Keloid Therapy Research Articles

The deubiquitinating enzyme USP37 promotes keloid fibroblasts proliferation and collagen production by regulating the c-Myc expression.

Previous research testifies that c-Myc may promote keloid fibroblast proliferation and collagen accumulation. Ubiquitin-specific peptidase 37 (USP37)-mediated deubiquitination and stabilisation of c-Myc are vital for lung cancer proliferation, while the potential role of USP37 in keloid fibroblasts is not investigated. Elevated USP37, c-Myc, and Collagen I content were detected in keloid tissue with RT-PCR or ELISA assay. USP37 over-expression plasmids or USP37 short hairpin RNAs (shRNAs) were transfected into keloid fibroblasts with Lipofectamine 3000 to decipher the role of USP37 in keloid fibroblasts. USP37 overexpression could promote the proliferation of keloid fibroblasts with increased c-Myc and Collagen I expression. On the other hand, USP37 shRNAs inhibited the proliferation of keloid fibroblasts with diminished c-Myc and Collagen I expression. It was worth noting that C-Myc overexpression promoted the proliferation of keloid fibroblasts inhibited by USP37 shRNAs with increasing Collagen I expression. All of these results demonstrate that USP37 could regulate c-Myc to promote the proliferation and collagen deposit of keloid fibroblasts, and USP37 could be targeted in future keloid therapy.

Retrospective Study on the Effect of Adipose-Derived Stem Cells on the Proliferation and Apoptosis of Keloid Fibroblasts Through the Suppression of ITGA2.

Keloid is characterized by excessive collagen accumulation and fibroblast growth, which are fibroproliferative disorders of injured skin, causing functional limitations. Studies have shown that adipose-derived stem cells (ADSCs) inhibit the bioactivity and fibrosis of keloid fibroblasts. However, the molecular mechanism of this effect of ADSCs on keloid formation has not been fully elucidated. This in vitro study used fibroblasts obtained from keloids. A consensus gene co-expression network was constructed to focus on identifying consensus gene co-expression modules associated with keloid fibroblasts. Differentially expressed genes (DEGs) were identified between keloid fibroblasts and normal dermal fibroblasts. A functional enrichment analysis was also performed with the DAVID database. A weighted gene co-expression network analysis (WGCNA) was used to screen keloid-related modules using the "WGCNA" R package, followed by hub gene selection in modules from the Protein-protein interaction network through the STRING database. Keloid fibroblasts and ADSCs were extracted and cultured. Proliferation and apoptosis were examined using a 5-ethynyl-2-deoxyuridine (Edu) kit and flow cytometry. We identified 302 DEGs overlapping with a consensus analysis of clusters and a differential expression analysis between keloid fibroblasts and normal dermal fibroblasts. Most of these were involved in collagen binding, extracellular matrix organization, and the PI3K-Akt signaling pathway. WGCNA analysis selected a keloid-associated brown module. ITGA2 was identified as a novel marker in hub genes from the PPI network based on the degree and function of collagen modulation. Furthermore, the proliferation ability of keloid fibroblasts cultured in ADSC medium was inhibited while apoptosis was dramatically increased. Overexpression of ITGA2 reversed the decrease in ADSC-induced apoptosis and increased ADSC-reduced proliferation. Our study demonstrated that activation of ITGA2 plays a crucial role in ADSC-induced keloid fibroblast apoptosis and anti-proliferation effects. These results also improved our understanding of the molecular mechanism of the pathogenesis of keloid in response to ADSCs and may contribute to the further development of keloid therapy.

Keloid therapy: A neoteric comparative study.

