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Keloids in various races. A review of 175 cases

Alhady SM, Sivanantharajah K

Plast Reconstr Surg, 1969 Dec;44(6):564-6.
PMID: 5352921
Matched MeSH terms: Keloid/etiology; Keloid/epidemiology*; Keloid/pathology; Keloid/therapy
Clinical implications of single- versus multiple-site keloid disorder: a retrospective study in an Asian population

Park TH, Park JH, Tirgan MH, Halim AS, Chang CH

Ann Plast Surg, 2015 Feb;74(2):248-51.
PMID: 24681623 DOI: 10.1097/SAP.0b013e3182a2b537

There is strong evidence of genetic susceptibility in individuals with keloid disorder. The purpose of this cross-sectional study was to determine the clinical relevance of our proposed variables on the multiplicity of keloids by further investigating the presence of other keloids and a family history.

Matched MeSH terms: Keloid/ethnology; Keloid/genetics*; Keloid/pathology
Fulltext Antiproliferative effect of methanolic extraction of tualang honey on human keloid fibroblasts

Nurul Syazana MS, Halim AS, Gan SH, Shamsuddin S

BMC Complement Altern Med, 2011;11:82.
PMID: 21943200 DOI: 10.1186/1472-6882-11-82

Keloid is a type of scar which extends beyond the boundaries of the original wound. It can spread to the surrounding skin by invasion. The use of Tualang honey is a possible approach for keloid treatment. The objective of this study was to determine the antiproliferative effect of methanolic extraction of Tualang honey to primary human keloid fibroblasts and to identify the volatile compounds in methanol extraction of Tualang honey.

Matched MeSH terms: Keloid/drug therapy*; Keloid/physiopathology
Fulltext Keloid scarring: understanding the genetic basis, advances, and prospects

Halim AS, Emami A, Salahshourifar I, Kannan TP

Arch Plast Surg, 2012 May;39(3):184-9.
PMID: 22783524 DOI: 10.5999/aps.2012.39.3.184

Keloid disease is a fibroproliferative dermal tumor with an unknown etiology that occurs after a skin injury in genetically susceptible individuals. Increased familial aggregation, a higher prevalence in certain races, parallelism in identical twins, and alteration in gene expression all favor a remarkable genetic contribution to keloid pathology. It seems that the environment triggers the disease in genetically susceptible individuals. Several genes have been implicated in the etiology of keloid disease, but no single gene mutation has thus far been found to be responsible. Therefore, a combination of methods such as association, gene-gene interaction, epigenetics, linkage, gene expression, and protein analysis should be applied to determine keloid etiology.

Matched MeSH terms: Keloid
Keloids - the sebum hypothesis revisited

Fong EP, Bay BH

Med Hypotheses, 2002 Apr;58(4):264-9.
PMID: 12027517

The aetiology of the keloid scar has not been completely elucidated. Numerous hypotheses have been proposed in the past to explain the unusual characteristics of the keloid scar. While we do know that there is excessive and ongoing collagen-deposition, the exact triggering stimulus is a subject of conjecture. We present some of our photographic records of keloids and electron microscopic findings of keloid edges and reiterate the sebum hypothesis. We also attempt to explain the features of keloids in the light of the present knowledge of immunology and cell biology.

Matched MeSH terms: Keloid/etiology*; Keloid/immunology; Keloid/pathology
Cryotherapy: A Successful Monotherapy for Earlobe Keloids

Muthanna AM, Al-Qubati YA

Malays Fam Physician, 2020;15(3):83-85.
PMID: 33329867

A keloid represents an excessive overgrowth of skin beyond the boundaries of an injury. Earlobe keloids usually follow ear piercing and can become large, sometimes producing remarkable disfigurement. Surgical excision, pressure dressing, intralesional corticosteroid injection, cryosurgery, radiation, and lasers have all been used to treat earlobe keloids. However, none has produced uniformly satisfactory results. Combinations of more than one modality have also been employed to yield successful outcomes. We describe cryotherapy as a single modality to treat seven-year-old, multiple earlobe keloids. Three cryotherapy sessions with two freezing-thawing cycles of 30-40 seconds' freezing time and two minutes' thawing time, undertaken one month apart, resulted in complete flatness of the keloids and no recurrence after 5 years. We also evaluate keloid-related and operational factors that determine the success of cryotherapy as a monotherapy for earlobe keloids.

