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Search on : collagen and type and v [Words]
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[PMID]: 29496505
[Au] Autor:Lee A; Karamichos D; Onochie OE; Hutcheon AEK; Rich CB; Zieske JD; Trinkaus-Randall V
[Ad] Address:Department of Biochemistry, Boston University School of Medicine, 80 E. Concord St., Boston, MA, 02118, USA. Electronic address: rusna9632@gmail.com.
[Ti] Title:Hypoxia modulates the development of a corneal stromal matrix model.
[So] Source:Exp Eye Res;170:127-137, 2018 Feb 27.
[Is] ISSN:1096-0007
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Deposition of matrix proteins during development and repair is critical to the transparency of the cornea. While many cells respond to a hypoxic state that can occur in a tumor, the cornea is exposed to hypoxia during development prior to eyelid opening and during the diurnal sleep cycle where oxygen levels can drop from 21% to 8%. In this study, we used 2 three-dimensional (3-D) models to examine how stromal cells respond to periods of acute hypoxic states. The first model, a stromal construct model, is a 3-D stroma-like construct that consists of human corneal fibroblasts (HCFs) stimulated by a stable form of ascorbate for 1, 2, and 4 weeks to self-assemble their own extracellular matrix. The second model, a corneal organ culture model, is a corneal wound-healing model, which consists of wounded adult rat corneas that were removed and placed in culture to heal. Both models were exposed to either normoxic or hypoxic conditions for varying time periods, and the expression and/or localization of matrix proteins was assessed. No significant changes were detected in Type V collagen, which is associated with Type I collagen fibrils; however, significant changes were detected in the expression of both the small leucine-rich repeating proteoglycans and the larger heparan sulfate proteoglycan, perlecan. Also, hypoxia decreased both the number of Cuprolinic blue-positive glycosaminoglycan chains along collagen fibrils and Sulfatase 1, which modulates the effect of heparan sulfate by removing the 6-O-sulfate groups. In the stromal construct model, alterations were seen in fibronectin, similar to those that occur in development and after injury. These changes in fibronectin after injury were accompanied by changes in proteoglycans. Together these findings indicate that acute hypoxic changes alter the physiology of the cornea, and these models will allow us to manipulate the conditions in the extracellular environment in order to study corneal development and trauma.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  2 / 8370 MEDLINE  
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[PMID]: 29517852
[Au] Autor:Amer J; Salhab A; Doron S; Morali G; Safadi R
[Ad] Address:Liver and Gastroenterology Units, Hadassah University Medical Center, Jerusalem, Israel.
[Ti] Title:A novel flow cytometry tool for fibrosis scoring through hepatic stellate cell differentiation.
[So] Source:Cytometry A;, 2018 Mar 08.
[Is] ISSN:1552-4930
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hepatic stellate cells (HSCs) are a central fibrogenic cell type that contributes to collagen accumulation during chronic liver disease. Peripheral blood lymphocytes from HCV patients are phagocytized by HSCs and induce their differentiation. This study aimed to characterize HSCs differentiation using a flow cytometry tool for fibrosis scoring. NK cells from healthy donors and from patients with chronic HCV with various severities of fibrosis were co-cultured with a human HSC line (LX2). LX2 phagocytosis of NK cells were stained for NK cells (CD45/CD56/CD3) and NK activation marker (CD107a) as well as INF-γ, apoptosis (Annexin-V) and α-smooth-muscle-actin (αSMA, as a marker of LX2 activation). In addition, reactive oxygen species (ROS) and the senescence marker P15 were analyzed prior to flow cytometry analysis. LX2 mono-cultures demonstrated a homogenous cell-population according to size (forward-scattered; FSC), granularity and αSMA expressions. However, on their co-culture with NK cells, the HSCs formed four subpopulations, which were stratified by αSMA intensities and cell size. NK cells isolated from heathy donors did not activate LX2-cells. In contrast, HCV exposed to NK cells from both F1 and F4 fibrosis grade patients, showed elevated CD107a and INF-γ levels and increased αSMA intensities in two of the four cell populations, with fibrosis scoring showing a linear correlation with αSMA intensities and NK phagocytosis. The αSMA /Size HSCs sub-population showed higher proliferation following F4-NK cells with higher phagocytosis ability, suggesting an active/regulatory population. The αSMA /Size subpopulations showed low proliferation and phagocytosis capacity, and were correlated with higher apoptosis, increased ROS and P15 intensities, suggesting senescing cells. Taken together, NK cells lead to heterogeneous differentiation of HSCs. Flow-cytometry may provide a novel means of characterizing HSCs in relation to the severity of liver fibrosis. © 2017 International Society for Advancement of Cytometry.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1002/cyto.a.23202

  3 / 8370 MEDLINE  
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[PMID]: 29517678
[Au] Autor:Zeng XT; Liu XP; Liu TZ; Wang XH
[Ad] Address:Department of Urology.
