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  • Title: Comparison of numerical and phenotypic leukocyte changes during constant hydrocortisone infusion in normal humans with those in thermally injured patients.
    Author: Calvano SE, Albert JD, Legaspi A, Organ BC, Tracey KJ, Lowry SF, Shires GT, Antonacci AC.
    Journal: Surg Gynecol Obstet; 1987 Jun; 164(6):509-20. PubMed ID: 3589906.
    Abstract:
    Twenty-four to 48 hours after thermal injury, percentages and number of T X mu or T4 lymphocytes decrease with little or no change in T X gamma or T8 cells. Additionally, the plasma hydrocortisone level is extremely elevated. Since administration of hydrocortisone to normal humans also produces a specific decrease in T X mu or T4 lymphocytes, it was hypothesized that burn induced elevations of hydrocortisone were responsible for the decrease in T X mu/T4 cells. In this study, normal humans were administered constant infusions of hydrocortisone for six hours, such that plasma levels were increased to an extent that mimics those 24 to 48 hours after thermal injury. Before, during and after infusion, percentages and numbers of lymphocytes, monocytes, granulocytes and T3, T4, T8, T11, HLA-DR and Leu7 lymphocytes were quantified by flow cytometry. Results were compared with those for patients with burns. The plasma hydrocortisone level rose to 49.0 micrograms per deciliter during infusion, similar to the mean of 47.5 micrograms per deciliter for patients with burns. Infused volunteers showed significant lymphopenia, monocytopenia and granulocytosis. Additionally, there were significant decreases in percentages of T3, T4 and T11 lymphocytes, no significant changes in percentages of T8 or HLA-DR and an increase in percentages of Leu7+ cells. These changes in lymphocyte subsets mimicked those of burn patients. Numbers of T3, T4 and T11 cells significantly decreased during hydrocortisone infusion while numbers of T8, HLA-DR and Leu7 lymphocytes did not change. Burn patients showed decreased numbers of T3 and T4 cells, but this T3/T4 lymphopenia was not as great as during hydrocortisone infusion. These results support the hypothesis that elevation of hydrocortisone is responsible for the lymphocyte phenotypic changes that occur in the early postburn period.
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