Increased Serum Parathyroid Hormone Research Articles

Serum concentrations of 25-hydroxyvitamin D and its association with bone mineral density and serum parathyroid hormone levels during winter in urban males from Guiyang, Southwest China.

Serum vitamin D (25-hydroxyvitamin D (25OHD)) may influence serum parathyroid hormone (PTH) levels and bone mineral density (BMD). In the present study, we assessed serum 25OHD concentration and its association with PTH and BMD in urban males from Guiyang (N26.57°), the capital city of Guizhou province, Southwest China. We recruited 634 males aged >20 years from the Guiyang Health Measures Survey, and stratified them into three groups according to age: young (20-39 years), middle aged (40-59 years) and older (60-79 years). We measured serum concentrations of 25OHD, PTH levels and BMD of the lumbar spine (L1-L4), femoral neck and total hip. In addition, we also explored the relationship between 25OHD and lifestyle, socio-economic characteristics and medical history by applying covariance analysis and locally weighted regression plots. The results showed that serum 25OHD was 75 nmol/l in 12·6 % of the subjects. Higher level of serum PTH was detected in relation to lower concentrations of serum 25OHD up to 50 nmol/l. A negative correlation between serum 25OHD and PTH concentrations was observed (r -0·207, P=0·003). Mean concentration of serum PTH increased gradually and plateaued while concentrations of serum 25OHD decreased to 50 nmol/l. Gradual increase in serum PTH was observed as 25OHD concentration was <25 nmol/l (P=0·004). BMD values at all sites were greater in the higher serum 25OHD concentration group. This study shows that low concentrations of serum 25OHD were common in males, and bone health was likely to be improved when serum 25OHD values were between 30 and 50 nmol/l.

Accuracy of Dual Phase Single-Photon Emission Computed Tomography/Computed Tomography in Primary Hyperparathyroidism: Correlation With Serum Parathyroid Hormone Levels

PurposeThe objectives of this study were: 1) to determine the accuracy of dual-phase 99mTc -methoxyisobutylisonitrile (MIBI) with single-photon emission computed tomography/computed tomography (SPECT/CT) for the preoperative localization of parathyroid adenomas in the setting of primary hyperparathyroidism; 2) to determine the accuracy of localization for ectopic glands; and 3) to assess the relationship between accuracy and serum parathyroid hormone (PTH) levels. MethodsEighty-eight patients who underwent 99mTc-MIBI SPECT/CT imaging for primary hyperparathyroidism at our institution over a 27-month period were retrospectively assessed. The preoperative SPECT/CT results were compared to intraoperative findings (within 1 year of imaging). The relationship between serum PTH level (within 3 months) and SPECT/CT accuracy was then evaluated. ResultsAccuracy indices for the retrothyroid subgroup were sensitivity 86.7%, specificity 96.4%, positive predictive value 98.1%, negative predictive value 77.1%, and accuracy 89.8%. Accuracy indices for ectopic parathyroid adenomas were sensitivity 81.5%, specificity 100%, positive predictive value 100%, negative predictive value 92.4%, and accuracy 94.3%. For the overall group, SPECT/CT demonstrated a sensitivity of 85.1% and a PPV of 98.7%. SPECT/CT correctly identified the abnormal parathyroid gland in 60% of patients with a normal serum PTH (<6.9 pmol/L), 73% between 6.9-9.9 pmol/L, 86% between 10.0-14.9 pmol/L, 100% between 15.0-19.9 pmol/L, 88% between 20.0-24.5 pmol/L, and 100% of patients with a PTH greater than 25.0 pmol/L. ConclusionsDual-phase 99mTc- MIBI with SPECT/CT is an accurate and reliable means to correctly localize both retrothyroid and ectopic parathyroid adenomas for the purpose of surgical planning. The accuracy of SPECT/CT increases with increasing serum PTH levels.

The fibroblast growth factor receptor mediates the increased FGF23 expression in acute and chronic uremia.

