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      Changes in bone mineral density and bone turnover markers in patients undergoing hematopoietic stem cell transplant

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          Abstract

          Introduction:

          Hematopoietic stem cell transplant (HSCT) is frequently complicated by endocrine abnormalities and loss of bone mass. This prospective study was conducted to evaluate the bone loss post-HSCT.

          Materials and Methods:

          A total of 50 patients was evaluated pretransplantation, and 25 had HSCT (17 males, 8 females; 19 allogenic, 6 autologous). Bone mineral density (BMD) and bone markers were measured at baseline, 3–6 months and 12 months.

          Results:

          The mean age and body mass index were 25.1 ± 16.3 years and 19.4 ± 4.5 kg/m 2, respectively. There were 15 adults (60%), and 10 adolescents (40%). There was a significant decline in BMD from the baseline at total femur (−8.7%; P < 0.0001), femoral neck (−5.0%; P = 0.003), femoral trochanter (−6.0%; P = 0.001), and Ward's triangle (−9.9%; P < 0.0001) at 6 months posttransplantation. From the 6 months to 12 months, there was a significant improvement in BMD at above sites except at Ward's triangle. The decline in BMD was nonsignificant at the whole body (−0.3%, P = 0.748) and the lumbar spine (−2.7%, P = 0.130) at 6 months posttransplant. Younger patients with allogenic graft and steroid use are more likely to have significant loss of BMD at hip posttransplant. Serum osteocalcin decreased, and N-telopeptide increased at 3–6 months, which return to baseline at 1-year posttransplant.

          Conclusions:

          A significant bone loss is observed at 6 months in patients with post-HSCT. The bone loss occurs predominantly at cortical bone. There is recovery of bone mass at 12 months posttransplant except at Ward's triangle. Bone loss after HSCT is multifactorial.

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          A meta-analysis of the association of fracture risk and body mass index in women.

          Didier Hans, Heikki Kröger, Fernando Rivadeneira … (2013)
          Several recent studies suggest that obesity may be a risk factor for fracture. The aim of this study was to investigate the association between body mass index (BMI) and future fracture risk at different skeletal sites. In prospective cohorts from more than 25 countries, baseline data on BMI were available in 398,610 women with an average age of 63 (range, 20-105) years and follow up of 2.2 million person-years during which 30,280 osteoporotic fractures (6457 hip fractures) occurred. Femoral neck BMD was measured in 108,267 of these women. Obesity (BMI ≥ 30 kg/m(2) ) was present in 22%. A majority of osteoporotic fractures (81%) and hip fractures (87%) arose in non-obese women. Compared to a BMI of 25 kg/m(2) , the hazard ratio (HR) for osteoporotic fracture at a BMI of 35 kg/m(2) was 0.87 (95% confidence interval [CI], 0.85-0.90). When adjusted for bone mineral density (BMD), however, the same comparison showed that the HR for osteoporotic fracture was increased (HR, 1.16; 95% CI, 1.09-1.23). Low BMI is a risk factor for hip and all osteoporotic fracture, but is a protective factor for lower leg fracture, whereas high BMI is a risk factor for upper arm (humerus and elbow) fracture. When adjusted for BMD, low BMI remained a risk factor for hip fracture but was protective for osteoporotic fracture, tibia and fibula fracture, distal forearm fracture, and upper arm fracture. When adjusted for BMD, high BMI remained a risk factor for upper arm fracture but was also a risk factor for all osteoporotic fractures. The association between BMI and fracture risk is complex, differs across skeletal sites, and is modified by the interaction between BMI and BMD. At a population level, high BMI remains a protective factor for most sites of fragility fracture. The contribution of increasing population rates of obesity to apparent decreases in fracture rates should be explored. © 2014 American Society for Bone and Mineral Research.
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            Bone loss in the lower leg during 35 days of bed rest is predominantly from the cortical compartment.

