International Osteoporosis Foundation, Nyon 45 Cooper C, Cole ZA

International Osteoporosis Foundation, Nyon 45. Cooper C, Cole ZA, Holroyd CR, Earl SC, Harvey NC, Dennison EM, the IOF CSA Working Group on Selleck Alvespimycin fracture Epidemiology (2011) Secular trends in the incidence of hip and other osteoporotic fractures. Osteoporos Int 22:1277–1288PubMedCrossRef 46. Gullberg B, Johnell O, Kanis JA (1997) World-wide projections for hip fractures. Osteoporos Int 7:407–413PubMedCrossRef 47. Johansson H, Clark P, Carlos F, Oden A, McCloskey EV, Kanis JA (2011) Increasing age- and sex-specific rates of hip fracture in Mexico: a survey of the Mexican institute Selleckchem 4SC-202 of social security. Osteoporos Int 22:2359–2364PubMedCrossRef

48. Zingmond DS, Melton LJ 3rd, Silverman SL (2004) Increasing hip fracture incidence in California Hispanics, 1983 to 2000. Osteoporos Int 15:603–610PubMedCrossRef 49. Tuzun S, Eskiyurt N, Akarirmak U et al (2012) Incidence of hip fracture and prevalence of osteoporosis in Turkey: the FRACTURK study. Osteoporos Int 23:949–955PubMedCrossRef 50. Hagino H,

Furukawa K, Fujiwara S et al (2009) Recent trends in the incidence and lifetime risk of hip fracture in Tottori, Japan. Osteoporos Int 20:543–548PubMedCrossRef 51. Ross PD, Norimatsu H, Davis JW et al (1991) A comparison of hip fracture incidence among native Japanese, Japanese Americans, and American Caucasians. Am J Epidemiol 133:801–809PubMed 52. Bacon WE, Hadden WC (2000) Occurrence of hip fractures and socioeconomic position. J Aging Health 12:193–203PubMedCrossRef 53. Kanis JA, Passmore R (1989) Calcium supplementation of the diet—I. Br Med J 296:137–140CrossRef 54. Kanis JA, Passmore R (1989) Calcium supplementation of the diet—II. Br Med Enzalutamide J 296:205–208CrossRef”
“Dear Editor, We read with interest the comments by Aguilera et al. [1] regarding our recently published case report in Osteoporosis International [2]. To our knowledge, this is the

first case described in the literature involving development of post-liver transplantation (LT) de novo autoimmune hepatitis (AIH), following parathyroid hormone 1-34 [PTH(1-34) or teriparatide] and 1-84 [PTH(1-84)] administration for severe osteoporosis. The exact mechanisms linking PTH with AIH are not clarified. However, we hypothesized that Kuppfer cells in the liver, which are implicated in PTH degradation and which express the PTH/PTH-related protein type 1 receptor, play a key role in the pathogenesis of AIH, since they also produce interleukin-6 Baricitinib [2]. First of all, we thank Aguilera et al. for their interest in our paper. We appreciate their own work on this topic, which was unfortunately not cited in this article. Regarding the exact time that our patient developed de novo AIH after LT, this was 3 years, as we state in the text. We agree, as stated in the paper, that the assessment of serum autoantibodies directed against the cytosolic enzyme glutathione S-transferase T1 (GSTT1) and GSTT1 donor/recipient mismatch constitute a major factor implicated in the pathogenesis of de novo AIH in post-LT patients.

Comments are closed.