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Effect of low-dose prednisone on leukocyte counts and subpopulations in patients with rheumatoid arthritis.

Leukocytosis is a clinical laboratory hallmark of bacterial infection, a common complication in patients with rheumatoid arthritis (RA). Corticosteroids are known to increase white blood cell counts (WBC), and their use may be a potential confounder in RA patients suspected of concomitant bacterial infection. Up to 75% of patients with RA are estimated to use corticosteroids as part of their therapeutic scheme. In our center, 85% of patients had a current or past history of treatment with these drugs. In this hospital-based, observational cross-sectional retrospective study, 157 consecutive patients with RA (American College of Rheumatology criteria) were receiving (n 91) or not (n 66) daily doses of oral prednisone. Average prednisone dose was 6.1 2.7 mg. Groups were comparable except for a lower frequency of treatment with methotrexate and chloroquine in the prednisone-untreated group (data not shown) and in younger age in the prednisone-treated group (Table 1). Inclusion criteria were age between 18 and 80 years, and disease duration equal or longer than 6 months. Exclusion criteria were acute or chronic infectious processes or the presence of any of the following conditions within the 2 months prior to entry: diabetic ketoacidosis, hyperthyroidism, acute or subacute thyroiditis, Cushing syndrome, pheochromocytoma, myeloproliferative or lymphoproliferative disease, recent coronary disease events, trauma, use of lithium, beta adrenergic agonists, or intraarticular injection of corticosteroids. Venous blood samples were obtained in the morning by routine techniques and read in a Coulter GEN-STM hematology analyzer with AccuGate software (Beckman Coulter Inc., Fullerton, CA). The study was approved by the Bioethics Committee of the Hospital Universitario de Caracas and all patients signed an informed consent. WBC and neutrophil counts were significantly higher, whereas lymphocyte counts were lower in patients receiving oral prednisone (Table 1). Thirteen of 91 patients receiving prednisone versus 6 of 66 patients not receiving prednisone showed leukocytosis (NS, 2 test). After excluding this subgroup of patients with leukocytosis, patients on prednisone still showed higher number of WBC ( 0.23, P 0.03). There were no differences in the proportions of patients with or without neutrophilia in both groups. No differences were seen in monocyte or eosinophil total counts. WBC or eosinophil counts did not correlated with disease activity (as measured by DAS28) or with the use of disease modifying antirheumatic drugs (data not shown). There was a direct correlation between prednisone dose and WBC total counts (R 0.23, P 0.01) as well as neutrophil counts (R 0.22, P 0.01). To control for the contribution of other demographic and clinical covariates, we performed multiple regression analysis confirming that only prednisone dose was significantly associated with higher leukocyte counts ( 348.67, Standard Error SE 154.61) and higher neutrophil counts ( 387.93, SE 148.14). These results confirm an effect of corticosteroids on WBC and neutrophil counts in patients with RA. However, within the range of prednisone doses used by our patients, neither leukocytosis nor neutrophilia were seen as an effect attributable to prednisone treatment. According to our results low-dose prednisone regimens seem not to have a significant impact on circulating blood leukocytes. Therefore, in any RA patient being treated with low-dose prednisone, the appearance of leukocytosis or neutrophilia should warrant the search for other causes.