Factors related to curved femur in elderly Japanese women

Background: Multiple factors are involved in the development of atypical femoral fractures, and excessive curvature of the femur is thought to be one of them. However, the pathogenesis of femoral curvature is unknown. We evaluated the influence of factors related to bone metabolism and posture on the development of femoral curvature.

Methods: A total of 139 women participated in the present study. Curvatures were measured using antero-posterior and lateral radiography of the femur. We evaluated some bone and vitamin D metabolism markers in serum, the bone mineral density (BMD), lumbar spine alignment, and pelvic tilt.

Results: We divided the women into two groups, curved and non-curved groups, based on the average plus standard deviation as the cut-off between the groups. When univariate logistic regression analysis was performed to detect factors affecting femoral curvature, the following were identified as indices significantly affecting the curvature: age of the patients, serum concentrations of calcium, intact parathyroid hormone, pentosidine, homocysteine and 25-hydroxyvitamin D (25(OH)D), and BMD of the proximal femur (P?<?0.05) both in the lateral and anterior curvatures. When we used multivariate analyses to assess these factors, only 25(OH)D and age (lateral and anterior standardized odds ratio: 0.776 and 0.385, and 2.312 and 4.472, respectively) affected the femoral curvature (P?<?0.05).

Conclusion: Femoral curvature is strongly influenced by age and serum vitamin D.     

阿德福韦酯致低磷性骨软化病1例的护理

近年来,口服抗乙肝病毒的核苷类似物因具有较强的抗病毒作用和较好的耐受性已被临床广泛应用。但随着疗程的增加,某些不良反应逐渐显现并引起人们的关注。阿德福韦酯的肾毒性具有剂量和时间相关性,多见于30mg／d以上剂量以及有基础肾功能损害的患者。阿德福韦酯等核苷类似物的肾毒性作用靶点位于肾近曲小管,可导致肾小管病变。目前认为这类药物的肾毒性发生主要与肾小管阴离子转运蛋白-1(HOAT-1)对药物的聚集作用和药物对线粒体的毒性有关。阿德福韦酯等以原型通过肾小管主动分泌方式由肾脏排泄,HOAT- 1对阿德福韦酯等有较强的亲和力,可主动摄取阿德福韦酯,使其在肾脏近曲小管部位有较高的药物浓度[1-2],抑制细胞线粒体DNA的合成,导致近曲小管线粒体DNA减少甚至耗竭,线粒体功能显著降低,从而影响肾小管的重吸收和分泌功能,临床上表现为肾近曲小管功能障碍[3-4]。这种阿德福韦酯等相关性的肾小管病,其临床表现一般较轻,极少数重症患者可表现为显著的肾性低血磷症及骨质疏松[5-6]、肾小管性酸中毒、肾性电解质紊乱、低磷性骨软化症[7]等。     

Aluminum Contamination in Parenteral Nutrition Admixtures for Low‐Birth‐Weight Preterm Infants in Mexico

Background: Aluminum contamination from intravenous solutions still represents an unsolved clinical and biochemical problem. Increased aluminum intake constitutes a risk factor for the development to metabolic bone disease, anemia, cholestasis, and neurocognitive alterations. Low‐birth‐weight preterm infants (LBWPIs) are one of the most exposed populations for aluminum toxicity. Methods: To determine the presence of aluminum in components employed in the preparation of parenteral nutrition (PN) admixtures in Mexico and compare with the maximal aluminum recommended intake from the Food and Drug Administration. Results: Cysteine, trace elements, levocarnitine, phosphate, and calcium salts tested positive for aluminum contamination. All components analyzed were contained in glass vials. Total aluminum intake for 2 sample PN admixtures were calculated in basis to cover nutrition requirements of 2 hypothetical LBWPIs. Aluminum contents, stratified in micrograms per kilogram of weight, exceeded maximal aluminum recommendations, particularly for the very LBWPIs. Substituting sodium phosphate for potassium phosphate salts reduced aluminum intake by 52.7%. Calcium gluconate was the leading aluminum contamination source and confers the greatest risk for aluminum overdose, even with the salt substitution of potassium phosphate by sodium phosphate salts. Adding cysteine and trace elements might increase aluminum content in PN admixtures. Conclusion: Cysteine, trace elements, phosphate, and gluconate salts are the main sources of aluminum in PN prepared in Mexico. Substituting sodium phosphate for potassium phosphate salts reduces aluminum intake but does not resolve aluminum contamination risk. Mineral salts contained in plastic vials should be explored as an additional measure to reduce aluminum contamination.     

