No abstract

Helicobacter pylori (HP) infection is a common and persistent disorder acting as a major cofactor for the development of upper gastrointestinal diseases and several extraintestinal disorders including osteoporosis. However, no prospective study assessed the effects of HP on bone health and fracture risk. We performed a HP screening in a population‐based cohort of 1149 adults followed prospectively for up to 11 years. The presence of HP infection was assessed by serologic testing for serum antibodies to HP and the cytotoxin associated gene‐A (CagA). The prevalence of HP infection did not differ among individuals with normal bone mineral density (BMD), osteoporosis, and osteopenia. However, HP infection by CagA‐positive strains was significantly increased in osteoporotic (30%) and osteopenic (26%) patients respect to subjects with normal BMD (21%). Moreover, anti‐CagA antibody levels were significantly and negatively associated with lumbar and femoral BMD. Consistent with these associations, patients affected by CagA‐positive strains had a more than fivefold increased risk to sustain a clinical vertebral fracture (HR 5.27; 95% CI, 2.23–12.63; p < .0001) and a double risk to sustain a nonvertebral incident fracture (HR 2.09; 95% CI, 1.27–2.46; p < .005). Reduced estrogen and ghrelin levels, together with an impaired bone turnover balance after the meal were also observed in carriers of CagA‐positive HP infection. HP infection by strains expressing CagA may be considered a risk factor for osteoporosis and fractures. Further studies are required to clarify in more detail the underlying pathogenetic mechanisms of this association. © 2020 American Society for Bone and Mineral Research (ASBMR).

Context Intravenous aminobisphosphonates (N-BPs) can induce an acute phase reaction (APR) in up to 40% to 70% of first infusions, causing discomfort and often requiring intervention with analgesics or antipyretics. Objective Our aim was to explore the risk factors of APR in a large sample of patients with Paget’s disease of bone (PDB) and to assess the possible preventive effects of vitamin D administration. Methods An observational analysis was performed in 330 patients with PDB at the time of N-BP infusion. Then, an interventional study was performed in 66 patients with active, untreated PDB to evaluate if vitamin D administration (oral cholecalciferol 50 000 IU/weekly for 8 weeks before infusion) may prevent APR. Results In a retrospective study, APR occurred in 47.6% and 18.3% of naive or previously treated patients, respectively. Its prevalence progressively increased in relation to the severity of vitamin D deficiency, reaching 80.0% in patients with 25-hydroxyvitamin D (25OHD) levels below 10 ng/mL (relative risk (RR) = 3.7; 95% confidence interval (CI) 2.8–4.7, P &lt; .0001), even in cases previously treated with N-BPs. Moreover, APR occurred more frequently in patients who experienced a previous APR (RR = 2.8; 95% CI 1.5–5.2; P &lt; .001) or in carriers of SQSTM1 mutation (RR = 2.3; 95% CI 1.3–4.2; P = .005). In the interventional study, vitamin D supplementation prevented APR in most cases, equivalent to a RR of 0.31 (95% CI 0.14–0.67; P &lt; .005) with respect to prevalence rates of the observational cohort. A similar trend was observed concerning the occurrence of hypocalcemia. Conclusions The achievement of adequate 25OHD levels is recommended before N-BP infusion in order to minimize the risk of APR or hypocalcemia in PDB.

Bone loss and bone fractures are common complications after organ transplantation. Many factors contribute to the pathogenesis of transplant osteoporosis, such as bone disease preceding transplantation, immunosuppressive medications, and nutritional and lifestyle factors. This study aimed to assess the incidence of vertebral fractures before and after lung and heart transplantation. This longitudinal study analyzed 213 electronic medical records of patients who underwent lung transplantation (n = 128) and heart transplantation (n = 85) at Siena University Medical Center between January 2000 and December 2018. In lung and heart transplant recipients, the bone mineral density in the femoral sub-regions show a significant decrease at post-transplantation and at follow up visits. In both lung and heart recipients, we found an increase in the fracture incidence in the first period after transplantation (19.5% vs. 50.4% in lung recipients; 9.6% vs. 25.7% in heart recipients). Moreover, in lung recipients, vertebral fractures were predicted primarily by age, BMD at the femur, and any history of fracture. In heart recipients, vertebral fractures were predicted only by history of fracture. Our study supports the recommendations for pre-transplant osteoporosis screening in patients undergoing lung transplants, and in the first period after transplantation in heart transplant recipients.

Purpose It is well established that thyroiditis and other thyroid disorders can be induced by COVID-19 infection, but there is limited information about the autoimmune/inflammatory syndrome induced by adjuvants (ASIA) after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination. We report two cases of thyrotoxicosis following SARS-CoV-2 vaccine. Methods and results Two young health care peoples (wife and husband) received a first dose of SARS-CoV-2 vaccine, and few weeks later developed clinical manifestations of thyroid hyperactivity, with increased thyroid hormone levels on thyroid function tests, suppressed thyroid-stimulating hormone and negative antithyroid antibodies, despite being healthy before vaccination. They were diagnosed at the 4th week after first dose of SARS-Cov-2 vaccine as silent thyroiditis and followed without treatment, since their symptoms were not severe. At the 6th week, the patients became wholly asymptomatic and their thyroid function returned to normal. Conclusions Thyrotoxicosis can occur after SARS-CoV-2 vaccination probably related to silent thyroiditis.