A common observation in patients with severe acute respiratory syndrome (SARS) has been pronounced lymphopenia with reported prevalence of 69-6%1
Glucocorticoids have a profound effect on circulating T lymphocytes,3
which may involve their movement out of the intra-vascular compartment.4
Glucocorticoids are also used therapeutically in lymphoproliferative diseases, because of their cytolethal actions. In the study by Lee and colleagues,1
use of steroids may account for the decreasing trend in lymphocyte count over the 7 days of treatment. Booth and colleagues2
only used steroids in 40% of the patients, less than half of whom received them during the first 48 h. Therefore, some of the lymphopenia reported by Booth and colleagues2
may be associated with use of steroids, but it does not account for all the patients, and certainly not for the lymphopenia at the initial presentation.
Any critical illness is accompanied by the activation of the hypothalamic-pituitary-adrenal axis resulting in increased adrenocorticotropic hormone (ACTH) and cortisol to maintain the integrity of the vasculature and modulate the actions of proinflammatory and anti-inflammatory cytokines.5
In a healthy person under severe stress, pituitary ACTH can easily cause the adrenal cortex to release 225—440 mg per day of cortisol,5
which is equivalent to the dosage of methylprednisolone used by Lee and colleagues' that can drive T lymphocytes out of the peripheral circulation. Therefore, is the lymphopenia seen in some of the SARS patients an indication of the integrity of the status of the hypothalamic-pituitary-adrenal axis? More importantly, are the patients without lymphopenia, adrenal insufficient?
The answers to these questions need to be addressed urgently, because they may have a bearing on whether to use glucocorticoids in the treatment of SARS. Thompson5
has provided a helpful review of glucocorticoids and acute lung injury.