Background: Rheumatoid arthritis (RA) and metabolic syndrome (MetS) are chronic conditions that share common inflammatory mechanisms. Both diseases can lead to an impairment of the bone microarchitecture. The aims of our study were to evaluate clinical, metabolic, and bone parameters in RA patients with or without MetS (MetS+, MetS−) and potential correlations between the glico-lipidic profile, RA disease activity, and bone status. Methods: A total of thirty-nine RA female post-menopausal patients were recruited (median age 66.6 ± 10.4, disease duration 3 ± 2.7). Anthropometric data, medical history, and current treatment were recorded along with basal blood tests, bone, and lipid metabolism biomarkers. RA disease activity and insulin resistance were evaluated through standard scores. Quantitative assessment of the bone (bone mineral density—BMD) was performed by dual-energy-X ray absorption (DXA), whereas bone quality was quantified with the trabecular bone score (TBS). Results: No statistically significant differences concerning both BMD and TBS were detected between the MetS+ and MetS− RA patients. However, the MetS+ RA patients exhibited significantly higher disease activity and lower serum 25-hydroxyvitamin D [25(OH)D] concentrations (respectively, p = 0.04 and p = 0.01). In all RA patients, a significant negative correlation emerged between the BMD of the femoral trochanter with plasmatic triglycerides (TG) concentrations (r = −0.38, p = 0.01), whereas the lumbar BMD was positively correlated with the abdominal waist (AW) and fasting glucose (FG) concentrations. On the other hand, the TBS was negatively correlated with insulin concentrations, FG, and RA disease activity (respectively, r = −0.45, p = 0.01, r = −0.40, p = 0.03, r = −0.37, p = 0.04), the last one was further negatively correlated with 25-OHD serum concentrations (r = −0.6, p = 0.0006) and insulin-resistance (r = 0.3, p = 0.04). Conclusions: Bone quantity (BMD) and quality (TBS) do not seem significantly changed among MetS+ and MetS− RA patients; however, among MetS+ patients, both significantly higher disease activity and lower vitamin D serum concentrations were observed. In addition, the significant negative correlations between the alterations of metabolic parameters limited to the TBS in all RA patients might suggest that qualitative bone microarchitecture impairments (TBS) might manifest despite unchanged BMD values.

Vitamin D modulates bisphosphonate (BP) efficacy, but its contribution to bone mineral density (BMD) after BP discontinuation is not known. To address this topic, we performed a retrospective analysis of postmenopausal women exposed to alendronate (ALN) to treat osteoporosis who regularly continued the supplementation of cholecalciferol or calcifediol at recommended doses. In the ninety-six recruited women (age 61.1 ± 6.9 years), ALN was administered for 31.2 ± 20.6 months and then discontinued for 33.3 ± 18.9 months. The modification of 25(OH)D serum levels over time was associated with a change of alkaline phosphatase (r = −0.22, p = 0.018) and C-terminal collagen type 1 telopeptide (r = −0.3, p = 0.06). Women in the tertile of the highest increase in 25(OH)D level showed a 5.7% BMD gain at lumbar spine, that was twice as great in comparison with participants with a lower 25(OH)D variation. At a multiple regression analysis, BMD change was associated with time since menopause (ß = 2.28, SE 0.44, p < 0.0001), FRAX score for major fracture (ß = −0.65, SE 0.29, p = 0.03), drug holiday duration (ß = −2.17, SE 0.27, p < 0.0001) and change of 25(OH)D levels (ß = 0.15, SE 0.03, p = 0.0007). After ALN discontinuation, improving the vitamin D status boosts the ALN tail effect on BMD.

Background:Vitamin D repletion is known to maximize the response to bisphosphonates (BPs) in terms of both bone mineral density (BMD) changes and anti-fracture efficacy. The contribute of vitamin to BMD after discontinuation of BPs has been poorly investigated.Objectives:To explore whether change of vitamin D status may contribute to the tail effect of alendronate (ALE) on BMD.Methods:Participants in this retrospective study were postmenopausal osteoporotic women exposed to ALE. Either cholecalciferol or calcifediol have been administered, as vitamin D supplementation in accordance to good clinical practice, during ALE treatment and after ALE discontinuation. BMD was evaluated by Dual-energy X-ray absorptiometry (DXA) at lumbar spine and femoral site. Vitamin D status has been checked by measuring 25(OH)D serum levels through HPLC. Surrogate bone formation and resorption markers (i.e. C-terminal telopeptide of type I collagen (CTX) and alkaline phosphatase (ALP), respectively) were also evaluated. The Fracture Risk Assessment Tool (FRAX) served to estimate the participants’ 10-year fracture risk for major osteoporotic and hip fracture.Results:88 postmenopausal osteoporotic women (age 61.14 ± 6.96 yr.) were included in the final analysis. The 10-year probability of major and hip fractures was 18.31±11.51 and 8.60 ± 10.55 %, respectively. Participants were exposed to ALE treatment for 31.27 ± 20.69 months; then they stopped treatment for 33.33 ± 18.97 months. Change of BMD was inversely related to drug holiday (r=-0.27, p=0.005). Modification of 25(OH)D was inversely associated with change of ALP (r=-0.22, p=0.018) and CTX levels (r=-0.3, p=0.06). By distributing participants in tertiles according to variation of 25(OH)D levels over time, women allocated in the tertile with the higher increase of 25(OH)D showed a 5.7% BMD gain that was two times larger in comparison with participants with lower increase of 25(OH)D. At a multiple regression analysis, after correcting for ALE treatment duration, bone turn-over marker modifications, BMI and age at menopause, BMD change at lumbar spine was significantly associated with time since menopause (ß=2.28, SE 0.44, p<0.0001), FRAX score (ß=-0.65, SE 0.29, p=0.03), drug holiday duration (ß=-2.17, SE 0.27, p<0.0001) and change of 25(OH)D levels (ß=0.15 SE 0.03, p=0.0007).Conclusion:After ALE discontinuation, modification of BMD are strictly associated with change of vitamin D status.Disclosure of Interests:None declared