scholarly journals Is Preptin a New Bone Metabolism Parameter in Hemodialysis Patients?

Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 341
Author(s):  
Małgorzata Kałużna ◽  
Krzysztof Pawlaczyk ◽  
Krzysztof Schwermer ◽  
Krzysztof Hoppe ◽  
Aisha Yusuf Ibrahim ◽  
...  

Background: Preptin is a bone-anabolic pancreatic peptide hormone. Its role in bone metabolism has been studied in rats and in patients with diabetes, but its levels and significance in bone metabolism in hemodialyzed (HD) patients is unknown. Methods: The relationships between preptin and anthropometric and biochemical parameters related to bone metabolism were studied in 73 patients on chronic hemodialysis (48 males, 25 females; mean age of 57 years; HD vintage of 69.7 months). Of these subjects, 36 patients had diabetes or impaired glucose tolerance (DM/IGT), and 37 patients had normal glucose tolerance (NGT). Dual-energy X-ray absorptiometry of the femoral neck and lumbar spine were also performed. Results: No differences were observed in preptin levels between DM/IGT and NGT HD patients. Preptin was positively correlated with HD vintage (r = 0.312, p = 0.007). Negative correlations between preptin and bone mineral density (BMD), T-score, and Z-score in the lumbar spine (L2-L4) were observed (r = −0.319, p = 0.009; r = −0.341, p = 0.005; r = −0.375, p = 0.002). Preptin was positively correlated with parathormone (PTH) levels (r = 0.379, p < 0.001) and osteocalcin levels (r = 0.262, p = 0.027). Conclusions: The results indicate that preptin may reflect on bone and mineral metabolism disturbances seen in HD patients. The significant correlation of preptin with PTH and osteocalcin suggests that preptin may be important in indirect measurement of bone turnover in HD patients.

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1895
Author(s):  
Francesca Marini ◽  
Francesca Giusti ◽  
Federica Cioppi ◽  
Davide Maraghelli ◽  
Tiziana Cavalli ◽  
...  

Primary hyperparathyroidism (PHPT) is the most common endocrinopathy in multiple endocrine neoplasia type 1 (MEN1). Persistent levels of increased parathyroid hormone (PTH) result in a higher incidence of osteopenia and osteoporosis compared to the general population. Surgical removal of hyper-functioning parathyroid tissue is the therapy of choice. This retrospective study evaluated the effect of parathyroidectomy (PTX) on bone metabolism and bone mass in two series of patients with MEN1 PHPT and sporadic PHPT (sPHPT) by comparing bone metabolism-related biochemical markers and bone mineral density (BMD) before and after surgery. Our data confirmed, in a higher number of cases than in previously published studies, the efficacy of PTX, not only to rapidly restore normal levels of PTH and calcium, but also to normalize biochemical parameters of bone resorption and bone formation, and to improve spine and femur bone mass, in both MEN1 PHPT and sPHPT. Evaluation of single-patient BMD changes after surgery indicates an individual variable bone mass improvement in a great majority of MEN1 PHPT patients. In MEN1 patients, PTX is strongly suggested in the presence of increased PTH and hypercalcemia to prevent/reduce the early-onset bone mass loss and grant, in young patients, the achievement of the bone mass peak; routine monitoring of bone metabolism and bone mass should start from adolescence. Therapy with anti-fracture drugs is indicated in MEN1 patients with BMD lower than the age-matched normal values.


2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Jui-Hua Huang ◽  
Fu-Chou Cheng ◽  
Hsu-Chen Wu

The aim of this study is to investigate the impact of serum Mg on bone mineral metabolism in chronic kidney disease (CKD) patients with or without diabetes. A total of 56 CKD patients not receiving dialysis were recruited and divided into two groups, one group of 27 CKD patients with diabetes and another group of 29 CKD patients without diabetes. Biochemical determinations were made, and the estimated glomerular filtration rate (eGFR) was measured. Bone mineral density was measured by dual-energy X-ray absorptiometry. Serum Mg was inversely correlated with serum CaP=0.023and positively correlated with serum parathyroid hormone (PTH)P=0.020, alkaline phosphataseP=0.044, and phosphateP=0.040in the CKD patients with diabetes. The CKD patients with diabetes had lower serum albumin and a higher proportion of hypomagnesemia and osteoporosis than the nondiabetic patients didP<0.05. Serum Mg was inversely correlated with eGFR in the CKD patients with or without diabetesP<0.05. Serum Mg showed an inverse correlation with 25-hydroxyvitamin D in CKD patients without diabetesP=0.006. Furthermore, the diabetic CKD patients with low serum Mg had a lower iPTHP=0.007and a higher serum Ca/Mg ratioP<0.001than the other CKD patients. The lower serum Mg subgroup showed a higher incidence of osteoporosis than the moderate and higher serum Mg subgroups did (66.7%, 39.4%, and 29.4%, resp.). In conclusion, low serum Mg may impact iPTH and exacerbates osteoporosis in CKD patients, particularly with diabetes.


2017 ◽  
Vol 2 (3) ◽  
pp. 41-46
Author(s):  
Jimpei Miyakawa ◽  
Satoru Taguchi ◽  
Motofumi Suzuki ◽  
Kaori Endo ◽  
Yorito Nose ◽  
...  

