Bone loss in chronic liver diseases:Could healthy liver be a requirement for good bone health?

Given that the liver is involved in many metabolic mechanisms,it is not surprising that chronic liver disease(CLD)could have numerous complications.Secondary osteoporosis and increased bone fragility are frequently overlooked complications in CLD patients.Previous studies implied that up to one-third of these individuals meet diagnostic criteria for osteopenia or osteoporosis.Recent publications indicated that CLD-induced bone fragility depends on the etiology,duration,and stage of liver disease.Therefore,the increased fracture risk in CLD patients puts a severe socioeconomic burden on the health system and urgently requires more effective prevention,diagnosis,and treatment measures.The pathogenesis of CLD-induced bone loss is multifactorial and still insufficiently understood,especially considering the relative impact of increased bone resorption and reduced bone formation in these individuals.It is essential to note that inconsistent findings regarding bone mineral density measurement were previously reported in these individuals.Bone mineral density is widely used as the“golden standard”in the clinical assessment of bone fragility although it is not adequate to predict individual fracture risk.Therefore,microscale bone alterations(bone microstructure,mechanical properties,and cellular indices)were analyzed in CLD individuals.These studies further support the thesis that bone strength could be compromised in CLD individuals,implying that an individualized approach to fracture risk assessment and subsequent therapy is necessary for CLD patients.However,more well-designed studies are required to solve the bone fragility puzzle in CLD patients.

Glucagon-like peptide-1 receptor agonists:Exploring the mechanisms from glycemic control to treatment of multisystemic diseases

This editorial takes a deeper look at the insights provided by Soresi and Giannitrapani,which examined the therapeutic potential of glucagon-like peptide-1 receptor agonists(GLP-1RAs)for metabolic dysfunction-associated fatty liver disease.We provide supplementary insights to their research,highlighting the broader systemic implications of GLP-1RAs,synthesizing the current understanding of their mechanisms and the trajectory of research in this field.GLP-1RAs are revolutionizing the treatment of type 2 diabetes mellitus and beyond.Beyond glycemic control,GLP-1RAs demonstrate cardiovascular and renal protective effects,offering potential in managing diabetic kidney disease alongside renin–angiotensin–aldosterone system inhibitors.Their role in bone metabolism hints at benefits for diabetic osteoporosis,while the neuroprotective properties of GLP-1RAs show promise in Alzheimer's disease treatment by modulating neuronal insulin signaling.Additionally,they improve hormonal and metabolic profiles in polycystic ovary syndrome.This editorial highlights the multifaceted mechanisms of GLP-1RAs,emphasizing the need for ongoing research to fully realize their therapeutic potential across a range of multisystemic diseases.

Burden of bone disease in chronic pancreatitis:A systematic review and meta-analysis

BACKGROUND Bone disease is an under-recognized cause of morbidity in chronic pancreatitis(CP).Over the past decade,publications of original studies on bone disease in CP has warranted synthesis of the evidence to ascertain the true burden of the problem.AIM To quantify the prevalence of osteopenia,osteoporosis,and fragility fractures in CP patients and investigate the associated clinical features and outcomes.METHODS A systematic search identified studies investigating bone disease in CP patients from Cochrane Library,Embase,Google Scholar,Ovid Medline,PubMed,Scopus,and Web of Science,from inception until October 2022.The outcomes included prevalence of osteopenia,osteoporosis,and fragility fractures,which were metaanalyzed using a random-effects model and underwent metaregression to delineate association with baseline clinical features.RESULTS Twenty-one studies were included for systematic review and 18 studies were included for meta-analysis.The pooled prevalence of osteopenia and osteoporosis in CP patients was 41.2%(95%CI:35.2%-47.3%)and 20.9%(95%CI:14.9%-27.6%),respectively.The pooled prevalence of fragility fractures described among CP was 5.9%(95%CI:3.9%-8.4%).Metaregression revealed significant association of pancreatic enzyme replacement therapy(PERT)use with prevalence of osteoporosis[coefficient:1.7(95%CI:0.6-2.8);P<0.0001].We observed no associations with mean age,sex distribution,body mass index,alcohol or smoking exposure,diabetes with prevalence of osteopenia,osteoporosis or fragility fractures.Paucity of data on systemic inflammation,CP severity,and bone mineralization parameters precluded a formal metaanalysis.CONCLUSION This meta-analysis confirms significant bone disease in patients with CP.Other than PERT use,we observed no patient or study-specific factor to be significantly associated with CP-related bone disease.Further studies are needed to identify confounders,at-risk population,and to understand the mechanisms of CP-related bone disease and the implications of treatment response.