Keloids are considered disorders of fibroproliferation characterized by accumulation of collagen fibers in hypodermis and dermis, caused by inflammation, surgery, and trauma. The main goal of the study was to approach a better modality for the treatment of keloids by comparing the effects and the side effects of intralesional cryotherapy and intralesional injection of bleomycin. This interventional, comparative clinical trial was conducted on 60 cases and was divided equally into the group (A), combined group who were subjected to intralesional bleomycin followed by cryotherapy in the same session, group (B) who were subjected to intralesional injection of bleomycin, and group (C) intralesional cryotherapy. All cases were subjected to clinical examination, complete history taking, dermatological examination, examination, and evaluation of scar lesion using the Vancouver scar scale. There was a statistically significant decrease in pliability among the combined group. Also, pliability decreased in the bleomycin group and cryotherapy, but this decrease wasn't statistically significant. Our results revealed that there was a statistically significant decrease in lesion height among all the studied groups, but the decrease was more among the combined group. Intralesional cryotherapy was effective as intralesional bleomycin. Combined therapy was a valid and more effective technique with few adverse effects than either alone for keloids as it achieved a decrease in volumes of scars or accompanied symptoms.

Targeting the Akt/PI3K/mTOR signaling pathway for complete eradication of keloid disease by sunitinib

Keloid disease is a nodular lesion, tumor-like but not cancerous, and characterized of excessive proliferation of fibroblasts and deposition of extracellular matrix (ECM) components. This condition often causes itching, pain and cosmetic disfigurement, significantly reducing patient quality of life. To date, no universally effective therapies are available, possibly due to inadequate understanding of keloid pathogenesis. As an oral small-molecule inhibitor of certain tyrosine kinase receptors, sunitinib has shown significant therapeutic effects in renal cell carcinoma (RCC) and gastrointestinal stromal tumor (GIST). However, it has never been tested if keloid therapy can be effective for the management of keloids. This study thus aims to explore the potential of sunitinib for keloid treatment. Keloid-derived fibroblasts (KFs) were successfully isolated and demonstrated proliferative advantage to normal skin-derived fibroblasts (NFs). Additionally, sunitinib showed specific cytotoxicity and inhibition of invasion, and induced cell cycle arrest and significant apoptosis in KFs. These effects were accompanied by complete suppression of ECM component expression, including collagen types 1 and 3, upregulation of autophagy-associated LC3B and significant suppression of the Akt/PI3K/mTOR pathway. Moreover, a keloid explant culture model was successfully established and used to test the therapeutic efficacy of sunitinib on keloid formation in nude mice. Sunitinib was found to induce complete regression of keloid explant fragments in nude mice, showing significantly higher therapeutic efficacy than the most commonly used intralesional drug triamcinolone acetonide (TAC). These data suggest that sunitinib effectively inhibits keloid development through suppression of the Akt/PI3K/mTOR pathway and thus can be potentially developed as a monotherapy or combination therapy for the effective treatment of keloid disease.

Hydration and hypoxic-occlusion therapy (gel-wrap treatment) for hypertrophic scars and keloids

Keloids and hypertrophic scars are pathological fibroproliferative disorders characterized by excessive collagen deposition. The affected skin becomes raised and thickened, forming firm pink or red plaques. Common causes include trauma, burn, and surgery. Multiple studies on keloids and hypertrophic scars have been reported previously, leading to the development of various therapeutic approaches for them, most of which remain clinically unsatisfactory. In this study, three patients underwent the gel-wrap treatment: the gel (manufactured by ITO Co Ltd.) was applied to the lesion and the affected skin was wrapped with a polyvinylidene chloride film (Saran Wrap; Asahi Kasei Corporation). Satisfactory results were noted in all three cases. The gel-wrap treatment is more convenient and inexpensive than existing therapeutic approaches. Furthermore, reducing thymic stromal lymphopoietin seems crucial for the treatment of keloids and hypertrophic scars.

TSP1 promotes fibroblast proliferation and extracellular matrix deposition via the IL6/JAK2/STAT3 signalling pathway in keloids.

