Skip to main content
Erschienen in: Inflammation 2/2012

01.04.2012

Elevated Expression of β1,4-Galactosyltransferase-I in Cartilage and Synovial Tissue of Patients with Osteoarthritis

verfasst von: Wei Liu, Zhiming Cui, Youhua Wang, Xinhui Zhu, Jianbo Fan, Guofeng Bao, Junjun Qiu, Dawei Xu

Erschienen in: Inflammation | Ausgabe 2/2012

Einloggen, um Zugang zu erhalten

Abstract

Osteoarthritis (OA) is considered a complex illness, characterized by cartilage degeneration, secondary synovial membrane inflammation, and subchondral bone sclerosis. Previous studies have shown β1,4-galactosylransferase-I (β1,4-GalT-I) to be a key inflammatory mediator that participates in the initiation and maintenance of inflammatory reaction in diseases. In the present study, we investigated the expression and possible biological function of β1,4-GalT-I in the cartilage and synovial tissue of OA patients. Cartilage and synovial tissue samples from OA patients and healthy controls were stained for β1,4-GalT-I. Reverse transcription-polymerase chain reaction was used to observe the expression of β1,4-GalT-I, and western blot was carried out for E-selectin. The interaction between β1,4-GalT-I and E-selectin was analyzed by double labeling immunohistochemistry and immunoprecipitation. The expression of β1,4-GalT-I increased in the cartilage and synovial tissue of OA patients compared with healthy controls. E-selectin was overexpressed and was correlated with β1,4-GalT-I in OA cartilage and synovial tissue. These data suggest that β1,4-GalT-I may play an important role in the inflammatory processes in cartilage and synovial tissue of patients with OA.
Literatur
1.
Zurück zum Zitat Pritzker, K.P., S. Gay, S.A. Jimenez, K. Ostergaard, J.P. Pelletier, P.A. Revell, D. Salter, and W.B. van den Berg. 2006. Osteoarthritis cartilage histopathology: grading and staging. Osteoarthritis and Cartilage 14: 13–29.PubMedCrossRef Pritzker, K.P., S. Gay, S.A. Jimenez, K. Ostergaard, J.P. Pelletier, P.A. Revell, D. Salter, and W.B. van den Berg. 2006. Osteoarthritis cartilage histopathology: grading and staging. Osteoarthritis and Cartilage 14: 13–29.PubMedCrossRef
2.
Zurück zum Zitat Martel-Pelletier, J., and J.P. Pelletier. 2005. New insights into the major pathophysiological processes responsible for the development of osteoarthritis. Seminars in Arthritis and Rheumatism 34: 6–8.PubMedCrossRef Martel-Pelletier, J., and J.P. Pelletier. 2005. New insights into the major pathophysiological processes responsible for the development of osteoarthritis. Seminars in Arthritis and Rheumatism 34: 6–8.PubMedCrossRef
3.
Zurück zum Zitat Lavigne, P., M. Benderdour, D. Lajeunesse, P. Reboul, Q. Shi, J.P. Pelletier, J. Martel-Pelletier, and J.C. Fernandes. 2005. Subchondral and trabecular bone metabolism regulation in canine experimental knee osteoarthritis. Osteoarthritis and Cartilage 13: 310–317.PubMedCrossRef Lavigne, P., M. Benderdour, D. Lajeunesse, P. Reboul, Q. Shi, J.P. Pelletier, J. Martel-Pelletier, and J.C. Fernandes. 2005. Subchondral and trabecular bone metabolism regulation in canine experimental knee osteoarthritis. Osteoarthritis and Cartilage 13: 310–317.PubMedCrossRef
4.
Zurück zum Zitat Adams, M.E. 1989. Cartilage hypertrophy following canine anterior cruciate ligament transection differs among different areas of the joint. Journal of Rheumatology 16: 818–824.PubMed Adams, M.E. 1989. Cartilage hypertrophy following canine anterior cruciate ligament transection differs among different areas of the joint. Journal of Rheumatology 16: 818–824.PubMed
5.
Zurück zum Zitat Pelletier, J.P., J. Martel-Pelletier, F. Mehraban, and C.J. Malemud. 1992. Immunological analysis of proteoglycan structural changes in the early stage of experimental osteoarthritic canine cartilage lesions. Journal of Orthopaedic Research 10: 511–523.PubMedCrossRef Pelletier, J.P., J. Martel-Pelletier, F. Mehraban, and C.J. Malemud. 1992. Immunological analysis of proteoglycan structural changes in the early stage of experimental osteoarthritic canine cartilage lesions. Journal of Orthopaedic Research 10: 511–523.PubMedCrossRef