Bone alterations in inflammatory bowel diseases

Inflammatory bowel diseases(IBDs)are characterized by a multifactorial partially unknown etiology that involves genetic,immunological and environmental factors.Up to 50%of IBD patients experience at least one extraintestinal manifestation;among them is the involvement of bone density which is referred to as metabolic bone disease(MBD),including osteopenia and osteoporosis.Bone alterations in IBDs population appear to have a multifactorial etiology:Decreased physical activity,inflammation-related bone resorption,multiple intestinal resections,dietary malabsorption of minerals and vitamin D deficiency,genetic factors,gut-bone immune signaling interaction,steroid treatment,microbiota and pathogenic micro-organisms interaction,and dietary malabsorption of minerals,that,all together or individually,may contribute to the alteration of bone mineral density.This review aims to summarize the prevalence and pathophysiology of metabolic bone alterations in IBD subjects outlining the main risk factors of bone fragility.We also want to underline the role of the screening and prophylaxis of bone alterations in Crohn’s disease and ulcerative colitis patients and the importance of treating appropriately MBD.

Roles and regulation of bone morphogenetic protein-7 in kidney development and diseases

The gene encoding bone morphogenetic protein-7(BMP7) is expressed in the developing kidney in embryos and also in the mature organ in adults. During kidney development, expression of BMP7 is essential to determine the final number of nephrons in and proper size of the organ. The secreted BMP7 acts on the nephron progenitor cells to exert its dual functions: To maintain and expand the progenitor population and to provide them with competence to respond to differentiation cues, each relying on distinct signaling pathways. Intriguingly, in the adult organ, BMP7 has been implicated in protection against and regeneration from injury. Exogenous administration of recombinant BMP7 to animal models of kidney diseases has shown promising effects in counteracting inflammation, apoptosis and fibrosis evoked upon injury. Although the expression pattern of BMP7 has been well described, the mechanisms by which it is regulated have remained elusive and the processes by which the secretion sites of BMP7 impinge upon its functions in kidney development and diseases have not yet been assessed. Understanding the regulatory mechanisms will pave the way towards gaining better insight into the roles of BMP7, and to achieving desired control of the gene expression as a therapeutic strategy for kidney diseases.

Non-alcoholic fatty liver disease connections with fat-free tissues: A focus on bone and skeletal muscle

The estimates of global incidence and prevalence of non-alcoholic fatty liver disease(NAFLD) are worrisome, due to the parallel burden of obesity and its metabolic complications. Indeed, excess adiposity and insulin resistance represent two of the major risk factors for NAFLD; interestingly, in the last years a growing body of evidence tended to support a novel mechanistic perspective, in which the liver is at the center of a complex interplay involving organs and systems, other than adipose tissue and glucose homeostasis. Bone and the skeletal muscle are fat- free tissues which appeared to be independently associated with NAFLD in several cross-sectional studies. The deterioration of bone mineral density and lean body mass, leading to osteoporosis and sarcopenia, respectively, are age-related processes. The prevalence of NAFLD also increases with age. Beyond physiological aging, the three conditions share some common underlying mechanisms, and their elucidations could be of paramount importance to design more effective treatment strategies for the management of NAFLD. In this review, we provide an overview on epidemiological data as well as on potential contributors to the connections of NAFLD with bone and skeletal muscle.

Andrias davidianus bone peptides alleviates hyperuricemia-induced kidney damage in vitro and in vivo

