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BACKGROUND: Keloids are benign proliferative scars that form as a result of dysregulated growth and collagen deposition in response to cutaneous injury. Laser therapies have emerged as promising options for the treatment of keloids, with performance varying by laser type and lesion characteristics. PURPOSE: To assess the combined continuous wave and repetitive fractionated CO2 laser treatment of keloids. METHODS: A retrospective chart review of 22 cases of keloid scars treated with combined CO2 laser modes. A single session of continuous wave followed by five sessions of fractional delivery. Efficacy was assessed using the Patient and Observer Scar Assessment Scale (POSAS) and the Vancouver Scar Scale. The Numeric Rating Scale was used to assess patient satisfaction and pain. RESULTS: Most patients were female (77.3%) with skin type IV (72.7%), age was 24.3 ± 9.3 years, most keloids were located on the earlobe (56.5%) or arm or hand (17.4%), size ranged from 5 to 10 cm, and time since injury ranged from 3 months to 35 years. No serious adverse events were reported. At 6 months, significant improvements from baseline occurred in all characteristics, scar color (4.8 ± 2.8 to 1.9 ± 1.1), rigidity (5.0 ± 2.8 vs. 5.4 ± 2.8), thickness (5.4 ± 2.8 vs. 2.0 ± 1.1), and irregularity (5.9 ± 2.4 vs. 1.9 ± 0.9). The Vancouver scores followed a similar trend. Patient-rated overall improvement from 37 ± 17.6 at baseline to 16.1 ± 8.5 at 6 months, and improvement in associated pain and pruritus. CONCLUSION: Combination of two ablative laser delivery modes within a single laser platform provided for effective and safe keloid management and left patients highly satisfied.

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Keloid is the maximum expression of pathological fibroproliferative skin wound healing, whose pathophysiology is not yet fully understood. Its occurrence in the perineum and genitalia is uncommon. A systematic review was carried out regarding the occurrence and treatment of keloids on the penis. An illustrative case was also reported. The review used the PRISMA checklist and was registered in PROSPERO. The entire literature period up to April 2023 was searched in the EMBASE/Elsevier, Cochrane, Scopus, Medline, BVS, SciELO, and Lilacs databases. The inclusion criteria embraced primary studies, clinical trials, prospective or retrospective cohorts, case series, case-control studies and case reports. Three hundred and sixty-one studies were found and 12 of them were included, consisting of 9 case reports and 3 case series. The most common triggering factor for keloid formation was circumcision, in 11 of the cases, of which more than half occurred in prepubescent children. Several therapies, associated or isolated, were used to treat the cases. Only one of the reported patients had scar recurrence after surgical treatment. Studies with better scientific evidence are needed to understand the involvement of keloids in male genitalia. However, keloid formation in this topography is rare, making it difficult to carry out more elaborate studies.

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SUMMARY: Keloid scar is a unique benign fibroproliferative tumor of the human skin. Previously, it was reported that early growth response 1 (EGR1), a transcription factor, promotes keloid fibrosis; however, the mechanism by which EGR1 modulates keloid formation was not elaborated. In this research, the specific function and the microRNA (miRNA) regulatory network of EGR1 in keloids was examined. Keloid fibroblasts (KFs) were transfected with EGR1-small interfering RNA (siEGR1), EGR1-overexpression plasmid (pcDNA3.1-EGR1), and microRNA (miR-183-5p)-mimics to regulate the expression of EGR1 and miR-183-5p. The study employed dual-luciferase reporter assays to explore the targeting regulation of miR-183-5p on EGR1. Additionally, Western blotting, flow cytometry, qRT-PCR, cell count kit-8 (CCK-8), transwell, and wound healing assays, and RNA sequencing were conducted. EGR1 was upregulated in KFs, and EGR1 silencing diminished proliferation, fibrosis, migration, invasion, and apoptosis of cells. In KFs, the expression of miR- 183-5p was reduced, leading to the inhibition of cell proliferation, migration, and invasion. Conversely, it enhanced apoptosis. By targeting EGR1, miR-183-5p partially counteracted the impact of EGR1 on migration, invasion, and fibrosis in KFs. The findings imply that miR-183-5p suppresses keloid formation by targeting EGR1. As a result, EGR1 holds promise as a potential therapeutic target for preventing and treating keloids.