[Ti] Title:The clinical significance of COL5A2 in patients with bladder cancer: A retrospective analysis of bladder cancer gene expression data.
[So] Source:Medicine (Baltimore);97(10):e0091, 2018 Mar.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The present study was aimed to investigate the relationship between the expression of collagen type V alpha 2 chain (COL5A2) and clinical outcomes of patients with bladder cancer.Chi-square test and log-rank-based survival analysis were performed to assess the correlation of COL5A2 expression with clinical characteristics and survivals of patients with bladder cancer using GSE13507. Gene set enrichment analysis was conducted to study the relevant mechanisms.Bladder cancer patients in COL5A2 low expression group were associated with better invasiveness (P < .0001), tumor grade (P = .001), T staging (P < .0001), N staging (P = .002), cancer specific survival (P < .0001), overall survival (P < .0001), and a trend of better M staging (P = .053) than those in COL5A2 high expression group.COL5A2 might affect the progression of bladder cancer through "Coagulation," "Hypoxia," "Apical junction," "Ultraviolet response," "Epithelial mesenchymal transition," "Angiogenesis," "KRAS (KRAS proto-oncogene, GTPase) signaling,""Complement,""IL2-STAT5-signaling," "Inflammatory response," "IL6-JAK-STAT3-signaling," "Myogenesis," "TNF α signaling," "Apoptosis," and "Hedgehog-signaling."Our results demonstrated that COL5A2 was correlated with poor clinical outcomes and survivals of patients with bladder cancer, suggesting that it could be regarded as a biomarker of bladder cancer.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Process
[do] DOI:10.1097/MD.0000000000010091

  4 / 8370 MEDLINE  
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[PMID]: 29361086
[Au] Autor:Truffi M; Sorrentino L; Monieri M; Fociani P; Mazzucchelli S; Bonzini M; Zerbi P; Sampietro GM; Di Sabatino A; Corsi F
[Ad] Address:Department of Biomedical and Clinical Sciences "L. Sacco", University of Milan, Milan, Italy.
[Ti] Title:Inhibition of Fibroblast Activation Protein Restores a Balanced Extracellular Matrix and Reduces Fibrosis in Crohn's Disease Strictures Ex Vivo.
[So] Source:Inflamm Bowel Dis;24(2):332-345, 2018 Jan 18.
[Is] ISSN:1536-4844
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Background: Crohn's disease (CD) is a chronic bowel inflammation that ultimately leads to fibrosis, for which medical therapy is currently unavailable. Fibrotic strictures in CD are characterized by excessive extracellular matrix (ECM) deposition, altered balance between matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs), and overexpression of fibroblast activation protein (FAP), a marker of active fibroblasts. Here we investigated the role of FAP-targeted therapy in ECM remodeling in CD strictures ex vivo. Methods: Bowel specimens were obtained from stenotic and nonstenotic ileal segments from 30 patients with fibrostenotic CD undergoing surgery. FAP expression was evaluated in isolated mucosal myofibroblasts by immunoblotting and flow cytometry. Bowel tissue cultures were treated with anti-FAP antibody, and soluble collagen, TIMP-1, and MMPs were measured in tissue culture supernatants by immunoblotting. Anti-FAP-treated myofibroblasts were analyzed for TIMP-1 expression by immunoblotting, for migratory potential by wound healing assay, and for apoptosis by Annexin V staining. Results: Myofibroblasts from stenotic CD mucosa showed upregulation of FAP expression when compared with nonstenotic mucosa. Treatment of stenotic tissues with anti-FAP antibody induced a dose-dependent decrease in collagen production, particularly affecting type I collagen. The treatment also reduced TIMP-1 production in CD strictures, without altering MMP-3 and MMP-12 secretion. Accordingly, anti-FAP treatment inhibited TIMP-1 expression in stenotic CD myofibroblasts and enhanced myofibroblast migration without affecting survival. Conclusions: FAP inhibition reduced type I collagen and TIMP-1 production by CD strictures ex vivo without compromising uninvolved bowel areas. These results suggest that targeting FAP could reconstitute ECM homeostasis in fibrostenotic CD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1093/ibd/izx008

  5 / 8370 MEDLINE  
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[PMID]: 29490295
[Au] Autor:Cao H; Umbach AT; Bissinger R; Gawaz M; Lang F
[Ad] Address:Department of Internal Medicine III, Tübingen, Germany.