Keloids are benign fibroproliferative diseases with abnormally proliferated bulges beyond the edge of the skin lesions, and they are characterized by uncontrolled fibroblast proliferation and excessive extracellular matrix deposition in the dermis. However, the definite mechanisms that increase fibroblast proliferation and collagen deposition in keloids remain unclear. Thrombospondin 1 (TSP1) has been suggested to play an important role in wound healing and fibrotic disorders, but its role in keloids is unknown. In this study, we aimed to clarify the specific role of TSP1 in keloids and explore the potential mechanism. Our results demonstrated that TSP1 was highly expressed in keloid lesions compared to normal skin. Knockdown of TSP1 in keloid fibroblasts decreased cell proliferation and collagen I deposition. Exogenous TSP1 treatment increased cell proliferation and collagen I deposition in normal fibroblasts. We further investigated the underlying mechanism and found that TSP1 promoted fibroblast proliferation and extracellular matrix deposition by upregulating the IL6/JAK2/STAT3 pathway. Moreover, we verified that TSP1 expression was positively correlated with IL6/STAT3 signalling activity in keloids. Taken together, our findings indicate that TSP1 promotes keloid development via the IL6/JAK2/STAT3 signalling pathway and blocking TSP1 may represent a potential strategy for keloid therapy.

The Inhibition of Adipose-Derived Stem Cells on the Invasion of Keloid Fibroblasts.

Background: Keloids represent the dysregulation of cutaneous wound healing caused by aberrant fibroblast activities. Adipose-derived stem cells have been recognized as a promising treatment for keloids. However, the molecular mechanisms have not been fully elucidated.Objectives: to explicitly demonstrate the relationship between adipose-derived stem cells alleviating keloids and alterations of Col-1, Col-3, CTGF, and P-4-HB.Methods: Skin biopsies were obtained from 10 keloid patients and 9 healthy volunteers. Fibroblasts isolated from all samples were divided into two groups, one co-cultured with adipose-derived stem cells and the other grown independently. We compared the wound-healing rates, fibroblast survival rates, apoptosis rates, mRNA expressions, and protein levels of Col-1, Col-3, CTGF, and P-4-HB between separated groups.Results: We found no significant differences between normal fibroblasts and keloid fibroblasts in terms of wound-healing rate, survival rate, or apoptosis rate at the baseline. With adipose-derived stem cells, wound-healing rate and survival rate of normal fibroblasts were promoted, whereas in keloid fibroblasts, they were reduced. The apoptosis rate of normal fibroblasts and keloid fibroblasts were restrained, with the restraint in keloid fibroblasts being more evident. The protein levels of Col-3, CTGF, and P-4-HB were lower in keloid fibroblasts co-cultured with adipose-derived stem cells than in normal fibroblasts under similar conditions.Conclusions: Adipose-derived stem cells strongly suppressed keloid fibroblasts' proliferative and invasive behavior. However, adipose-derived stem cells negatively regulated keloid fibroblast apoptosis. Adipose-derived stem cells can be a potential keloid therapy worth further investigation.

Keloid Excision with Debulking Technique on the Lobule Auricle Sinistra

Introduction: Keloids are fibroproliferative lesions caused by abnormal wound healing and are characterized by excessive collagen deposits that cannot heal spontaneously. Keloid in the ear is a challenging condition to be treated by doctors, especially the large ones. This condition has a psychosocial impact on the patient and a consideration for appearance is often the main reason for patients seeking to cure keloids, although there is a high possibility of keloid recurrence. Out of various keloid therapy options, one method that can be done is surgical excision therapy with debulking technique. Case report: A case of keloids in left ear lobule measuring 2.5 cm × 3 cm is reported after the patient does ear piercing with complaints of slight itch and aesthetical disturbance. Keloids enlarge 6 months after piercing. The case is treated by debulking excision surgery using local anesthesia Pehacain® (lidocaine 2% + adrenaline 1:80,000). At the end of the wound closure, 40 mg of triamcinolone acetone is given. It is regiven one week after the stitches are removed and repeatedly every 2 weeks for 4 times. Excision surgical results are good and the patient feels satisfied. Conclusion: Excision surgery with debulking technique is chosen because of the large size of the lesion and to ensure there is no residual keloid tissue at the site of predilection. Corticosteroid injection is given immediately after excision to decrease fibroblast proliferation, collagen and glycosaminoglycan synthesis and suppress proinflammatory mediators in order to prevent keloid recurrence.

Genetics and Epigenetics of Keloids.

