The purpose of this document, a result of the harmonisation and revision of Guidelines published separately by the SIMFER, SIOMMMS/SIR, and SIOT associations, is to provide practical indications based on specific levels of evidence and various grades of recommendations, drawn from available literature, for the management of osteoporosis and for the diagnosis, prevention, and treatment of fragility fractures. These indications were discussed and formally approved by the delegates of the Italian Scientific Associations involved in the project (SIE, SIGG, SIMFER, SIMG, SIMI, SIOMMMS, SIR, and SIOT).

Data on treatment of glucocorticoid-induced osteoporosis (GIO) in men are scarce. We performed a randomized, open-label trial in men who have taken glucocorticoids (GC) for ≥3 months, and had an areal bone mineral density (aBMD) T-score ≤ –1.5 standard deviations. Subjects received 20 μg/d teriparatide (n = 45) or 35 mg/week risedronate (n = 47) for 18 months. Primary objective was to compare lumbar spine (L1–L3) BMD measured by quantitative computed tomography (QCT). Secondary outcomes included BMD and microstructure measured by high-resolution QCT (HRQCT) at the 12th thoracic vertebra, biomechanical effects for axial compression, anterior bending, and axial torsion evaluated by finite element (FE) analysis from HRQCT data, aBMD by dual X-ray absorptiometry, biochemical markers, and safety. Computed tomography scans were performed at 0, 6, and 18 months. A mixed model repeated measures analysis was performed to compare changes from baseline between groups. Mean age was 56.3 years. Median GC dose and duration were 8.8 mg/d and 6.4 years, respectively; 39.1% of subjects had a prevalent fracture, and 32.6% received prior bisphosphonate treatment. At 18 months, trabecular BMD had significantly increased for both treatments, with significantly greater increases with teriparatide (16.3% versus 3.8%; p = 0.004). HRQCT trabecular and cortical variables significantly increased for both treatments with significantly larger improvements for teriparatide for integral and trabecular BMD and bone surface to volume ratio (BS/BV) as a microstructural measure. Vertebral strength increases at 18 months were significant in both groups (teriparatide: 26.0% to 34.0%; risedronate: 4.2% to 6.7%), with significantly higher increases in the teriparatide group for all loading modes (0.005 < p < 0.015). Adverse events were similar between groups. None of the patients on teriparatide but five (10.6%) on risedronate developed new clinical fractures (p = 0.056). In conclusion, in this 18-month trial in men with GIO, teriparatide showed larger improvements in spinal BMD, microstructure, and FE-derived strength than risedronate.

Objective: FSH, via its receptor (FSHR), influences bone remodeling and osteoclast proliferation and activity. The aim of this study was to evaluate the influence of two single nucleotide polymorphisms (SNPs) of the FSHR gene on bone mineral density (BMD) and bone turnover markers (bone alkaline phosphatase and type I collagen C-telopeptides) in postmenopausal women. Methods: Two hundred and eighty-nine unrelated postmenopausal women were genotyped for the SNPs rs1394205 and rs6166. BMD was estimated using dual-energy X-ray absorptiometry and quantitative ultrasound (QUS) methodologies. Results: AA rs6166 women showed a lower BMD (femoral neck and total body), lower stiffness index (calcaneal QUS), and higher serum levels of bone turnover markers compared to GG rs6166 women. The prevalence of osteoporosis was significantly higher in AA rs6166 women compared with GG rs6166 women. These results were not influenced by circulating levels of FSH and estrogens. Conclusion: The SNP rs6166 of the FSHR gene significantly influences BMD in postmenopausal women. In particular, AA rs6166 women are at increased risk of postmenopausal osteoporosis compared with GG rs6166 women, independently of circulating levels of FSH and estrogens. Previous studies have demonstrated that this SNP influences cell and tissue response to hyperstimulation of FSHR in vivo and in vitro. Our study results appear in agreement with these experimental data and with known biological actions of FSH/FSHR system in bone homeostasis.

Background: Abdominal aortic aneurysm (AAA) is considered a manifestation of atherosclerosis, however there are epidemiologic, biochemical, and structural differences between occlusive atherosclerosis and AAA. The pathogenesis of AAA involves several factors, fi rst of all destruction of collagen and elastin in the aortic wall. Classical risk factors may infl uence the evolution and development of AAA, though no consistent association has been found. Aims of the study were to evaluate associations between risk factors and to establish the prevalence of carotid, peripheral vascular and coronary atherosclerosis in patients with AAA. Methods: We studied 98 patients with AAA (Group 1) awaiting surgery compared with high cardiovascular risk population having two or more risk factors (n = 82 Group 2). We evaluated traditional risk factors and we studied by eco-doppler and echocardiography the presence of carotid peripheral and coronaric atherosclerosis in two groups. Results: We found a higher incidence of AAA in males (p Ͻ 0.01). The prevalence of infrarenal AAA was signifi cantly higher than suprarenal AAA (81 vs 17 p Ͻ 0.001). No differences in total cholesterol (199 ± 20 vs. 197 ± 25 mg/dl), low-density lipoprotein (142 ± 16 vs. 140 ± 18 mg/dl), triglycerides (138 ± 45 vs. 144 ± 56 mg/dl), glycemia (119 ± 15 vs. 122 ± 20 mg/dl), and fi brinogen (388 ± 154 vs. 362 ± 92 mg/dl) were found between groups. We demonstrated signifi cant differences for cigarette smoking (p Ͻ 0.002), systolic and diastolic blood pressure (150 ± 15 vs. 143 ± 14 mmHg and 88 ± 6 vs. 85 ± 7 mmHg, p Ͻ 0.0001 and p Ͻ 0.05, respectively) and high sensititivity C reactive protein (2.8 ± 1.3 vs. 1.3 ± 0.7 mg/dl, p Ͻ 0.001). High-density lipoprotein (HDL) cholesterol levels were signifi cant greater in Group 1 than Group 2 (p Ͻ 0.003). Subgroups of patients with AAA and luminal thrombus showed higher fi brinogen levels (564 ± 235 vs. 341 ± 83 mg/dl, p Ͻ 0.001) and lower HDL than in controls (46.6 ± 6.5 vs. 52.1 ± 7.8 mg/dl, p Ͻ 0.01). We did not fi nd any difference in body mass index, or prevalence of coronary and peripheral atherosclerosis between groups. Conversely, we found higher prevalence of carotid atherosclerosis in Group 2 (9% vs. 25%, p Ͻ 0.004). Conclusion: Our AAA patients had fewer and different risk factors respect to patients with atherosclerosis. Only elevated blood pressure, C reactive protein, and smoking showed a signifi cant association with AAA. Atherosclerosis in other arterial districts did not differ respect to subjects with high cardiovascular risk. Our results confi rm the hypothesis that AAA and atherosclerosis are two different pathological entities with different risk profi les.

Rosacea and chronic urticaria are two common skin disorders existing in idiopathic forms. A role of Helicobacter pylori bacterium infection in the aetiopathogenesis of rosacea or chronic urticaria has been suggested although still controversial. The aim of the present study was to establish a relationship between H. pylori infection and rosacea chronic urticaria by means of an immunoproteomic investigation. We analyzed immunoglobulin A (IgA)-, IgG-, and IgE-mediated immune-responses against H. pylori antigens and we identified some bacterial immunoresponsive proteins. A general IgA- and IgE-mediated immune response against antioxidative bacterial proteins was observed. A correlation between the bacterial occurrence and skin diseases pathogenesis is discussed.