[Ti] Title:Inhibition of Collagen Related Peptide Induced Platelet Activation and Apoptosis by Ceritinib.
[So] Source:Cell Physiol Biochem;45(4):1707-1716, 2018.
[Is] ISSN:1421-9778
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:BACKGROUND/AIMS: The anaplastic lymphoma (tyrosine) kinase (ALK) inhibitor ceritinib triggers apoptosis of tumor cells and eryptosis of erythrocytes. Blood platelets may similarly enter a state resembling apoptosis, which could be triggered by activation with collagen related peptide (CRP). CRP-induced platelet apoptosis is characterized by cell membrane scrambling with phosphatidylserine exposure to the platelet surface and cell shrinkage, preceded by externalization of Ca2+ channel Orai1, increase of cytosolic Ca2+-activity ([Ca2+]i), formation of reactive oxygen species (ROS), and caspase activation. The present study explored whether ceritinib triggers platelet apoptosis and/or modifies the CRP induced apoptosis. METHODS: Platelets isolated from wild-type mice were exposed for 30 minutes to ceritinib (1.5 µg/ml) without or with 2.5 - 15 min pretreatment with CRP (2 µg/ml or 5 µg/ml). Flow cytometry was employed to estimate cytosolic Ca2+-activity ([Ca2+]i) from Fluo-3 fluorescence, ROS abundance from 2',7'-dichlorodihydrofluorescein diacetate fluorescence, platelet degranulation from P-selectin abundance, integrin activation from αIIbß3 integrin abundance, caspase activity utilizing an Active Caspase-3 Staining kit, phosphatidylserine abundance from annexin-V-binding, platelet volume from forward scatter and aggregation utilizing staining with CD9-APC and CD9-PE. RESULTS: In the absence of CRP, ceritinib slightly, but significantly decreased [Ca2+]i without significantly modifying the other measured parameters. CRP significantly increased [Ca2+]i, ROS abundance, P-selectin abundance, activated αIIbß3 integrin, annexin-V-binding, caspase activity as well as aggregation and decreased cell volume, all effects significantly blunted in the presence of ceritinib. CONCLUSIONS: The present observations uncover a novel, unexpected effect of ceritinib, i.e. inhibition of CRP-induced platelet activation and apoptosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:In-Process
[do] DOI:10.1159/000487778

  6 / 8370 MEDLINE  
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[PMID]: 29506241
[Au] Autor:Hendee KE; Sorokina EA; Muheisen SS; Reis LM; Tyler RC; Markovic V; Cuturilo G; Link BA; Semina EV
[Ad] Address:Department of Pediatrics and Children's Research Institute.
[Ti] Title:PITX2 deficiency and associated human disease: insights from the zebrafish model.
[So] Source:Hum Mol Genet;, 2018 Mar 01.