6.
Zurück zum Zitat Pelletier, J.P., J. Martel-Pelletier, R.D. Altman, L. Ghandur-Mnaymneh, D.S. Howell, and J.F. Jr Woessner. 1983. Collagenolytic activity and collagen matrix breakdown of the articular cartilage in the Pond-Nuki dog model of osteoarthritis. Arthritis and Rheumatism 26: 866–874.PubMedCrossRef Pelletier, J.P., J. Martel-Pelletier, R.D. Altman, L. Ghandur-Mnaymneh, D.S. Howell, and J.F. Jr Woessner. 1983. Collagenolytic activity and collagen matrix breakdown of the articular cartilage in the Pond-Nuki dog model of osteoarthritis. Arthritis and Rheumatism 26: 866–874.PubMedCrossRef
7.
Zurück zum Zitat McDevitt, C., E. Gilbertson, and H. Muir. 1977. An experimental model of osteoarthritis; early morphological and biochemical changes. Journal of Bone Joint Surgery (British) 59: 24–35. McDevitt, C., E. Gilbertson, and H. Muir. 1977. An experimental model of osteoarthritis; early morphological and biochemical changes. Journal of Bone Joint Surgery (British) 59: 24–35.
8.
Zurück zum Zitat Apweiler, R., H. Hermjakob, and N. Sharon. 1999. On the frequency of protein glycosylation, as deduced from analysis of the SWISS-PROT database. Biochimica et Biophysica Acta 1473: 4–8.PubMedCrossRef Apweiler, R., H. Hermjakob, and N. Sharon. 1999. On the frequency of protein glycosylation, as deduced from analysis of the SWISS-PROT database. Biochimica et Biophysica Acta 1473: 4–8.PubMedCrossRef
9.
Zurück zum Zitat Furukawa, K., and T. Sat. 1999. Beta-1,4-galactosylation of N-glycans is a complex process. Biochimica et Biophysica Acta 1473: 54–66.PubMedCrossRef Furukawa, K., and T. Sat. 1999. Beta-1,4-galactosylation of N-glycans is a complex process. Biochimica et Biophysica Acta 1473: 54–66.PubMedCrossRef
10.
Zurück zum Zitat Shur, B.D., S. Evans, and Q. Lu. 1998. Cell surface galactosyltransferase: current issues. Glycoconjugate Journal 15: 537–548.PubMedCrossRef Shur, B.D., S. Evans, and Q. Lu. 1998. Cell surface galactosyltransferase: current issues. Glycoconjugate Journal 15: 537–548.PubMedCrossRef
11.
Zurück zum Zitat Hathaway, H.J., and B.D. Shur. 1992. Cell surface beta 1,4-galactosyltransferase functions during neural crest cell migration and neurulation in vivo. The Journal of Cell Biology 117: 369–382.PubMedCrossRef Hathaway, H.J., and B.D. Shur. 1992. Cell surface beta 1,4-galactosyltransferase functions during neural crest cell migration and neurulation in vivo. The Journal of Cell Biology 117: 369–382.PubMedCrossRef
12.
Zurück zum Zitat Eckstein, D.J., and B.D. Shur. 1992. Cell surface beta-1,4-galactosyltransferase is associated with the detergent-insoluble cytoskeleton on migrating mesenchymal cells. Experimental Cell Research 201: 83–90.PubMedCrossRef Eckstein, D.J., and B.D. Shur. 1992. Cell surface beta-1,4-galactosyltransferase is associated with the detergent-insoluble cytoskeleton on migrating mesenchymal cells. Experimental Cell Research 201: 83–90.PubMedCrossRef
13.
Zurück zum Zitat Miller, D.J., M.B. Macek, and B.D. Shur. 1992. Complementarity between sperm surface beta-1,4-galactosyltransferase and egg-coat ZP3 mediates sperm-egg binding. Nature 357: 589–593.PubMedCrossRef Miller, D.J., M.B. Macek, and B.D. Shur. 1992. Complementarity between sperm surface beta-1,4-galactosyltransferase and egg-coat ZP3 mediates sperm-egg binding. Nature 357: 589–593.PubMedCrossRef
14.
Zurück zum Zitat Evans, S.C., L.C. Lopez, and B.D. Shur. 1993. Dominant negative mutation in cell surface beta 1,4-galactosyltransferase inhibits cell-cell and cell-matrix interactions. The Journal of Cell Biology 120: 1045–1057.PubMedCrossRef Evans, S.C., L.C. Lopez, and B.D. Shur. 1993. Dominant negative mutation in cell surface beta 1,4-galactosyltransferase inhibits cell-cell and cell-matrix interactions. The Journal of Cell Biology 120: 1045–1057.PubMedCrossRef
15.
