What is the primary effect of long-term corticosteroid therapy in patients?

Long-term corticosteroid therapy primarily leads to suppressive effects on cortisol production. This is due to the negative feedback mechanism that corticosteroids exert on the hypothalamic-pituitary-adrenal (HPA) axis. When high doses of corticosteroids are administered over an extended period, the body's own production of cortisol is inhibited because the body senses that there is already sufficient cortisol present, resulting in decreased stimulation of the adrenal glands. This suppression can lead to secondary adrenal insufficiency if corticosteroids are withdrawn abruptly or if the therapy is not tapered properly.

In contrast to this primary effect, the other options represent responses that can happen in various contexts but are not the primary responses associated with long-term corticosteroid use. For example, long-term corticosteroid use actually tends to decrease, rather than increase, the immune response, thereby making animals more susceptible to infections. Tissue repair may be impaired rather than enhanced during prolonged steroid therapy due to potential inhibition of inflammatory processes that are critical for healing. Finally, glucose levels often increase rather than decrease, as corticosteroids stimulate gluconeogenesis and can lead to insulin resistance, resulting in hyperglycemia over time. Thus, the primary effect of long-term corticosteroid therapy is indeed the suppression of cortisol production.