Serum FGF23 is markedly elevated in chronic kidney disease and has been associated with poor long-term outcomes. FGF23 expression is increased by activation of the FGF receptor 1 (FGFR1) in rats with normal renal function and in vitro in bone-derived osteoblast-like cells. We studied the regulation of FGF23 by FGFR1 in vivo in acute and chronic uremia in mice and rats. Folic acid-induced acute kidney injury increased calvaria FGF23 mRNA and serum FGF23 and parathyroid hormone (PTH) levels at 6 h. The FGFR1 receptor inhibitor PD173074 prevented the folic acid-induced increase in both FGF23 mRNA and serum levels but had no effect on serum PTH levels. A more prolonged uremia due to an adenine high-phosphorus diet for 14 days resulted in high levels of FGF23 mRNA and serum FGF23 and PTH. PD173074 decreased serum FGF23 and mRNA levels with no effect on PTH in the adenine high phosphorus-induced uremic rats. Therefore, a derangement in FGF23 regulation starts early in the course of acute kidney injury, is in part independent of the increase in serum PTH, and involves activation of FGFR1. It is possible that FGFR1 in the osteocyte is activated by locally produced canonical FGFs, which are increased in uremia. This is the first demonstration that activation of FGFR1 is essential for the high levels of FGF23 in acute and chronic experimental uremia.

Phosphorylation of Ribosomal Protein S6 Mediates Mammalian Target of Rapamycin Complex 1-Induced Parathyroid Cell Proliferation in Secondary Hyperparathyroidism.

Secondary hyperparathyroidism is characterized by increased serum parathyroid hormone (PTH) level and parathyroid cell proliferation. However, the molecular pathways mediating the increased parathyroid cell proliferation remain undefined. Here, we found that the mTOR pathway was activated in the parathyroid of rats with secondary hyperparathyroidism induced by either chronic hypocalcemia or uremia, which was measured by increased phosphorylation of ribosomal protein S6 (rpS6), a downstream target of the mTOR pathway. This activation correlated with increased parathyroid cell proliferation. Inhibition of mTOR complex 1 by rapamycin decreased or prevented parathyroid cell proliferation in secondary hyperparathyroidism rats and in vitro in uremic rat parathyroid glands in organ culture. Knockin rpS6(p-/-) mice, in which rpS6 cannot be phosphorylated because of substitution of all five phosphorylatable serines with alanines, had impaired PTH secretion after experimental uremia- or folic acid-induced AKI. Uremic rpS6(p-/-) mice had no increase in parathyroid cell proliferation compared with a marked increase in uremic wild-type mice. These results underscore the importance of mTOR activation and rpS6 phosphorylation for the pathogenesis of secondary hyperparathyroidism and indicate that mTORC1 is a significant regulator of parathyroid cell proliferation through rpS6.

Serum parathyroid hormone and active vitamin D in chronic periodontitis

To study the association between periodontitis and serum parathyroid hormone (PTH) and the response of PTH to periodontal therapy in type 1 diabetic patients (T1DM). We also investigated the PTH-1,25(OH)2 D axis in the T1DM group. Periodontal health status was recorded in 54 periodontitis patients and 30 periodontally healthy controls (case-control data). Data were also collected from patients with type 1 diabetes mellitus at the baseline (n=76) and after periodontal therapy (intervention data) (n=53). Periodontitis was not associated with serum PTH in the case-control data or at the baseline of the intervention data. A post-therapy increase in serum PTH was found in 61% of the T1DM patients; in patients with moderate or severe periodontitis (n=26) the average increase was 0.6pmol/l (p=0.016) and in patients with no or mild periodontitis (n=27) 0.2pmol/l (p=0.250). In 47% of the T1DM patients, an increase in PTH was associated with an increase in serum 1,25(OH)2 D. An association between serum PTH and periodontal infection was found only after periodontal therapy in T1DM patients. This post-treatment response in serum PTH may partly explain the previously reported increase in serum 1,25(OH)2 D.

