Improving benefit-harm assessment of glucocorticoid therapy incorporating the patient perspective: The OMERACT glucocorticoid core domain set

Tieu, Joanna; Cheah, Jonathan; Black, Robert; Christensen, Robin; Ghosh, Nina; Richards, Pamela; Robson, Joanna; Shea, Beverley; Simon, Lee S.; Singhi, Jasvinder A.; Tugwell, Peter; Boers, Maarten; Garibay, Marco A.Alba; Campochiaro, Corrado; Décary, Simon; Witt, Maarten de; Fernandez, Anthony P.; Keen, Helen; King, Lauren; Hinojosa‐Azaola, Andrea; Hofstetter, C. Richard; Gaydukova, I.; George, Michael; Gupta, Latika; Lyne, Suellen; Makol, Ashima; Mukhtyar, Chetan; Oo, Win Min; Petri, Michelle; Pisaniello, Huai Leng; Sattui, Sebastian E.; Russell, Oscar; Teixeira, Vítor; Toupin‐April, Karine; Uhunmwangho, Courage; Whitstock, Margaret T.; Yip, Kevin; McDermott, Michael; Goodman, Susan M.; Hill, Catherine

doi:10.1016/j.semarthrit.2021.06.010

Cited by 11 publications

(1 citation statement)

References 12 publications

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“…We do not have mechanistic hypothesis for decreased weight gain when the animals were hyperphagic and showed insulin resistance. SPI-62 appeared to attenuate the second phase, CORT-associated accelerated weight gain, which is a core concern expressed by patients with endogenous hypercortisolism (25) or who take GC medicines (26). To date, SPI-62 has not been administered for 5 weeks or longer to mice in the absence of CORT, hence, no inference can be made regarding an independent subchronic or chronic effect of SPI-62 on weight in mice.…”

Section: Discussionmentioning

confidence: 99%

The 11β-hydroxysteroid dehydrogenase type 1 inhibitor SPI-62 prevents morbidity in a mouse model of Cushing’s syndrome

Pan,

Hou,

et al. 2024

Preprint

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Abstract11β-hydroxysteroid dehydrogenase type 1 (HSD-1) inhibitors represent a potential therapeutic approach for patients with Cushing’s syndrome, autonomous cortisol secretion (ACS), or iatrogenic glucocorticoid (GC) excess. We assessed whether the HSD-1 inhibitor SPI-62 prevents GC-associated morbidity in a mouse Cushing’s syndrome model. Corticosterone (CORT) was administered to mice for 5 weeks. Animals who received CORT were randomized between vehicle and 3 SPI-62 regimens. A control group received neither CORT nor SPI-62. Body weight was measured daily to enable weight-based SPI-62 administration. Food consumption by pair-housed animals was reported weekly. Insulin sensitivity was evaluated by fasting homeostatic model assessment of insulin resistance. Adiposity and skeletal myopathy were measured using magnetic resonance imaging and post-mortem weights of fat depots and skeletal muscles. Grip strength was measured with a digital meter. Ambulation behavior in an open field maze was assessed. Post-mortem dermal thickness was quantified. Skin structure was evaluated by histology. CORT was associated with decreased insulin sensitivity, increased adiposity, skeletal myoatrophy, reduced grip strength, decreased dermal thickness, and skin structural changes. A trend of increased food consumption and an unexpected biphasic weight change were observed with CORT. SPI-62 attenuated all observed adverse effects in a dose-dependent manner. In general, results for the high SPI-62 regimen were similar as those in animals who received no CORT, suggesting that full HSD-1 inhibition should be maintained throughout a dose interval to mitigate the effects of glucocorticoid excess.

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Section: Discussionmentioning

confidence: 99%

The 11β-hydroxysteroid dehydrogenase type 1 inhibitor SPI-62 prevents morbidity in a mouse model of Cushing’s syndrome

Pan,

Hou,

et al. 2024

Preprint

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Short-term induction glucocorticoids and disease-modifying anti-rheumatic drugs (DMARD) therapy for rheumatoid arthritis

Hepworth

Lee

Pardo

et al. 2021

Cochrane Database of Systematic Reviews

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The Burden of Glucocorticoids: Patterns of Use, Adverse Health Conditions, and Health Care Use in Two Cohorts With Systemic Lupus Erythematosus

Katz,

Pedro,

Park

et al. 2024

ACR Open Rheumatology

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ObjectiveGlucocorticoids (GCs) can be beneficial from both clinical and patient perspectives, but side effects are well documented. We examined patterns of GC use over 15 years (2006–2021) and occurrence of adverse health conditions (AHCs) and health care use by GC exposure in two longitudinal cohorts with systemic lupus erythematosus (SLE).MethodsData from the Lupus Outcomes Study (LOS; 2003–2015) and FORWARD cohort (2015–2021) were used. AHCs examined were diabetes, osteoporosis, nontraumatic fractures, cataracts, and infections. Health care use measures examined were the number of rheumatology and other provider visits, hospitalizations, and specific diagnostic tests. Kaplan–Meier analyses examined time to occurrence of each AHC. Cox regression analyses estimated the risk of occurrence of AHCs, controlling for covariates by GC use and by GC dose (0, 1–5, 5–7.5, and ≥7.5 mg).ResultsGC use was relatively consistent over time. At baseline, individuals who used GCs in the LOS were more likely to report osteoporosis (adjusted odds ratio [aOR] 1.7, 95% confidence interval [CI] 1.2–2.6) and cataracts (aOR 1.6, 95% CI 1.04–2.6); individuals who used GCs in the FORWARD cohort were more likely to report diabetes (aOR 5.1, 95% CI 2.2–12.0), osteoporosis (aOR 4.5, 95% CI 2.6–8.0), and fractures (aOR 6.5, 95% CI 3.8–11.1). Individuals who used high doses of GCs in the LOS had greater incidence of osteoporosis, fracture, and cataracts. In the FORWARD cohort, a significant difference in incidence was noted only for infections. In both cohorts, individuals who used GCs had more rheumatology and other physician visits, and greater risk of hospitalization.ConclusionDespite recommendations on steroid sparing, a large portion of people with SLE appear to remain on steroids. These analyses provide additional evidence of the potential health and health care burden of GC use, underscoring the need for other effective treatments for individuals with SLE.

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Improving benefit-harm assessment of glucocorticoid therapy incorporating the patient perspective: The OMERACT glucocorticoid core domain set

Cited by 11 publications

References 12 publications

The 11β-hydroxysteroid dehydrogenase type 1 inhibitor SPI-62 prevents morbidity in a mouse model of Cushing’s syndrome

The 11β-hydroxysteroid dehydrogenase type 1 inhibitor SPI-62 prevents morbidity in a mouse model of Cushing’s syndrome

Short-term induction glucocorticoids and disease-modifying anti-rheumatic drugs (DMARD) therapy for rheumatoid arthritis

The Burden of Glucocorticoids: Patterns of Use, Adverse Health Conditions, and Health Care Use in Two Cohorts With Systemic Lupus Erythematosus

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