[Is] ISSN:1460-2083
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The PITX2 (paired-like homeodomain 2) gene encodes a bicoid-like homeodomain transcription factor linked with several human disorders. The main associated congenital phenotype is Axenfeld-Rieger syndrome, type 1 (ARS), an autosomal dominant condition characterized by variable defects in the anterior segment of the eye, an increased risk of glaucoma, craniofacial dysmorphism and dental and umbilical anomalies; in addition to this, one report implicated PITX2 in ring dermoid of the cornea and a few others described cardiac phenotypes. We report three novel PITX2 mutations- c.271C>T, p.(Arg91Trp); c.259T>C, p.(Phe87Leu); and c.356delA, p.(Gln119Argfs*36)- identified in independent families with typical ARS characteristics and some unusual features such as corneal guttata, Wolf-Parkinson-White syndrome, and hyperextensibility. To gain further insight into the diverse roles of PITX2/pitx2 in vertebrate development, we generated various genetic lesions in the pitx2 gene via TALEN-mediated genome editing. Affected homozygous zebrafish demonstrated congenital defects consistent with the range of PITX2-associated human phenotypes: abnormal development of the cornea, iris, and iridocorneal angle; corneal dermoids; and craniofacial dysmorphism. In addition, via comparison of pitx2M64*and wild-type embryonic ocular transcriptomes we defined molecular changes associated with pitx2 deficiency, thereby implicating processes potentially underlying disease pathology. This analysis identified numerous affected factors including several members of the Wnt pathway and collagen type I and V gene families. These data further support the link between PITX2 and the WNT pathway and suggest a new role in regulation of collagen gene expression during development.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:Publisher
[do] DOI:10.1093/hmg/ddy074

  7 / 8370 MEDLINE  
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[PMID]: 28458336
[Au] Autor:Nakamura Y; Suzuki T; Kamimura M; Ikegami S; Uchiyama S; Kato H
[Ad] Address:Department of Orthopaedic Surgery, Shinshu University School of Medicine.
[Ti] Title:Alfacalcidol Increases the Therapeutic Efficacy of Ibandronate on Bone Mineral Density in Japanese Women with Primary Osteoporosis.
[So] Source:Tohoku J Exp Med;241(4):319-326, 2017 04.
[Is] ISSN:1349-3329
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:Bisphosphonates (BPs) increase bone mineral density (BMD) through the inhibition of osteoclast activity. Among BPs, ibandronate (IBN) is a strong inhibitor of bone resorption. However, the effects of a vitamin D analogue, alfacalcidol (ALF), on IBN treatment for osteoporosis is unknown. Fifty-three treatment-naïve post-menopausal women with primary osteoporosis were recruited and divided into IBN-treatment group (IBN group) and IBN with ALF group (IBN/ALF group). IBN (1.0 mg) was intravenously injected once a month, with or without oral ALF (1.0 µg/day). Ultimately, 19 subjects in IBN group and 26 in IBN/ALF group were analyzed. Bone turnover markers were examined at 4, 6, 12, and 18 months, and BMD was measured at 6, 12, and 18 months. Compared with pre-treatment, bone turnover markers significantly decreased in both groups after 4 months. The levels of serum N-terminal propeptide of type-1 procollagen and tartrate-resistant acid phosphatase-5b, and urinary N-terminal telopeptide of type-I collagen were significantly lower in IBN/ALF group than those in IBN group at 12 months. Lumbar 1-4 (L)-BMD significantly increased from 6 months in IBN/ALF group and at 18 months in IBN group. L-BMD was significantly higher in IBN/ALF group (6.6% increase) than in IBN group (3.4%) at 18 months. Total hip (H)-BMD significantly increased from 6 months in IBN/ALF group and tended to improve in IBN group. H-BMD was significantly higher in IBN/ALF group (4.8%) than in IBN group (3.2%) at 18 months. In conclusion, treatment with ALF in combination with IBN improves BMD in post-menopausal women with osteoporosis.
[Mh] MeSH terms primary: Bone Density Conservation Agents/therapeutic use
Bone Density/drug effects
Diphosphonates/therapeutic use
Hydroxycholecalciferols/therapeutic use
Osteoporosis/drug therapy
[Mh] MeSH terms secundary: Absorptiometry, Photon
Administration, Intravenous
Administration, Oral
Aged
Asian Continental Ancestry Group
Drug Synergism
Female
Hip/diagnostic imaging
Humans
Hydroxycholecalciferols/adverse effects
Postmenopause
Tartrate-Resistant Acid Phosphatase/blood
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Bone Density Conservation Agents); 0 (Diphosphonates); 0 (Hydroxycholecalciferols); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase); UMD7G2653W (ibandronic acid); URQ2517572 (alfacalcidol)
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:IM
[Da] Date of entry for processing:170502
[St] Status:MEDLINE
[do] DOI:10.1620/tjem.241.319

  8 / 8370 MEDLINE  
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[PMID]: 29400583
[Au] Autor:Liu C; Liu D; Wang Y; Li Y; Li T; Zhou Z; Yang Z; Wang J; Zhang Q
[Ad] Address:a Institute of Biomedical and Pharmaceutical Technology, Fuzhou University , Fuzhou , PR China.