Hyperuricemia(HUA)is a vital risk factor for chronic kidney diseases(CKD)and development of functional foods capable of protecting CKD is of importance.This paper aimed to explore the amelioration effects and mechanism of Andrias davidianus bone peptides(ADBP)on HUA-induced kidney damage.In the present study,we generated the standard ADBP which contained high hydrophobic amino acid and low molecular peptide contents.In vitro results found that ADBP protected uric acid(UA)-induced HK-2 cells from damage by modulating urate transporters and antioxidant defense.In vivo results indicated that ADBP effectively ameliorated renal injury in HUA-induced CKD mice,evidenced by a remarkable decrease in serum UA,creatinine and blood urea nitrogen,improving kidney UA excretion,antioxidant defense and histological kidney deterioration.Metabolomic analysis highlighted 14 metabolites that could be selected as potential biomarkers and attributed to the amelioration effects of ADBP on CKD mice kidney dysfunction.Intriguingly,ADBP restored the gut microbiome homeostasis in CKD mice,especially with respect to the elevated helpful microbial abundance,and the decreased harmful bacterial abundance.This study demonstrated that ADBP displayed great nephroprotective effects,and has great promise as a food or functional food ingredient for the prevention and treatment of HUA-induced CKD.

Growth and bone health in paediatric patients with Crohn's disease receiving subcutaneous tumor necrosis factor antibody

AIM:To study whether adalimumab(ADA) was associated with improvement in growth,bone mineraldensity(BMD) and bone metabolism.METHODS:In children with Crohn's disease(CD) there is a high prevalence of growth failure and reduced BMD.Treatment with infliximab is associated with an improvement in growth.Anthropometry,paediatric CD activity index(PCDAI),bone markers and BMD was measured in 18 patients(72% females) one year before and after start of ADA with a median age of 14.4 years(range:5-19 years) at treatment start.Outcomes were indicators of growth with treatment as well as interval growth.RESULTS:Eleven(61%) children experienced catchup growth after ADA.PCDAI significantly decreased from 52.1 ± 16 to 30.4 ± 23(P ≤ 0.001).Post ADA,body mass index(BMI) standard deviation score(SDS) 0.1[range:2.7-(-0.8)] vs-1 [range:0.1-(-3.6)],P = 0.04 and △BMI SDS in children 0.3 [range:0.7-(-0.2)] vs-1.1 [range:1.2-(-2.3)],P = 0.01 in remission were significantly higher compared to those with moderate to severe inflammation.The main predictors for growth were 25-hydroxycholecalciferol and for bone mineralisation weight and height SDS.ADA had no significant influence on bone markers and BMD.CONCLUSION:Next to improvement of PCDAI,half of the children achieved a positive catch-up growth.A better nutritional status with improvement in BMI and weight is positive predictor for improved growth and bone mineralisation.

Clinical benefits of biochemical markers of bone turnover in Egyptian children with chronic liver diseases

AIM： To investigate the association between serum insulin-like growth factor 1 （IGF-1）, osteocalcin, and parathyroid hormone （PTH） levels with the etiology and clinical condition of patients with chronic liver disease. METHODS： Eighty children with hepatocellular damage were divided into 3 groups according to the etiology of disease infection： bilharziasis （9 patients）, hepatitis B virus （HBV, 12 patients） and hepatitis C virus （HCV, 29 patients）. The Child score index was found as A in 24 patients, B in 22 patients, C in 4 patients. Thirty healthy children served as control group.HBsAg, HBcAbIgM, HBcAbIgG, and anti-HCV were detected using ELISA technique. HCV-RNA was measured by reverse transcription polymerase chain reaction （RT-PCR）. Antibllharzial antibodies were detected by indirect haemagglutination test. Liver function tests were performed using autoanalyser. Serum IGF-1, osteocalcin and PTH levels were measured by ELISA technique. Abdominal ultrasonography was also conducted. RESULTS： Serum IGF-1 level was significantly lower in all patient groups with liver diseases, while serum osteocalcin and PTH levels were significantly elevated in patients with HBV and HCV infections compared with the control group. Serum osteocalcin and PTH concentrations were measured with the severity of liver disease from Child A to C. Child A patients unexpectedly showed significantly reduced IGF-1 levels in comparison to patients staged as Child B or C. Serum osteocalcin level was negatively correlated with albumin （14.7 ± 0.54 vs 3.6 ± 0.10, P 〈 0.05）, while that for PTH was positively correlated with total protein （70.1 ± 2.17 vs 6.7 ± 0.10, P 〈 0.05） in patients with HCV infection.

