Bone Metabolism In Patients Research Articles

Консервативне лікування порушень метаболізму кісткової тканини у хворих на вітамін-D-залежний рахіт I типу

Мета: визначити вплив консервативної терапії на генетично зумовлені порушення метаболізму кісткової тканини у хворих на вітамін-D-залежний рахіт (ВDЗР) І типу. Матеріал і методи. На базі консультативно-поліклінічного відділу ДУ «Інститут травматології та ортопедії НАМНУ» було обстежено та проліковано 48 пацієнтів із діагнозом «вітамін-D-залежний рахіт І типу». Консервативне лікування пацієнтів з рахітоподібними захворюваннями проводилось в 4 етапи. Перший етап включав в себе повне обстеження пацієнта на кальцій, фосфор крові та сечі, визначення рівня кальцидіолу та кальцитріолу крові, показників паратиреоїдного гормона та остеокальцину, а також маркера кісткоутворення P1NP і остеорезорбції B-CTx. На першому етапі в обов’язковому порядку діти проходили генетичне дослідження для виявлення змін (поліморфізму) в алелях рецепторів до вітаміну D та колагену першого типу. Обстеження на наступних етапах проводилось в повному обсязі, окрім генетичних досліджень. Результати. Всебічне вивчення метаболізму вітаміну D і біохімічних показників життєдіяльності кісткової тканини у хворих на ВDЗР І типу дозволило впритул підійти до розуміння деяких питань патогенезу та сутності остеомаляційних і в подальшому остеопоротичних змін різного ступеня, об’єктивувати ці зміни у відповідних показниках біохімічного дослідження та залежно від змін розробити різні схеми медикаментозної корекції порушень кісткового обміну за даного захворювання. Висновки. Для медикаментозного лікування ВDЗР І типу альфакальцидол є препаратом вибору, бо має можливість трансформуватись печінкою в кальцитріол, обійшовши генетично пошкоджене ниркове 1α-гідроксилювання. На підставі вивчення біохімічних показників у пацієнтів з вітамін-D-залежним рахітом І типу розроблено патогенетично обґрунтовану ефективну медикаментозну терапію ортопедичних проявів, що включає холекальциферол (80 000 Од/міс) та альфакальцидол (7,5 мкг/міс). Запропоноване лікування дає значне покращення метаболізму кісткової тканини, що відображається в біохімічних і клінічних показниках вже після першого 3-місячного етапу лікування (p < 0,05).

Результати моніторингу біохімічних маркерів кісткового метаболізму у хворих із пухлинами кісток після ендопротезування та лікування бісфосфонатами

В статті повідомляється про моніторинг біохімічних маркерів кісткового метаболізму після застосування препарату групи бісфосфонатів при комбінованому лікуванні хворих із пухлинами кісток. Порівнюються дві групи хворих: група практично здорових пацієнтів і група хворих із доброякісними та злоякісними пухлинами кісток, яким виконано ендопротезування та лікування бісфосфонатами. В результаті дослідження маркерів кісткового метаболізму (Ca2+, TRAP-5b, ендостатин) у хворих із пухлинами кісток встановлено, що нормалізація вмісту Ca2+ в крові, а також інтенсивне зниження активності TRAP-5b та концентрації ендостатину свідчать про довгострокову активацію остеобластів і прискорену мінералізацію кісткового матриксу.

Analysis of the Effect of Liraglutide on Bone Metabolism in Patients with Type 2 Diabetes Mellitus

Analysis of the Effect of Liraglutide on Bone Metabolism in Patients with Type 2 Diabetes Mellitus

Bone microarchitecture and metabolism in elderly male patients with signs of intravertebral cleft on MRI.

