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BACKGROUND AND OBJECTIVE: Lasers have a favorable synergistic effect when combined with other modalities of treatment against keloids. Different types of lasers have been used with triamcinolone infiltration, resulting in promising success rates. The purpose of this study is to describe our first experience treating earlobe keloids with 980 nm laser diode excision followed by triamcinolone infiltration and present our outcomes after 24 months of follow-up. STUDY DESIGN/MATERIALS AND METHODS: A retrospective chart review of 11 patients with 14 earlobe keloids treated with excision using a 980 nm laser diode followed by triamcinolone acetonide infiltration, between January 2015 and May 2016. Database included demographics, Fitzpatrick skin type, laterality, lesion size, and postoperative visits information. Outcomes were assessed in terms of keloid recurrence rates, complications, and patient subjective aesthetical result satisfaction after 24 months of follow-up. RESULTS: All procedures were technically completed, and follow-up accomplished without attrition. One (7.14%) patient experienced keloid recurrence after the third month. Four (28.57%) patients experienced early wound dehiscence, successfully treated with debridement and re-suture. Self-assessment of aesthetical result was considered "very good" in 64.28% of patients. CONCLUSION: Surgical excision with 980 nm laser diode followed by triamcinolone infiltration is well-tolerated and shows favorable results treating earlobe keloids, and can be considered a first-line treatment. Comparison between different types of lasers and control groups in large clinical trials is warranted in order to obtain strong clinical evidence for clear indications and recommendations. Lasers Surg. Med. © 2020 Wiley Periodicals LLC.

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BACKGROUND:: A single, effective therapeutic regimen for keloids has not been established yet, and the development of novel therapeutic approaches is expected. Butyrate, a short-chain fatty acid, and docosahexaenoic acid (DHA), a ω-3 polyunsaturated fatty acid, play multiple anti-inflammatory and anticancer roles via their respective mechanisms of action. OBJECTIVE:: In this study, we evaluated the antifibrogenic effects of their single and combined use on keloid fibroblasts. METHODS:: Keloid fibroblasts were treated with butyrate (0-16 mM) and/or DHA (0-100 µM) for 48 or 96 h. RESULTS:: Butyrate inhibited cell proliferation, and α-smooth muscle actin (α-SMA) and type III collagen expressions, with inhibition of the transforming growth factor (TGF)-ß1 and TGF-ß type I receptor expressions and increased prostaglandin E2 with upregulation of cyclooxygenase-1 expression with induction of histone acetylation. DHA inhibited α-SMA, type III collagen, and TGF-ß type I receptor expressions. Then, the butyrate/DHA combination augmented the antifibrogenic effects, resulting in additional inhibition of α-SMA, type I and III collagen expressions, with strong disruption of stress fiber and apoptosis induction. Moreover, the butyrate/DHA combination inhibited the cyclooxygenase-2 expression, suggesting stronger anti-inflammatory effect than each monotherapy. STUDY LIMITATIONS:: Activation in keloid tissue is affected not only by fibroblasts but also by epithelial cells and immune cells. Evaluation of the effects by butyrate and DHA in these cells or in an in vivo study is required. CONCLUSION:: This study demonstrated that butyrate and docosahexaenoic acid have antifibrogenic effects on keloid fibroblasts and that these may exert therapeutic effects for keloid.

