Glucocorticoids in the treatment of rheumatic diseases: An update on the mechanisms of action

Buttgereit, Frank; Straub, Rainer H.; Wehling, Martin; Burmester, Gerd‐Rüdiger

doi:10.1002/art.20583

Cited by 301 publications

(246 citation statements)

References 66 publications

(91 reference statements)

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“…Physicochemical changes cause interactions between biologic membranes, and this possibly contributes to the therapeutic effect [28]. Glucocorticoids can change the physicochemical properties of biological membranes, especially plasma and mitochondrial membranes.…”

Section: Non-specific Nongenomic Effectsmentioning

confidence: 99%

“…Glucocorticoids can change the physicochemical properties of biological membranes, especially plasma and mitochondrial membranes. Glucocorticoids are thought to intercalate into these membranes and change the function of membraneassociated proteins, thereby affecting lipid peroxidation and membrane permeability [28,29]. In immune cells, the interaction of glucocorticoids with plasma membranes results in rapidly reduced calcium and sodium cycling across the membranes, which, in turn, is thought to contribute to immunosuppression and the reduction of inflammation.…”

Section: Non-specific Nongenomic Effectsmentioning

confidence: 99%

“…Three nongenomic mechanisms with different speeds have been defined for glucocorticoids [28][29][30]. Non-genomic effects may prepare the cell for subsequent glucocorticoid-induced genomic changes, bridge the gap between the early need of change and the delay in the expression of genomic effects and may induce specific changes that in some instances are opposite to those induced by genomic mechanisms.…”

Section: Introductionmentioning

confidence: 99%

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Section: Non-specific Nongenomic Effectsmentioning

confidence: 99%

Section: Non-specific Nongenomic Effectsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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et al. 2015

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“…Corticosteroids are powerful antiinflammatory drugs used to suppress the effects of the immune response of any origin: autoimmune diseases, allergy or transplant rejection. One of the most commonly used is prednisone, synthetic analogue of cortisol presenting mineralocorticoid action in addition to the glucocorticoid effect [14]. In plasma, cortisol is linked to corticosteroid binding protein (CBG) and albumin, and prednisone circulates free or weakly bound to albumin.…”

Section: Steroid Therapymentioning

confidence: 99%

Glomerulonephritis, Pathogenetic Mechanisms and Therapeutic Options: An Overview

Russo

Musto²,

Testorio³

et al. 2014

J Nephrol Ther

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Introduction: Most forms of human glomerulonephritis (GN) result from immunologic mechanisms that are mediated by the actions of multiple elements of both the innate and adaptive immune systems, thereby resulting in different clinical manifestations. The treatment of immune-mediated kidney disease is based on steroids and immunosuppressive drugs that interfere with the immune processes. These groups of drugs have led to significant benefits, but severe side effects are still frequent. Monoclonal antibodies directed against molecules of inflammation or several cellular components have emerged in clinical practice. Plasmapheresis and new methods to reduce the risks associated with the procedure with standard therapies may be combined. Moreover new therapeutic options have been proposed, as the use of natural anti-inflammatory cytokines or intracellular signaling reducing inflammation.

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“…GC modulate different metabolic pathways by activating cytosolic and membrane-bound GCreceptors as well as nonspecific interaction of GC with cell membranes thus conferring genomic and non-genomic effects [14]. Therefore, GC mediate effects on every cell in the body.…”

Section: Glucocorticoidsmentioning

confidence: 99%

Perioperative management of immunosuppression in rheumatic diseases—what to do?

Härle¹,

Straub

Fleck

2009

Rheumatol Int

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To stop or not to stop immunosuppressive therapy in the perioperative setting puts the clinician to a challenge. The risk of potential wound infection with possible septic or even lethal consequences needs to be weight against exacerbation of the rheumatic disease.However, exacerbation of autoimmune inflammatory activity needs to be treated with increasing immunosuppressive medication, thus leading to enhanced risk of local and systemic infection as well.Unfortunately, up to now there is no data from randomized, double-blind controlled clinical trials available on how to steer immunosuppressive therapy in the perioperative setting, making evidence-based recommendations difficult. Neither is there good evidence, if the risk of infectious complications under immunosuppressive therapy differs according to the type and localization of surgery performed. Finally, immunosuppressive co-medication, like glucocorticoid dosage, is not adequately addressed in the available studies, making interpretation of these studies even more problematic. Therefore, a decision has to be made on an individual basis. We discuss the available data on DMARD and biologics therapy in the perioperative setting and describe our own perioperative management with different DMARDs and biologics.

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Glucocorticoids in the treatment of rheumatic diseases: An update on the mechanisms of action

Cited by 301 publications

References 66 publications

Signal Transduction Pathways in use of Dexamethasone Implant in the Eye

Signal Transduction Pathways in use of Dexamethasone Implant in the Eye

Glomerulonephritis, Pathogenetic Mechanisms and Therapeutic Options: An Overview

Perioperative management of immunosuppression in rheumatic diseases—what to do?

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