Glucocorticoids (GCs) induce insulin synthesis but oppose its effects on glucose metabolism, thus predisposing to or exacerbating, if present, diabetes mellitus. These effects take place because of decreased peripheral utilization of glucose and increased gluconeogenesis induction in the liver. GC enhances effects on lipolysis and protein catabolism, thus increasing the substrates for gluconeogenesis (Schimmer and Parker 1996). GCs have an impact on lipid metabolism by enhancing the lipolytic effect of catecholamines and growth hormone, and they induce a centripetal body fat redistribution (Orth and Kovacs 1998). One study showed that the administration of prednisone for 14 days in healthy men increased the levels of very-low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides (Ettinger and Haz-zard 1988). Another study showed that increasing the prednisone dose by 10 mg daily was associated with a 7.5-mg/dL increase in cholesterol levels (Petri et al. 1994). GCs induce peripheral neutrophilia and elevate white blood cell counts by reducing neu-trophil migration to tissues (Boumpas et al. 1993). Because of these effects of GCs, before starting therapy, it is recommended to check the baseline lipid panel (total cholesterol, low-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, and triglyceride levels), complete blood cell count, and serum glucose and potassium levels. Thereafter, serum or urine glucose levels should be checked every 3-6 months. Since corticosteroids promote the excretion of water, some of its mineralocorticoid effects include hypokalemia, which should also be monitored.

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