Radiotherapy for a rare phosphaturic mesenchymal tumor in the middle ear presenting with oncogenic osteomalacia: A case report

Rationale:Phosphaturic mesenchymal tumor (PMT) is a rare neoplasm causing oncogenic osteomalacia. Surgery remains the definitive treatment for PMT, and radiotherapy is seldom employed. However, surgery for PMT involving the head and neck is often difficult due to the local invasion and complicated anatomy. We report the first case of PMT, which was successfully treated with the combination of radiotherapy and supplementation of activated vitamin D.Patient concerns:A 55-year-old woman suffered from pain in the hip and bilateral femur. Serum phosphate and calcium decreased to abnormal levels. Serum alkaline phosphatase and fibroblast growth factor 23 increased to abnormal levels. The hearing loss of the right ear had continued and a middle ear tumor was revealed.Diagnoses:Subsequent biopsy provided the diagnosis of PMT that caused oncogenic osteomalacia. These clinical and pathological characteristics were consistent with and provided the final diagnosis of benign PMT.Interventions:Surgery of the PMT was difficult and the patient underwent radiotherapy. The prescribed dose was 36 Gy in 10 fractions. Simultaneously, the patient started supplementation of 1,25-dihydroxyvitamin D3 (1–2 μg/day) and continued for 2 years.Outcomes:Near-complete resolution of the symptoms was achieved and abnormal laboratory values recovered. At 5 years of follow-up, the irradiated tumor showed no regrowth. Severe hearing loss of the right ear was not observed.Lessons:Radiotherapy was effective for the PMT and could be an important treatment option for inoperable cases.     

Experimental evidence for the effects of calcium and vitamin D on bone: a review

Animal models fed low calcium diets demonstrate a negative calcium balance and gross bone loss while the combination of calcium deficiency and oophorectomy enhances overall bone loss. Following oophorectomy the dietary calcium intake required to remain in balance increases some 5 fold, estimated to be approximately 1.3% dietary calcium. In the context of vitamin D and dietary calcium depletion, osteomalacia occurs only when low dietary calcium levels are combined with low vitamin D levels and osteoporosis occurs with either a low level of dietary calcium with adequate vitamin D status or when vitamin D status is low in the presence of adequate dietary calcium intake. Maximum bone architecture and strength is only achieved when an adequate vitamin D status is combined with sufficient dietary calcium to achieve a positive calcium balance. This anabolic effect occurs without a change to intestinal calcium absorption, suggesting dietary calcium and vitamin D have activities in addition to promoting a positive calcium balance. Each of the major bone cell types, osteoblasts, osteoclasts and osteocytes are capable of metabolizing 25 hydroxyvitamin D (25D) to 1,25 dihydroxyvitamin D (1,25D) to elicit biological activities including reduction of bone resorption by osteoclasts and to enhance maturation and mineralization by osteoblasts and osteocytes. Each of these activities is consistent with the actions of adequate circulating levels of 25D observed in vivo.     

A noncompetitive enzyme immunoassay (hetero-two-site enzyme immunoassay) for salmon calcitonin: Determination of the bioavailability of subcutaneous salmon calcitonin and its correlation with the hypocalcemic activity in rats

A noncompetitive enzyme immunoassay method (hetero-two-site enzyme immunoassay) for salmon calcitonin (SCT) and its usability for the pharmacokinetic study are described. The method in brief proceeds as follows: centrifugal filtration through a polysaccharide membrane to remove plasma proteins, biotinylation, trapping onto an anti-SCT IgG-coated polystyrene ball, acid elution, coupling with affinity-purified anti-SCT Fab¹-peroxidase conjugate, final trapping onto streptavidin-coated polystyrene balls, and measurement of peroxidase activity bound to the balls by fluorometry. The practical detection limit of SCT was 0.1 pg (30 amol)/assay and 2 pg/ml as the assay sample's concentration, which was at least fivefold lower than those previously reported by competitive radioimmunoassays. The application of this method has enabled us to 1) directly estimate the bioavailability of SCT dosed subcutaneously at the therapeutic levels (1.2 and 4.7 μg/kg) for its antiosteoporotic effect as compared to an intravenous dose (1.2 μg/kg) and 2) search for the relationship between blood level and the hypocalcemic activity of SCT. The pharmacokinetic parameters of subcutaneous SCT (1.2 and 4.7 μg/kg) thus estimated were as follows: the area under the blood concentration-time curve (AUC) = 89 and 550 pg hr/ml, and mean residence time (MRT) = 44 and 65 minutes, respectively, when the AUC for an intravenous SCT (1.2 μg/kg) = 160 pg hr/ml and the MRT = 10 minutes. © 1996 Wiley-Liss, Inc.     

Tumor-induced osteomalacia caused by a massive phosphaturic mesenchymal tumor of the acetabulum: A case report

We report a case of tumor-induced osteomalacia (TIO) caused by a massive phosphaturic mesenchymal tumor (PMT) of the acetabulum. A 68-year-old woman presented with progressive bone pain of the rib cage, and polyarthralgia and back pain for 3 years. She was diagnosed with hypophosphatemic osteomalacia because laboratory testing was remarkable for low serum phosphorus and a low level of 1,25(OH)2 vitamin D. Three years later, her hip radiograph revealed an osteolytic lesion of the acetabulum. Magnetic resonance imaging of the acetabulum showed a massive lesion. Laboratory data showed hypophosphatemia and an elevated serum level of fibroblast growth factor 23 (FGF-23). Samples obtained with open biopsy showed a low-grade spindle cell neoplasm with FGF-23 positivity, identified by using immunohistochemical staining, confirming the diagnosis of a PMT mixed connective tissue variant. Curettage of the tumor was performed, and the defects were filled with bone allografts. The hip joint was reconstructed with total hip arthroplasty using a Muller support ring. To our knowledge, this report represents the first documented case of massive PMT of the acetabulum causing TIO.