Glucose tolerance, insulin sensitivity and  -cell function in patients with rheumatoid arthritis treated with or without low-to-medium dose glucocorticoids

Hoes, Jos N.; Goes, Marlies C van der; Raalte, Daniël H. van; Zijl, N.J. van der; Uyl, Debby den; Lems, Willem F.; Lafeber, Floris; Jacobs, Johannes W. G.; Welsing, Paco M J; Diamant, Michaëla; Bijlsma, J. W. J.

doi:10.1136/ard.2011.151464

Cited by 98 publications

(94 citation statements)

References 28 publications

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“…In our study, short-term prednisolone exposure did not aggravate the already present severe insulin resistance. Similarly, in a previous study, chronic GC treatment in patients with rheumatoid arthritis did not further decrease insulin sensitivity compared with patients without GC-use (39).…”

Section: Clinical Study R E Van Genugten and Othersmentioning

confidence: 99%

Does dipeptidyl peptidase-4 inhibition prevent the diabetogenic effects of glucocorticoids in men with the metabolic syndrome? A randomized controlled trial

Genugten

Raalte

Muskiet

et al. 2014

European Journal of Endocrinology

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Objective: Anti-inflammatory glucocorticoid (GC) therapy often induces hyperglycemia due to insulin resistance and islet-cell dysfunction. Incretin-based therapies may preserve glucose tolerance and pancreatic islet-cell function. In this study, we hypothesized that concomitant administration of the dipeptidyl peptidase-4 inhibitor sitagliptin and prednisolone in men at high risk to develop type 2 diabetes could protect against the GC-induced diabetogenic effects. Design and methods: Men with the metabolic syndrome but without diabetes received prednisolone 30 mg once daily plus sitagliptin 100 mg once daily (nZ14), prednisolone (nZ12) or sitagliptin alone (nZ14) or placebo (nZ12) for 14 days in a double-blind 2!2 randomized-controlled study. Glucose, insulin, C-peptide, and glucagon were measured in the fasted state and following a standardized mixed-meal test. b-cell function parameters were assessed both from a hyperglycemic-arginine clamp procedure and from the meal test. Insulin sensitivity (M-value) was measured by euglycemic clamp. Results: Prednisolone increased postprandial area under the curve (AUC)-glucose by 17% (P!0.001 vs placebo) and postprandial AUC-glucagon by 50% (P!0.001). Prednisolone reduced 1st and 2nd phase glucose-stimulated-and combined hyperglycemia-arginine-stimulated C-peptide secretion (all P%0.001). When sitagliptin was added, both clamp-measured b-cell function (PZNS for 1st and 2nd phase vs placebo) and postprandial hyperglucagonemia (PZNS vs placebo) remained unaffected. However, administration of sitagliptin could not prevent prednisolone-induced increment in postprandial glucose concentrations (P!0.001 vs placebo). M-value was not altered by any treatment. Conclusion: Fourteen-day treatment with high-dose prednisolone impaired postprandial glucose metabolism in subjects with the metabolic syndrome. Concomitant treatment with sitagliptin improved various aspects of pancreatic islet-cell function, but did not prevent deterioration of glucose tolerance by GC treatment.

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Section: Clinical Study R E Van Genugten and Othersmentioning

confidence: 99%

Does dipeptidyl peptidase-4 inhibition prevent the diabetogenic effects of glucocorticoids in men with the metabolic syndrome? A randomized controlled trial

Genugten

Raalte

Muskiet

et al. 2014

European Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…As already described, RA patients tend to have decreased insulin sensitivity and impaired b-cell function when compared to control subjects of comparable age with normal glucose tolerance. Low doses of prednisolone have been shown to acutely affect carbohydrate metabolism [117] and GC-induced hyperglycemia is common in individuals with or without diabetes [114]. However, within the context of RA, the long-term effects of low-dose GC are not clear and longitudinal studies are required in this area.…”

Section: Effects Of Gcs On Glycaemiamentioning

confidence: 99%

“…The mechanisms underlying the effect remain poorly understood, but appear to include increases in gluconeogenesis and hepatic glucose output, as well as inducing insulin resistance [116]. In a cross-sectional analysis of patients with established RA and without type 2 diabetes mellitus, tests showed that there was no difference between chronic GC users and GCnaïve patients in terms of glucose tolerance, insulin sensitivity and b-cell function [117]. As already described, RA patients tend to have decreased insulin sensitivity and impaired b-cell function when compared to control subjects of comparable age with normal glucose tolerance.…”

Section: Effects Of Gcs On Glycaemiamentioning

confidence: 99%

Balancing benefits and risks of glucocorticoids in rheumatic diseases and other inflammatory joint disorders: new insights from emerging data. An expert consensus paper from the European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO)

et al. 2016

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Purpose This consensus review article considers the question of whether glucocorticoid (GC) therapy is still relevant in the treatment of rheumatic diseases, with a particular focus on rheumatoid arthritis (RA), and whether its side effects can be adequately managed. Recent basic and clinical research on the molecular, cellular and clinical effects of GCs have considerably advanced our knowledge in this field. An overview of the subject seems appropriate.

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“…The principal rationale for this treatment regimen is to achieve a higher therapeutic effect than that achieved with conventional oral steroid doses, while minimizing toxicity (4).…”

Section: To the Editormentioning

confidence: 99%

Hyperglycemia and methylprednisolone: Comment on the article by den Uyl et al

Martínez-Martínez¹,

Martínez-Lozano²,

Abud-Mendoza³

2012

Arthritis & Rheumatism

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Glucose tolerance, insulin sensitivity and -cell function in patients with rheumatoid arthritis treated with or without low-to-medium dose glucocorticoids

Abstract: Objectives

Cited by 98 publications

References 28 publications

Does dipeptidyl peptidase-4 inhibition prevent the diabetogenic effects of glucocorticoids in men with the metabolic syndrome? A randomized controlled trial

Does dipeptidyl peptidase-4 inhibition prevent the diabetogenic effects of glucocorticoids in men with the metabolic syndrome? A randomized controlled trial

Balancing benefits and risks of glucocorticoids in rheumatic diseases and other inflammatory joint disorders: new insights from emerging data. An expert consensus paper from the European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO)

Hyperglycemia and methylprednisolone: Comment on the article by den Uyl et al

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