Intravertebral cleft (IVC) is a common but not unique imaging manifestation in Kümmell's disease. To date, great controversy exists regarding the specific mechanisms of IVC. In this study, we aimed to investigate the characteristics of microarchitecture and metabolism in patients with IVC and to analyse the correlations between degree of vertebral collapse and risk factors. A total of 79 elderly men were included in this study. We divided all patients into two groups: the IVC group (30 patients) and the non-IVC group (49 patients). We compared the differences in microarchitecture and bone turnover marker (BTM) serum concentrations between the groups and analysed risk factors affecting vertebral collapse by using the Mann-Whitney U test and Spearman's correlation test. Quantitative analysis of the microarchitecture showed higher content of necrotic bone (p < 0.001) and lower content of lamellar bone (p < 0.001) in the IVC group. Analysis of BTMs identified lower concentration of N-terminal propeptide of type I collagen (PINP, p = 0.002) and higher concentration of β-isomerized C-terminal telopeptide (β-CTX, p < 0.001) in the IVC group. The correlation analysis showed that lamellar bone content (p < 0.001) and spine T-score (p = 0.011) were significantly correlated with the degree of vertebral collapse. IVC is a radiological feature of excessive bone resorption by higher activities of osteoclasts and decreased bone remodelling ability by lower activities of osteoblasts. Histomorphological feature in patients with IVC is delayed callus mineralisation, which may increase the risk of vertebral collapse. • A key histomorphological feature in patients with IVC is delayed callus mineralisation, which may aggravate the degree of vertebral collapse. • We investigated bone metabolism in patients with IVC to evaluate the activities of osteoclasts and osteoblasts directly. • We propose a novel hypothesis for the pathogenesis of IVC: bone resorption by higher activity of osteoclasts and decreased callus mineralisation ability by lower activity of osteoblasts are the main mechanisms leading to IVC.

Мінеральна щільність та метаболізм кісткової тканини у разі тиреотоксикозу

Introduction. Hyperthyroidism is a pathological condition of the body due to increased of thyroid hormones in blood. The prevalence of this pathology increases with age. In the age period from 40 to 60 years it is 0.45%, and after 60 years the risk of the disease increases and is 1.4%. Aim is to analyze the condition of bone tissue in the conditions of thyrotoxicosis on the basis of literature data. Materials and methods are content analysis of the literature on studies of mineral density and bone metabolism in patients with thyrotoxicosis syndrome. Results. Thyroid hormones at physiological concentrations have an important role in skeletal development, reaching peak bone mass and maintaining bone mass during adulthood. It is proved that the effect of thyroid hormone on bone cells is carried out by hormone-receptor interactions. Receptors for thyroid hormones and TSH are found on osteoblasts and osteoclasts, which testifies to their direct action on the cell. The presence of calcium in the skeleton is mainly determined the bone mineral density. Hyperthyroidism is associated with negative calcium balance. When thyrotoxicosis decrease the bone density is observed in 10–20% of patients. This is due to a violation of bone remodeling by increasing metabolism with a disproportionate increase in bone resorption and increased bone formation, but the activation of bone formation cannot fully compensate for the loss of bone mass in the background enhanced resorption. With increasing severity of hyperthyroidism concentration in serum alkaline phosphatase, osteocalcin, and osteoprotegerin growth factor FGF-23 of fibroblasts, indicating increased bone metabolism accompanied by activation of bone resorption. When reducing subclinical hyperthyroidism TSH with normal T3 and T4, or elevated levels of thyroid hormones in the suppression of TSH. It is associated with decreased bone mineral density, increased fragility of bones with a high risk of fractures. Conclusions. Skeletal development and maintenance is regulated by a normal balance of thyroid hormones. Hyperthyroidism is associated with a prolonged cycle of bone remodeling, increased resorption and bone formation. However, the activation of bone formation observed in thyrotoxicosis is not able to fully compensate for the loss of bone mass against the background of increased resorption, which leads to osteoporosis and increased risk of fractures.

Serum granulocyte-macrophage colony-stimulating factor (GM-CSF) is increased in patients with active radiographic axial spondyloarthritis and persists despite anti-TNF treatment

