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      Effects and safety of triamcinolone acetonide-controlled common therapy in keloid treatment: a Bayesian network meta-analysis

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          Triamcinolone acetonide (TAC) is used frequently in the treatment of keloid scars, but has presented controversial results. In this study, we aim to evaluate the effectiveness of TAC compared with other common therapies used in keloid treatment.


          MEDLINE, Embase, Web of Science and the Cochrane Library databases were searched until January 2018. Key data were extracted from eligible randomized controlled trials. Both pairwise and network meta-analyses were conducted for synthesizing data from eligible studies.


          Ten randomized controlled trials were included in this meta-analysis. The relative risk of keloids associated with seven adjuvants was analyzed, including placebo, pulsed dye laser (PDL), 5-fluorouracil (5-FU), silicone, verapamil, TAC+5-FU and TAC+5-FU+PDL. Patients treated with the following adjuvants appeared to not have significantly reduced risk of keloid in relation to those treated with TAC: placebo (OR=1.86, 95% CI 1.12–2.61), PDL (OR=1.32, 95% CI 0.53–3.30), 5-FU (OR=1.13, 95% CI 0.48–2.68), silicone (OR=1.28, 95% CI 0.59–2.78), verapamil (OR=1.86, 95% CI 0.67–5.14), TAC+5-FU (OR=0.77, 95% CI 0.38–1.58) and TAC+5-FU+PDL (OR=0.80, 95% CI 0.16–4.03). The surface under the cumulative ranking curve values for each adjuvant were as follows: TAC, 59.9%; placebo, 17.4%; PDL, 46.3%; 5-FU, 48.9%; silicone, 56.2%; verapamil, 84.7%; TAC+5-FU, 68.5% and TAC+5-FU+PDL, 18.1%.


          There were no differences between the efficacy of TAC and other common therapies in keloid treatment. TAC also acts as an effective alternative modality in the prevention and treatment of keloids. Incorporating adjuvants particularly verapamil appeared to be significantly associated with a decreased risk of keloids.

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          Most cited references 31

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          Wound healing: an overview of acute, fibrotic and delayed healing.

          Acute wounds normally heal in a very orderly and efficient manner characterized by four distinct, but overlapping phases: hemostasis, inflammation, proliferation and remodeling. Specific biological markers characterize healing of acute wounds. Likewise, unique biologic markers also characterize pathologic responses resulting in fibrosis and chronic non-healing ulcers. This review describes the major biological processes associated with both normal and pathologic healing. The normal healing response begins the moment the tissue is injured. As the blood components spill into the site of injury, the platelets come into contact with exposed collagen and other elements of the extracellular matrix. This contact triggers the platelets to release clotting factors as well as essential growth factors and cytokines such as platelet-derived growth factor (PDGF) and transforming growth factor beta (TGF-beta). Following hemostasis, the neutrophils then enter the wound site and begin the critical task of phagocytosis to remove foreign materials, bacteria and damaged tissue. As part of this inflammatory phase, the macrophages appear and continue the process of phagocytosis as well as releasing more PDGF and TGF beta. Once the wound site is cleaned out, fibroblasts migrate in to begin the proliferative phase and deposit new extracellular matrix. The new collagen matrix then becomes cross-linked and organized during the final remodeling phase. In order for this efficient and highly controlled repair process to take place, there are numerous cell-signaling events that are required. In pathologic conditions such as non-healing pressure ulcers, this efficient and orderly process is lost and the ulcers are locked into a state of chronic inflammation characterized by abundant neutrophil infiltration with associated reactive oxygen species and destructive enzymes. Healing proceeds only after the inflammation is controlled. On the opposite end of the spectrum, fibrosis is characterized by excessive matrix deposition and reduced remodeling. Often fibrotic lesions are associated with increased densities of mast cells. By understanding the functional relationships of these biological processes of normal compared to abnormal wound healing, hopefully new strategies can be designed to treat the pathological conditions.
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                Author and article information

                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                29 May 2018
                : 14
                : 973-980
                [1 ]Department of Aesthetic Plastic and Burn Surgery, West China Hospital, Sichuan University, Chengdu, People’s Republic of China
                [2 ]Department of Pancreatic Surgery, West China Hospital, Sichuan University, Chengdu, People’s Republic of China
                Author notes
                Correspondence: Zhengyong Li, Department of Aesthetic Plastic and Burn Surgery, West China Hospital, Sichuan University, No 37 Guo Xue Xiang, Wuhou, 610041 Chengdu, Sichuan, People’s Republic of China, Tel +86 156 2905 4695, Email 15629054695m@ 123456sina.cn
                © 2018 Zhang et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Original Research


                keloid, triamcinolone acetonide, randomized controlled trial, network meta-analysis


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