Over the last few years, there has been experimental evidence for the existence of cross-talking between bone remodeling and
glucose metabolism. Whether this experimental model can be translated to humans is still debated, and it is also unclear whether the modulation of bone turnover by anti-osteoporotic drugs may lead to changes in
glucose metabolism. The aim of this 12-month prospective study was to investigate whether treatment of
glucocorticoid-induced
osteoporosis (GIO) with bipshosphonates or
teriparatide may influence serum
glycated hemoglobin (HbA1c) and fasting plasma
glucose. One-hundred-eleven patients (70 F, 41 M, median age 70, range: 55-89) chronically treated with
glucocorticoids were evaluated for changes in serum HbA1c and fasting plasma
glucose during treatment with
bisphosphonates (45 cases) or
teriparatide (33 cases) as compared to those occurring during treatment with
calcium and
vitamin D alone (33 cases). In patients treated with
teriparatide, but not in those treated with
bisphosphonates or
calcium and
vitamin D alone, a statistically significant (p=0.01) decrease in serum HbA1c was observed during the follow-up, the change being greater (p=0.01) in patients with diabetes as compared to those without diabetes. In most cases, the decrease of serum HbA1c was relatively limited and in some patients the improvement of
glucose homeostasis was concomitant with implementation of anti-diabetic treatments. Fasting plasma
glucose did not change significantly during either
bisphosphonates or
teriparatide treatments. In conclusion, currently used bone active drugs may produce limited effects on
glucose metabolism in patients with GIO. Interestingly, the bone anabolic drug
teriparatide was shown to be associated with some improvement in serum HbA1c in this clinical context.