[Ti] Title:Glycol chitosan/oxidized hyaluronic acid hydrogels functionalized with cartilage extracellular matrix particles and incorporating BMSCs for cartilage repair.
[So] Source:Artif Cells Nanomed Biotechnol;:1-12, 2018 Feb 05.
[Is] ISSN:2169-141X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:In this article, we fabricated a bioactive hydrogel composed of glycol chitosan (G-CS) and oxidized hyaluronic acid (OHA) via Schiff base reaction. Cartilage extracellular matrix (ECM) particles with different concentrations were used to functionalize G-CS/OHA (S1) hydrogel. The results demonstrated that S3 (G-CS/OHA/ECM 2% w/v) hydrogel exhibited the most suitable compression strength and provided the optimal environment for proliferation of bone marrow mesenchymal stem cells (BMSCs). To assess the chondroinductivity of ECM in vitro, we compared the chondrogenesis of BMSCs in S1 (G-CS/OHA) and S3 (G-CS/OHA/ECM 2% w/v) hydrogels. The results confirmed that the higher levels of glycosaminoglycans (GAGs) and collagen type II (COL II) were accumulated in S3 hydrogel. In vivo, cartilage defects of rats generated most mature tissue within BMSCs-laden S3 hydrogel (S3/BMSCs group). The tissues were more integrative and contained higher levels of COL II and GAGs compared to the other groups. All these results suggested that the G-CS/OHA hydrogel functionalized with ECM particles is a good candidate biomaterial to be applied in cartilage tissue engineering.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:Publisher
[do] DOI:10.1080/21691401.2018.1434662

  9 / 8370 MEDLINE  
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[PMID]: 29251812
[Au] Autor:Zhang C; Kelkar A; Nasirikenari M; Lau JTY; Sveinsson M; Sharma UC; Pokharel S; Neelamegham S
[Ad] Address:Department of Chemical and Biological Engineering, State University of New York, Buffalo, NY, USA.
[Ti] Title:The physical spacing between the von Willebrand factor D'D3 and A1 domains regulates platelet adhesion in vitro and in vivo.
[So] Source:J Thromb Haemost;16(3):571-582, 2018 Mar.
[Is] ISSN:1538-7836
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Essentials The role of von Willebrand factor (VWF) domains in regulating platelet adhesion was studied in vivo. Multimeric VWF with spacers at the N- and C-terminus of VWF-A1 were systematically tested. N-terminal modified VWF avidly bound platelet GpIbα, causing VWD Type2B like phenotype in mice. Novel anti-D'D3 mAbs suggest that changes at the D'D3-A1 interface may be biologically relevant. SUMMARY: Background Previous ex vivo studies using truncated VWF (von Willebrand factor) suggest that domain-level molecular architecture may control platelet-GpIbα binding function. Objective We determined if this is the case with multimeric VWF in vivo. Methods Full-length human VWF ('hV') was modified with a 22-amino acid mucinous stretch at either the N-terminus of VWF-A1 to create 'hNV' or C-terminus to yield 'hCV'. This extends the physical distance between VWF-A1 and the adjacent domains by ~6 nm. Similar mucin inserts were also introduced into a human-murine chimera ('h[mA1]V') where murine-A1 replaced human-A1 in hV. This yielded 'h[mA1]NV' and 'h[mA1]CV', with N- and C-terminal inserts. The constructs were tested ex vivo and in vivo. Results Mucin insertion at the N-terminus, but not C-terminus, in both types of constructs resulted in >50-fold increase in binding to immobilized GpIbα. N-terminal insertion also resulted in greater shear-induced platelet activation, more thrombus formation on collagen, enhanced platelet accumulation and slower platelet translocation on immobilized VWF in microfluidics assays. Hydrodynamic injection-based expression of h[mA1]NV, but not h[mA1]V or h[mA1]CV, in VWF mice caused profound thrombocytopenia, reduced plasma VWF concentrations, lower multimer distribution, and incessant tail bleeding that is reminiscent of von Willebrand disease type 2B. Platelet plugs were noted in the portal veins and hepatic arteries. An anti-D'D3 mAb DD3.3 that displays enhanced binding to VWF containing the N-terminal mucin insert also exhibited increased binding to wild-type VWF under shear and upon ristocetin addition. Conclusion Conformation changes at the VWF D'D3-A1 interface may be a key regulator of thrombosis in vivo. Structural features at the A1-A2 interface are likely of less significance.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:In-Data-Review
[do] DOI:10.1111/jth.13927

  10 / 8370 MEDLINE  
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[PMID]: 29488480
[Au] Autor:Skripnikova IA; Kosmatova OV; Abirova ES; Novikov VE; Murashko LM
[Ad] Address:National Medical Research Center for Preventive Medicine, Ministry of Health of Russia, Moscow, Russia.