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The aim of this study was to evaluate the effect of intralesional tamoxifen on keloids, particularly on the concentration of fibroblasts, dermal inflammatory infiltrate, and collagen degeneration. A prospective study was carried out to evaluate keloids in 13 patients of both genders pre- and post-treatment with intralesional tamoxifen. Two samples of keloid lesions were obtained by 4-mm punch biopsies during the study: the first at the time of diagnostic confirmation of keloid and the other eight weeks later at the end of intralesional tamoxifen treatment. The biopsy samples were placed in 10% buffered formalin for HE staining and morphological and morphometric study. The degree of collagen fiber reduction and inflammatory infiltration were analyzed. Student's t-test was used for statistical analysis of the mean number of fibroblasts before and following tamoxifen treatment ( P < 0.05). The degree of collagen fiber reduction and inflammatory infiltration were absent before treatment and present in 100% of cases after treatment, while the mean number of fibroblasts was significantly lower after intralesional tamoxifen treatment ( P < 0.0001). We conclude that intralesional administration of tamoxifen promoted an inflammatory stimulus and collagen fiber reduction as well as a significant reduction in the number of fibroblasts that produce collagen. Impact statement Effective treatment of keloid that is a commonly recurrent dermatosis is very difficult, even after standard treatment. Standard treatment consists of partial resection of the lesion (shaving excision), in addition to local corticosteroid injection. Therefore, there is interest in alternative forms of topical treatment, e.g., selective estrogen receptor modulators, particularly tamoxifen has demonstrated in vitro studies to be a promising drug. Nevertheless, there is scarcity of publications on the effects of intralesional tamoxifen on keloids have been found, leading us to the conception of the present study. In this study, tamoxifen has proven to be an interesting alternative drug for the topical treatment of keloid, allowing us to conclude that the intralesional application of tamoxifen in keloids promotes a variable but ever-present inflammatory stimulus, associated with intense reduction of collagen fiber, in addition to a significant decrease in the number of fibroblasts that produce collagen and are involved in disease maintenance.

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Abstract: Background: A single, effective therapeutic regimen for keloids has not been established yet, and the development of novel therapeutic approaches is expected. Butyrate, a short-chain fatty acid, and docosahexaenoic acid (DHA), a ω-3 polyunsaturated fatty acid, play multiple anti-inflammatory and anticancer roles via their respective mechanisms of action. Objective: In this study, we evaluated the antifibrogenic effects of their single and combined use on keloid fibroblasts. Methods: Keloid fibroblasts were treated with butyrate (0-16 mM) and/or DHA (0-100 µM) for 48 or 96 h. Results: Butyrate inhibited cell proliferation, and α-smooth muscle actin (α-SMA) and type III collagen expressions, with inhibition of the transforming growth factor (TGF)-β1 and TGF-β type I receptor expressions and increased prostaglandin E2 with upregulation of cyclooxygenase-1 expression with induction of histone acetylation. DHA inhibited α-SMA, type III collagen, and TGF-β type I receptor expressions. Then, the butyrate/DHA combination augmented the antifibrogenic effects, resulting in additional inhibition of α-SMA, type I and III collagen expressions, with strong disruption of stress fiber and apoptosis induction. Moreover, the butyrate/DHA combination inhibited the cyclooxygenase-2 expression, suggesting stronger anti-inflammatory effect than each monotherapy. Study limitations: Activation in keloid tissue is affected not only by fibroblasts but also by epithelial cells and immune cells. Evaluation of the effects by butyrate and DHA in these cells or in an in vivo study is required. Conclusion: This study demonstrated that butyrate and docosahexaenoic acid have antifibrogenic effects on keloid fibroblasts and that these may exert therapeutic effects for keloid.

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BACKGROUND: The current treatment of keloids includes surgery, intralesional steroids, and radiotherapy, among others. Radiotherapy is not recommended in children due to its effects on growing tissues. Our aim was to study intralesional triamcinilone therapy of keloids in children and analyze the impact of body location, age of the lesion, and etiology of the keloid on clinical response. METHODS: We conducted a prospective clinical trial with patients 1 to 14 years of age evaluated for keloid treatment. A soft tissue ultrasound was performed to measure the keloid volume, prior to intralesional infiltration with triamcinolone acetonide. A posttreatment ultrasound quantified the volume differences attributed to therapy. For the analysis, Mann-Whitney/Wilcoxon test for paired samples and a multiple regression analysis were performed. RESULTS: Twenty-one patients with a total of 25 keloids were enrolled, with a median age of 12 years (range 6-14 yrs). The initial lesional volume was 1.25 cc (range 0.2-6.3 cc) and the final volume was 0.2 cc (range 0.0-1.53 cc), corresponding to 82.7% of size reduction (p < 0.001). Regarding the relationships between response and body location, etiology and age of the lesion, the multiple regression analyses obtained p-values of 0.46, 0.16, and 0.87, respectively. One patient failed to improve. Average follow-up was 30 months. CONCLUSIONS: Triamcinolone acetonide is highly effective for the treatment of pediatric keloids. There is no relationship between clinical response and the factors evaluated, such as lesion location, etiology and age of the keloid.