Matched MeSH terms: Keloid
Fulltext Effect of Kelulut Honey on the Cellular Dynamics of TGFβ-Induced Epithelial to Mesenchymal Transition in Primary Human Keratinocytes

Nordin A, Chowdhury SR, Saim AB, Bt Hj Idrus R

Int J Environ Res Public Health, 2020 05 06;17(9).
PMID: 32384749 DOI: 10.3390/ijerph17093229

Over-induction of epithelial to mesenchymal transition (EMT) by tumor growth factor beta (TGFβ) in keratinocytes is a key feature in keloid scar. The present work seeks to investigate the effect of Kelulut honey (KH) on TGFβ-induced EMT in human primary keratinocytes. Image analysis of the real time observation of TGFβ-induced keratinocytes revealed a faster wound closure and individual migration velocity compared to the untreated control. TGFβ-induced keratinocytes also have reduced circularity and display a classic EMT protein expression. Treatment of 0.0015% (v/v) KH reverses these effects. In untreated keratinocytes, KH resulted in slower initial wound closure and individual migration velocity, which sped up later on, resulting in greater wound closure at the final time point. KH treatment also led to greater directional migration compared to the control. KH treatment caused reduced circularity in keratinocytes but displayed a partial EMT protein expression. Taken together, the findings suggest the therapeutic potential of KH in preventing keloid scar by attenuating TGFβ-induced EMT.

Matched MeSH terms: Keloid
Association of TGFβ1 and SMAD4 variants in the etiology of keloid scar in the Malay population

Emami A, Halim AS, Salahshourifar I, Yussof SJ, Khoo TL, Kannan TP

Arch. Dermatol. Res., 2012 Sep;304(7):541-7.
PMID: 22805880 DOI: 10.1007/s00403-012-1262-0

Keloid is a complex condition with environmental and genetic risk-contributing factors. Two candidate genes, TGFβ1 and SMAD4, located in the same signaling pathway are highly expressed in the keloid fibroblast cells. In a case-control design, TGFβ1 haplotypes showed association with the risk of keloid in the present study. The CC haplotype, composed of both c.29C>T and -509T>C variants, was observed more frequently among cases (Corrected p = 0.037, OR = 2.07, 95 % CI = 0.87-4.93), showing a 4.5-fold increased risk for keloid. The AG genotype of the SMAD4 c.5131A>G variant showed a trend of significance (p = 0.0573, OR = 1.75, 95 % CI = 0.99-3.13). Taken together, either of these variants is most probably causative at the expression level or is in linkage disequilibrium with other causative variants in a complex pattern together with the environmental factors that contribute to the condition. To the best of our knowledge, there is only one documented report on a relationship between TGFβ1 and keloid with no association within the Caucasian population, while there have not been any reports for SMAD4. Therefore, the present study is likely the first research showing a significant association between TGFβ1 variants and keloids in the Malay population.

Matched MeSH terms: Keloid/genetics*
A Randomized, Single-Blind Trial of Clobetasol Propionate 0.05% Cream Under Silicone Dressing Occlusion Versus Intra-Lesional Triamcinolone for Treatment of Keloid

Nor NM, Ismail R, Jamil A, Shah SA, Imran FH

Clin Drug Investig, 2017 Mar;37(3):295-301.
PMID: 27888448 DOI: 10.1007/s40261-016-0484-x

BACKGROUND AND OBJECTIVE: Keloid is conventionally treated with intra-lesional (IL) triamcinolone, which is highly operator dependent and has its own adverse effects. Topical steroid and silicone dressings are a patient friendly and non-invasive treatment alternative. We therefore sought to determine the efficacy and safety of topical clobetasol propionate (Dermovate(®)) 0.05% cream under occlusion with Mepiform(®) silicone dressing compared to IL triamcinolone in the treatment of keloid.
METHODS: This was a prospective, randomised, observer-blinded study. Two keloids on the same site were randomly assigned to receive either daily topical clobetasol propionate 0.05% cream under occlusion with silicone dressing (Scar 1) or monthly IL triamcinolone injection (Scar 2). Efficacy was assessed using patient and observer scar assessment scale (POSAS) at 4-weekly intervals up to 12 weeks. Dimension of keloid and adverse effects were also assessed.
RESULTS: A total of 34 scars from 17 patients completed the study. There was significant improvement of POSAS at 12 weeks compared to baseline within each treatment group. However, there was no statistically significant difference in POSAS at 12 weeks between the two treatments. Keloid dimensions showed a similar trend of improvement by week 12 with either treatment (p = 0.002 in Scar 1, p = 0.005 for Scar 2). However, there was no significant difference between the treatment. In the IL triamcinolone group, all patients reported pain and 70.6% observed necrotic skin reaction. There was a significantly higher rate of adverse effects such as erythema (41.2 vs. 17.6%), hypopigmentation (35.3 vs. 23.5%), telangiectasia (41.2 vs. 17.6%) and skin atrophy (23.5 vs. 5.9%) documented in the IL triamcinolone group when compared to clobetasol propionate 0.05% cream under occlusion with silicone dressing.
CONCLUSION: Clobetasol propionate 0.05% cream under occlusion with silicone dressing is equally effective and has fewer adverse effects compared to IL triamcinolone. Hence, it may be used as an alternative treatment for keloid particularly in patients with low pain threshold, needle phobia and those who prefers home-based treatment.

