Can we manage lupus nephritis without chronic corticosteroids administration?

Lightstone, Liz; Doria, Andrea; Wilson, Hannah R; Ward, Frank; Larosa, Maddalena; Bargman, Joanne M.

doi:10.1016/j.autrev.2017.11.002

Cited by 40 publications

(24 citation statements)

References 63 publications

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“…Remission rates at 48 weeks were 49.45% and 39.8% in both voclosporin groups [ 28 ]. Even patients in the control arm of the AURA trial had remission rates higher than those in previous studies such as ALMS [ 29 ] and LUNAR [ 30 , 31 ].…”

Section: Introductionmentioning

confidence: 72%

“…Thus, current evidence, based on large observational cohorts and a few clinical trials, supports the idea that low-medium initial doses of prednisone (i.e., ≤30 mg/day) are at least as effective as high-dose schemes and with a better safety profile [ 31 , 33 ]. MP pulses offer additional potency and allow the use of lower doses of prednisone.…”

Section: Introductionmentioning

confidence: 99%

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Glucocorticoids in Systemic Lupus Erythematosus. Ten Questions and Some Issues

Porta

Danza

Saavedra

et al. 2020

JCM

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Since the discovery of glucocorticoids (GCs), their important anti-inflammatory effect, rapid mechanism of action, low cost, and accessibility have made them one of the mainstays of treatment for Systemic lupus erythematosus (SLE). Although their use has allowed controlling the disease and reducing acute mortality in severe conditions, the implementation of a scheme based on high doses for long periods has inevitably been accompanied by an increase in adverse effects and infections, including long-term damage. The objective of this review is to answer some important questions that may arise from its use in daily clinical practice, and to propose a paradigm based on the use of methylprednisolone pulses followed by medium-low doses and a rapid decrease of prednisone.

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Section: Introductionmentioning

confidence: 72%

Section: Introductionmentioning

confidence: 99%

Glucocorticoids in Systemic Lupus Erythematosus. Ten Questions and Some Issues

Porta

Danza

Saavedra

et al. 2020

JCM

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“…As an active agent, ACTH exerts direct anti-inflammatory effects directly through melanocortin (M)-1-5 receptors, which leads to nuclear factor kappa B inhibition, as well as indirect effects via stimulation of cortisol release [ 55 ]. While contemporary pharmaceuticals have shifted towards B cell depletion and other B cell-directed modalities, the HPA axis continues to be relevant in the treatment of severe SLE and synthetic hormones targeting the HPA axis have greatly decreased morbidity and mortality since their widespread use [ 56 ]. For these reasons, studies like ours help to clearly define nuances in HPA axis dysfunction, which could assist with more effective drug regimens.…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide Challenge Reveals Hypothalamic-Pituitary-Adrenal Axis Dysfunction in Murine Systemic Lupus Erythematosus

Pham

Mathis

2018

Brain Sciences

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Crosstalk between the brain and innate immune system may be dysregulated in systemic lupus erythematosus (SLE), a chronic autoimmune disease that presents with dysautonomia and aberrant inflammation. The hypothalamic-pituitary-adrenal (HPA) axis is an endogenous neuro-endocrine-immune pathway that can regulate inflammation following activation of vagal afferents. We hypothesized that chronic inflammatory processes in SLE are in part due to HPA axis dysfunction, at the level of either the afferent vagal-paraventricular nuclei (PVN) interface, the anterior pituitary, and/or at the adrenal glands. To study this, we challenged female control and SLE mice with lipopolysaccharide (LPS) and measured c-Fos expression as an index of neuronal activation, plasma adrenocorticotrophic hormone (ACTH) as an index of anterior pituitary function, and plasma corticosterone as an index of adrenal function. We found that c-Fos expression in the PVN, and plasma ACTH and corticosterone were comparable between unchallenged SLE and control mice. PVN c-Fos was increased similarly in control and SLE mice three hours after LPS challenge; however, there were no changes in plasma ACTH amongst any experimental groups post inflammatory challenge. Plasma corticosterone was markedly increased in LPS-challenged SLE mice compared to their vehicle-treated counterparts, but not in controls. Paradoxically, following LPS challenge, brain and spleen TNF-α were elevated in LPS-challenged SLE mice despite heightened plasma corticosterone. This suggests that, despite normal c-Fos expression in the PVN and activation of the HPA axis following LPS challenge, this cumulative response may not adequately defend SLE mice against inflammatory stimuli, leading to abnormally heightened innate immune responses and peripheral inflammation.

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“…doses of methylprednisolone bolus (500 mg each) and 2 doses of Rituximab 1 g on days 1 and 15, followed by maintenance treatment with mycophenolate mofetil [23]. After 5 years of follow-up, the majority of these patients are still in remission with preserved renal function [24].…”

Section: Editorialmentioning

confidence: 99%