BackgroundAccumulating evidence supports the role of monocytes and neutrophils in radiographic axSpA (r-axSpA). Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a growth factor for both leukocyte lineages and a pro-inflammatory cytokine activating myeloid cells and promoting osteoclastogenesis. It acts through the JAK-STAT pathway. We measured serum GM-CSF and markers of bone metabolism in patients with r-axSpA before and after anti-TNF treatment.MethodsPatients with active r-axSpA despite treatment with NSAIDs, all eligible for treatment with a biologic agent, were recruited. Healthy donors were sampled as controls. Serum was collected before (baseline) and after 4–6 months (follow-up) of anti-TNF treatment and the following molecules were measured with ELISA: GM-CSF, sclerostin (SOST), and dickkopf-1 (Dkk-1).ResultsTwelve r-axSpA patients (7 males, 5 females, median age 37 years) with a median disease duration of 1 year and 16 age- and sex-matched controls were included. At baseline, patients had mean BASDAI 6.3±2 and ASDAS 3.2±0.7, which decreased to 4.1±1.7 and 2.2±0.6 at follow-up, respectively. At baseline, r-axSpA patients had significantly higher mean serum levels of GM-CSF (150 vs 62pg/ml, p=0.049), significantly lower Dkk-1 (1228 vs 3052pg/ml, p=0.001), but similar levels of SOST (369 vs 544pg/ml, p=0.144) compared to controls. Anti-TNF treatment did not affect GM-CSF, Dkk-1, or SOST levels. Spearman correlation analysis showed that GM-CSF correlated positively with ASDAS at baseline (r=0.61, p=0.039), while no correlations were identified between bone markers (Dkk-1, SOST) on one hand and GM-CSF or disease activity indices on the other.ConclusionsGM-CSF is increased in patients with active AS and strongly correlates with disease activity. TNF inhibition does not affect GM-SCF levels, despite improving disease activity. GM-CSF may represent an important pathway responsible for residual inflammation during TNF blockade, but also a potential target of JAK inhibitors, explaining their efficacy in r-axSpA.

Effect of High-Dose Glucocorticoids on Markers of Inflammation and Bone Metabolism in Patients with Primary Glomerular Disease

Background: Glucocorticoids are one of the most commonly used drugs for treatment of inflammatory and autoimmune diseases. Sirtuin-1 (SIRT-1) belongs to the family of proteins involved in protection against inflammation and oxidative stress. A role of SIRT-1 in regulation of bone metabolism during high-dose steroid therapy is unknown. Objectives: The study assessed influence of high doses of intravenous corticosteroids on plasma inflammation and bone markers in patients with primary glomerular disease. Methods: The study included 40 patients (25 M, 15 F; mean age 53.1 ± 14 years) with chronic kidney disease (mean estimated glomerular filtration rate, 58.9 ± 31.3 mL/min). The main inclusion criterion was clinical and histopathological diagnosis of primary glomerular disease and urine protein excretion >2.0 g/24 h. The patients received intravenous pulses of methylprednisolone 20–30 mg/kg/day for three consecutive days followed by oral prednisone 0.8–1.0 mg/kg/day. The blood was taken before administration of methylprednisolone to assess plasma SIRT-1, sclerostin, calcium, phosphate, and parathormone; and first-morning urine sample was taken for measurement of calcium, phosphate, and albumin to creatinine ratio. The same laboratory tests were repeated after 4, 7, and 30 days during steroid therapy. Results: Plasma SIRT-1 increased significantly during steroid administration. Plasma sclerostin did not change significantly. There was a significant linear negative correlation between changes in SIRT-1 levels and sclerostin throughout the study. In a multiple regression model, changes of plasma sclerostin induced by steroid therapy explained the largest part of variance of respective changes of plasma SIRT-1. Conclusions: Plasma SIRT-1 increase during high-dose corticosteroid therapy is negatively related to the change of plasma sclerostin that may suggest a protective role of SIRT-1 against the negative effects of steroid therapy on bone.

The role of IL-6 and osteoprotegerin in bone metabolism in patients with Graves' disease.

Increased bone turnover is a hallmark of hyperthyroidism. The underlying factors of how thyroid hormones affect bone cells are still under the spotlight. Previous studies indicated serum osteoprotegerin (OPG), receptor activator of NF-kB ligand (RANKL), and interleukin-6 (IL-6) as mediators of the effect of thyroid hormones on bone metabolism. Ultimately, the present research aimed to examine the association of IL-6 with OPG and RANKL in patients with hyperthyroidism. We carried out this study with 39 newly diagnosed and untreated Graves' patients and 43 healthy controls. In addition to routine tests, we measured serum OPG, RANKL, and IL-6 levels. Mean age and sex distribution were similar in both groups. The hyperthyroid group had significantly higher OPG (p = 0.002) and IL-6 (p < 0.001) levels, but RANKL levels were significantly lower in this group (p < 0.001). We found OPG not to correlate with free T4 and T3, while it had a moderate and negative correlation with thyrotropin (TSH) (r = -0.372, p = 0.001). IL-6 had no correlation with OPG but positively correlated with free T4 (r = 0.445, p < 0.001) and free T3 (r = 0.326, p = 0.035). It also negatively correlated with RANKL (r = -0.247, p = 0.033). Maintaining skeletal development and integrity is partially regulated by a normal balance of thyroid hormones. We concluded that increases in serum OPG and IL-6 levels accompanied hyperthyroidism. However, excessive levels of the hormones might cause drops in serum RANKL levels. Our results suggested that OPG, RANKL, and IL-6 might be involved in the cross-talking among immunity, thyroid function, and bone metabolism in the case of hyperthyroidism.