Zurück zum Zitat Huang, Q., B.D. Shur, and P.C. Begovac. 1995. Overexpressing cell surface beta 1.4-galactosyltransferase in PC12 cells increases neurite outgrowth on laminin. Journal of Cell Science 108(Pt 2): 839–847.PubMed Huang, Q., B.D. Shur, and P.C. Begovac. 1995. Overexpressing cell surface beta 1.4-galactosyltransferase in PC12 cells increases neurite outgrowth on laminin. Journal of Cell Science 108(Pt 2): 839–847.PubMed
16.
Zurück zum Zitat Asano, M., S. Nakae, N. Kotani, N. Shirafuji, A. Nambu, N. Hashimoto, H. Kawashima, M. Hirose, M. Miyasaka, S. Takasaki, and Y. Iwakura. 2003. Impaired selectin-ligand biosynthesis and reduced inflammatory responses in beta-1,4-galactosyltransferase-I-deficient mice. Blood 102: 1678–1685.PubMedCrossRef Asano, M., S. Nakae, N. Kotani, N. Shirafuji, A. Nambu, N. Hashimoto, H. Kawashima, M. Hirose, M. Miyasaka, S. Takasaki, and Y. Iwakura. 2003. Impaired selectin-ligand biosynthesis and reduced inflammatory responses in beta-1,4-galactosyltransferase-I-deficient mice. Blood 102: 1678–1685.PubMedCrossRef
17.
Zurück zum Zitat Mori, R., T. Kondo, T. Nishie, T. Ohshima, and M. Asano. 2004. Impairment of skin wound healing in beta-1,4-galactosyltransferase-deficient mice with reduced leukocyte recruitment. American Journal of Pathology 164: 1303–1314.PubMedCrossRef Mori, R., T. Kondo, T. Nishie, T. Ohshima, and M. Asano. 2004. Impairment of skin wound healing in beta-1,4-galactosyltransferase-deficient mice with reduced leukocyte recruitment. American Journal of Pathology 164: 1303–1314.PubMedCrossRef
18.
Zurück zum Zitat Xu, D., Z. Cui, W. Liu, R. Tao, T. Tao, A. Shen, and Y. Wang. 2010. Tumor necrosis factor-alpha up-regulates the expression of beta1,4-galactosyltransferase-I in human fibroblast-like synoviocytes. Inflammation. doi:10.1007/s10753-010-9260-x. Xu, D., Z. Cui, W. Liu, R. Tao, T. Tao, A. Shen, and Y. Wang. 2010. Tumor necrosis factor-alpha up-regulates the expression of beta1,4-galactosyltransferase-I in human fibroblast-like synoviocytes. Inflammation. doi:10.​1007/​s10753-010-9260-x.
19.
Zurück zum Zitat Wang, Y., D. Xu, R. Tao, H. Wang, Q. Wang, and A. Shen. 2010. beta1,4-Galactosyltransferase-I contributes to the inflammatory processes in synovial tissue of patients with rheumatoid arthritis. Inflammation Research 59: 1009–1018.PubMedCrossRef Wang, Y., D. Xu, R. Tao, H. Wang, Q. Wang, and A. Shen. 2010. beta1,4-Galactosyltransferase-I contributes to the inflammatory processes in synovial tissue of patients with rheumatoid arthritis. Inflammation Research 59: 1009–1018.PubMedCrossRef
20.
Zurück zum Zitat Wang, H., D. Xu, R. Tao, X. Ni, A. Shen, and Y. Wang. 2010. β1,4-Galactosyltransferase-I in synovial tissue of collagen-induced rat model of rheumatoid arthritis. Clin Exp Med. doi:10.1007/s10238-010-0121-6. Wang, H., D. Xu, R. Tao, X. Ni, A. Shen, and Y. Wang. 2010. β1,4-Galactosyltransferase-I in synovial tissue of collagen-induced rat model of rheumatoid arthritis. Clin Exp Med. doi:10.​1007/​s10238-010-0121-6.
21.
Zurück zum Zitat Altman, R., E. Asch, D. Bloch, G. Bole, D. Borenstein, K. Brandt, W. Christy, T.D. Cooke, R. Greenwald, and M. Hochberg. 1986. Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association. Arthritis Rheum 29: 1039–1049.PubMedCrossRef Altman, R., E. Asch, D. Bloch, G. Bole, D. Borenstein, K. Brandt, W. Christy, T.D. Cooke, R. Greenwald, and M. Hochberg. 1986. Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association. Arthritis Rheum 29: 1039–1049.PubMedCrossRef
22.
Zurück zum Zitat Ebnet, K., and D. Vestweber. 1999. Molecular mechanisms that control leukocyte extravasation: the selectins and the chemokines. Histochemistry and Cell Biology 112: 1–23.PubMedCrossRef Ebnet, K., and D. Vestweber. 1999. Molecular mechanisms that control leukocyte extravasation: the selectins and the chemokines. Histochemistry and Cell Biology 112: 1–23.PubMedCrossRef
23.
Zurück zum Zitat Kotani, N., M. Asano, Y. Iwakura, and S. Takasaki. 2001. Knockout of mouse beta 1,4-galactosyltransferase-1 gene results in a dramatic shift of outer chain moieties of N-glycans from type 2 to type 1 chains in hepatic membrane and plasma glycoproteins. Biochemical Journal 357: 827–834.PubMedCrossRef Kotani, N., M. Asano, Y. Iwakura, and S. Takasaki. 2001. Knockout of mouse beta 1,4-galactosyltransferase-1 gene results in a dramatic shift of outer chain moieties of N-glycans from type 2 to type 1 chains in hepatic membrane and plasma glycoproteins. Biochemical Journal 357: 827–834.PubMedCrossRef