Epigenetic regulation by long noncoding RNAs in osteo-/adipogenic differentiation of mesenchymal stromal cells and degenerative bone diseases

Bone is a complex tissue that undergoes constant remodeling to maintain homeostasis,which requires coordinated multilineage differentiation and proper proliferation of mesenchymal stromal cells(MSCs).Mounting evidence indicates that a disturbance of bone homeostasis can trigger degenerative bone diseases,including osteoporosis and osteoarthritis.In addition to conventional genetic modifications,epigenetic modifications(i.e.,DNA methylation,histone modifications,and the expression of noncoding RNAs)are considered to be contributing factors that affect bone homeostasis.Long noncoding RNAs(lncRNAs)were previously regarded as‘transcriptional noise’with no biological functions.However,substantial evidence suggests that lncRNAs have roles in the epigenetic regulation of biological processes in MSCs and related diseases.In this review,we summarized the interactions between lncRNAs and epigenetic modifiers associated with osteo-/adipogenic differentiation of MSCs and the pathogenesis of degenerative bone diseases and highlighted promising lncRNA-based diagnostic and therapeutic targets for bone diseases.

Fractional Order Nonlinear Bone Remodeling Dynamics Using the Supervised Neural Network

This study aims to solve the nonlinear fractional-order mathematical model(FOMM)by using the normal and dysregulated bone remodeling of themyeloma bone disease(MBD).For themore precise performance of the model,fractional-order derivatives have been used to solve the disease model numerically.The FOMM is preliminarily designed to focus on the critical interactions between bone resorption or osteoclasts(OC)and bone formation or osteoblasts(OB).The connections of OC and OB are represented by a nonlinear differential system based on the cellular components,which depict stable fluctuation in the usual bone case and unstable fluctuation through the MBD.Untreated myeloma causes by increasing the OC and reducing the osteoblasts,resulting in net bone waste the tumor growth.The solutions of the FOMM will be provided by using the stochastic framework based on the Levenberg-Marquardt backpropagation(LVMBP)neural networks(NN),i.e.,LVMBPNN.The mathematical performances of three variations of the fractional-order derivative based on the nonlinear disease model using the LVMPNN.The static structural performances are 82%for investigation and 9%for both learning and certification.The performances of the LVMBPNN are authenticated by using the results of the Adams-Bashforth-Moulton mechanism.To accomplish the capability,steadiness,accuracy,and ability of the LVMBPNN,the performances of the error histograms(EHs),mean square error(MSE),recurrence,and state transitions(STs)will be provided.

Role of fibroblast growth factor receptor 1 in the bone development and skeletal diseases

Accumulating data suggest that FGFs/FGFR1 plays essential roles in the bone development and human skeletal diseases. Conditional inactivation of fgfrl caused different phenotypes displaying in different cells or specific organs and revealed some novel functions of FGFR1 in bone development. Fgfrl mutation mainly induced 2 types of human skeletal diseases, craniosynostosis syndrome and dysplasias. Similar mutation of fgfrl in mouse model just mimicked the phenotype that happened in human. These fa- cilitate the investigation on the underlying mechanism of the diseases. Here we mainly focused on the ad- vance of FGFR1 function in the bone development and its mutation caused skeletal diseases.

Surgical treatment of metastatic bone disease of the distal extremities

Metastatic bone disease of the distal extremities,also known as acrometastasis,is very rare.Thus,there is very limited information regarding the clinical manifestations and methods of surgical treatment.The current available literature shows that acrometastases are often encountered in the context of advanced disease and are thus associated with poor patient survival.As metastatic bone disease is generally uncurable,the goal of surgical treatment is to provide the patient with good function with as few complications as possible.In this article,we discuss the clinical manifestation of acrometastases,the methods of surgical intervention,and the expected clinical outcome.Non-surgically managed pathological fractures generally remain ununited;therefore,conservative treatment is reserved for patients with poor general condition or dismal prognosis.The current evidence suggests that in lesions of the lower arm and leg,osteosynthesis(plate and screw fixation or intramedullary nail)is the most common method of reconstruction,whereas local excision or amputation are more commonly used in cases of more distal lesions(such as ankle,foot and hand).Following surgery most patients receive adjuvant radiotherapy,even though its role is poorly documented.Close collaboration between orthopedic surgeons and medical oncologists is necessary to improve patient care and treatment outcome.Further studies are needed in order to provide stronger clinical evidence and improve decision-making,in an effort to optimize the patients’quality of life and avoid the need for revision surgery.

Bone destruction of orbital wall in idiopathic orbital inflammatory pseudotumor:does it always imply malignancy?