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OBJECTIVE: to assess the effects of injectable triamcinolone on keloid scars length, height and thickness, and on the number of cells undergoing apoptosis. METHODS: This study consists in a prospective, controlled, randomized, single-blinded clinical trial, conducted with fifteen patients with ear keloids divided into two groups: group 1 - seven patients undergoing keloid excisions, and group 2 - eight patients undergoing keloid excisions after three sessions of infiltration with one ml of Triamcinolone hexacetonide (20mg/ml) with three week intervals between them and between the last session and surgery. The two groups were homogeneous regarding age, gender and evolution of the keloid scar. The keloid scars of patients in group 2 were measured for the length, height and thickness before triamcinolone injection and before surgery. A blinded observer performed morphological detailing and quantification of cells in hematoxylin-eosin-stained surgical specimens. An apoptotic index was created. RESULTS: The apoptotic index in group 1 was 56.82, and in group 2, 68.55, showing no significant difference as for apoptosis (p=0.0971). The reduction in keloid dimensions in Group 2 was 10.12% in length (p=0.6598), 11.94% in height (p=0.4981) and 15.62% in thickness (p=0.4027). CONCLUSION: This study concluded that the infiltration of triamcinolone in keloid scars did not increase the number of apoptosit and did not reduce keloids' size, length, height or thickness.

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OBJECTIVE: To evaluate the combined treatment of ear lobe keloids. METHODS: We studied 46 consecutive patients with 81 ear lobe keloids. Patients underwent local infiltration of triamcinolone acetonide (TCN) at concentrations of 40 mg/ml (Group 1), 20 mg/ml (Group 2) and 10mg/ml (Group 3). The volume of TCN infiltrate varied according to the size of the lesion. Treatment consisted of three monthly injections before surgery, excision of keloid in the fourth month and perioperative infiltration, followed by two more leaks TCN within two months. Patients used earrings pressure on the scar after operation for four months. The pressure exerted by earrings in the ear lobe was measured electronically. Post-treatment follow-up of patients was 24 months. RESULTS: TCN at concentrations of 20mg/ml and 40 mg/ml were effective for the treatment of keloids, no difference between the groups (p = 0.58). However, patients in which TCN was infiltrated the 10mg/ml had poor involution of keloid and the study of this group was stopped. CONCLUSION: the combination of infiltration TCN month to 20 mg/mL (1.2mg to 2.0mg per mm3 TCN injury), surgical excision and pressure application device is effective for treatment of keloid ear lobe.

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While treatment of keloids and hypertrophic scars normally shows modest results, we found that treatment with bleomycin was more promising. The present study was divided into two parts. In the first part the aim was to show the results using a combination of bleomycin and triamcinolone acetonide per cm2 (BTA). In the second part the objective was to determine the response to both drugs in large keloids that were divided into 1 cm2 squares, treating each square with the dose previously used. In the first part of the study, the clinical response of 37 keloids ranging from 0.3 to 1.8 cm2 treated with BTA were followed up over a period of 1- 2 years. 0.375 IU bleomycin and 4 mg triamcinolone acetonide were injected every 3 months. In the second part of the study we reviewed the clinical response in six patients with large keloids. The monthly dose administered never exceeded 3 IU of bleomycin. The first study showed 36 keloids (97.29%) softening after the first dose. In the second study, 5 showed different responses (the response was complete in the four smaller keloids). The largest keloid needed 9 doses to achieve an improvement of 70%. In conclusion, combined treatment with 0.375 IU of bleomycin and 4mg of triamcinolone acetonide to 1 cm2 was considered to be an acceptable procedure for the treatment of keloids. The best results were obtained in keloids over 1 cm2 or when divided into 1 cm2 square areas. Larger series need to be performed in order to confirm these results..

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