PubMed · 15035138
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Masako Ito. 2004. [DXA].. https://pubmed.ncbi.nlm.nih.gov/15035138/
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OBJECTIVE: Osteoporosis is a common disorder with a strong genetic component. We investigated the correlations between bone mineral density (BMD) and four gene polymorphisms (-308G>A tumor necrosis factor alpha (TNF-alpha), -34T>C CYP 17, *141T>C urokinase, and -627C>A interleukin 10 (IL-10) promoter), and their relationship to osteoporosis in postmenopausal women. STUDY DESIGN: These polymorphisms were determined using polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP) analysis. BMD of the lumbar spine and proximal femur were measured using dual-energy X-ray absorptiometry. RESULTS: The prevalence of each genotype was as follows: (1) 79.3% A/A, 16.6% A/G, and 4.1% G/G in -308G>A TNF-alpha; (2) 18.9% T/T, 52.1% T/C, and 29% C/C in -34T>C CYP 17; (3) 86.4% C/C and 13.6% C/T in *141T>C urokinase; (4) 46.2% A/A, 45% A/C, and 8.8% C/C in -627C>A IL-10 promoter. Subjects with genotype C/C in -627C>A IL-10 promoter had lower BMD values and a significantly greater risk for osteoporosis (OR 8.1, 95% CI 1.5-42.8) at the lumbar spine compared with subjects with genotype A/C in -627C>A IL-10 promoter, after adjustment for potential confounders. CONCLUSION: The RsaI IL-10 promoter gene polymorphism is associated with reduced BMD and predisposes women to osteoporosis at the lumbar spine.
With decrease of serum PTH in hemodialysis (HD) patients, other factors besides parathyroid hormone (PTH) become important in regulating bone metabolism. We investigated which serum bone metabolic marker is the best to predict the bone mineral density (BMD) reduction in HD patients with serum PTH<180 pg/ml. The bone formation markers, bone alkaline phosphatase (BAP), intact osteocalcin (OC), and N-terminal propeptide of type I collagen (PINP), and the bone resorption markers, deoxypyridinoline (DPD), pyridinoline (PYD), and beta-crossLaps (beta-CTx) were measured in serum from 137 HD patients. BMD of all patients was measured twice, approximately 1.5 years before and 1.5 years after measurement of their markers of bone metabolism. In all 137 HD patients, serum BAP was the only marker significantly higher in those with BMD reduction than in those without. In 42 diabetes mellitus (DM) HD patients with serum PTH<180 pg/ml, hypothetically low bone turnover state, serum BAP was again the only marker to discriminate those with BMD reduction from those without. At serum PTH<60 pg/ml, serum BAP retained tendency toward higher value. These findings suggest that serum BAP might be the most sensitive to identify small changes of bone metabolism in low bone turnover state. Retrospective study confirmed the usefulness of serum BAP in clinical practice by significantly higher values in those with bone loss at PTH<180 pg/ml even in under routine sample handling. In conclusion, serum BAP is a clinically useful bone formation marker to predict the BMD reduction in DM HD patients with low level of PTH.
OBJECTIVES: A double-blind, randomized, placebo-controlled trial was conducted in women with postmenopausal osteoporosis to evaluate effects on biochemical markers and urinary excretion of zinc (Zn) of calcitonin therapy. METHODS: Patients were required to have a bone mineral density (BMD) of 2.5 S.D. or more below the young adult mean either at the postero-anterior lumbar spine or at the femoral neck. Subjects were eligible for our study if they were 50 years or older, with at least 5 years of menopause, and in good general health as determined by medical history and a routine clinical blood analysis. The patients were randomly assigned to receive intranasal salmon calcitonin (200 IU/day; 50 patients) or placebo (50 patients). All patients received supplemental calcium (1000 mg/day). Additionally, 40 age-matched, demographically similar, healthy postmenopausal women were also selected as controls. Measurements of cross-linked N-telopeptides of type I collagen (uNTx), osteocalcin (sOC), and urinary zinc concentration were done. All parameters were measured before therapy and again after 1, 3 and 6 months. RESULTS: After 3 and 6 months of treatment, a higher decrease of most indices was observed in the calcitonin group. A statistically significant decrease occurred in the levels of sOC, uNTx and uZn after 3 and 6 months in patients receiving calcitonin therapy (P<0.05). Levels of sOC and uNTx in calcitonin group were significantly different after 3 and 6 months from both placebo and baseline values of calcitonin group (P<0.05). Levels of sOC, uNTx and uZn decreased about 40, 46 and 37%, respectively, in calcitonin group at 6 months after the start of treatment. CONCLUSIONS: Our study suggests that values of uNTx, uZn and sOC were significantly lower in the patient group than those in control group and in postmenopausal women with osteopororsis, calcitonin reduces the concentrations of uNTx, uZn and sOC.