Psychological stress enhances keloid development via stress hormone-induced abnormal cytokine profiles and inflammatory responses

Yang, Yating; Wu, Xiaoli; Liu, Wei

doi:10.20517/2347-9264.2020.24

Cited by 5 publications

(5 citation statements)

References 67 publications

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“…8 In addition to the initial cutaneous trauma (e.g., burn, sharp injury, operation scar, acne, and/or insect bite), psychological stress has been hypothesized as a risk factor for keloid growth due to the stress hormone. 9 Differential diagnoses of keloid include hypertrophic scar and dermatofibrosarcoma protuberans (DFSP). 6 Hypertrophic scar is characterized by a heightened or thickened scar occurring after trauma or inflammation with growth within the initial insult and may regress after a few months to years.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Intralesional Triamcinolone Acetonide Alone with Intralesional Triamcinolone Acetonide-5-Fluorouracil Combination Injection in Keloid: A Case Report

Mawu,

Marlyn Grace Kapantow,

Oktavia Reymond L. Sondakh

et al. 2024

AMCR

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Keloids are abnormal cutaneous wound healing responses extending beyond the borders of the initial wound, usually appearing pink-purplish to hyperpigmented nodules or plaques with a hard consistency, irregular shape, uneven border, and smooth shiny surface. Most often occur on the chest, shoulder, upper arms, earlobes, and cheeks. This case report aims to compare a case of keloid treated with intralesional triamcinolone acetonide (TAC) alone with intralesional triamcinolone acetonide-5-fluorouracil (TAC + 5-FU) combination injection. A 21-year-old Minahasa male complains of growing pruritic scars in the back area and right and left upper arms since five years ago. Physical examination of the right and left upper arms revealed multiple hyperpigmented nodules and plaques, irregularly shaped, smooth, and shiny surfaces with defined borders and varying sizes. A clinical diagnosis of keloid was made. Treatment was initiated with weekly intralesional TAC alone on the left upper arm vs. intralesional TAC + 5-FU combination injection on the right upper arm. The evaluation was made based on the clinical and modified Vancouver scar scale. One of the most commonly used therapeutic options for keloid is TAC. However, the combination of TAC + 5-FU may be opted for due to its mechanism through the corticosteroid mechanism of action in conjunction with the antimetabolite activity of 5-FU. The combination may yield a more effective and faster outcome with fewer side effects. Intralesional combination TAC + 5-FU injection may be a therapeutic option for keloid with minimal side effects.

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Section: Discussionmentioning

confidence: 99%

Comparison of Intralesional Triamcinolone Acetonide Alone with Intralesional Triamcinolone Acetonide-5-Fluorouracil Combination Injection in Keloid: A Case Report

Mawu,

Marlyn Grace Kapantow,

Oktavia Reymond L. Sondakh

et al. 2024

AMCR

View full text Add to dashboard Cite

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“…Meanwhile, Hochman et al [23] described keloid as a psycho-mediated disease that could influence mental health through a "brain-skin connection." Stress hormones can activate keloid formation and aggravate lesion hypoxia through α-Adrenergic receptors (α-ARs), upregulate IL-6 to promote fibrosis via activating β-Adrenergic receptors, and dysregulate lesion immune and inflammatory responses to aggravate keloids [24]. Therefore, focusing on treating itch and pain in keloid patients is necessary.…”

Section: Discussionmentioning

confidence: 99%

An Open-Label, Uncontrolled, Single-Arm Clinical Trial of Tofacitinib, an Oral JAK1 and JAK3 Kinase Inhibitor, in Chinese Patients with Keloid

Chen,

Feng,

Pan

et al. 2023

Dermatology

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Background: The keloid treatment is still a thorny and complicated clinical problem, especially in multiple keloids induced by wound, severe burn, ethnic background or cultural behaviors, or unexplained skin healing. Mainstream treatments have limited efficacy in treating multiple keloids. As no oral treatment with painlessness and convenience is available, oral treatment strategies should be formulated. Objectives: This study aimed to investigate the efficacy and therapeutic mechanism of oral tofacitinib in keloid patients. Methods: We recruited the 7 patients with keloid scars and prescribed 5 mg of tofacitinib twice a day orally with a maximum follow-up of 12 weeks. The Patient and Observer Scar Assessment Scale (POSAS), the Vancouver scar scale (VSS), ANTERA 3D camera, and the DUB Skin Scanner 75 were used to assess the characteristics of the lesion. Immunohistochemistry was performed to evaluate collagen synthesis, proliferation, and relative molecular pathways. Moreover, the effects of tofacitinib were assessed on keloid fibroblast in vitro. Results: After 12 weeks of oral tofacitinib, significant improvement in POSAS, VSS, and Dermatology Life Quality Index (DLQI) scores was observed (p < 0.05). The volume, lesion height, and dermis thickness of the keloid decreased (p < 0.05). Moreover, significant decreases in the expression of collagen I, Ki67, p-STAT 3, and p-SMAD2 were observed after 12 weeks of administration. In vitro experiments suggested that tofacitinib treatment inhibits fibroblast proliferation and collagen I synthesis via suppression of STAT3 and SMAD2 pathway. Conclusion: Tofacitinib, a new candidate oral drug for keloid, could reduce keloid lesion volume by inhibiting collagen synthesis and inhibiting fibroblast proliferation, and alleviate itch and pain to obtain a better life quality.

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“…In addition, high levels of GCs can cause neuronal dysfunction in the brain. [ 66 , 67 ] Dysregulated vagal inhibition is also observed in CS, whereby the cholinergic anti-inflammatory pathways acting via the vagal nerve are inhibited, resulting in reduced release of anti-inflammatory cytokines and an increase in inflammation in the body. This decrease in vagal tone can lead to increased intestinal permeability and may promote systemic inflammation.…”

Section: Chronic Stress Stress System and Gliomamentioning

confidence: 99%

Chronic stress as an emerging risk factor for the development and progression of glioma

Yi,

Lin,

She

et al. 2024

Chinese Medical Journal

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Gliomas tend to have a poor prognosis and are the most common primary malignant tumors of the central nervous system. Compared with patients with other cancers, glioma patients often suffer from increased levels of psychological stress, such as anxiety and fear. Chronic stress (CS) is thought to impact glioma profoundly. However, because of the complex mechanisms underlying CS and variability in individual tolerance, the role of CS in glioma remains unclear. This review suggests a new proposal to redivide the stress system into two parts. Neuronal activity is dominant upstream. Stress-signaling molecules produced by the neuroendocrine system are dominant downstream. We discuss the underlying molecular mechanisms by which CS impacts glioma. Potential pharmacological treatments are also summarized from the therapeutic perspective of CS.

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Psychological stress enhances keloid development via stress hormone-induced abnormal cytokine profiles and inflammatory responses

Abstract: Psychological stress enhances keloid development via stress hormone-induced abnormal cytokine profiles and inflammatory responses.

Cited by 5 publications

References 67 publications

Comparison of Intralesional Triamcinolone Acetonide Alone with Intralesional Triamcinolone Acetonide-5-Fluorouracil Combination Injection in Keloid: A Case Report

Comparison of Intralesional Triamcinolone Acetonide Alone with Intralesional Triamcinolone Acetonide-5-Fluorouracil Combination Injection in Keloid: A Case Report

An Open-Label, Uncontrolled, Single-Arm Clinical Trial of Tofacitinib, an Oral JAK1 and JAK3 Kinase Inhibitor, in Chinese Patients with Keloid

Chronic stress as an emerging risk factor for the development and progression of glioma

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