La cicatriz queloide es un tumor fibroproliferativo benigno único de la piel humana. Anteriormente, se informó que la respuesta de crecimiento temprano 1 (EGR1), un factor de transcripción, promueve la fibrosis queloide; sin embargo, no se explicó el mecanismo por el cual EGR1 modula la formación de queloides. En esta investigación, se examinó la función específica y la red reguladora de microARN (miARN) de EGR1 en queloides. Se transfectaron fibroblastos queloides (KF) con ARN de interferencia pequeño de EGR1 (siEGR1), plásmido de sobreexpresión de EGR1 (pcDNA3.1-EGR1) y miméticos de microARN (miR-183-5p) para regular la expresión de EGR1 y miR-183. -5p. El estudio empleó ensayos de indicador de luciferasa dual para explorar la regulación dirigida de miR-183-5p en EGR1. Además, se realizaron pruebas de transferencia Western, citometría de flujo, qRT-PCR, kit de recuento celular-8 (CCK-8), transwell y curación de heridas, y secuenciación de ARN. EGR1 estaba regulado positivamente en KF, y el silenciamiento de EGR1 disminuyó la proliferación, fibrosis, migración, invasión y apoptosis de las células. En KF, la expresión de miR- 183-5p se redujo, lo que llevó a la inhibición de la proliferación, migración e invasión celular. Por el contrario, mejoró la apoptosis. Al apuntar a EGR1, miR-183-5p contrarrestó parcialmente el impacto de EGR1 en la migración, invasión y fibrosis en KF. Los hallazgos implican que miR-183-5p suprime la formación de queloides al apuntar a EGR1. Como resultado, EGR1 es prometedor como objetivo terapéutico potencial para prevenir y tratar los queloides.

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Keloidal or nodular scleroderma (NS) is a variant of localized scleroderma (LS) frequently seen in patients with limited or diffuse systemic sclerosis (SSc). It presents as raised, firm plaques or nodules with extensive dermal fibrosis and hyalinized collagen bundles. We present a patient with SSc who presented with this rare entity.

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Introdução: Com o passar dos anos a técnica de mamoplastia de aumento foi sendo aprimorada. Novos instrumentos para auxílio cirúrgico foram adicionados, incluindo o uso de afastadores luminosos para produção de túneis subcutâneos e descolamento subglandular ou retromuscular. Por essa técnica, em um só estágio, é possível obter o formato, volume e simetria adequada das mamas, assim como correção da flacidez abdominal, com cicatriz localizada apenas no abdome. Objetivo: Demonstrar a experiência do Serviço de Cirurgia Plástica do Hospital do Servidor Público Municipal de São Paulo com a técnica cirúrgica de inclusão dos implantes mamários através da dermolipectomia abdominal. Método: Foram selecionados prontuários de pacientes operadas entre março de 2011 e novembro de 2021 que foram submetidas à inclusão dos implantes mamários através da abdominoplastia. Resultados: A amostra deste estudo foi constituída por 24 pacientes do sexo feminino, com média de idade de 37,6 ± 8,1 anos, e IMC médio de 23,5 ± 2,0 kg/m2, todas submetidas à abdominoplastia concomitantemente ao aumento das mamas. Em média, foram colocadas próteses no volume de 293,5 ± 32,2 ml e o peso dos retalhos uma média de 734,2 ± 320,0 g. A duração média das cirurgias foi de 205,9 ± 34 minutos. Avaliando as complicações relacionadas aos procedimentos, deiscência associada à cicatriz hipertrófica foi observada em 3 pacientes (12,5%), contratura capsular em 3 (12,5%), formação de queloide em 2 (8%), ruptura de prótese em 1 (4%), granuloma na cicatriz em 1 (4%), seroma em 1 (4%), e rippling associado à ptose de grau I em 1 (4%). Conclusão: Este levantamento pontual demonstrou que a inclusão dos implantes mamários através da dermolipectomia abdominal traz excelentes resultados, eliminando as cicatrizes mamárias e com baixa taxa de complicações. Palavras-chave: Cirurgia plástica. Implantes de mama. Mamoplastia. Abdominoplastia. Procedimentos de Cirurgia Plástica.

