Keloids

Jagdeo, Jared; Kerby, Eva; Glass, Donald A.

doi:10.1001/jamadermatol.2020.4705

Cited by 18 publications

(15 citation statements)

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“…From a translational point of view, this study shows a new potential direction for clinical treatment of keloids. Currently, the most common therapeutic regimens are surgical excision, intradermal corticosteroid injection, laser or radiation therapy, pressure dressings, and combinations of them (1, 61, 62). For example, only approximately 50% of keloids respond to corticosteroid treatment, whereas nearly 100% regrow after surgery used as the sole therapy (62).…”

Section: Discussionmentioning

confidence: 99%

Commensal microbiome dysbiosis elicits IL-8 signaling to drive fibrotic skin disease

Zhang,

Peng,

Huang

et al. 2023

Preprint

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SUMMARYCommensal bacteria are core players in wound healing whose function in the opposite pathophysiological process-scarring is presently unclear. Here, we document the association between bacteria and a specific skin fibrotic disease-keloid, which might offer a promising avenue for translational practice.ABSTRACTWound healing is an intensely studied topic involved in many relevant pathophysiological processes, including fibrosis. Despite the large interest in fibrosis, the network that related to commensal microbiota and skin fibrosis remain mysterious. Here, we pay attention to keloid, a classical yet intractable skin fibrotic disease to establish the association between commensal microbiota to scaring tissue. Our histological data reveal the presence of microbiota in the keloids. 16S rRNA sequencing characterize microbial composition and divergence between the pathological and normal skin tissue. Moreover, the data show elevation of interleukin-8 both in the circulation and keloid tissue, which elicited the collagen accumulation and migratory program of dermal fibroblasts via CXCR1/2 receptor. Our research provides insights into the pathology of human fibrotic diseases, advocating commensal bacteria and IL-8 signaling as useful targets in future interventions of recurrent keloid disease.

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Section: Discussionmentioning

confidence: 99%

Commensal microbiome dysbiosis elicits IL-8 signaling to drive fibrotic skin disease

Zhang,

Peng,

Huang

et al. 2023

Preprint

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“…Common sites for keloids formation include the chest, shoulders, back, and ears. 9 Keloids can cause symptoms such as pruritus, pain, and tenderness to touch. As surgical removal has a high risk of recurrence, nonsurgical approaches are recommended.…”

Section: Discussionmentioning

confidence: 99%

Effect of Epidermoid Cysts on the Efficacy of Intralesional Corticosteroid Therapy for Hypertrophic Scars and Keloids: A Prospective Pilot Study

Xu,

Bao,

Liu

et al. 2023

Dermatol Surg

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BACKGROUND Patients with hypertrophic scars (HSs) or keloids occasionally have epidermoid cysts (ECs), and the effect of ECs on the effectiveness of intralesional corticosteroids (ILCs) treatment in these patients has not been reported. OBJECTIVE This study aims to evaluate the influence of ECs on the outcomes of ILCs treatment in patients with HSs or keloids. MATERIALS AND METHODS This prospective study included 572 patients with keloids (n = 461) or HSs (n = 111). Patients received intralesional triamcinolone acetonide injection (0.05 mL/injection) at a concentration of 40 mg/mL and every 28 days for 4 sessions, with a 1-year follow-up. RESULTS A higher incidence of ECs was observed in keloid patients (16.92%) compared with HSs patients (7.21%). Keloid patients with ECs were older (p = .008) and had a longer disease duration (p = .0148), higher Vancouver scar scale (VSS) scores (p = .04), and greater thickness (p = .006). Keloid patients with ECs showed less improvement in VSS scores (p < .0001) and thickness (p < .0001) after ILCs treatment, with a higher recurrence rate (p < .0001). The overall complication rate in keloid patients with ECs after ILCs treatment was 49.51%. CONCLUSION Epidermoid cysts under keloids were associated with a poor response to ILCs therapy. Therefore, it is recommended to incorporate ultrasonography as a routine examination for keloid patients to aid in better decision making in clinical practice.

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“…The disease has an extensive effect on patients' quality of life and, if left untreated in the joints, may have an influence on motor function. Keloid scar formation is assumed to be caused by a number of factors, including chronic inflammation and immunological dysfunction, although there is considerable evidence of aberrant epigenetic modulation which results in keloid scar development 1–3 . The most important remaining issue is: what abnormalities in normal skin epigenetics cause keloid development and progression?…”

Section: Introductionmentioning

confidence: 99%

Identification of novel biomarkers of ferroptosis involved in keloid based on bioinformatics analysis

Yuan,

Meijia,

Rong

et al. 2024

International Wound Journal

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Keloid is a fibroproliferative disease of unknown aetiology, which has a significant impact the quality of life of patients. Ferroptosis plays an important role in the occurrence and development of fibrosis, but there is still a lack of research related to keloids. The objective of this work was to identify the hub genes related to ferroptosis in keloid to better understand the keloid process. The microarray data (GSE7890 GSE145725, and GSE44270) (23 keloid and 22 normal fibroblast) were analysed via the gene expression comprehensive database (GEO). Only GSE7890 met the FerrDB database. Cell cycle and pathway analysis were performed with gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was performed to differentially expressed genes (DEG). The differential genes were confirmed in other GEO datasets (GSE145725 and GSE44270), and multi‐fibrosis‐gene correlation analysed. To validate these hub genes, quantitative real‐time PCR (qRT‐PCR) was conducted. A total of 581 DEGs were screened, with 417 genes down‐regulated and 164 genes up‐regulated, with 11 ferroptosis genes significantly up‐regulated in both keloid and normal tissue, and 6 genes are consistent with our findings and are associated with multiple fibrosis genes. The qRT‐PCR results and tissues of normal skin and keloid agreed with our predictions. Our findings provide new evidence for the ferroptosis‐related molecular pathways and biomarker of keloid.

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Keloids

Cited by 18 publications

References 0 publications

Commensal microbiome dysbiosis elicits IL-8 signaling to drive fibrotic skin disease

Commensal microbiome dysbiosis elicits IL-8 signaling to drive fibrotic skin disease

Effect of Epidermoid Cysts on the Efficacy of Intralesional Corticosteroid Therapy for Hypertrophic Scars and Keloids: A Prospective Pilot Study

Identification of novel biomarkers of ferroptosis involved in keloid based on bioinformatics analysis

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