Significance: Keloid scarring is cosmetically disfiguring, psychosocially distressing, and can be physically disabling. The pathophysiology of keloid formation is poorly understood and subsequently, treatment options are ill defined, limited, and largely unsatisfactory. Therefore, in view of its unsatisfactory and recalcitrant management, keloid therapy is often seen as a financial burden affecting both patients and the health care systems. Recent Advances: Increased research on the genetic and epigenetic mechanisms in keloids has broadened our understanding of keloid pathobiology. Epigenetic mechanisms, mainly DNA methylation, histone modification, and noncoding RNAs, are currently being widely investigated. Advances in genetic sequencing technology and reduced cost have aided this endeavor. Studies on blood and patient-derived keloid tissue are being done with therapeutic agents targeting epigenetic and genetic markers with the shared goal of identifying the pathways underlying the initiation and maintenance of keloids. These advances have informed us of multiple complex molecular pathways implicated in keloids, which are yet to be fully elucidated. Critical Issues: Improved understanding of the genetic and epigenetic causes implicated in keloids will enhance our knowledge of this enigmatic disorder and likely lead to the development of therapeutic targets based on the available clinical and experimental studies. Due to the incomplete knowledge of molecular targets involved in keloid scarring pathways, therapeutics is still lagging for this clinically and scientifically important condition. Future Directions: Focused research on the identification of molecular targets and mechanistic pathways implicated in keloids is required to generate novel antifibrotic therapeutic options to decrease or eradicate recurrence of the disease as well as associated morbidity and improve the quality of life of those affected with keloids.

The Role of Interleukin 10 in Keloid Therapy: A Literature Review.

Keloids are pathological wound healing responses to dermal injuries. These scars may lead to considerable morbidity, but treatments remain challenging for physicians. Interleukin 10 (IL-10), a potent anti-inflammatory cytokine, plays a prominent role in fetal scarless regenerative healing; therefore, it may become a more targeted and effective therapy for keloids. This review aimed to obtain an overview of the background of keloid and IL-10 functions as its promising forthcoming treatment. Studies were sought from Pubmed, ScienceDirect, PLOS, and Clinical Key. Keywords are interleukin 10, keloid, and wound healing as Medical Subject Headings terms. Keloids and fetal scarless healing represent 2 opposing ends of the tissue repair spectrum. Promising multiple animal models have demonstrated successful regenerative healing promotion through IL-10 overexpression by its ability to minimize inflammatory wound microenvironment, downregulate transforming growth factor β/SMAD signaling pathway, increase extracellular matrix breakdown, and regulate extracellular matrix. These results have led to the development of clinical trials investigating human recombinant IL-10. Interleukin 10 has the potential to become a more targeted and promising therapy of keloids owing to its pleiotropic effects.

Targeted inhibition of YAP/TAZ alters the biological behaviours of keloid fibroblasts.

Abnormal activation of fibroblasts plays a crucial role in keloid development. However, the mechanism of fibroblast activation remains to be determined. YAP/TAZ are key molecules in the Hippo signalling pathway that promote cell proliferation and inhibit apoptosis. Here, we show that keloid fibroblasts have higher levels of YAP/TAZ mRNA and proteins on primary culture. Targeted knockdown of endogenous YAP or TAZ significantly inhibited cell proliferation, reduced cell migration, induced cell apoptosis and down-regulated collagen1a1 production by keloid fibroblasts. Moreover, we demonstrate that verteporfin, an inhibitor of YAP/TAZ, has similar but stronger inhibitory effects on fibroblasts compared to YAP/TAZ knockdown. Our study provides evidence that YAP/TAZ may be involved in the pathogenesis of keloids. Targeted inhibition of YAP/TAZ could change the biological behaviours of fibroblasts and can potentially be used as therapy for keloids.

Treatment of Keloids Using Plasma Skin Regeneration Combined with Radiation Therapy Under the Evaluation of Patient and Observer Scar Assessment Scale.