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Keloids and hypertrophic scars are abnormal responses to wound-healing. While hypertrophic scars remain limited to the areas of trauma, keloids most often develop over several years, growing out from the limits of the initial wound area. Both lesions may cause itching, burning, and pain, and they may lead to significant impairment of self-esteem, socialization, and quality of life. Although they might be observed in all races, they are far more common in Africans and African descendants than in Caucasians.We extensively reviewed their treatment, including compression with pressure garments, occlusion with siliconized and non-siliconized gel sheets, gels, corticosteroid and antineoplastic injections, and the use of lasers and intense pulsed light (IPL) therapy. We also reviewed new therapies, including botulinum toxin injection, and addressed outcomes of various studies. (SKINmed. 2022;20:432-443).

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Fibrosis is a common pathophysiological response of many tissues and organs subjected to chronic injury. Despite the diverse aetiology of keloid, lacaziosis and localized scleroderma, the process of fibrosis is present in the pathogenesis of all of these three entities beyond other individual clinical and histological distinct characteristics. Fibrosis was studied in 20 samples each of these three chronic cutaneous inflammatory diseases. An immunohistochemical study was carried out to explore the presence of α-smooth muscle actin (α-SMA) and vimentin cytoskeleton antigens, CD31, CD34, Ki67, p16; CD105, CD163, CD206 and FOXP3 antigens; and the central fibrotic cytokine TGF-ß. Higher expression of vimentin in comparison to α-SMA in all three lesion types was found. CD31- and CD34-positive blood vessel endothelial cells were observed throughout the reticular dermis. Ki67 expression was low and almost absent in scleroderma. p16-positive levels were higher than ki67 and observed in reticular dermis of keloidal collagen in keloids, in collagen bundles in scleroderma and in the external layers of the granulomas in lacaziosis. The presence of α-actin positive cells and rarely CD34 positive cells, observed primarily in keloids, may be related to higher p16 antigen expression, a measure of cell senescence. Low FOXP3 expression was observed in all lesion types. CD105-positive cells were mainly found in perivascular tissue in close contact with the adventitia in keloids and scleroderma, while, in lacaziosis, these cells were chiefly observed in conjunction with collagen deposition in the external granuloma layer. We did not find high involvement of CD163 or CD206-positive cells in the fibrotic process. TGF-ß was notable only in keloid and lacaziosis lesions. In conclusion, we have suggested vimentin to be the main myofibroblast general marker of the fibrotic process in all three studied diseases, while endothelial-to-mesenchymal transition (EndoMT) and mesenchymal stem cells (MSCs) and M2 macrophages may not play an important role.

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ABSTRACT: Insulin-derived amyloidosis (AIns) is a rare iatrogenic subtype of cutaneous amyloidosis occurring at frequent insulin injection sites. Here, we describe 2 cases of AIns accompanied by acanthosis nigricans (AN)-like changes, a rare finding which has been reported fewer than 5 times in the literature. We also report the first case of an AIns nodule being misdiagnosed as a keloid. Both of our patients presented with asymptomatic, hyperkeratotic, pigmented plaques at frequent insulin injection sites, and histopathologic examination showed (1) nodular aggregates of amyloid demonstrating apple-green birefringence with Congo red staining and (2) AN-like features, such as epidermal papillomatosis, hyperkeratosis, and hyperpigmentation. Accurate diagnosis of AIns is crucial, because repeated insulin injection into a nodule can impair glycemic control. However, misdiagnosis is common, as observed with our second patient, whose AIns nodule was misdiagnosed by an outside provider as a keloid, perhaps because of the presence of AN-like features. Our case report adds to the limited but growing body of literature on AIns and significantly increases the number of reported cases of AIns with AN-like features, an even rarer phenomenon.

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