AIM:To assess the clinical presentations and outcomes of idiopathic orbital inflammatory pseudotumor(IOIP)patients with orbital wall bone destruction(OWBD)and to propose an expanded classification system that includes bone destruction.METHODS:The study retrospectively reviewed clinical presentations,imaging findings,treatment modalities,and outcomes of six patients diagnosed histopathologically with IOIP and OWBD at the Beijing Tongren Hospital,Capital Medical University between October 2018 and June 2021.RESULTS:Over two years,6(10%)of 60 IOIP patients at our hospital exhibited OWBD,but this may overrepresent severe cases.The cohort consisted of three men and three women,aged 17 to 60y(mean 35.5±16.1y).Presenting symptoms included proptosis,eyelid swelling,decreased visual acuity with pain,and palpable mass.Imaging revealed multiple anatomical structures involved with the medial wall being the most common site of bone destruction.Histopathological examination showed classic type in five patients and sclerosing type in one patient.All patients underwent surgical resection followed by methylprednisolone treatment.Follow-up(mean 30.3±3.1mo)indicated three patients had no recurrence,while others had varying degrees of symptom persistence or recurrence.CONCLUSION:IOIP with bone destruction is a rare but significant subtype that mimics malignancy,leading to potential diagnostic and therapeutic challenges.Our findings suggest that complete surgical resection combined with adjunctive glucocorticoid therapy can yield favorable outcomes.However,larger-scale studies are needed to further optimize therapeutic approaches.

Hematological picture of pediatric Sudanese patients with visceral leishmaniasis and prediction of leishmania donovani parasite load

BACKGROUND Visceral leishmaniasis(VL)is a systemic protozoan infection caused by Leishmania donovani(L.donovani)and transmitted by sand flies,causing macrophage invasion in the liver,spleen,and bone marrow.Diagnosis of VL is currently based on clinical signs,symptoms,and specific in-vitro markers and bone marrow investigations.However,VL's specific hematological and bone marrow manifestation in Sudanese pediatric patients is not well studied.AIM To examine the blood and bone marrow characteristics in pediatric patients from Sudan who have VL.METHODS This is a retrospective hospital-based study with a sample of 107 consecutive Sudanese pediatric patients.The data focused on hematological and bone marrow results.We included only the completed records of the pediatric patients with VL in the Tropical Disease Teaching Hospital in Khartoum,Sudan from the period of 2016 to 2020.RESULTS The majority of pediatric patients included in this study are below 5-years-old(n=59,55.2%).Moreover,anemia,thrombocytopenia,and leukopenia were among the prevalent characteristics in the population under study.To further analyze the data,we developed a machine learning model using boosted forest algorithms to predict L.donovani parasites load,with a mean accuracy of 0.88 for the training dataset and an accuracy of 0.46,0.50,and 0.74 for mild,moderate,and severe L.donovani parasite load in the validation dataset.CONCLUSION This study shows that the most common bone marrow change among Sudanese VL children was increased chronic inflammatory cells(n=88,82.2%)with present macrophage hemophagocytes(n=103,96.3%).While anemia and thrombocytopenia were the most common hematological changes.These results will hopefully lead to an early diagnosis and hence better management for Sudanese pediatric patients with suspected VL.

Intracerebroventricular transplanted bone marrow stem cells survive and migrate into the brain of rats with Parkinson's disease

In this study, 6-hydroxydopamine was stereotaxically injected into the right substantia nigra compact and ventral tegmental area of rats to establish Parkinson＇s disease models. The rats then received a transplantation of bone marrow stromal cells that were previously isolated, cultured and labeled with 5-bromo-2＇-deoxyuridine in vitro. Transplantation of the bone marrow stromal cells significantly decreased apomorphine-induced rotation time and the escape latency in the Morris water maze test as compared with rats with untreated Parkinson＇s disease. Immunohistochemical staining showed that, 5-bromo-2＇-deoxyuridine-immunoreactive cells were present in the lateral ventricular wall and the choroid plexus 1 day after transplantation. These immunoreactive cells migrated to the surrounding areas of the lateral cerebral ventricle along the corpus callosum. The results indicated that bone marrow stromal cells could migrate to tissues surround the cerebral ventricle via the cerebrospinal fluid circulation and fuse with cells in the brain, thus altering the phenotype of cells or forming neuron-like cells or astrocytes capable of expressing neuron-specific proteins. Taken together, the present findings indicate that bone marrow stromal cells transplanted intracerebroventricularly could survive, migrate and significantly improve the rotational behavior and cognitive function of rats with experimentally induced Parkinson＇s disease.