24.
Zurück zum Zitat Wittenberg, R.H., R.E. Willburger, K.S. Kleemeyer, and B.A. Peskar. 1993. In vitro release of prostaglandins and leukotrienes from synovial tissue, cartilage, and bone in degenerative joint diseases. Arthritis and Rheumatism 36: 1444–1450.PubMedCrossRef Wittenberg, R.H., R.E. Willburger, K.S. Kleemeyer, and B.A. Peskar. 1993. In vitro release of prostaglandins and leukotrienes from synovial tissue, cartilage, and bone in degenerative joint diseases. Arthritis and Rheumatism 36: 1444–1450.PubMedCrossRef
25.
Zurück zum Zitat Pelletier, J.P., J. Martel-Pelletier, and S.B. Abramson. 2001. Osteoarthritis, an inflammatory disease: potential implication for the selection of new therapeutic targets. Arthritis and Rheumatism 44: 1237–1247.PubMedCrossRef Pelletier, J.P., J. Martel-Pelletier, and S.B. Abramson. 2001. Osteoarthritis, an inflammatory disease: potential implication for the selection of new therapeutic targets. Arthritis and Rheumatism 44: 1237–1247.PubMedCrossRef
26.
Zurück zum Zitat Nakamura, H., S. Yoshino, T. Kato, J. Tsuruha, and K. Nishioka. 1999. T-cell mediated inflammatory pathway in osteoarthritis. Osteoarthritis and Cartilage 7: 401–402.PubMedCrossRef Nakamura, H., S. Yoshino, T. Kato, J. Tsuruha, and K. Nishioka. 1999. T-cell mediated inflammatory pathway in osteoarthritis. Osteoarthritis and Cartilage 7: 401–402.PubMedCrossRef
27.
Zurück zum Zitat Martel-Pelletier, J., N. Alaaeddine, and J.P. Pelletier. 1999. Cytokines and their role in the pathophysiology of osteoarthritis. Frontiers in Bioscience 4: 694–703.CrossRef Martel-Pelletier, J., N. Alaaeddine, and J.P. Pelletier. 1999. Cytokines and their role in the pathophysiology of osteoarthritis. Frontiers in Bioscience 4: 694–703.CrossRef
28.
Zurück zum Zitat Caron, J.P., J.C. Fernandes, J. Martel-Pelletier, G. Tardif, F. Mineau, C. Geng, and J.P. Pelletier. 1996. Chondroprotective effect of intraarticular injections of interleukin-1 receptor antagonist in experimental osteoarthritis. Suppression of collagenase-1 expression. Arthritis and Rheumatism 39: 1535–1544.PubMedCrossRef Caron, J.P., J.C. Fernandes, J. Martel-Pelletier, G. Tardif, F. Mineau, C. Geng, and J.P. Pelletier. 1996. Chondroprotective effect of intraarticular injections of interleukin-1 receptor antagonist in experimental osteoarthritis. Suppression of collagenase-1 expression. Arthritis and Rheumatism 39: 1535–1544.PubMedCrossRef
29.
Zurück zum Zitat Mapp, P.I., P.S. Avery, D.F. McWilliams, J. Bowyer, C. Day, S. Moores, R. Webster, and D.A. Walsh. 2008. Angiogenesis in two animal models of osteoarthritis. Osteoarthritis and Cartilage 16: 61–69.PubMedCrossRef Mapp, P.I., P.S. Avery, D.F. McWilliams, J. Bowyer, C. Day, S. Moores, R. Webster, and D.A. Walsh. 2008. Angiogenesis in two animal models of osteoarthritis. Osteoarthritis and Cartilage 16: 61–69.PubMedCrossRef
30.
Zurück zum Zitat Honorati, M.C., L. Cattini, and A. Facchini. 2004. IL-17, IL-1beta and TNF-alpha stimulate VEGF production by dedifferentiated chondrocytes. Osteoarthritis and Cartilage 12: 683–691.PubMedCrossRef Honorati, M.C., L. Cattini, and A. Facchini. 2004. IL-17, IL-1beta and TNF-alpha stimulate VEGF production by dedifferentiated chondrocytes. Osteoarthritis and Cartilage 12: 683–691.PubMedCrossRef
31.
Zurück zum Zitat Bonnet, C.S., and D.A. Walsh. 2005. Osteoarthritis, angiogenesis and inflammation. Rheumatology (Oxford, England) 44: 7–16.CrossRef Bonnet, C.S., and D.A. Walsh. 2005. Osteoarthritis, angiogenesis and inflammation. Rheumatology (Oxford, England) 44: 7–16.CrossRef
32.
Zurück zum Zitat Lowe, J.B. 2003. Glycan-dependent leukocyte adhesion and recruitment in inflammation. Current Opinion in Cell Biology 15: 531–538.PubMedCrossRef Lowe, J.B. 2003. Glycan-dependent leukocyte adhesion and recruitment in inflammation. Current Opinion in Cell Biology 15: 531–538.PubMedCrossRef