Background: While semiannual 60 mg denosumab is a common treatment for osteoporosis, impact of monthly 120 mg denosumab, the common treatment protocol for bone metastases from solid tumors, on bone metabolism is unclear.Materials and Methods: We reviewed 15 patients with bone-metastatic prostate cancer who initiated monthly 120 mg denosumab in conjunction with androgen deprivation therapy between 2013 and 2014. Bone mineral density (BMD) was measured at lumbar spine and femoral neck using dual energy X-ray absorptiometry (DXA), before treatment and annually thereafter. Bone metabolism markers, including urine N-terminal telopeptide (uNTx) and bone type alkaline phosphatase (BAP), were monitored monthly.Results: Twelve of 15 (80%) patients had evaluable DXA before treatment, and of them, eight underwent DXA after a year of initiation without discontinuation of denosumab. Percent changes in BMD from baseline were +6.2% at lumbar spine and +7.6% at femoral neck, both of which were significant increases (both P<0.01). Bone metabolism markers were evaluable in 11 (73%) patients: uNTx decreased rapidly, while BAP declined gradually after initiating denosumab. These effects were similar to those seen by the standardized dose for osteoporosis in previous literature. There were no denosumab-related severe adverse events during the follow-up period. Conclusions: The impact of monthly 120 mg denosumab on bone metabolism was significant, but almost equivalent to that of the standard dose for osteoporosis (60mg semiannually) in bone-metastatic prostate cancer undergoing androgen deprivation therapy. Whereas the higher dose has reportedly reduced skeleton-related events, the effect on bone metabolism seemed plateaued or showed no dose-dependency.


2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Sain S. Safarova

Aim. The study aims to develop a practical model for screening bone turnover state in patients with diabetes and evaluate its clinical usefulness to identify diabetic osteopathy. Materials. The study was conducted in 2015–2017 in the Endocrinology Department of the Therapeutic Clinic of AM University. A total of 235 patients were assessed in the study (98 with T1DM and 137 with T2DM). 89 nondiabetic subjects served as controls. Bone mineral density (BMD) [by dual energy X-ray absorptiometry (DXA)] and serum markers of bone remodeling [aminoterminal propeptide of procollagen type I (P1NP) and c-terminal telopeptide of type I collagen (CTX)], parathyrin, and 25(OH)D were measured in all 235 patients. Results. Our results show that patients with T2DM have lower b-CTx values and relatively higher levels of P1NP, reflecting less pronounced changes in bone metabolism compared to patients with T1DM, regardless of age or duration of the disease. Osteoporosis was detected in 50% of patients with T1DM, compared to 13% of patients with T2DM. Conclusion. In some cases, bone remodeling markers are useful for improving the assessment of the state of bone tissue in early stages of diabetes, while alterations in bone microarchitecture may not always be captured by bone mineral density measurements.


PLoS ONE ◽  
2021 ◽  
Vol 16 (5) ◽  
pp. e0251912
Author(s):  
Mayuko Hori ◽  
Kaoru Yasuda ◽  
Hiroshi Takahashi ◽  
Chikao Yamazaki ◽  
Kunio Morozumi ◽  
...  

Introduction Bone mineral density (BMD) measured with dual-energy X-ray absorptiometry (DXA) can be used to predict fractures, but its clinical utility has not been fully established in chronic kidney disease (CKD) patients. Magnesium is an essential trace element. Although magnesium is associated with the risk of fractures in non-CKD populations, the relationship is unknown in CKD patients. Methods BMD and serum magnesium levels were measured in 358 stable outpatients undergoing maintenance hemodialysis therapy. The primary outcome was fragility fracture. Patients were divided into groups according to the median level of magnesium and the normal threshold value of lumbar spine BMD. Results During the median follow-up period of 36 months, 36 (10.0%) fractures occurred. The cumulative incidence rates of fractures were 17.6% and 5.2% [adjusted hazard ratio (aHR) 2.31, 95% confidence interval (CI) 1.03–5.17, P = 0.030] in the lower (<2.6 mg/dL) and higher (≥2.6 mg/dL) magnesium (Mg) groups, respectively, and 21.2% and 7.3% (aHR 2.59, 95% CI 1.09–6.16, P = 0.027) in the low- and high-BMD groups, respectively. The lower-Mg and low-BMD group had a 9.21-fold higher risk of fractures (95% CI; 2.35–47.00; P = 0.0010) than the higher-Mg and high-BMD group. Furthermore, adding both magnesium levels and lumbar spine BMD levels to the established risk factors significantly improved the prediction of fractures (C-index: 0.784 to 0.830, p = 0.041). Discussion/Conclusions The combination of serum magnesium and lumbar spine BMD can be used for fracture risk stratification and synergistically improves the prediction of fractures in CKD patients.


2019 ◽  
Vol 104 (10) ◽  
pp. 4341-4346 ◽  
Author(s):  
Ying Yang ◽  
Min Wang ◽  
Jingzhi Tong ◽  
Zuoliang Dong ◽  
Min Deng ◽  
...  

