Search

Severe osteoporosis, a situation with fractures, can worsen in the case of poor response to usual therapies, such as bisphosphonates associated with calcium and vitamin D, especially if bone turnover is strongly suppressed. One way of inverting the poor evolution of non-responders is to use Teriparatide. The case of a non-responder is reported, with considerations about the possibility of detecting these patients before a new fracture takes place.

Aim: Non-invasive assessment of bone geometry, biomechanics, and mineral content in postmenopausal women by peripheral quantitative Computed Tomography (pQCT)., Material and Methods: Total, trabecular and cortical mineral density (totBMD, cortBMD, trabBMD), and the geometrical (total area, trabecular area, cortical area) and biomechanical properties of bone (strength-strain index, cortical thickness) were assessed in 93 consecutive post-menopausal women (mean age: 63+/-7 yrs; age at menopause: 49+/-6 yrs; years since menopause: 14+/-9 yrs) by pQCT at the ultradistal radius of non-dominant forearm., Results: Compared with 50 healthy women at peak of bone mass, volumetric total, trabecular and cortical bone densities were significantly reduced in postmenopausal subjects (TotBMD: 318+/-106 mg/cm3 vs ctr 442+/-100, -28%, p<0.001; TrabBMD: 117+/-59 mg/cm3 vs ctr: 203+/-47, -42%, p<0.001; CorBMD: 764+/-159 mg/cm3 vs 921+/-111, -17%, p<0.001). The bone loss was greater in trabecular bone. Cortical area (0.7+/-0,1 cm2 vs ctr: 0.8+/-0.1, -12.5%, p<0.001), cortical thickness (0.151+/-0.02 cm vs ctr: 0.169+/-0.03, -11%, p<0.001), and strength-strain index (686+/-207 mm3 vs ctr: 883+/-165, -22%, p<0.001) were significantly lower in post-menopausal women in comparison with the controls. Years since menopause and age showed a significant negative correlation with bone mineral densities and biomechanical parameters., Conclusions: In post-menopausal women pQCT showed: 1) osteopoenia in all bone compartments, greater at the trabecular level, related to age and years since menopause; 2) reduced cortical density and cortical thickness, consistent with a reduced ability of bone to absorb loading forces; 3) reduced strength-strain index, indicative of inability to adapt to mechanical use and augmented risk for fracture. We conclude that pQCT is a valuable tool for measuring the true volumetric mineral density and the geometrical and biomechanical indexes of bone, which could be proposed in current clinical practice for the assessment of osteoporosis.

No satisfactory treatment is available for metabolic bone disease associated with primary biliary cirrhosis. On the basis of the similarities to postmenopausal osteoporosis, the rationale exists for calcitonin to be tested in clinical studies in patients with primary biliary cirrhosis-associated osteoporosis. We evaluated the effect of calcitonin on bone metabolism and mineral density in 25 women with primary biliary cirrhosis and severe osteopenia. After 6 mo of observation, patients received a synthetic calcitonin or a control treatment consisting of less than one hundredth of the recommended dose of porcine calcitonin. The two treatments were administered in sequence to each patient for two 6-mo periods, with a 3-mo washout between them, according to a crossover design. After the observation period, oral calcium supplementation was started. Bone mineral density was measured by dual-photon absorptiometry of the lumbar spine at study entry and at the beginning and the end of each treatment period. During the observation period bone mineral density fell by 3.5% whereas during the following 6 mo it increased in both the patients who received calcitonin (4.3%) and those who received the control treatment (4.9%). Conversely, after the crossover, bone mineral density decreased during both calcitonin (-2.7%) and control treatment (-2.9%). A significant difference was observed between the two periods but not between the two treatments or between the two sequences of treatment administration. In conclusion, our findings indicate that parenterally administered calcitonin for 6 mo is ineffective in halting bone loss in patients with primary biliary cirrhosis-associated metabolic bone disease, whereas calcium supplementation may have a transient beneficial effect.