Comparative effect and safety of verapamil in keloid and hypertrophic scar treatment: a meta-analysis

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Abstract

Background

Keloids and hypertrophic scars are the most common types of pathological scarring. Traditionally, keloids have been considered as a result of aberrant wound healing, involving excessive fibroblast participation that is characterized by hyalinized collagen bundles. However, the usefulness of this characterization has been questioned. In recent years, studies have reported the appropriate use of verapamil for keloids and hypertrophic scars.

Methods

Searches were conducted on the databases Medline, Embase, Cochrane, PubMed, and China National Knowledge Infrastructure from 2006 to July 2016. State12.0 was used for literature review, data extraction, and meta-analysis. Treatment groups were divided into verapamil and nonverapamil group. Nonverapamil group includes steroids and intense pulsed light (IPL) therapy. Total effective rates include cure rate and effective rate. Cure: skin lesions were completely flattened, became soft and symptoms disappeared. Efficacy: skin lesions subsided, patient significantly reduced symptoms. Inefficient definition of skin was progression free or became worse. Random-effects model was used for the meta-analysis.

Results

Six studies that included 331 patients with keloids and hypertrophic scars were analyzed. Analysis of the total effective rate of skin healing was performed. The total effective rates in the two groups were 54.07% (verapamil) and 53.18% (nonverapamil), respectively. The meta-analysis showed that there was no difference between the two groups. We also compared the adverse reactions between the verapamil treatment group and the steroids treatment group in two studies, and the result indicated that the verapamil group showed less adverse reactions.

Conclusion

There were no differences between the application of verapamil and nonverapamil group in keloids and hypertrophic scars treatment. Verapamil could act as an effective alternative modality in the prevention and treatment of keloid and hypertrophic scars. A larger number of studies are required to confirm our conclusion.

Most cited references 40

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

Robert F. Diegelmann, Melissa Evans (2004)

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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The most current algorithms for the treatment and prevention of hypertrophic scars and keloids.

Rei Ogawa (2010)

Previous reports on the treatment of hypertrophic scars and keloids have not described clear algorithms for multimodal therapies. This article presents an evidence-based review of previous articles and proposes algorithms for the treatment and prevention of hypertrophic scars and keloids. The methodologic quality of the clinical trials was evaluated, and the baseline characteristics of the patients and the interventions that were applied and their outcomes were extracted. Important factors that promote hypertrophic scar/keloid development include mechanical forces on the wound, wound infection, and foreign body reactions. For keloids, the treatment method that should be used depends on whether scar contractures (especially joint contractures) are present and whether the keloids are small and single, or large and multiple. Small and single keloids can be treated radically by surgery with adjuvant therapy (which includes radiation or corticosteroid injections) or by nonsurgical monotherapy (which includes corticosteroid injections, cryotherapy, laser, and antitumor/immunosuppressive agents such as 5-fluorouracil). Large and multiple keloids are difficult to treat radically and are currently only treatable by multimodal therapies that aim to relieve symptoms. After a sequence of treatments, long-term follow-up is recommended. Conservative therapies, which include gel sheeting, taping fixation, compression therapy, external and internal agents, and makeup (camouflage) therapy, should be administered on a case-by-case basis. The increase in the number of randomized controlled trials over the past decade has greatly improved scar management, although these studies suffer from various limitations. The hypertrophic scar/keloid treatment algorithms that are currently available are likely to be significantly improved by future high-quality clinical trials.

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Keloids and Hypertrophic Scars: Update and Future Directions

Chenyu Huang, George Murphy, Satoshi Akaishi … (2013)

Summary: The development of cutaneous pathological scars, namely, hypertrophic scars (HSs) and keloids, involves complex pathways, and the exact mechanisms by which they are initiated, evolved, and regulated remain to be fully elucidated. The generally held concepts that keloids and HSs represent “aberrant wound healing” or that they are “characterized by hyalinized collagen bundles” have done little to promote their accurate clinicopathological classification or to stimulate research into the specific causes of these scars and effective preventative therapies. To overcome this barrier, we review here the most recent findings regarding the pathology and pathogenesis of keloids and HSs. The aberrations of HSs and keloids in terms of the inflammation, proliferation, and remodeling phases of the wound healing process are described. In particular, the significant roles that the extracellular matrix and the epidermal and dermal layers of skin play in scar pathogenesis are examined. Finally, the current hypotheses of pathological scar etiology that should be tested by basic and clinical investigators are detailed. Therapies that have been found to be effective are described, including several that evolved directly from the aforementioned etiology hypotheses. A better understanding of pathological scar etiology and manifestations will improve the clinical and histopathological classification and treatment of these important lesions.

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Author and article information

Journal

Journal ID (nlm-ta): Ther Clin Risk Manag

Journal ID (iso-abbrev): Ther Clin Risk Manag

Journal ID (publisher-id): Therapeutics and Clinical Risk Management

Title: Therapeutics and Clinical Risk Management

Publisher: Dove Medical Press

ISSN (Print): 1176-6336

ISSN (Electronic): 1178-203X

Publication date Collection: 2016

Publication date (Electronic): 09 November 2016

Volume: 12

Pages: 1635-1641

Affiliations

Department of Dermatology, Yanbian University Affiliated hospital, Yanji, Jilin, People’s Republic of China

Author notes

Correspondence: Zhehu Jin, Department of Dermatology, Yanbian University Affiliated Hospital, 1327 Juzi Street, Yanji, Jilin 133000, People’s Republic of China, Tel +86 433 266 0009, Email huzejinjz@ 123456126.com

Article

Publisher ID: tcrm-12-1635

DOI: 10.2147/TCRM.S118748

PMC ID: 5108599

SO-VID: 5f9db8e8-874a-4a5f-913a-eb87b21a9fab

License:

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.

Comparative effect and safety of verapamil in keloid and hypertrophic scar treatment: a meta-analysis

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Abstract

Background

Methods

Results

Conclusion

Most cited references 40

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

The most current algorithms for the treatment and prevention of hypertrophic scars and keloids.

Keloids and Hypertrophic Scars: Update and Future Directions

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