PurposeKeloids are caused by uncontrolled excessive proliferation of fibrous tissue. Multiple treatment strategies including steroid injection, surgical excision, laser therapy and radiation therapy have been reported. Few studies have evaluated the performance of plasma skin regeneration (PSR) in the treatment of keloid. This study aimed to evaluate the effectiveness of PSR combined with radiation therapy for keloids on different body parts.Patients and MethodsA total of 71 patients with 98 keloids were enrolled in this study. Keloids <4 mm thick underwent single-dose PSR, while keloids ≥4 mm thick were administered compound betamethasone injection beforehand. Radiation therapy was administered after 24 hours and again 7 days later after PSR. The outcome was evaluated using the patient and observer scar assessment scale at 12 months post-treatment.ResultsPatient-reported average scores for all keloids significantly decreased from 35.05±9.94 to 21.84±7.04 (p < 0.05). Keloids on face and neck, chest, and back responded better than those on shoulders and limbs. The recurrence rate was observed to be 15.3% (15 out of 98). Adverse effects were mild.ConclusionPSR combined with radiation therapy is an effective and safe strategy to treat keloids. Location could be a factor that affects curative effects.

The Effectiveness of Depigmentation, Interleukin-1B, and Transforming Growth Factor-B Antibodies in Activating and Increasing Collagenase in Keloid as Adjuvant Therapy After Scar Excision

Background: Keloid is an abnormal scar in previously traumatic skin after going through the wound healing process. One hundred million cases have been found in developing countries with the main complaint of scar appearances. To overcome this problem, 24 literatures from various journals and textbooks are reviewed. Reviews: Keloid formation is based on high melanin amount which inhibits the collagenase enzyme. Moreover, the high melanin amount would block interleukin (IL)-1B work resulting in collagen synthesis and collagenase reduction. Depigmentation effort with 4% hydroquinone is implemented to reduce the amount of melanin presented in the skin. With melanin reduction, IL-1B can work optimally by inhibiting fibroblast growth in keloid tissue without affecting on normal skin. It also induces Matrix Metalloproteinase (MMP)-1 which is an interstitial collagenase. IL-1B has an opposing effect compared to Transforming Growth Factor (TGF)-B, thus TGF-B antibody is needed to potentiate IL-1B therapeutic effect. TGF-B antibody can neutralize TGF-B ligand and avB6 integrin resulting in blocking of COL1A1 gene expression which is responsible for MMP-1 production and type-I collagen synthesis. These three components are combined in cream with liposome as a drug carrier. This combination is applicated for adjuvant therapy after scar excision. Liposomes are chosen because of their high biocompatibility, low toxicity, and low biodegradability. Liposomes also can release slowly in the extravascular area such as skin. This advantage may carry drug components effectively to the target location. Summary: The combination of depigmentation, IL-1B, and TGF-B antibodies has a potency to be developed as a future adjuvant therapy of keloid.

Combined versus single treatment regimens for keloid therapy using serial intralesional corticosteroid injections, surgical excision, silicone- and/or cryotherapy

Efficacy comparison of several regimens in treating keloids as combined or standalone therapies could provide essential information for selecting appropriate therapy. This study retrospectively evaluated the treatment efficacy of corticosteroid injections, excision, silicone, cryotherapy, or combinations of these for treating keloids. Additionally, the use of corticosteroid injection schemes and combined cryotherapy regimens were analysed.Retrospective chart analysis was performed on 204 keloids treated patients at the plastic surgery department of the Máxima Medical Centre between 2009 and 2018. The patient's age, gender, treatment, anatomic location, scar aetiology, previous therapy, scar recurrence, additional therapy, and follow-up duration were retrieved. Treatment efficacy was assessed through treatment failure, defined by the recurrence or lack of response. Kaplan–Meier and Cox survival analyses were performed to compare treatment efficacy between the different regimens.Monotherapies exhibited a significantly higher chance of treatment failure (HR 2.4, 95% CI 1.4–4.2, p<0.05) when compared to combined therapies.Sporadic corticosteroid injections demonstrated more treatment failure overall (HR 3.5 95% CI 1,6–7,3; p=0.001), but did not differ significantly from injection schemes.Combined cryotherapy efficacy did not differ significantly from the other combined regimens (HR 1,6 95% CI 0,5–5,1; p=0.401).Combined therapies exhibited clear superiority over monotherapies. Sporadic corticosteroid injections demonstrated inferior results compared to all other therapies. Combined cryotherapy cases were insufficient, and more data are required for proper assessment. Future prospective assessments of corticosteroid injection schemes and combined regimens are warranted.