Parathyroid-specific deletion of dicer-dependent microRNAs abrogates the response of the parathyroid to acute and chronic hypocalcemia and uremia

MicroRNAs (miRNAs) down-regulate gene expression and have vital roles in biology but their functions in the parathyroid are unexplored. To study this, we generated parathyroid-specific Dicer1 knockout (PT-Dicer(-/-) ) mice where parathyroid miRNA maturation is blocked. Remarkably, the PT-Dicer(-/-) mice did not increase serum parathyroid hormone (PTH) in response to acute hypocalcemia compared with the >5-fold increase in controls. PT-Dicer(-/-) glands cultured in low-calcium medium secreted 5-fold less PTH at 1.5 h than controls. Chronic hypocalcemia increased serum PTH >4-fold less in PT-Dicer(-/-) mice compared with control mice with no increase in PTH mRNA levels and parathyroid cell proliferation compared with the 2- to 3-fold increase in hypocalcemic controls. Moreover, uremic PT-Dicer(-/-) mice increased serum PTH and FGF23 significantly less than uremic controls. Therefore, stimulation of the parathyroid by both hypocalcemia and uremia is dependent upon intact dicer function and miRNAs. In contrast, the PT-Dicer(-/-) mice responded normally to activation of the parathyroid calcium-sensing receptor (Casr) by both hypercalcemia and a calcimimetic that decreases PTH secretion, demonstrating that they are dicer-independent. Therefore, miRNAs are essential for the response of the parathyroid to both acute and chronic hypocalcemia and uremia, the major stimuli for PTH secretion.

Bone density in apheresis donors and whole blood donors.

Apheresis donation using citrate causes acute decrease in serum calcium and increase in serum parathyroid hormone. Long-term consequences, such as decrease in bone mineral density (BMD), are not known. In this study, we compared the BMD of 20 postmenopausal apheresis donors (mean donation number 115 times in up to 15 years) with that of 20 whole blood donors (for 15 years or more) aged 55-70. BMD in the lumbar spine was not lower in apheresis donors than in blood donors (mean ± SD 1.00 ± 0.18 vs. 0.92 ± 0.12, P = 0.09). In the hip, BMD was not different between the groups.

Changes in Bone Metabolism in Morbidly Obese Patients After Bariatric Surgery: A Meta-Analysis.

The aim is to evaluate via meta-analysis bone metabolism and bone mineral density (BMD) in morbidly obese patients before and after bariatric surgery. We searched Medline, EMBASE, and the Cochrane Library for relevant studies published before January 2014. The following outcomes were evaluated: serum calcium, serum parathyroid hormone (PTH), serum 25-hydroxyvitamin D [25(OH)D], serum or urinary N-telopeptide (NTX), bone-specific alkaline phosphatase (BSAP), and bone mineral density (BMD). Ten studies, including 344 patients, met our inclusion criteria. Results showed a significant decrease in serum calcium (MD = -0.10, 95 %CI -0.14 to -0.07, P < 0.00001) and increase in serum PTH (MD = 12.41, 95 %CI 6.51 to 18.31, P < 0.00001) but no significant difference in serum 25(OH)D (MD = 1.35, 95 %CI -1.12 to 3.83, P = 0.28) following bariatric surgery. There were significant increases in serum or urinary NTX (MD = 18.49, 95 %CI 3.33 to 33.66, P = 0.02) and BSAP (MD = 7.47, 95 %CI 0.21 to 14.72, P = 0.04) but a significant decrease in BMD (MD = -0.08, 95 %CI -0.13 to -0.04, P < 0.00001) after bariatric surgery. BMD was significantly decreased, while bone turnover was elevated, and bone remodeling was accelerated following bariatric surgery. Basal bone metabolism should be evaluated preoperatively. To prevent secondary hyperparathyroidism and bone loss, calcium and vitamin D should be monitored closely and supplemented accordingly after the surgery.

Zinc Deficiency Increases Serum Concentrations of Parathyroid Hormone through a Decrease in Serum Calcium and Induces Bone Fragility in Rats.