Change in tartrate-resistant acid phosphatase isoform 5b levels, a marker of bone metabolism, in patients with chronic hepatitis B treated with tenofovir alafenamide.

Hepatitis B virus (HBV) infection is associated with the risk of osteoporosis and bone mineral density (BMD) loss. Tenofovir alafenamide (TAF) is associated with a slightly lower degree of BMD loss compared with tenofovir disoproxil, without loss of the excellent anti-HBV effects. The aim of the present study was to verify the effect of bone metabolism in patients with HBV treated with TAF. A total of 87 patients were treated with TAF. Of these, 32 patients were treatment naïve, and 55 patients were treated with entecavir (ETV) for at least 1 year, after which ETV was switched to TAF. At the start of TAF and after 1 year, BMD in the lumbar and neck of the femur, tartrate-resistant acid phosphatase isoform 5b (TRACP-5b) levels as a marker of bone metabolism and serum inorganic phosphorus (P) were compared to estimate bone metabolism. Serum creatinine (Cr), cystatin C, urine protein and β2 microglobulin levels were evaluated to estimate kidney function. Treatment with TAF for 1 year decreased TRACP-5b levels, particularly in patients with bone disease, except for a minimal significant change (MSC; decrease of 12.4%) in TRACP-5b levels. The change in rate of TRACP-5b levels were positively associated with changes in P, Cr-estimated glomerular filtration rate and TRACP-5b levels at the start of TAF. Logistic regression analysis showed that increased BMD in the lumbar region contributed to the switch from ETV to TAF. TAF induced a decrease in TRACP-5b levels in patients with HBV. Bone disease was a contributing factor for MSC. Since TRACP-5b can be used as a marker of bone metabolism and fractures, TAF may exhibit potential in preventing fractures in patients with HBV.

Особливості метаболізму кісткової тканини у хворих на остеоартроз, цукровий діабет 2-го типу та при їх поєднанні