Association Between Knee Alignment,Disease Severity and Subchondral Trabecular Bone Microarchitecture in Patients with Knee Osteoarthritis

Objective Most patients with knee osteoarthritis(OA)have alignment deformity with the change of Hip-knee-ankle(HKA)angle.The knee alignment influences load distribution at the tibial plateau.Meanwhile,change of subchondral trabecular bone microstructure is related to load bearing and OA progression.However,the relationship between knee alignment on the changes of subchondral trabecular bone microstructure and OA severity have been poorly investigated.The main goal of this work was to investigate variation in tibial plateaus subchondral trabecular bone microstructure in knee OA patients and their association with the severity of OA with the change of knee alignment.Methods Seventy-one knee OA patients planning to undergo total knee arthroplasty were enrolled in this study.The HKA angle and OA disease severity(OARSI score,compartment-specific Kellgren-Lawrence(K-L)grade and OARSI Atlas grade)based on full-leg standing posteroanterior radiographs were evaluated preoperatively in all patients.The tibial plateau collected during surgery was first used for micro-computed tomography(μCT)to analyze the subchondral trabecular bone microstructures,and then used for pathological sections to analyze cartilage degeneration(OARSI score).Pearson and spearman correlations were used to examine linear relationships between knee alignment,OA disease severity and subchondral trabecular bone microstructure.Patients were then divided into group I(HKA angle exceeds 0°in the valgus direction),group II(varus angle<10°)and group III(varus angle≥10°).The differences in subchondral trabecular bone microstructural parameters between the three groups were analyzed by the one-way ANOVA with a post hoc Tukey test.Results HKA angle was significantly correlated with all tibial plateau subchondral trabecular bone microstructure parameters.Regardless of the medial or lateral tibia,HKA angle was most strongly correlated with bone volume fraction(BV/TV),M:(r=0. 613,P<0.01);L:(r=-0.490,P<0.01).In addition,for the media-to-lateral ratios(M:L)of the subchondral trabecular bone microstructure parameters,the HKA angle is positively correlated with M:L BV/TV(r=0.658,P<0.01),M:L trabecular number(Tb.N)(r=0.525,,P<0.01),M:L trabecular thickness(Tb.Th)(r=0.636,P<0.01),and negatively correlated with M:L trabecular separation(Tb.Sp)(r=-0.636,P<0.01)and M:L Specific Bone Surface(BS/BV)(r=-0.792,P<0.01).The BV/TV,Tb.N,and Tb.Th of the medial tibia were sequentially incremented in the order of groupⅠ,Ⅱ,Ⅲof knee alignment,while the Tb.Sp and BS/BV were decreased in this order.The lateral tibia is the opposite.In addition,most of the severity indices of OA are associated with subchondral trabecular bone microstructures,of which OARSI score and BV/TV in medial tibia are the most relevant(r=0.787,P<0.01).HKA angle is significantly correlated with all OA severity grades in medial compartment,but only with OARSI score and Bone sclerosis grade in lateral compartment.Conclusions Tibial plateau subchondral trabecular bone microarchitecture is associated with the HKA angle and OA severity.With the increase of varus angle and the severity of OA,the subchondral trabecular bone in medial tibia has more obvious sclerosis changes and vice versa,suggesting that knee malalignment may promote abnormal subchondral trabecular bone remodeling by altering joint load distribution,thereby affecting the progression of OA.

Potential efficacy and mechanism of medicinal plants on chronic kidney disease-associated vascular calcification:a review

Vascular calcification is a crucial risk factor that affects the incidence and mortality of cardiovascular disease in chronic kidney disease patients.Modern medicine relies on calcium-phosphorus binding agents,calcium mimetics,active vitamin D,and hemodialysis to prevent and treat vascular calcification,however,their efficacy is unsatisfactory and adverse reactions often occur.Medical plant therapy can act as an integrative regulator in patients with chronic kidney disease-associated vascular calcification,which can significantly improve patients’symptoms,but its specific mechanism has not been fully elucidated yet.In this paper,we reviewed the domestic and international theoretical studies on the pathogenesis mechanism of chronic kidney disease-associated vascular calcification in recent years,summarized eight active ingredients of medicinal plants as well as four compound formulas for improving chronic kidney disease-associated vascular calcification,and explored the mechanism of action of herbal medicine,which will provide a new strategy for promoting the prevention and treatment of vascular calcification.