We hypothesized that a zinc-deficient diet alters the mineral (calcium, magnesium, and phosphorus) components of bones, as well as hormones related to bone remodeling, and negatively affects bone metabolism. Four-week-old male Wistar rats were randomly assigned to one of three groups for 4 wk: a zinc-adequate group (C, 30 ppm); a zinc-deficient group (ZD, 1 ppm); and a pair-fed group (PF, 30 ppm), which was pair-fed to the ZD group. Bone mineral density and bone mechanical properties were reduced in the ZD group compared to the C and PF groups. Compared with the C and PF groups, serum osteocalcin, a bone formation marker, was reduced in the ZD group. Conversely, urine deoxypyridinoline, a bone resorption marker, was increased in the ZD group compared to the C and PF groups. Calcium and phosphorus concentrations in bone were not different among all groups. The bone magnesium concentration was significantly higher in the ZD group than in the PF and C groups. Interestingly, compared with the C and PF groups, the ZD group showed a reduction in serum calcium concentration along with an increase in serum parathyroid hormone (PTH) concentration. Although serum 1,25-dihydroxycholecalciferol concentration was significantly higher in the ZD and PF groups than in the C group, the rate of apparent calcium absorption was significantly lower in the ZD group than in the C and PF groups. Therefore, zinc deficiency is suspected to cause an increase in serum PTH concentration owing to an inability to maintain calcium homeostasis, resulting in bone fragility.

Effects of Dietary Calcium Supplementation on Bone Metabolism, Kidney Mineral Concentrations, and Kidney Function in Rats Fed a High-Phosphorus Diet.

We investigated the effects of dietary calcium (Ca) supplementation on bone metabolism, kidney mineral concentrations, and kidney function in rats fed a high-phosphorus (P) diet. Wistar strain rats were randomly divided into 4 dietary groups and fed their respective diets for 21 d: a diet containing 0.3% P and 0.5% Ca (C), a diet containing 1.5% P and 0.5% Ca (HP), a diet containing 0.3% P and 1.0% Ca (HCa), or a diet containing 1.5% P and 1.0% Ca (HPCa). Compared to the C group, the high-P diet increased serum parathyroid hormone concentration, markers of bone turnover, receptor activator of NF-κB ligand mRNA expression of the femur, kidney Ca and P concentrations, urinary N-acetyl-β-D-glucosaminidase activity, and urinary β2-microglobulin excretion, and decreased bone mineral content and bone mineral density of the femur and tibia. Dietary Ca supplementation improved the parameters of bone metabolism and kidney function in rats fed the high-P diet, while there were no significant differences in kidney Ca or P concentrations between the HP and HPCa groups. These results suggest that dietary Ca supplementation prevented the bone loss and decline in kidney function induced by a high-P diet, whereas dietary Ca supplementation did not affect kidney mineral concentrations in rats fed the high-P diet.

Knockout of Nuclear High Molecular Weight FGF2 Isoforms in Mice Modulates Bone and Phosphate Homeostasis

We previously reported that targeted overexpression of the fibroblast growth factor 2 (FGF2) high molecular weight (HMW) isoforms in osteoblastic lineage cells in mice resulted in phenotypic changes, including dwarfism, rickets, osteomalacia, hypophosphatemia, increased serum parathyroid hormone, and increased levels of the phosphatonin FGF23 in serum and bone. This study examined the effects of genetically knocking out the FGF2HMW isoforms (HMWKO) on bone and phosphate homeostasis. HMWKO mice were not dwarfed and had significantly increased bone mineral density and bone mineral content in femurs and lumbar vertebrae when compared with the wild-type (WT) littermates. Micro-computed tomography analysis of femurs revealed increased trabecular bone volume, thickness, number, and connective tissue density with decreased trabecular spacing compared with WT. In addition, there was significantly decreased cortical porosity and increased cortical thickness and sub-periosteal area in femurs of HMWKO. Histomorphometric analysis demonstrated increased osteoblast activity and diminished osteoclast activity in the HMWKO. In vitro bone marrow stromal cell cultures showed there was a significant increase in alkaline phosphatase-positive colony number at 1 week in HMWKO. At 3 weeks of culture, the mineralized area was also significantly increased. There was increased expression of osteoblast differentiation marker genes and reduced expression of genes associated with impaired mineralization, including a significant reduction in Fgf23 and Sost mRNA. Normal serum phosphate and parathyroid hormone were observed in HMWKO mice. This study demonstrates a significant negative impact of HMWFGF2 on biological functions in bone and phosphate homeostasis in mice.

