Osteoporosis Treatment After Osteoporotic Fractures: Data From a Single Medical Center.

OBJECTIVE: Most patients do not receive osteoporosis treatment after osteoporotic fracture. This study reviewed osteoporosis treatment after osteoporotic fractures in a center without a Fracture Liaison Service. METHODS: We identified all patients with hip, vertebral, humeral or radial fractures, evaluated in Meir Medical Center, in 2017. The exclusion criteria were not a Clalit Health Services member, high-energy fracture or 30-day postoperative mortality. The primary endpoint was osteoporosis drugs issued within 12 months of fracture. Secondary endpoints included bone densitometry and 1-year mortality. RESULTS: Five-hundred-eighty-two patients (average age 78.6 ± 11.1 years, 75.8% women) were included. There were 321 (55.5%) hip, 84 (14.1%) humeral, 33 (5.6%) vertebral, and 144 (24.7%) radial fractures. Osteoporosis drugs were issued to 26.5% of the patients; those with humeral fractures received the least (21.4%) and vertebral, the most (30.3%; P = .51). Bone densitometry was performed in 23.2% of patients. One-year mortality after hip fracture was 12.1%, followed by humeral (3.6%; P < .05). Logistic regression showed that previous treatment (odds ratio [OR] = 7.4; 95% confidence interval [CI] 3.6-15.2), bone densitometry (OR = 4.4; 95% CI 2.6-7.4) and endocrinology visit (OR = 2.6; 95% CI, 1.4-4.6) were the most important factors associated with treatment. CONCLUSION: Fewer than one third of patients received pharmacotherapy within 1 year after fracture. Because pharmacotherapy reduces future fractures and mortality, we recommend that medical staff who care for patients with fracture adopt practical and effective strategies to increase treatment rates among patients with osteoporotic fractures.

[OSTEOPOROSIS AND DIABETES - IN WHICH WAY ARE THEY RELATED?]

INTRODUCTION: Diabetes and osteoporosis are common diseases with growing prevalence in the aging population. Many recent studies have reported an association between diabetes mellitus and an increased osteoporotic fracture rate. Compared to control subjects, decreased bone mineral density has been observed in patients with type 1 diabetes mellitus, while those with type 2 diabetes display a unique skeletal phenotype of increased bone mineral density, but impaired architectural structure and mineral properties. Accumulation of advanced glycation end products changes collagen structure and suppression of bone turnover causes impairment of repair and adaptation mechanisms. These seem to be significant factors impairing bone strength. In addition, longer disease duration, disease complications, insulin use and increased falls, as well as the use of drugs like thiazolidinediones for treatment, are all reported risk factors for fractures among patients with diabetes. Conventional diagnostic tools, including DXA measurements and the fracture risk assessment (FRAX) tool, seem to underestimate fracture risk so that for every FRAX, the actual risk of fracture is higher in the diabetic patient. Despite the unique pathophysiology of bone disease in patients with diabetes, as far as we know, existing drug treatments for osteoporosis are as effective as in patients without diabetes. Therefore, physicians should be aware of the higher risk for osteoporotic fracture among patients with diabetes and treat them according to the clinical algorithms used for all patients.