[Ti] Title:Opyt primeneniia preparata Prolia u patsientok s postmenopauzal'nym osteoporozom v klinicheskoi praktike. [Experience in using Prolia in patients with postmenopausal osteoporosis in clinical practice].
[So] Source:Ter Arkh;89(12. Vyp. 2):190-196, 2017.
[Is] ISSN:0040-3660
[Cp] Country of publication:Russia (Federation)
[La] Language:rus
[Ab] Abstract:AIM: To evaluate the efficiency and safety of long-term Prolia therapy in patients with postmenopausal osteoporosis (OP). SUBJECTS AND METHODS: The open prospective study enrolled 98 women (mean age, 68±9 years; mean menopause duration, 17±4 years) with postmenopausal OP, who were followed up in an outpatient setting at the National Medical Research Center for Preventive Medicine and who had been treated with denosumab 60 mg subcutaneously every 6 months for 12 months or more. The maximum follow-up period was 4 years: 48, 29, 11, and 10 patients were treated for 12, 24, 36, and 48 months, respectively. The patients were allocated into 2 groups: those who received and those who had not previously received antiosteoporotic therapy. Bone mineral density (BMD) was measured using dual-energy X-ray densitometry of the lumbar spine (L -L ) and proximal femur (PF). The ten-year probability of major osteoporotic fractures was estimated once in 72 patients not previously receiving antiosteoporotic therapy before the prescription of denosumab. RESULTS: In the patients not previously receiving therapy, the median 10-year probability of major fractures using the FRAX algorithm was 14.9%; that of femoral neck (FN) fractures was 3.7%. During denosumab treatment, the BMD increase in the lumbar spine was 4.2% at 12 months, 7.5% at 24 months, was 8.8% at 36 months; that in FN was 3.1, 3.9, and 5.3%, that in PF was 2.8, 4.1, and 5%; and that in the 1/3 forearm was 0.9, 1.4, and 2.6%, respectively (p < 0.001). In the persons receiving and not previously receiving the therapy, the BMD increase was similar, i.e. there was an additional positive effect when switching to denosumab. The decrease in the serum concentration of C-terminal telopeptide of type I collagen (CTX-I) was 54% at 6 months after initiation of denosumab therapy (p < 0.001) and 72% at 12 months (p<0.001); and the achieved marker level remained unchanged at 48 months. Transition from the OP zone to osteopenia one was noted in 23 patients with low BMD (T-score -2.5 SD) in L -L and in 12 patients with that in FN at 12 months of denosumab therapy and this was in 25 patients at 24 months. Nine-eight patients receiving the first Prolia injection refused to continue treatment on their own; adverse events were not the reason for drug discontinuation. CONCLUSION: Therapy with denosumab was effective in increasing BMD in routine outpatient practice and in allowing 25% of patients to achieve target values of this indicator. The marked decrease in the level of the bone resorption marker STX suggested that the drug had antiresorptive potency. The frequency of adverse reactions was low, confirming the good tolerability and safety profile of the drug. The convenience of the scheme and route of drug administration contributed to strict compliance with the doctor's recommendations. Denosumab was effective in increasing BMD not only in untreated patients, but also in those who had previously received antiosteoporotic therapy. The pharmacokinetic characteristics of denosumab, which contribute to its uniform distribution in trabecular and cortical bone tissue, regardless of active bone remodeling, and the fact that the clearance of the drug is independent of kidney function offer an advantage of administering the drug to patients with significant loss of FN and radius BMD and of reducing kidney function.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180228
[Lr] Last revision date:180228
[St] Status:In-Data-Review
[do] DOI:10.17116/terarkh20178912190-196


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