Protective effects of water fraction of Fructus Ligustri Lucidi extract against hypercalciuria and trabecular bone deterioration in experimentally type 1 diabetic mice

Ethnopharmacological relevanceFructus Ligustri Lucidi (FLL), the fruit of Ligustrum lucidum Ait, is a commonly prescribed herb to nourish the endocrine and renal systems and to strengthen the bones in Traditional Chinese Medicine. This study was aimed to determine the effects of water fraction of FLL ethanol extract (WF-EE) on urinary calcium excretion and trabecular bone properties in type 1 diabetic mice. Materials and methodsThe DBA/2J mice with type 1 diabetes induced by streptozotocin injection were orally administered with WF-EE. After 6 weeks of treatment, the level of biomarkers, including serum calcium, parathyroid hormone (PTH), and fibroblast growth factor-23 (FGF-23) and urine calcium, was measured. Micro-CT was performed to detect trabecular bone properties of the proximal tibial metaphysis. The expression of active calcium transporting proteins in kidney and duodenum was determined by RT-PCR, immunoblotting and immunostaining. ResultsType 1 diabetes induced hypercalciuria and trabecular bone deterioration. The WF-EE could significantly inhibit hypercalciuria and ameliorate the micro-structure of trabecular bone as well as increase serum PTH and FGF-23 levels in type 1 diabetic mice. The gene expressions of active calcium transporting proteins in duodenum were up-regulated, and the gene and protein expressions of calcium-sensing receptor (CaSR) in kidney were dramatically down-regulated in diabetic mice in response to the treatment with WF-EE. ConclusionsThe present study demonstrated the protective effects of the water fraction of Fructus Ligustri Lucidi ethanol extract against hypercalciuria and trabecular bone deterioration in experimentally type 1 diabetic mice, and the underlying mechanism may be attributed to its regulations on duodenal calcium transporting proteins and renal CaSR.

Decreased cortical thickness, as estimated by a newly developed ultrasound device, as a risk for vertebral fracture in type 2 diabetes mellitus patients with eGFR of less than 60 mL/min/1.73 m2.

SummaryCortical porosity is increasingly recognized as an important risk for fracture in DM patients. The present study demonstrated that decreased cortical thickness, assessed using a newly developed quantitative ultrasonic bone densitometry, is a significant risk factor for vertebral fractures in type 2 diabetes mellitus patients with stage 3 or higher chronic kidney disease, but not in those without.IntroductionCortical porosity is increasingly recognized as an important risk factor for fracture in type 2 diabetes mellitus (T2DM) patients as well as in stage 3 chronic kidney disease (CKD) patients in whom serum parathyroid hormone (PTH) starts to increase. The present study aimed to clarify whether the coexistence of CKD might affect the relationship of decreased cortical thickness (CoTh) in the development of vertebral fractures (VF) in T2DM patients.MethodsIn this cross-sectional study, trabecular bone mineral density (TrBMD), elastic modulus of trabecular bone (EMTb), and CoTh were estimated with a new quantitative ultrasound bone densitometry in 173 T2DM patients. VFs were identified radiographically.ResultsThirty-nine patients (22.5 %) had VF. Those with estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 (low eGFR) showed a significantly higher VF rate (32.4 %) than those with eGFR ≥60 mL/min/1.73 m2 (high eGFR, 16.2 %). Serum PTH was significantly higher with low eGFR than with high eGFR. In those with high eGFR, EMTb was significantly lower in VF(+) than VF(−). In those with low eGFR, TrBMD, EMTb, and CoTh were significantly lower in VF(+) than in VF(−). In a multivariate logistic regression analysis, EMTb was independently and significantly associated with VF in T2DM patients with a high eGFR, in contrast to those with only CoTh with VF in T2DM with low eGFR.ConclusionThis study demonstrated CoTh as a factor independently associated with VF in T2DM patients with low eGFR and increasing serum PTH levels.Electronic supplementary materialThe online version of this article (doi:10.1007/s00198-014-2843-x) contains supplementary material, which is available to authorized users.