Актуальність. Остеоартроз (ОА) є одним із найчастіших захворювань суглобів, що характеризується періодичними загостреннями, наявністю больового синдрому різного ступеня вираженості, прогресуючим перебігом та призводить до деформації суглобів, зниження їх функції та погіршення якості життя хворих. Важливим є зв’язок ОА з низкою метаболічних порушень, а саме вуглеводного та ліпідного обміну. Мета дослідження — вивчення параметрів метаболізму кісткової тканини у хворих на ОА, цукровий діабет (ЦД) 2-го типу та при їх поєднанні в осіб із різним фенотипом, а також взаємозв’язок між показниками маркерів метаболізму кісткової тканини та рівнем прозапальних цитокінів. Матеріали та методи. До дослідження було включено 104 пацієнти (31 чоловік та 73 жінки) з ОА, ЦД 2-го типу та поєднанням ОА та ЦД 2-го типу з різним фенотипом, середній вік яких становив 54,02 ± 0,67 року. Контрольну групу становили 20 практично здорових осіб. Дослідження включало визначення рівня остеоасоційованих елементів (Ca, P, Mg), С-реактивного протеїну (СРП), остеокальцину, кальцитоніну, фактора некрозу пухлин α (ФНП-α) та інтерлейкіну-1β (ІЛ-1β). Усім хворим на ОА було проведене рентгенологічне дослідження суглобів. Результати. Вірогідно вищі показники рівня остеокальцину було визначено у хворих у контрольній групі та в пацієнтів з OA на відміну від пацієнтів з встановленим діагнозом ЦД 2-го типу. Тобто для остеокальцину справедливим є такий ряд: конт­роль = ОА &gt; ЦД 2-го типу = ОА + ЦД 2-го типу = ОА + ЦД 2-го типу + ожиріння. Відмінності в значеннях інших показників метаболізму кісткової тканини між досліджуваними п’ятьма групами були менш вираженими, що не дозволяло сформувати для них єдиний ряд. Дослідження рівня цитокінів показало їх вірогідне підвищення у всіх обстежених хворих на відміну від контрольної групи (р &lt; 0,001). Установлено зв’язок показників метаболізму кісткової тканини з підвищеними рівнями прозапальних цитокінів. У хворих із коморбідною патологією та ожирінням було визначено найбільшу кількість вірогідних кореляційних зв’язків, а саме: між остеокальцином та ФНП-α (r = –0,78; p &lt; 0,05), ІЛ-1β (r = –0,75; p &lt; 0,05), СРП (r = –0,46; p &lt; 0,05), між Са та ФНП-α (r = 0,67; p &lt; 0,05), ІЛ-1β (r = 0,59; p &lt; 0,05), між кальцитоніном та ФНП-α (r = 0,56; p &lt; 0,05), ІЛ-1β (r = 0,46; p &lt; 0,05), СРП (r = 0,42; p &lt; 0,05), між Mg та ФНП-α (r = –0,47; p &lt; 0,05). Результати канонічного аналізу між показниками активності цитокінів і метаболізму кісткової тканини дозволяють стверджувати, що між цитокінами і характеристиками метаболізму кісткової тканини існує вірогідний зв’язок (канонічна кореляція = 0,52; p &lt; 0,05), найбільший внесок до якого з показників активності цитокінів, що визначали, вносить ІЛ-1β, а з показників метаболізму кісткової тканини — рівень остеокальцину. Висновки. Отримані дані дозволяють зробити висновки про певну роль системного запалення в порушенні метаболізму кісткової тканини, що може впливати на прогресування перебігу ОА.

Low serum levels of bone turnover markers are associated with perirenal fat thickness in patients with type 2 diabetes mellitus.

BackgroundObesity is known as a common risk factor for osteoporosis and type 2 diabetes mellitus (T2DM). Perirenal fat, surrounding the kidneys, has been reported to be unique in anatomy and biological functions. This study aimed to explore the relationship between perirenal fat and bone metabolism in patients with T2DM.MethodsA total of 234 patients with T2DM were recruited from September 2019 to December 2019 in the cross-sectional study. The biochemical parameters and bone turnover markers (BTMs) were determined in all participants. Perirenal fat thickness (PrFT) was performed by ultrasounds via a duplex Doppler apparatus. Associations between PrFT and bone metabolism index were determined via correlation analysis and regression models.ResultsThe PrFT was significantly correlated with β-C-terminal telopeptides of type I collagen (β-CTX) (r = −0.14, P < 0.036), parathyroid hormone (iPTH) (r = −0.18, P ≤ 0.006), and 25 hydroxyvitamin D (25-OH-D) (r = −0.14, P = 0.001). Multivariate analysis confirmed that the association of PrFT and β-CTX (β = −0.136, P = 0.042) was independent of other variables.ConclusionThis study showed a negative and independent association between PrFT and β-CTX in subjects with T2DM, suggesting a possible role of PrFT in bone metabolism. Follow-up studies and further research are necessary to validate the associations and to elucidate the underlying mechanisms.

Вміст вітаміну D і стан кісткового метаболізму при синдромі тиреотоксикозу (огляд літератури)

В огляді літератури наведені дані досліджень вмісту вітаміну D і стану кісткового метаболізму у хворих із синдромом тиреотоксикозу. Підсумовуючи результати досліджень, проведених різними авторами, слід відзначити важливість нормального балансу гормонів щитоподібної залози для розвитку скелета й забезпечення мінеральної щільності кісткової тканини.

Hybrid deep learning model for risk prediction of fracture in patients with diabetes and osteoporosis.