Keloid after orthopedic surgery: prevention, current therapy modalities, and emerging therapies modalities

Keloid is a benign fibroproliferative tissue growth that exceeds the initial wound margins. It is caused by the disruption in the wound healing phase with increased fibroblast activity and excess collagen deposition. Keloid usually develops after tissue trauma. Orthopedic surgery inevitably causes tissue trauma that will lead to the formation of keloids in a few patients. Keloids can cause cosmetic and functional problems, thus interfere with a person's quality of life. Keloid therapy modalities are mainly divided into three, which are prophylactic therapy modalities, current therapy modalities, and emerging therapy modalities that are being developed. This literature review aims to evaluate further prevention, current therapy modalities, and emerging therapies modalities in Keloid following orthopedic surgery.

Laser Speckle Contrast Imaging for the Objective Assessment of Blood Perfusion in Keloids Treated With Dual-Wavelength Laser Therapy.

Most of the widely used methods for the assessment of keloid treatment are subjective grading scales based on the opinion of an individual clinician or patient. There is a growing need for objective methods to evaluate keloid treatment. This study aimed to evaluate the value of laser speckle contrast imaging (LSCI) as an objective method for the assessment of dual-wavelength laser therapy for keloids. This prospective study included 21 patients with 54 keloids. All patients were treated with a combined 585-nm pulsed dye laser and 1,064 nm neodymium-doped yttrium aluminum garnet dual-wavelength laser at 4 weeks to 6 weeks intervals. Keloids were assessed using the Vancouver Scar Scale (VSS) and LSCI. The total VSS score significantly decreased after 4 sessions of treatment (p < .05). Blood perfusion in keloids as measured by LSCI was significantly reduced after treatment (p < .05). The improvement of chest keloids in terms of the total VSS score and blood perfusion was significantly greater than that of scapular keloids (p < .05). There was a positive correlation between decreased perfusion and reduced total VSS score (R2 = 0.84). Blood perfusion in keloids significantly decreased after dual-wavelength laser therapy. Laser speckle contrast imaging is a promising objective method for assessing the improvement of keloids treated with laser therapy.

Identification of drug compounds for keloids and hypertrophic scars: drug discovery based on text mining and DeepPurpose.

BackgroundKeloids (KL) and hypertrophic scars (HS) are forms of abnormal cutaneous scarring characterized by excessive deposition of extracellular matrix and fibroblast proliferation. Currently, the efficacy of drug therapies for KL and HS is limited. The present study aimed to investigate new drug therapies for KL and HS by using computational methods.MethodsText mining and GeneCodis were used to mine genes closely related to KL and HS. Protein-protein interaction analysis was performed using Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and Cytoscape. The selection of drugs targeting the genes closely related to KL and HS was carried out using Pharmaprojects. Drug-target interaction prediction was performed using DeepPurpose, through which candidate drugs with the highest predicted binding affinity were finally obtained.ResultsOur analysis using text mining identified 69 KL- and HS-related genes. Gene enrichment analysis generated 25 genes, representing 7 pathways and 130 targeting drugs. DeepPurpose recommended 14 drugs as the final drug list, including 2 phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) inhibitors, 10 prostaglandin-endoperoxide synthase 2 (PTGS2) inhibitors and 2 vascular endothelial growth factor A (VEGFA) antagonists.ConclusionsDrug discovery using in silico text mining and DeepPurpose may be a powerful and effective way to identify drugs targeting the genes related to KL and HS.

Emerging and Novel Therapies for Keloids: A compendious review.

