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Intralesional vs. contact cryosurgery in treatment of keloids: a clinical and immunohistochemical study
Author(s) -
AbdelMeguid Azza M.,
Weshahy Ahmed Hany,
Sayed Doaa S.,
Refaiy Abeer E.M.,
Awad Sara M.I.
Publication year - 2015
Publication title -
international journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 93
eISSN - 1365-4632
pISSN - 0011-9059
DOI - 10.1111/ijd.12667
Subject(s) - cryosurgery , medicine , keloid , immunohistochemistry , tenascin , vascular endothelial growth factor , dermatology , cryotherapy , surgery , vegf receptors , pathology , extracellular matrix , fibronectin , biology , microbiology and biotechnology
Abstract Background Cryosurgery is a safe and effective treatment of keloids. Intralesional cryosurgery has been shown to bring about significant improvement in keloids. The histopathological and immunohistochemical changes in keloids following cryosurgery are not well‐assessed. Methods Twenty‐three patients with 66 keloids were treated with either the contact (cryoprobe) method or intralesional cryosurgery. Keloid specimens were obtained before treatment and after two sessions of treatment for evaluation of keloid pathology and immunohistochemical changes in expression of vascular endothelial growth factor ( VEGF ) and tenascin C induced by both cryosurgical techniques. Results A better therapeutic response was detected after intralesional cryosurgery (excellent response [ ER ], 87%) than contact cryosurgery ( ER , 60%; P  < 0.05). The intralesional technique achieved higher rates of flattening after the first two sessions ( ER in 61.3% and 22.9%, respectively; P  <   0.05) and caused fewer side effects compared with the contact method. Both cryosurgical methods resulted in a significant decrease in VEGF and tenascin C expression in keloids. Conclusions Intralesional cryosurgery is superior to contact cryosurgery in terms of efficacy and safety. Both techniques may have beneficial effects on keloids, at least partially, through the modulation of VEGF and tenascin C expression.

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