            Jörn Rittweger, Boštjan Šimunič, Giancarlo Bilancio … (2009)
            Immobilization-induced bone loss is usually greater in the epiphyses than in the diaphyses. The larger fraction of trabecular bone in the epiphyses than in the diaphyses offers an intuitive explanation to account for this phenomenon. However, recent evidence contradicts this notion and suggests that immobilization-induced bone loss from the distal tibia epiphysis is mainly from the cortical compartment. The aim of this study was to establish whether this pattern of bone loss was a general rule during immobilization. We monitored various skeletal sites with different tissue composition during 5 weeks of immobilization. Ten healthy male volunteers with mean age of 24.3 years (SD 2.6 years) underwent strict horizontal bed rest. Bone scans were obtained during baseline data collection, at the end of bed rest and after 14 days of recovery by peripheral Quantitative Computed Tomography (pQCT). Sectional images were obtained from the distal tibia epiphysis (at 4% of the tibia's length), from the diaphysis (at 38%), from the proximal metaphysis (at 93%) and from the proximal epiphysis (at 98%), as well as from the distal femur epiphysis (at 4% of the femur's length) and from the patella. Relative bone losses were largest at the patella, where they amounted to -3.2% (SD 1.8%, p<0.001) of the baseline values, and smallest at the tibia diaphysis, where they amounted to -0.7% (SD 1.0%, p=0.019). The relative losses were generally larger from cortical than from trabecular compartments (p=0.004), and whilst all skeletal sites depicted such cortical losses, substantial trabecular losses were found only from the proximal tibia epiphysis. Results confirm that the differential losses from the various skeletal sites cannot be explained on the basis of trabecular vs. cortical tissue composition differences, but that endocortical circumference can account for the different amounts of bone loss in the tibia. The present study therefore supports the suggestion of the subendocortical layer as a transitional zone, which can readily be transformed into trabecular bone in response to immobilization. The latter will lead to cortical thinning, a factor that has been associated with the risk of fracture and with osteoarthritis.
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              Bone loss following hematopoietic stem cell transplantation: a long-term follow-up.

              Claudia M S Schulte, Dietrich W Beelen (2004)
              Transplantation-associated bone loss is a well-known phenomenon, however, effects of hematopoietic stem cell transplantation are insufficiently characterized. We conducted a prospective, unicentric, long-term follow-up in 280 patients undergoing allogeneic hematopoietic stem cell transplantation (HSCT). Bone mineral density (BMD) was measured before transplantation and then yearly for at least 4 years. Patients received vitamin D plus calcium until steroid withdrawal. Mean baseline BMD was normal. We demonstrated significant bone loss with nadir BMD at month 6 for the spine and at month 24 for total body and femoral neck. Average annual bone loss was 0.6% for spine, 0.4% for total body, 2.3% for femoral neck, and 3.5% for Ward triangle. While spine and total body BMD returned to baseline, bone loss at femoral neck sites was attenuated, but BMD did not return to baseline until month 48 (P <.0001 for femoral neck and Ward triangle). Univariate factor analysis of 15 potential risk factors for rapid bone loss revealed a positive correlation of bone loss with steroid and cyclosporine A use, baseline BMD, and loss of muscle mass (overwhelming power of steroid use in multifactor analysis). Such rapid BMD changes probably increase fracture risk consecutive to irreversible microarchitectural changes even if osteodensitometry shows long-term recovery.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Indian J Endocrinol Metab
                Journal ID (iso-abbrev): Indian J Endocrinol Metab
                Journal ID (publisher-id): IJEM
                Title: Indian Journal of Endocrinology and Metabolism
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 2230-8210
                ISSN (Electronic): 2230-9500
                Publication date (Print): May-Jun 2015
                Volume: 19
                Issue: 3
                Pages: 393-398
                Affiliations
                [1] Commandant, Military Hospital, Shillong, Meghalaya,, India
                [1 ] Department of Endocrinology, Army Hospital Research and Referral, New Delhi, India
                [2 ] Department of Hematology, Army Hospital Research and Referral, New Delhi, India
                Author notes
                Corresponding Author: Prof. M. K. Garg, Military Hospital, Shillong - 793 001, Meghalaya, India. E-mail: mkgargs@ 123456gmail.com
                Article
                Publisher ID: IJEM-19-393
                DOI: 10.4103/2230-8210.152785
                PMC ID: 4366780
                SO-VID: d5c4f9bd-49e7-43e8-89b0-7668ebe93dfa
                Copyright © Copyright: © Indian Journal of Endocrinology and Metabolism
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Subject: Original Article

                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: bone markers,bone mineral density,hematopoietic stem cell transplant
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: bone markers, bone mineral density, hematopoietic stem cell transplant

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