The fracture risk of patients with diabetes is higher than those of patients without diabetes due to hyperglycemia, usage of diabetes drugs, changes in insulin levels, and excretion, and this risk begins as early as adolescence. Many factors including demographic data (such as age, height, weight, and gender), medical history (such as smoking, drinking, and menopause), and examination (such as bone mineral density, blood routine, and urine routine) may be related to bone metabolism in patients with diabetes. However, most of the existing methods are qualitative assessments and do not consider the interactions of the physiological factors of humans. In addition, the fracture risk of patients with diabetes and osteoporosis has not been further studied previously. In this paper, a hybrid model combining XGBoost with deep neural network is used to predict the fracture risk of patients with diabetes and osteoporosis, and investigate the effect of patients' physiological factors on fracture risk. A total of 147 raw input features are considered in our model. The presented model is compared with several benchmarks based on various metrics to prove its effectiveness. Moreover, the top 18 influencing factors of fracture risks of patients with diabetes are determined.

Interrelationships Between Sclerostin, Secondary Hyperparathyroidism, and Bone Metabolism in Patients on Hemodialysis.

Sclerostin is an osteocyte-derived inhibitor of bone formation and is increased in kidney failure, but its role in the pathogenesis of renal bone disease remains unknown. We aimed to explore the association of serum sclerostin with bone metabolism in patients undergoing hemodialysis, with a particular focus on parathyroid hormone (PTH)-dependent and PTH-independent pathways. This cross-sectional and prospective cohort study included 654 patients undergoing hemodialysis at 10 facilities in Japan. We employed multivariable linear regression to explore whether sclerostin levels were associated with metacarpal bone mineral density (BMD), intact PTH, bone alkaline phosphatase (BAP), and tartrate-resistant acid phosphatase-5b (TRACP-5b). We employed mediation analyses to explore whether and to what extent the association of PTH with bone turnover markers is mediated by sclerostin. We also compared sclerostin levels between patients with and without previous or incident fractures. The median sclerostin level in hemodialysis patients was 3- to 4-fold higher than that in healthy individuals. Higher sclerostin levels were associated with higher metacarpal BMD and lower levels of intact PTH, BAP, and TRACP-5b. However, the relationships of sclerostin with bone turnover markers were substantially attenuated after adjustment for PTH. Mediation analysis suggested that the effects of PTH on bone turnover markers were mainly direct rather than mediated by sclerostin. Sclerostin levels were not associated with previous or incident fractures. These findings suggest that in patients undergoing dialysis, sclerostin has only a limited role in bone metabolism and may not mediate the effect of PTH on bone turnover.

Lean mass, magnesium, faecal calprotectin and glucocorticoid exposure as risk factors for low bone mineral density in inflammatory bowel disease patients.

Background and aimLow bone mineral density (BMD) is a common complication in patients with inflammatory bowel disease (IBD). However, debates are ongoing with regard to the other involved factors, especially in younger patients. This study aimed to evaluate the parameters that contribute to decreased BMD, focusing on premenopausal women and men aged <50 years.MethodsThis study included 81 patients with IBD and 81 age-, sex- and BMI-matched controls. Blood tests were conducted on IBD patients, and a dual-energy X-ray absorptiometry (DXA) scan was performed on both groups.ResultsLow BMD and fragility fracture were found to be more prevalent in IBD patients than in healthy subjects (49.3% vs 23.4%, P = 0.001 and 9.8% vs 1.2%, P = 0.01, respectively). Patients with low BMD were older, with a longer disease duration, higher faecal calprotectin (FC) levels and lower magnesium and lean mass (appreciated as appendicular skeletal muscle index (ASMI)). Multiple regression analysis revealed that ASMI, age and use of glucocorticoids were the independent parameters for decreased BMD. Although 91.3% of the patients had a 25-hydroxy vitamin D level of <30 ng/mL, it was not a statistically significant factor for decreased BMD.ConclusionIn our study, the levels of vitamin D did not seem to have an important impact on BMD. Conversely, FC, magnesium and lean mass are important factors, suggesting that good control of disease, adequate magnesium intake and increased lean mass can have a good impact on bone metabolism in patients with IBD.