Keloids are abnormal fibroproliferative scars with aggressive dermal growth expanding beyond the borders of the original injury. Different therapeutic modalities, such as corticosteroids, surgical excision, topical silicone gel sheeting, laser therapy, cryotherapy, photodynamic therapy and radiotherapy, have been used to treat keloids; however, none of these modalities has proven completely effective. Recently, researchers have devised several promising anti-keloid therapies including anti-hypertensive pharmaceuticals, calcineurin inhibitors, electrical stimulation, mesenchymal stem cell therapy, microneedle physical contact and ribonucleic acid-based therapies. The present review summarises emerging and novel treatments for keloids. PubMed® (National Library of Medicine, Bethesda, Maryland, USA), EMBASE (Elsevier, Amsterdam, Netherlands) and Web of Science (Clarivate Analytics, Philadelphia, Pennsylvania, USA) were searched for relevant literature published between January 1987 to June 2020. A total of 118 articles were included in this review. A deeper understanding of the molecular mechanisms underlying keloid scarring pathogenesis would open further avenues for developing innovative treatments.

Combination Between Surgical Excision and Pressure Therapy for Ear Keloids in a Pediatric Population: Clinical Results

Introduction: A single effective therapeutic option for ear keloids has yet to be discovered. Many treatments have been studied with variable effectiveness, side effects and complications. Pressure therapy using custom molded clip is a non-invasive treatment with minimal side effects. In the present study, the recurrence rate of a treatment protocol combining excisional surgery and pressure therapy on ear keloids is being studied in a pediatric population. Materials and Methods: The charts of 22 consecutive patients treated between January 2008 and January 2019 were reviewed. All patients were under 18 years of age and clinically diagnosed with, at least, one keloid of the ear. They all underwent complete surgical excision with primary closure followed by early postoperative pressure therapy using custom molded clips. The collected data included patient age at time of diagnosis and surgery, sex, skin type, familial and personal history, etiology and anatomical location of the keloid, and recurrence. Patients or parents were interviewed by phone call and reviewed by an independent examiner to evaluate the current evolution of their scar (s). Results: 22 patients were included in the study, representing a total of 26 keloids of the ear. The male to female ratio was of 3:4. The mean age at diagnosis was 9.7 years old. The mean follow-up time was 5.2 years. Four ears needed a single corticoid injection in addition to the initial protocol. Follow-up observations showed a recurrence rate of 15.4%. Conclusion: Excisional surgery combined with pressure therapy is an effective and well-tolerated treatment for ear keloids in a pediatric population. Although residual symptoms are sometimes observed, it seems to be better tolerated than other, more invasive, therapies.

A comparative study of the effectiveness and safety of injectable combination therapy of keloid and hypertrophic scars with 5-fluorouracil and betamethasone

therapy for their reliable removal. Standard methods of treatment often give unpredictable results, are accompanied by various complications, and require the use of expensive equipment.&#x0D; AIM: To investigate the efficacy and safety of intralesional injection of a combination of 5-fluorouracil (5-FU) and betamethasone for the treatment of keloids and hypertrophic scars.&#x0D; MATERIALS AND METHODS: The study involved 26 patients who were divided into two equal groups. Patients in group A received intralesional injections of betamethasone, and those in group B received 5-FU and betamethasone. Three injections were performed with an interval of 3 weeks. The scars were assessed at the beginning of the treatment, on the 3rd and 6th week during the treatment, and 4 and 16 weeks after the end of the treatment. The dynamics of scar condition was evaluated by the average decrease in the scar height and density, changes in subjective sensations, and the presence or absence of complications.&#x0D; RESULTS: At 4 weeks after the end of the therapy, the total effectiveness of reducing the initial scar height was significantly higher in group B (10 patients; 76.9%) than in group A (6; 46.1%). In the comparison of long-term results at 16 weeks after treatment, 92.3% of the patients from group B and 53.8% of the patients from group A showed cessation of scar growth, flattening and softening, diminished itching and pain, smoothing of the scar contour, and a decrease in the color of the border between the scar and surrounding tissues.&#x0D; CONCLUSIONS: The combination of betamethasone with 5-FU is safer and more effective than monotherapy with betamethasone or 5-FU in the treatment of keloid and hypertrophic scars, with a faster and more pronounced decrease in the height and density of the scar, erythema, and subjective sensations. This mode of therapy is characterized by a low relapse rate with prolonged follow-up. The article is of interest to practicing cosmetologists, dermatologists, and plastic surgeons.