Glucocorticoid Use and Abuse in SLE
Glucocorticoid Use and Abuse in SLE
Glucocorticoids (GCs) are potent anti-inflammatory and immunosuppressive agents. They act by two different mechanisms: the genomic and the non-genomic pathways. The genomic pathway is considered responsible for many adverse effects of GCs, most of them are time and dose dependent. Observational studies support a relationship between GCs and damage in SLE. GCs have been associated with the development of osteoporosis, osteonecrosis, cataracts, hyperglycaemia, coronary heart disease and cognitive impairment, among others. Although no clinical trial has compared high vs low doses of GCs, some studies have shown the efficacy of medium doses in severe forms of SLE. The dose below which treatment can be considered safe has not been defined, but daily doses <7.5 mg of prednisone seem to minimize adverse effects. Combination therapy with HCQ and the judicious use of immunosuppressive drugs help to keep prednisone therapy within those limits.
GCs are potent anti-inflammatory and immunosuppressive agents. They are widely used in clinical practice to treat systemic autoimmune diseases, and also a number of diverse conditions, such as asthma, skin diseases, allergic reactions and other systemic diseases. The utility of cortisone for the treatment of RA was proved by Hench et al., who was awarded the Nobel Prize for Medicine in 1950. Following Hench et al.'s initial discovery, new CSs have been developed. These new drugs have lower mineralocorticoid and higher GC activity, showing a higher anti-inflammatory potency. Despite their important clinical efficacy, GCs produce several adverse reactions, most are time and dose dependent, limiting their clinical usefulness. These adverse effects are particularly relevant in chronic diseases that require long treatment periods. A clear example is SLE and other autoimmune diseases.
In this article, we aim to critically review the relation between the dose of GCs, mainly prednisone and prednisolone, and their efficacy and unwanted side effects, based on the pharmacological basis of GC actions and specifically focusing on SLE. We will try to defend the idea that a sensible use of lower doses of prednisone is not associated with less clinical efficacy, while substantially reducing corticoid-related damage.
Abstract and Introduction
Abstract
Glucocorticoids (GCs) are potent anti-inflammatory and immunosuppressive agents. They act by two different mechanisms: the genomic and the non-genomic pathways. The genomic pathway is considered responsible for many adverse effects of GCs, most of them are time and dose dependent. Observational studies support a relationship between GCs and damage in SLE. GCs have been associated with the development of osteoporosis, osteonecrosis, cataracts, hyperglycaemia, coronary heart disease and cognitive impairment, among others. Although no clinical trial has compared high vs low doses of GCs, some studies have shown the efficacy of medium doses in severe forms of SLE. The dose below which treatment can be considered safe has not been defined, but daily doses <7.5 mg of prednisone seem to minimize adverse effects. Combination therapy with HCQ and the judicious use of immunosuppressive drugs help to keep prednisone therapy within those limits.
Introduction
GCs are potent anti-inflammatory and immunosuppressive agents. They are widely used in clinical practice to treat systemic autoimmune diseases, and also a number of diverse conditions, such as asthma, skin diseases, allergic reactions and other systemic diseases. The utility of cortisone for the treatment of RA was proved by Hench et al., who was awarded the Nobel Prize for Medicine in 1950. Following Hench et al.'s initial discovery, new CSs have been developed. These new drugs have lower mineralocorticoid and higher GC activity, showing a higher anti-inflammatory potency. Despite their important clinical efficacy, GCs produce several adverse reactions, most are time and dose dependent, limiting their clinical usefulness. These adverse effects are particularly relevant in chronic diseases that require long treatment periods. A clear example is SLE and other autoimmune diseases.
In this article, we aim to critically review the relation between the dose of GCs, mainly prednisone and prednisolone, and their efficacy and unwanted side effects, based on the pharmacological basis of GC actions and specifically focusing on SLE. We will try to defend the idea that a sensible use of lower doses of prednisone is not associated with less clinical efficacy, while substantially reducing corticoid-related damage.
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