Characteristics of bone metabolism in postmenopausal female patients with different types of idiopathic benign paroxysmal positional vertigo: A single-centre retrospective study

ObjectiveThe association between benign paroxysmal positional vertigo (BPPV) and impaired calcium metabolism has attracted widespread interest. Several studies have suggested that decreased bone mineral density (BMD) and serum 25-hydroxyvitamin D (25(OH)D) level are related to the occurrence and/or recurrence of BPPV; however, the characteristics of bone metabolism in patients with BPPV subtypes have not been fully investigated, and conclusions have been controversial. This study aimed to evaluate BMD and serum levels of 25(OH)D and bone turnover markers to clarify the characteristics of bone metabolism in patients with different types of BPPV. MethodWe retrospectively analysed the data of new-onset idiopathic postmenopausal female patients with BPPV at our institution from January 2016 to January 2020. The patients' demographic data including age, medication history, concomitant diseases, onset time, clinical form, laboratory indicators, such as serum levels of 25(OH)D, bone formation markers, namely, amino-terminal propeptide of type I procollagen (PINP) and osteocalcin (OC), bone resorption marker, namely, β-isomerized carboxy-terminal telopeptide of type I collagen (β-CTX), and BMD were collected and analysed. ResultsThis study included 201 consecutive postmenopausal female patients with BPPV. Among them, 138 were diagnosed with posterior semicircular canal BPPV, 42 were diagnosed with lateral semicircular canal canalolithiasis, and 21 were diagnosed with lateral semicircular canal cupulolithiasis. There were no significant differences in age distribution, body mass index, clinical history, levels of albumin, globulin, uric acid, creatinine, or blood urea nitrogen, lipid profiles (except high-density lipoprotein cholesterol) and routine blood parameters among these groups (P > 0.05). There were no significant differences in the mean T-score and BMD values of different sites or in the serum levels of 25(OH)D and bone turnover markers (PINP, OC and β-CTX) among the subgroups (P > 0.05). The proportion of reduction in BMD (T-score < −1 SD) and decreased serum vitamin D level (< 20 ng/ml) were not significantly different between the subgroups (P > 0.05). ConclusionThere were no significant differences in bone metabolism in postmenopausal female patients with different types of idiopathic BPPV.

The Impact of Glucagon-Like Peptide 1 Receptor Agonists on Bone Metabolism and Its Possible Mechanisms in Osteoporosis Treatment.

Diabetes mellitus and osteoporosis are closely related and have complex influencing factors. The impact of anti-diabetic drugs on bone metabolism has received more and more attention. Type 2 diabetes mellitus (T2DM) would lead to bone fragility, high risk of fracture, poor bone repair and other bone-related diseases. Furthermore, hypoglycemic drugs used to treat T2DM may have notable detrimental effects on bones. Thus, the clinically therapeutic strategy for T2DM should not only effectively control the patient’s glucose levels, but also minimize the complications of bone metabolism diseases. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are novel and promising drug for the treatment of T2DM. Some studies have found that GLP-1RAs may play an anti-osteoporotic effect by controlling blood sugar levels, promoting bone formation and inhibiting bone resorption. However, in clinical practice, the specific effects of GLP-1RA on fracture risk and osteoporosis have not been clearly defined and evidenced. This review summarizes the current research findings by which GLP-1RAs treatment of diabetic osteoporosis, postmenopausal osteoporosis and glucocorticoid-induced osteoporosis and describes possible mechanisms, such as GLP-1R/MAPK signaling pathway, GLP-1R/PI3K/AKT signaling pathway and Wnt/β-catenin pathway, that are associated with GLP-1RAs and osteoporosis. The specific role and related mechanisms of GLP-1RAs in the bone metabolism of patients with different types of osteoporosis need to be further explored and clarified.

Serum undercarboxylated osteocalcin levels are related to bone disease in hemodialysis and peritoneal dialysis patients

Objectives: In our study, we investigated whether the undercarboxylated osteocalcin (ucOC) is an indicator of bone turnover for patients treated with hemodialysis (HD) or peritoneal dialysis (PD). Furthermore, we have examined the relationships between ucOC levels and other bone inidicators such as osteocalcin (OC), bone specific alkaline phosphatase (B-ALP), calcitonin, vitamin D, intact parathyroid hormone (iPTH), calcium (Ca), phosphate (P), magnesium (Mg) and bone mineral density (BMD). Methods: Study group was consisted of 24 HD, 30 PD patients and 30 control subjects. ucOC measurements were based on precipitation of carboxylated OC with barium sulfate. After precipitation, ucOC was measured in supernatant by ELISA. Results: In chronic kidney disease (CKD), increased ucOC levels were present both in HD and PD groups. The ucOC levels in HD group were higher than those of PD group. ucOC levels in samples after HD were lower than in samples before HD. But there is no difference between groups for ucOC% levels. We observed that ucOC levels for CRF were higher compared to that of control group and statistically significant. ucOC levels were positively correlated with OC, B-ALP, ALP, iPTH, P and Mg levels. There were negative and significant correlations between ucOC levels and BMD values. ucOC has a good discrimination power for both high and low turnover ROD groups. Conclusions: ucOC is a useful marker to evaluation of bone metabolism in patients undergone hemodialysis or peritoneal dialysis in end-stage renal disease.

