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Cited by 1,044Adrenal Hormones and DisordersEstrogen and related hormone effectsStress Responses and Cortisol

Glucocorticosteroid Therapy: Mechanisms of Action and Clinical Considerations

FAUCI, ANTHONY S., DALE, DAVID C., BALOW, JAMES E.·1976·Annals of Internal Medicine
DOI 10.7326/0003-4819-84-3-304
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Abstract

The administration of glucocorticosteroids results in a wide range of effects on inflammatory and immunologically mediated disease processes. Glucocorticosteroids cause neutrophilic leukocytosis together with eosinopenia, monocytopenia, and lymphocytopenia. A principal mechanism whereby corticosteroids suppress inflammation is their impeding the access of neutrophils and monocytes to an inflammatory site. Granulocyte function is relatively refractory, whereas monocyte-macrophage function seems to be particularly sensitive to corticosteroids. Corticosteroid administration causes a transient lymphocytopenia of all detectable lymphocyte subpopulations, particularly the recirculating thymus-derived lymphocyte. The mechanism of this lymphocytopenia is probably a redistribution of circulating cells to other body compartments. There is considerable disagreement about the direct effects of corticosteroid administration on human lymphocyte function. The corticosteroid regimen should be adjusted to attain maximal therapeutic benefit with minimal adverse side effects. Often, alternate-day dosage regimens effectively maintain disease remission with minimization or lack of Cushingoid and infectious complications.

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Crossref · 10.7326/0003-4819-84-3-304

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122 of 122 references verified0 citation errors · 0 not checkable

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  • Greater levels of glucocorticoid are associated with higher numbers of circulating neutrophils, lower numbers of circulating lymphocytes, and a lower neutrophil-to-lymphocyte ratio.

    “Greater levels of glucocorticoid are associated with higher numbers of circulating neutrophils, lower numbers of circulating lymphocytes, and a lower neutrophil-to-lymphocyte (N/L) ratio-an overall marker of the trafficking of these cells (e.g., refs.22,23).”

    From Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk (2012) · cites this paper as [22]

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Authors
FAUCI, A. S., DALE, D. C., & BALOW, J. E.
Affiliations
Bethesda, Maryland
Corresponding author
FAUCI, ANTHONY S.
ORCID
FAUCI, ANTHONY S.
Venue
Annals of Internal Medicine
Publisher
American College of Physicians
Published
1976-03-01
Volume
84
Issue
3
Pages
304-315
ISSN
  • 0003-4819 (ISSN-L)
  • 1539-3704
DOI
10.7326/0003-4819-84-3-304
OpenAlex
W2076863034
Cited by
1,044
References
122
Citations by year
2026: 13 · 2025: 12 · 2024: 15 · 2023: 21 · 2022: 22 · 2021: 32 · 2020: 21 · 2019: 14 · 2018: 12 · 2017: 10 · 2016: 26 · 2015: 9 · 2014: 10 · 2013: 15 · 2012: 13
FWCI
8.34
Type
journal article
Language
en
Open access
closed
Licence
www.acpjournals.org/journal/aim/text-and-data-mining (tdm)
Locations
  • Annals of Internal Medicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
glucocorticoids, anti-inflammatory activity, immunosuppression, neutrophilia, lymphopenia, monocyte/macrophage function, granulocyte function, lymphocyte redistribution, corticosteroid adverse effects, alternate-day dosing, infection risk, inflammatory diseases
MeSH terms
Animals, Glucocorticoids, Granulocytes, Immunity, Cellular, Infections, Inflammation, Kinetics, Lymphocytes, T-Lymphocytes

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