Relationship between 25-hydroxyvitamin D concentrations, serum calcium, and parathyroid hormone in apparently healthy Syrian people

Vitamin D deficiency (25-hydroxyvitamin D (25OHD) <25 nmol/L) was common in a convenience sample of apparently healthy Syrian adults. Female gender, season, and concealing clothing were independent predictors of vitamin D deficiency. Community-based research is needed to identify vulnerable subgroups and inform public health actions. Optimal vitamin D status for bone health has been inferred from the determination of serum 25OHD levels below which there is an increase in serum parathyroid hormone (PTH). Studies worldwide showed high prevalence of hypovitaminosis D even in sunny countries. There is little evidence about its prevalence among Syrian adult population. We aimed to assess the serum levels of 25OHD and factors related to vitamin D inadequacy and its relation to serum PTH and calcium among apparently healthy adults. Serum 25OHD and PTH measurements were obtained from 372 subjects aged 18-62 years living in Damascus and its surroundings, between April 2011 and March 2013. Binary logistic regression was used to assess risk factors for hypovitaminosis D. The mean (standard deviation (SD)) 25OHD level was 24.7 (16.9) nmol/L [9.8 (6.7) ng/mL] and was higher in men than women (p < 0.001). Levels <25, <50, and <75 nmol/L were detected in 61, 90.1, and 99.2 % of the participants, respectively. Season influenced vitamin D status in men but not in women (p < 0.001). Female gender and wearing the veil (hijab) were independent predictors of vitamin D deficiency (25OHD <25 nmol/L). PTH was significantly higher below this threshold (p < 0.001). Serum 25OHD <25 nmol/L, sex, and age ≥ 35 years were statistically significant factors for PTH elevation. Vitamin D deficiency was highly prevalent in our sample. Further research is needed to identify population groups vulnerable for hypovitaminosis D and specify its predictors and inform the necessary public health measures.

Successful Detection and Removal of a Functional Parathyroid Adenoma in a Pony Using Technetium Tc 99m Sestamibi Scintigraphy

Successful Detection and Removal of a Functional Parathyroid Adenoma in a Pony Using Technetium Tc 99m Sestamibi Scintigraphy

Association between parathyroid hormone levels and inflammatory markers among US adults.

Background and Aims. High levels of parathyroid hormone (PTH) appear to be associated with an increased mortality. Previous studies concerning the relationship of inflammatory markers with hyperparathyroidism have yielded inconsistent results. This study investigated whether serum PTH concentrations were independently associated with several inflammatory markers among the US adults. Materials and Methods. Using data from the National Health and Nutrition Examination Survey, we examined the relation between serum PTH and C-reactive protein (CRP), red cell distribution width (RDW), and platelet-to-lymphocyte ratio (PLR) levels with weighted linear regression. Additionally, we examined the relation with increased modified Glasgow Prognostic Score (mGPS) by using weighted logistic regression. Results. CRP, RDW, and PLR values increased with increasing serum PTH concentration. After extensively adjusting for covariates, CRP and RDW increased linearly and across PTH categories (all P < 0.001), while PLR marginally increased (P = 0.190 and P = 0.095 using PTH as a categorical and continuous variable, resp.). The odds ratio of increased mGPS was 1.11 and 1.31 across PTH categories and with increasing PTH levels continuously. Conclusion. These nationally representative data indicate that serum PTH levels are independently associated with several inflammatory markers in the US population. The casual relationship between PTH levels and inflammation remains to be elucidated.