Abstract Context Evidence indicates that there is substantial impairment/loss of β-cell function/mass even before prediabetes. Elevated plasma proinsulin is a sign of β-cell dysfunction in patients with diabetes/prediabetes. However, the dynamic changes of glucose stimulated proinsulin secretion (GSPS) among nondiabetic individuals remain obscure. Objective To examine GSPS and glucose-stimulated insulin secretion (GSIS) among individuals with normal glucose tolerance (NGT) and impaired glucose tolerance (IGT) and to evaluate whether impaired GSPS is an early biomarker of β-cell impairment in individuals with NGT who have subthreshold postprandial plasma glucose (PPG). Design and Participants We evaluated GSPS and GSIS in 116 Chinese adults without diabetes (mean age ± SD, 33.31 ± 9.10 years; mean BMI, 25.24 ± 4.20 kg/m2) with fasting plasma glucose (FPG) < 5.6 mmol/L. Based on 2hPPG, the participants were divided into three groups: NGT1 (2hPPG < 6.67 mmol/L), NGT2 (6.67 ≤ 2hPPG < 7.78 mmol/L), and IGT (7.78 ≤ 2hPPG<11.1 mmol/L). We analyzed the association of GSIS and GSPS with commonly used indexes of β-cell function, insulin resistance and family history of diabetes. Results Although not diagnosed with prediabetes, the individuals with NGT2 have clinical characteristics and high diabetes risk factors similar to those of the IGT group. However, unlike individuals with IGT, NGT2 participants did not exhibit a delayed GSIS. Instead, GSPS was impaired in NGT2 groups but not in NGT1 group. Conclusions This study suggests that impaired GSPS, but not impaired GSIS, may serve as an early biomarker to identify a subpopulation of NGT with a high risk of diabetes.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A279-A280
Author(s):  
Maria Chang Villacreses ◽  
Panadeekarn Panjawatanan ◽  
Rudruidee Karnchanasorn ◽  
Horng-Yih Ou ◽  
Wei Feng ◽  
...  

Abstract It is generally acknowledged that fracture rate is higher in diabetic subjects than non-diabetic subjects. However, the impact of diabetes on bone is less clear due to contradictory results of bone mineral density (BMD) and fracture rate. To date, most of reports were based on the studies from relatively small sample sizes. To clarify the issues, we examined the fracture rates and BMD across a spectrum of glucose tolerance in a representative US population. The participants of the National Health and Nutrition Survey 2005–2010 were used in this study. Among adult subjects (age≥20 years old) with reported BMI, we were able to define the states of glucose tolerance in 31,073 subjects cording to the diagnostic criteria based on HbA1c, fasting glucose, and/or 2-h post-changed glucose with established diabetes and using diabetes medications, into normal glucose tolerance (NGT), abnormal glucose tolerance (AGT), and diabetes mellitus (DM). Those who received osteoporosis medications were excluded from BMD analysis. Fracture information was available in 15,547 subjects; validated hip BMD was available in 12,317 subjects; and validated lumbar spine BMD was available in 10,329 subjects. Fracture rates were compared among 3 groups of glucose tolerance states and odds ratio (OR) with 95% confidence intervals (95% CI) were calculated in reference to the NGT group with sample weighting. BMD was compared among 3 groups of glucose tolerance with consideration of covariates. The reported osteoporosis diagnosed rate differed among 3 groups of glucose tolerances (3.99%, 5.77%, and 8.41%, P&lt;0.001, for NGT, AGT, and DM respectively). Worsening states of glucose tolerance were associated increased fracture OR at Hip [AGT, 2.1770 (95% CI: 2.1732–2.1807) and DM, 2.7369 (95% CI: 2.7315–2.7423)], spine [AGT, 0.9924 (95% CI: 0.9912–0.9936); DM, 1.2405 (95% CI: 1.2387–1.2423)]. In contrast, a different trend was observed on the wrist fracture rate [AGT, 0.9556 (95% CI: 0.9551–0.9562); DM, 0.9053 (95% CI: 0.9045–0.9060)]. After adjustment for covariates, higher BMD was noted in AGT and DM when compared to NGT at total femur (NGT, 0.9760±0.0015 gm/cm2; AGT, 0.9853±0.0021 gm/cm2; DM 0.9847±0.0034 gm/cm2, mean±SE, P=0.001) and femoral neck (NGT, 0.8388±0.0015 gm/cm2; AGT, 0.8474±0.0020 gm/cm2; DM, 0.8496±0.0032 gm/cm2, P=0.0007) while no difference was found in lumbar spine BMD (NGT, 0.1.0441±0.0018 gm/cm2; AGT, 1.0406±0.0025 gm/cm2; DM, 1.0464±0.0041 gm/cm2, P=0.35). Our observed significant increased fracture risk at hip (OR: 2.7369) and lumbar spine (OR: 1.2405) in DM subjects when compared to NGT subjects. DM subjects had higher BMD at total femur and femoral neck than NGT subjects while no difference was noted at lumbar spine BMD when compared to NGT subjects. Further studies are required to explore the discrepancy between the increased fracture risk with higher BMDs in diabetes.


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