Glucocorticoids (Gcs) are widely used in the treatment of inflammatory diseases including skin, neurologic, pulmonary and rheumatic disorders. While this treatment is very efficient, the chronic use of systemic (oral and parenteral) glucocorticoid therapy is unfortunately associated with common adverse events (AEs) including secondary osteoporosis, osteonecrosis and muscle weakness. All of these adverse events are associated with an increased risk of fractures (1-3). Bone loss is potentially reversible with the tapering or cessation of glucocorticoid therapy and the withdrawal of Gcs treatment may lead to a reduction of fracture risk. A deleterious effect of Gcs on bone metabolism is caused by a direct inhibition of osteoblast differentiation and function, increased osteocyte apoptosis, secondary hypogonadism, negative calcium balance and myopathy (3). The elevated risk of fractures (long-term use of Gcs causes fractures in about 30 to 50% of patients) (1) and other adverse events such as obesity, insulin resistance, diabetes, cataracts and glaucoma, elevated blood pressure and cardiovascular diseases are similar to clinical symptoms of endogenous Cushing’s syndrome (2). So far, Gcs-induced adverse events including osteoporosis remain under diagnosed and undertreated in many countries (4).

International (1, 4, 5) and Polish experts (6) routinely recommend Vitamin D and calcium supplementation in the prevention and basic management of a primary (7) and secondary osteoporosis, including GIO (4).

Active metabolite of vitamin D, 1,25-dihydroxycholecalciferol increases intestinal calcium absorption, inhibits renal calcium excretion and regulates bone mineralisation. Due to pleiotropic role of vitamin D, low serum concentration of 25(OH)D (< 30 mg/ml) is associated with muscle weakness and atrophy with increased risk of falls (8, 9), osteomalacia, osteoporosis, respiratory infections, diabetes, elevated risk of cardiovascular diseases, autoimmune diseases, dental diseases and risk of cancer (8, 10). Low serum concentrations of 25(OH)D is often observed in elderly people (9, 11) and in patients suffering from rheumatoid arthritis (RA) and lupus (SLE) (12, 13). Most of these patients are at high risk of bone fractures because of the underlying disease and/or advanced age. Moreover, a number of patients with RA and SLE are treated with Gcs. Therefore, vitamin D supplementation in GIO prevention and treatment seems to be quite rational. The dosage of vitamin D should maintain serum concentration of 25(OH)D in the range of 30-50 ng/ml (11). Vitamin D is safe, is contraindicated in patients with hypercalcemia and sarcoidosis (14). Active metabolites alfacalcidol and calcitriol could be effective increasing vertebral BMD in GIO (1), but are not superior to native vitamin D and are not recommended for the prevention or treatment of GIO (1, 4, 5). It is worth noting that most studies and current guidelines advise that vitamin D supplementation should be combined with an adequate calcium intake (4-6, 14). Vitamin D plays an adjuvant role in the primary prevention and treatment, but bisphosphonates are considered to be the gold standard for the pharmacologic management of GIO (4, 5).