Bone Mineral Density in Patients with Newly Diagnosed Inflammatory Bowel Disease: Frequency and Risk Factors in Tunisian Population. Results of a Prospective Study

Background and Aims: Osteopenia and osteoporosis are frequently encountered with Inflammatory Bowel Disease (IBD). Our aims were to determine the prevalence of low bone mineral density (BMD) in patients with recently diagnosed IBD, and to assess predictive factors of reduced BMD. Patients and Methods: Prospective study conducted from January 2008 to December 2012 and involved patients with IBD treated in the Department of Gastroenterology of the Internal Security Forces Hospital. The data collected included: age, gender, body mass index (BMI), diagnostic delay, disease activity, and disease localization. Laboratory findings included serum calcium, phosphate, albumin, hemoglobin, and C-reactive protein. BMD was assessed by dual energy X-ray absorptiometry (DEXA) of the lumber spine and femoral neck. According to WHO criteria, osteopenia was defined as a T-score between -1 and -2 SD, and osteoporosis as a T-score less than -2 SD. Results: A total of 34 patients (17 men, 17 women) were enrolled. Mean age was 37.1 ± 13.8 years (range 16 - 62). Twenty-two patients (65%) had Crohn’s disease (CD) and 12 patients (35%) had ulcerative colitis (UC). Mean BMI was 20.5 ± 4 kg/m2. Low BMD occurred in 50% of patients (12 CD, 5 UC). Thirteen patients (38.2%) exhibited osteopenia and 4 patients (10.8%) showed osteoporosis. Mean vertebral T-score was -0.933 ± 1.41 (range -4.1 to 1.7) and BMD in this site was 1.079 ± 0.17 g/cm2 (range 0.674 to 1.380). Mean femoral T-score was -0.398 ± 1.2 (range -3.1 to 2.4) and BMD in this site was 0.990 ± 0.173 g/cm2 (range 0.633 to 1.600). There was a positive correlation between T-score and albuminemia. Low BMI was found to be predictive factor of reduced BMD at the moment of IBD diagnosis. However, no correlation was found between BMD and the other studied variables (age, gender, smoking, history of fracture, disease location, duration of disease, activity, small bowel resection, serum calcium level, phosphate, C-reactive protein and hemoglobin). Conclusion: Our study showed that the half of patients with IBD had a low BMD in newly diagnosed IBD patients. Low BMI and hypoalbuminemia were the major factors affecting BMD in these patients. Bone density measurement should be performed in all patients with IBD in an early stage of the disease.

Impact of bisphosphonate treatment on bone mineral density after kidney transplant

BACKGROUND Mineral bone disease is associated with chronic kidney disease and persists after kidney transplantation.Immunosuppressive treatment contributes to the patho-genesis of this disease.Bisphosphonate treatments have shown positive but inde-finite results.AIM To evaluate the effectiveness and safety of bisphosphonate treatment on post kidney transplantation bone mineral density(BMD).METHODS We included kidney transplant recipients(KTRs)whose BMD was measured after the operation but before the initiation of treatment and their BMD was measured at least one year later.We also evaluated the BMD of KTRs using two valid mea-surements after transplantation who received no treatment(control group).RESULTS Out of 254 KTRs,62(39 men)were included in the study.Bisphosphonates were initiated in 35 KTRs in total(20 men),1.1±2.4 years after operation and for a period of 3.9±2.3 years while 27(19 men)received no treatment.BMD improved significantly in KTRs who received bisphosphonate treatments(from-2.29±1.07 to-1.66±1.09,P<0.0001).The control group showed a non-significant decrease in BMD after 4.2±1.4 years of follow-up after surgery.Kidney function was not affected by bisphosphonate treatment.In KTRs with established osteoporosis,active treatment had a similar and significant effect on those with osteopenia or normal bone mass.CONCLUSION In this retrospective study of KTRs receiving bisphosphonate treatment,we showed that active treatment is effective in preventing bone loss irrespective of baseline BMD.