Long-term anti-epileptic drug therapy and metabolic bone disase in children

Epilepsy is a common chronic brain dysfunction in children. Studies have showed that antiepi- leptic drugs （AED） affect the hydroxylation of vitamin D in liver and kidney and inhibit the calcification of bone, mainly by up-regulating cytochrome oxidase P450 and promoting the resolution of vitamin D, and then increasing serum parathyroid hormone compensatory. Long-term use can cause children metabolic bone disease occurrence, clinical manifestations include bone pain, short stature, rickets, teeth agenesis, fracture, etc. AED firstly affect the hormones related to bone metabolism in vivo,so that the present researches focus on biochemical tests and meas- urement of sclerotin and bone density. In the children＇s long-term use of antiepileptic drug treatment at the same time,the application of Vitamin D,calcium and exercise can prevent the occurrence of metabolic bone disease. Key words: Antiepileptic drug; Metabolic bone disease in children

The Effect of Endogenous Parathyroid Hormone in Iliac Bone Structure and Turnover in Healthy Postmenopausal Women

Little is known about the effect of endogenous parathyroid hormone (PTH) on the skeleton in postmenopausal women without hyperparathyroidism. In this study, the effects of PTH on bone were investigated in iliac crest biopsies obtained from 37 healthy white postmenopausal women aged 50-73 years. The results showed that neither cancellous nor cortical bone structure changed with serum PTH levels. In cancellous bone, bone formation (wall thickness, osteoid surface, osteoblast surface, mineralizing surface, and mineral apposition rate) and turnover (bone formation rate at the surface, volume levels, and activation frequency) variables increased with increasing serum PTH levels (all p < 0.05) in univariate analysis. Multiple linear regressions, adjusted for serum 25-OHD, calcium, alkaline phosphatase, age, and BMI, showed that serum PTH level was independently associated with wall thickness, osteoid surface, osteoblast surface, mineralizing surface, and bone formation rate (all p < 0.05). In cortical bone, no histomorphometric variable was correlated with PTH levels. On the endosteal surface, some of the bone formation (osteoid surface, osteoblast surface, mineralizing surface) and turnover (bone formation rate at the bone surface levels and activation frequency) variables were positively correlated with PTH levels (all p < 0.05). None of these variables could be independently predicted by PTH status. We conclude that in healthy postmenopausal women endogenous PTH has a positive effect on bone formation on the cancellous surface. The effects of PTH on the endosteal surface are probably confounded by other factors.

Conjugated linoleic acid and calcium co-supplementation improves bone health in ovariectomised mice

Osteoporosis is a significant health concern for the elderly; conjugated linoleic acid (CLA) has been shown to improve overall bone mass when calcium is included as a co-supplement. However, potential effects of CLA and calcium on bone mass during a period of bone loss have not been reported. The purpose of this study was to determine how dietary calcium modulates the effects of conjugated linoleic acid (CLA) in preventing bone loss, using an ovariectomised mouse model. CLA supplementation significantly prevented ovariectomy-associated weight and fat mass gain, compared to non-supplemented controls. CLA significantly increased bone markers without major changes in bone mineral composition in the femur compared to respective controls. CLA treatment increased serum parathyroid hormone (PTH) significantly (p=0.0172), while serum 1,25-dihydroxyvitamin D3 concentration was not changed by CLA. Meanwhile, CLA significantly reduced femur tartrate resistant acid phosphatase (TRAP) activity, suggesting potential reduction of osteoclastogenesis. The data suggest that CLA, along with dietary calcium, has great potential to be used to prevent bone loss and weight gain associated with menopause.

Case Reports

Pseudohypoparathyroidism due to deficient end organ response to parathyroid hormone (PTH) is characterized by hypocalcemia, hyperphosphatemia and increased serum PTH. We report a case of an 8-year-old girl with pseudohypoparathyroidism without features of Albright's hereditary osteodystrophy. The case is of interest as the child on serial follow-up over a period of 2 years developed hypothyroidism. This is a rare feature seen in pseudohypoparathyroidism type1b.