop Rheumatoid Arthritis (RA) and RA disease severity. METHODS: The presence of GR polymorphisms was assessed in healthy controls (n = 5033), and in RA patients (n = 368). A second control group (n = 532) was used for confirmation of results. In RA patients, the relationship between GR polymorphisms and disease severity was examined. RESULTS: Carriers of the N363 S and BclI minor alleles had a lower risk of developing RA: odds ratio (OR) = 0.55 (95% confidence interval (CI) 0.32-0.96, P = 0.032) and OR = 0.73 (95% CI 0.58-0.91, P = 0.006), respectively. In contrast, 9? minor allele carriers had a higher risk of developing RA: OR = 1.26 (95% CI 1.00-1.60, P = 0.050). For ER22/23EK minor allele carriers a trend to an increased risk OR = 1.42 (95% CI 0.95-2.13, P = 0.086) was found. All ER22/23EK carriers (32/32) had erosive disease, while only 77% (259/336) of the non-carriers did (P = 0.008). In addition, ER22/23EK carriers were treated more frequently with anti-tumor necrosis factor-alpha (TNF?) therapy (P < 0.05). CONCLUSIONS: The minor alleles of the 9? and ER22/23EK polymorphisms seem to be associated with increased predisposition to develop RA. Conversely, the minor alleles of the N363 S and BclI polymorphisms are associated with reduced susceptibility to develop RA. These opposite associations suggest that constitutionally determined GC resistance may predispose to development of auto-immunity, at least in RA, and vice versa.