Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2008 Aug;71(2):298-301.
doi: 10.1016/j.mehy.2008.03.019. Epub 2008 Apr 29.

What caused lymphopenia in SARS and how reliable is the lymphokine status in glucocorticoid-treated patients?

N S Panesar  1
Affiliations

What caused lymphopenia in SARS and how reliable is the lymphokine status in glucocorticoid-treated patients?

N S Panesar. Med Hypotheses. 2008 Aug.

Abstract

Severe Acute Respiratory Syndrome (SARS) outbreak in 2002-03 caused morbidity in over 8000 individuals and mortality in 744 in 29 countries. Lymphopenia along with neutrophilia was a feature of SARS, as it is in respiratory syncytial virus (RSV) and Ebola infections, to name a few. Direct infestation of lymphocytes, neutrophils and macrophages by SARS coronavirus (CoV) has been debated as a cause of lymphopenia, but there is no convincing data. Lymphopenia can be caused by glucocorticoids, and thus any debilitating condition has the potential to induce lymphopenia via stress mechanism involving the hypothalamic-pituitary-adrenal axis. Cortisol levels are elevated in patients with RSV and Ebola, and cortisol was higher in SARS patients with lymphopenia before any steroid therapy. Glucocorticoids also down-regulate the production of proinflammatory lymphokines. Because of the insidious presentation, SARS was treated with antibacterial, antiviral and supra-physiological doses of glucocorticoids. Treatment with glucocorticoids complicated the issue regarding lymphopenia, and certainly calls into question the status of lymphokines and their prognostic implications in SARS.

PubMed Disclaimer

References

    1. Anand K., Ziebuhr J., Wadhwani P., Mesters J.R., Hilgenfeld R. Coronavirus main proteinase (3CLpro) structure: basis for design of anti-SARS drugs. Science. 2003;300:1763–1767. - PubMed
    1. Ho J.C., Ooi G.C., Mok T.Y. High-dose pulse versus nonpulse corticosteroid regimens in severe acute respiratory syndrome. Am J Respir Crit Care Med. 2003;168:1449–1456. - PubMed
    1. Sung J.J.Y., Wu A., Joynt G.M. Severe acute respiratory syndrome: report of treatment and outcome after a major outbreak. Thorax. 2004;59:414–420. - PMC - PubMed
    1. Lee N., Hui D., Wu A. A major outbreak of severe acute respiratory syndrome in Hong Kong. New Engl J Med. 2003;348:1986–1994. - PubMed
    1. Booth C.M., Matukas L.M., Tomlinson G.A. Clinical features and short-term outcomes of 144 patients with SARS in the greater toronto area. Jama. 2003;289:2801–2809. - PubMed

MeSH terms