Influence of hyperbaric oxygen therapy on bone metabolism in patients with neoplasm.

Hyperbaric oxygen therapy (HBOT) is useful in the treatment of complications due to radiotherapy in patients with neoplasm. Its effects on bone metabolism are unclear. In our study, we analyzed the effects of HBOT on bone remodeling in oncological patients with radiotherapy. Prospective clinical study in 23 patients with neoplasms undergoing treatment with HBOT due to complications of radiotherapy (hemorrhagic cystitis, proctitis or radionecrosis) and 25 patients with chronic anal fissure. The average number of HBOT sessions was 20 ± 5 (100% oxygen, 2.3 atmospheres and 90 min per day). Serum levels of aminoterminal propeptide of type I collagen (P1NP), C terminal telopeptide of type I collagen (CTX), alkaline phosphatase (AP), 25hydroxyvitamin D (25-OHD), parathyroid hormone (PTH), were measured at 3 time points: T0 (before beginning HBOT), T1 (at the end of HBOT) and T2 (6 months after HBOT). At baseline, the patients with neoplasm have higher bone turnover than those with anal fissure. These differences were 41% in CTX (0.238 ± 0.202 ng/mL in neoplasm and 0.141 ± 0.116 ng/mL in fissure; p = 0.04), 30% for PTH (46 ± 36 pg/mL in neoplasm and 32 ± 17 pg/mL in fissure; p = 0.04) and 15% for alkaline phosphatase (80 ± 24 U/L in neoplasm and 68 ± 16 U/L in fissure; p = 0.04). In the group with neoplasm, the values of P1NP decreased 6% after HBOT (T0: 49 ± 31 ng/mL, T2: 46 ± 12 ng/mL; p = 0.03). Also, there were non-significant decreases in PTH (-34%) and CTX (-30%). Patients with neoplasm and complications with radiotherapy have an increase in bone remodeling that may be diminished after HBOT.

Effects of endogenous GIP in patients with type 2 diabetes.

The insulinotropic effect of exogenous, intravenously infused glucose-dependent insulinotropic polypeptide (GIP) is impaired in patients with type 2 diabetes. We evaluated the effects of endogenous GIP in relation to glucose and bone metabolism in patients with type 2 diabetes using a selective GIP receptor antagonist and hypothesized that the effects of endogenous GIP were preserved. A randomized, double-blinded, placebo-controlled, crossover study. Ten patients with overweight/obesity and type 2 diabetes (mean±s.d.; HbA1c 52 ± 11 mmol/mol; BMI 32.5 ± 4.8 kg/m2) were included. We infused a selective GIP receptor antagonist, GIP(3-30)NH2 (1200 pmol/kg/min), or placebo (saline) during two separate, 230-min, standardized, liquid mixed meal tests followed by a meal ad libitum. Subcutaneous adipose tissue biopsies were analyzed. Compared with placebo, GIP(3-30)NH2 reduced postprandial insulin secretion (Δbaseline-subtracted area under the curve (bsAUC)C-peptide% ± s.e.m.; -14 ± 6%, P = 0.021) and peak glucagon (Δ% ± s.e.m.; -11 ± 6%, P = 0.046) but had no effect on plasma glucose (P = 0.692). Suppression of bone resorption (assessed by circulating carboxy-terminal collagen crosslinks (CTX)) was impaired during GIP(3-30)NH2 infusion compared with placebo (ΔbsAUCCTX; ±s.e.m.; -4.9 ± 2 ng/mL × min, P = 0.005) corresponding to a ~50% reduction. Compared with placebo, GIP(3-30)NH2 did not affect plasma lipids, meal consumption ad libitum or adipose tissue triglyceride content. Using a selective GIP receptor antagonist during a meal, we show that endogenous GIP increases postprandial insulin secretion with little effect on postprandial glycaemia but is important for postprandial bone homeostasis in patients with type 2 diabetes.