33.
Zurück zum Zitat McEver, R.P., K.L. Moore, and R.D. Cummings. 1995. Leukocyte trafficking mediated by selectin-carbohydrate interactions. Journal of Biological Chemistry 270: 11025–11028.PubMedCrossRef McEver, R.P., K.L. Moore, and R.D. Cummings. 1995. Leukocyte trafficking mediated by selectin-carbohydrate interactions. Journal of Biological Chemistry 270: 11025–11028.PubMedCrossRef
34.
Zurück zum Zitat Lowe, J.B. 1997. Selectin ligands, leukocyte trafficking, and fucosyltransferase genes. Kidney International 51: 1418–1426.PubMedCrossRef Lowe, J.B. 1997. Selectin ligands, leukocyte trafficking, and fucosyltransferase genes. Kidney International 51: 1418–1426.PubMedCrossRef
35.
Zurück zum Zitat Wilkins, P.P., R.P. McEver, and R.D. Cummings. 1996. Structures of the O-glycans on P-selectin glycoprotein ligand-1 from HL-60 cells. Journal of Biological Chemistry 271: 18732–18742.PubMedCrossRef Wilkins, P.P., R.P. McEver, and R.D. Cummings. 1996. Structures of the O-glycans on P-selectin glycoprotein ligand-1 from HL-60 cells. Journal of Biological Chemistry 271: 18732–18742.PubMedCrossRef
36.
Zurück zum Zitat Maemura, K., and M. Fukuda. 1992. Poly-N-acetyllactosaminyl O-glycans attached to leukosialin. The presence of sialyl Le(x) structures in O-glycans. Journal of Biological Chemistry 267: 24379–24386.PubMed Maemura, K., and M. Fukuda. 1992. Poly-N-acetyllactosaminyl O-glycans attached to leukosialin. The presence of sialyl Le(x) structures in O-glycans. Journal of Biological Chemistry 267: 24379–24386.PubMed
37.
Zurück zum Zitat Hiraoka, N., B. Petryniak, J. Nakayama, S. Tsuboi, M. Suzuki, J.C. Yeh, D. Izawa, T. Tanaka, M. Miyasaka, J.B. Lowe, and M. Fukuda. 1999. A novel, high endothelial venule-specific sulfotransferase expresses 6-sulfo sialyl Lewis(x), an L-selectin ligand displayed by CD34. Immunity 11: 79–89.PubMedCrossRef Hiraoka, N., B. Petryniak, J. Nakayama, S. Tsuboi, M. Suzuki, J.C. Yeh, D. Izawa, T. Tanaka, M. Miyasaka, J.B. Lowe, and M. Fukuda. 1999. A novel, high endothelial venule-specific sulfotransferase expresses 6-sulfo sialyl Lewis(x), an L-selectin ligand displayed by CD34. Immunity 11: 79–89.PubMedCrossRef
38.
Zurück zum Zitat Mori, R., T. Kondo, T. Nishima, and M. Asano. 2004. Impairment of skin wound healing in β1,4-galactosyltransferase-deficient mice with reduced leukocyte recruitment. American Journal of Pathology 164: 1303–1314.PubMedCrossRef Mori, R., T. Kondo, T. Nishima, and M. Asano. 2004. Impairment of skin wound healing in β1,4-galactosyltransferase-deficient mice with reduced leukocyte recruitment. American Journal of Pathology 164: 1303–1314.PubMedCrossRef
39.
Zurück zum Zitat Alon, R., and S. Feigelson. 2002. From rolling to arrest on blood vessels: leukocyte tap dancing on endothelial integrin ligands and chemokines at sub-second contacts. Seminars in Immunology 14: 93–104.PubMedCrossRef Alon, R., and S. Feigelson. 2002. From rolling to arrest on blood vessels: leukocyte tap dancing on endothelial integrin ligands and chemokines at sub-second contacts. Seminars in Immunology 14: 93–104.PubMedCrossRef
40.
Zurück zum Zitat Engelhardt, B., D. Vestweber, R. Hallmann, and M. Schulz. 1997. E- and P-selectin are not involved in the recruitment of inflammatory cells across the blood-brain barrier in experimental autoimmune encephalomyelitis. Blood 90: 4459–4472.PubMed Engelhardt, B., D. Vestweber, R. Hallmann, and M. Schulz. 1997. E- and P-selectin are not involved in the recruitment of inflammatory cells across the blood-brain barrier in experimental autoimmune encephalomyelitis. Blood 90: 4459–4472.PubMed
Metadaten
Titel
Elevated Expression of β1,4-Galactosyltransferase-I in Cartilage and Synovial Tissue of Patients with Osteoarthritis
verfasst von
Wei Liu
Zhiming Cui
Youhua Wang
Xinhui Zhu
Jianbo Fan
Guofeng Bao
Junjun Qiu
Dawei Xu
Publikationsdatum
01.04.2012
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 2/2012
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-011-9357-x

