Mineralocorticoid Dysfunction during Critical Illness

Nethathe, Gladness Dakalo; Cohen, Jérémy; Lipman, Jeffrey; Anderson, Ronald; Feldman, Charles

doi:10.1097/aln.0000000000003365

Cited by 15 publications

(14 citation statements)

References 156 publications

(232 reference statements)

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“…Glucocorticoids can also promote the formation of angiotensin II (Ang II), and up-regulate Ang II binding receptors in blood vessels, which further potentiate Ang II vasoconstrictor action. [12] Furthermore, glucocorticoids can bind to glucocorticoid receptors in VSMCs, thereby increasing the sensitivity of blood vessels to adrenergic agonists, and promoting further vasoconstriction. [13] Alternatively, they can also increase the proliferation of VSMCs, which promotes nutritive activity and leads to enhanced vasoconstriction.…”

Section: Discussionmentioning

confidence: 99%

Acute bilateral cerebral infarction in the presence of neuromyelitis optica spectrum disorder

Wang

Wang²,

Guo³

et al. 2020

Medicine

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Rationale: Neuromyelitis optica spectrum disorders (NMOSDs) are inflammatory demyelinating disorders of the central nervous system; they are characterized by severe optic neuritis and transverse myelitis. Intravenous methylprednisolone pulse (IVMP) therapy is an effective treatment that is administered to patients in the acute phase of NMOSD; this therapy has achieved remarkable results in clinical practice. However, there are no reports on NMOSD patients who have experienced an acute bilateral cerebral infarction while undergoing IVMP treatment. Patient concerns: We report on a 62-yr-old woman who was undergoing IVMP therapy for the primary diagnosis of NMOSD. Unexpectedly, the patient's existing limb weakness worsened, and she developed motor aphasia on the second day of IVMP treatment. Additionally, brain magnetic resonance imaging revealed acute bilateral cerebral infarction. Diagnosis: The patient's clinical manifestations, medical imaging results, and laboratory test results were taken into consideration; the final diagnosis was acute bilateral cerebral infarction in the presence of NMOSD. Interventions: Subsequent to the onset of acute cerebral infarction, the patient was immediately treated with oral aspirin, atorvastatin, and intravenous butylphthalide. The hormone dose was adjusted to an oral 60-mg/d dose for maintenance; this was followed by immunoadsorption plasmapheresis for 3 days, and double-filtration plasmapheresis for 2 days. Outcomes: Following treatment onset, the patient's ocular symptoms significantly improved, and her limb muscle strength gradually recovered. Two months after discharge, the patient's husband reported that she was able to walk with the help of others and take care of herself, and that there was no recurrence. Lessons: Medical professionals must be aware of the possibility of NMOSD patients with cerebrovascular risk factors suffering an acute cerebral infarction while undergoing high-dose IVMP therapy, as this therapy can exacerbate existing problems.

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Section: Discussionmentioning

confidence: 99%

Acute bilateral cerebral infarction in the presence of neuromyelitis optica spectrum disorder

Wang

Wang²,

Guo³

et al. 2020

Medicine

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“…It has been attributed to impaired adrenal response to increasing renin levels[ 51 - 53 ]. The recent demonstration of the reduced mortality in septic shock patients treated with adjunctive GCs combined with fludrocortisone[ 9 ], and the effectiveness of angiotensin II in treating vasodilatory shock[ 54 ] has renewed interest in the role of the MR in critical illness[ 55 ].…”

Section: Mrmentioning

confidence: 99%

“…Aldosterone and cortisol bind the MR and have a similar affinity for the MR. The binding of cortisol or aldosterone to the MR results in different cellular responses[ 55 ]. Under physiological conditions, plasma cortisol levels are 100 × higher than aldosterone levels, and most MRs are occupied by GCs.…”

Section: β-Hsdmentioning

confidence: 99%

Glucocorticoid and mineralocorticoid receptor expression in critical illness: A narrative review

Vassiliou¹,

Athanasiou²,

Vassiliadi³

et al. 2021

WJCCM

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The glucocorticoid receptor (GCR) and the mineralocorticoid receptor (MR) are members of the steroid receptor superfamily of hormone-dependent transcription factors. The receptors are structurally and functionally related. They are localized in the cytosol and translocate into the nucleus after ligand binding. GCRs and MRs can be co-expressed within the same cell, and it is believed that the balance in GCR and MR expression is crucial for homeostasis and plays a key role in normal adaptation. In critical illness, the hypothalamic-pituitary-adrenal axis is activated, and as a consequence, serum cortisol concentrations are high. However, a number of patients exhibit relatively low cortisol levels for the degree of illness severity. Glucocorticoid (GC) actions are facilitated by GCR, whose dysfunction leads to GC tissue resistance. The MR is unique in this family in that it binds to both aldosterone and cortisol. Endogenous GCs play a critical role in controlling inflammatory responses in critical illness. Intracellular GC concentrations can differ greatly from blood levels due to the action of the two 11β-hydroxysteroid dehydrogenase isozymes, type 1 and type 2. 11β-hydroxysteroid dehydrogenases interconvert endogenous active cortisol and intrinsically inert cortisone. The degree of expression of the two isozymes has the potential to dramatically influence local GC availability within cells and tissues. In this review, we will explore the clinical studies that aimed to elucidate the role of MR and GCR expression in the inflammatory response seen in critical illness.

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“…The rationale for the use of fludrocortisone was the possibility of concomitant primary adrenal insufficiency and downregulation of the mineralocorticoid receptor in septic shock. At the usual doses of hydrocortisone, however, there is activation of mineralocorticoid receptors and a sufficient mineralocorticoid activity, 46 with adequate activity by , that provides the homeostatic regulation of the receptor activity. 41 There are also relevant questions about the half-life of fludrocortisone (short) 47 and its absorption in critically ill patients (erratic).…”

Section: Summarizing the Evidencementioning

confidence: 99%

What Is the Role of Steroids for Septic Shock in 2021?

Nedel

Lisboa

Salluh

2021

Semin Respir Crit Care Med

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Corticosteroids have been used for decades in the adjunctive treatment of severe infections in intensive care. The most frequent scenario in intensive care is in septic shock, where low doses of glucocorticoids appear to restore vascular responsiveness to norepinephrine. There is a strong body of evidence suggesting that hydrocortisone reduces time on vasopressor, and may modulate the immune response. In this review, we explore the current evidence supporting the use of corticosteroids in septic shock, its benefits, and potential harms. In addition to landmark clinical trials, we will also describe new frontiers for the use of corticosteroids in septic shock which should be explored in future studies.

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Mineralocorticoid Dysfunction during Critical Illness

Cited by 15 publications

References 156 publications

Acute bilateral cerebral infarction in the presence of neuromyelitis optica spectrum disorder

Acute bilateral cerebral infarction in the presence of neuromyelitis optica spectrum disorder

Glucocorticoid and mineralocorticoid receptor expression in critical illness: A narrative review

What Is the Role of Steroids for Septic Shock in 2021?

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