scholarly journals Bone Loss in Celiac Disease Is Related to Secondary Hyperparathyroidism

1999 ◽  
Vol 14 (4) ◽  
pp. 652-657 ◽  
Author(s):  
Peter L. Selby ◽  
Michael Davies ◽  
Judith E. Adams ◽  
E. Barbara Mawer
2009 ◽  
Vol 42 (10) ◽  
pp. 25
Author(s):  
MICHELE G. SULLIVAN
Keyword(s):  

2007 ◽  
Vol 49 (3) ◽  
pp. 440-451 ◽  
Author(s):  
Aiji Yajima ◽  
Masaaki Inaba ◽  
Yoshihiro Tominaga ◽  
Akemi Ito

2000 ◽  
Vol 85 (9) ◽  
pp. 3011-3019 ◽  
Author(s):  
Munro Peacock ◽  
Guangda Liu ◽  
Mark Carey ◽  
Ronald McClintock ◽  
Walter Ambrosius ◽  
...  

Abstract Dietary supplements that prevent bone loss at the hip and that can be applied safely in the elderly are likely to reduce hip fractures. A daily dietary supplement of 750 mg calcium or 15 μg 25OH vitamin D3 on bone loss at the hip and other sites, bone turnover and calcium-regulating hormones were studied over 4 yr in elderly volunteers using a randomized, double-blind, placebo-controlled trial. Bone mineral density (BMD) was measured by dual x-ray absorptiometry and bone structure by radiographs. Calcium biochemistry and bone turnover markers were measured in blood and urine. The 316 women entering the trial had a mean age of 73.7 yr and the 122 men of 75.9 yr. Baseline median calcium intake was 546 mg/day, and median serum 25OH vitamin D3 was 59 nmol/L. On placebo, loss of BMD at total hip was 2% and femoral medulla expansion was 3% over 4 yr. Calcium reduced bone loss, secondary hyperparathyroidism, and bone turnover. 25OH vitamin D3 was intermediate between placebo and calcium. Fracture rates and drop-out rates were similar among groups, and there were no serious adverse events with either supplement. A calcium supplement of 750 mg/day prevents loss of BMD, reduces femoral medullary expansion, secondary hyperparathyroidism, and high bone turnover. A supplement of 15 μg/day 25OH vitamin D3 is less effective, and because its effects are seen only at low calcium intakes, suggests that its beneficial effect is to reverse calcium insufficiency.


2018 ◽  
Vol 90 (10) ◽  
pp. 89-93
Author(s):  
L.M. Krums ◽  
◽  
S.V. Bykova ◽  
E.A. Sabelnikova ◽  
Ts.V. Aminova ◽  
...  

1999 ◽  
Vol 92 (9) ◽  
pp. 937
Author(s):  
PL Selby ◽  
M Davies ◽  
JE Adams
Keyword(s):  

2007 ◽  
Vol 156 (3) ◽  
pp. 309-314 ◽  
Author(s):  
Robert J A Frost ◽  
Carolin Sonne ◽  
Uli Wehr ◽  
Hans-Ulrich Stempfle

Background: Cross-sectional studies have shown that more than 50% of patients with congestive heart failure (CHF) have decreased bone mineral density (BMD). There is limited knowledge about the longitudinal changes of BMD and how to treat bone loss in patients with CHF. Methods: The present study was a prospective, longitudinal trial in which 33 male patients with CHF (ejection fraction (EF): 30±11%) were assigned to 1000 mg calcium supplementation or no supplementation. BMD was measured at the lumbar spine (LS) and the femoral neck (FN) by dual-energy X-ray absorptiometry at baseline and after 12 months. Results: Osteopenia (LS 33% and FN 36%) and osteoporosis (LS 15% and FN 6%) were frequently seen in these patients; 70% showed impaired renal function, 42% secondary hyperparathyroidism, and 33% hypogonadism. Bone resorption markers were strongly elevated and correlated negatively with the EF. Patients without calcium supplementation revealed a reduction of BMD (LS 1.7% and FN 1.9%) within 12 months. The fracture incidence was 6%. Patients with calcium supplementation also demonstrated a 6% fracture incidence and a decrease in BMD (LS 1.2% and FN 1.6%), which was not significantly different from the untreated group. Loss of BMD at FN was only seen in patients with impaired renal function. Conclusions: Patients with CHF demonstrate a progressive decrease in BMD when compared with age-matched healthy individuals. Increased bone resorption due to renal insufficiency with consecutive secondary hyperparathyroidism is a main reason for BMD loss in CHF. Calcium supplementation alone cannot sufficiently prevent the decrease in BMD.


2005 ◽  
Vol 289 (5) ◽  
pp. E784-E793 ◽  
Author(s):  
Charles A. O'Brien ◽  
Robert L. Jilka ◽  
Qiang Fu ◽  
Scott Stewart ◽  
Robert S. Weinstein ◽  
...  

Continuous elevation of parathyroid hormone (PTH) increases osteoclast precursors, the number of osteoclasts on cancellous bone, and bone turnover. The essential molecular mediators of these effects are controversial, however, and both increased receptor activator of NF-κB ligand (RANKL) and IL-6 have been implicated. The goal of these studies was to determine whether continuous elevation of endogenous PTH alters IL-6 gene expression in vivo and whether IL-6 is required for PTH-induced bone loss. To accomplish this, we generated transgenic mice harboring a luciferase reporter gene under the control of IL-6 gene regulatory regions to allow accurate quantification of IL-6 gene activity in vivo. In these mice, induction of secondary hyperparathyroidism using a calcium-deficient diet did not alter IL-6-luciferase transgene expression, whereas RANKL mRNA expression was elevated in bone tissue. Moreover, secondary hyperparathyroidism induced an equivalent amount of bone loss in wild-type and IL-6-deficient mice, and PTH elevated RANKL mRNA and osteoclast formation to the same extent in bone marrow cultures derived from wild-type and IL-6-deficient mice. These results demonstrate that IL-6 is not required for the osteoclast formation and bone loss that accompanies continuous elevation of PTH.


2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i161-i161
Author(s):  
Lihua Ni ◽  
Rining Tang ◽  
Kaiyun Song ◽  
Liting wang ◽  
Meng Zuo ◽  
...  

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