Weitere Artikel der Ausgabe 2/2012

Inflammation 2/2012 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Notfall-TEP der Hüfte ist auch bei 90-Jährigen machbar

26.04.2024 Hüft-TEP Nachrichten

Ob bei einer Notfalloperation nach Schenkelhalsfraktur eine Hemiarthroplastik oder eine totale Endoprothese (TEP) eingebaut wird, sollte nicht allein vom Alter der Patientinnen und Patienten abhängen. Auch über 90-Jährige können von der TEP profitieren.

Niedriger diastolischer Blutdruck erhöht Risiko für schwere kardiovaskuläre Komplikationen

25.04.2024 Hypotonie Nachrichten

Wenn unter einer medikamentösen Hochdrucktherapie der diastolische Blutdruck in den Keller geht, steigt das Risiko für schwere kardiovaskuläre Ereignisse: Darauf deutet eine Sekundäranalyse der SPRINT-Studie hin.

Bei schweren Reaktionen auf Insektenstiche empfiehlt sich eine spezifische Immuntherapie

Insektenstiche sind bei Erwachsenen die häufigsten Auslöser einer Anaphylaxie. Einen wirksamen Schutz vor schweren anaphylaktischen Reaktionen bietet die allergenspezifische Immuntherapie. Jedoch kommt sie noch viel zu selten zum Einsatz.

Therapiestart mit Blutdrucksenkern erhöht Frakturrisiko

25.04.2024 Hypertonie Nachrichten

Beginnen ältere Männer im Pflegeheim eine Antihypertensiva-Therapie, dann ist die Frakturrate in den folgenden 30 Tagen mehr als verdoppelt. Besonders häufig stürzen Demenzkranke und Männer, die erstmals Blutdrucksenker nehmen. Dafür spricht eine Analyse unter US-Veteranen.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.