Matched MeSH terms: Keloid/drug therapy*
Fulltext Diabetic mastopathy: a case report and literature review

Neetu G, Pathmanathan R, Weng NK

Case Rep Oncol, 2010 Jul 16;3(2):245-251.
PMID: 20740205 DOI: 10.1159/000318641

Diabetic mastopathy is a rare fibroinflammatory breast disease characterized by lymphocytic lobulitis, ductitis, and perivasculitis with stromal fibrosis. This lesion often presents as a discretely palpable uni- or bilateral mass in long-standing type I diabetes and other autoimmune diseases. We report a case of insulin-dependent diabetic mastopathy, which presented clinically as an indeterminate breast lump suspicious for malignancy. The patient is a 36-year-old woman who had type 1 insulin-dependent diabetes mellitus. Mammography and ultrasonography raised a suspicion of malignancy, and an excisional biopsy was performed. A previous biopsy had shown no evidence of malignancy. Histopathological examination now showed dense keloid-like stromal fibrosis with epithelioid-like and spindly myofibroblasts and a characteristic lymphocytic infiltration around blood vessels in and around lobules and ducts, features consistent with diabetic mastopathy. The literature is briefly reviewed.

Matched MeSH terms: Keloid
Co-localization of LTBP-2 with FGF-2 in fibrotic human keloid and hypertrophic scar

Sideek MA, Teia A, Kopecki Z, Cowin AJ, Gibson MA

J Mol Histol, 2016 Feb;47(1):35-45.
PMID: 26644005 DOI: 10.1007/s10735-015-9645-0

We have recently shown that Latent transforming growth factor-beta-1 binding protein-2 (LTBP-2) has a single high-affinity binding site for fibroblast growth factor-2 (FGF-2) and that LTBP-2 blocks FGF-2 induced cell proliferation. Both proteins showed strong co-localisation within keloid skin from a single patient. In the current study, using confocal microscopy, we have investigated the distribution of the two proteins in normal and fibrotic skin samples including normal scar tissue, hypertrophic scars and keloids from multiple patients. Consistently, little staining for either protein was detected in normal adult skin and normal scar samples but extensive co-localisation of the two proteins was observed in multiple examples of hypertrophic scars and keloids. LTBP-2 and FGF-2 were co-localised to fine fibrous elements within the extracellular matrix identified as elastic fibres by immunostaining with anti-fibrillin-1 and anti-elastin antibodies. Furthermore, qPCR analysis of RNA samples from multiple patients confirmed dramatically increased expression of LTBP-2 and FGF-2, similar TGF-beta 1, in hypertrophic scar compared to normal skin and scar tissue. Overall the results suggest that elevated LTBP-2 may bind and sequester FGF-2 on elastic fibres in fibrotic tissues and modulate FGF-2's influence on the repair and healing processes.

Matched MeSH terms: Keloid/genetics*; Keloid/metabolism; Keloid/pathology
Is the Mitochondrial Function of Keloid Fibroblasts Affected by Cytoglobin?

Jusman SWA, Azzizah IN, Sadikin M, Hardiany NS

Malays J Med Sci, 2021 Apr;28(2):39-47.
PMID: 33958959 DOI: 10.21315/mjms2021.28.2.4

Background: A keloid is a benign skin tumour characterised by excessive proliferation of fibroblasts, a process that requires a sufficient amount of energy. The energy needs are associated with adequate oxygen (O2) flow and well-functioning mitochondria. It is known that cytoglobin (CYGB) has a function in O2 distribution. The aim of the present study was to explore whether the inhibition of CYGB expression caused impaired mitochondrial function of keloid fibroblasts.
Methods: An in vitro study was conducted on a keloid fibroblast derived from our previous study. The study was carried out in the laboratory of the Biochemistry & Molecular Biology Department, Faculty of Medicine, Universitas Indonesia (FMUI), from July to December 2018. CYGB expression was inhibited by small interfering ribonucleic acid (siRNA) and CYGB. Analysis of mitochondrial function was observed through peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), a mitochondrial biogenesis marker and the activity of the succinate dehydrogenase (SDH) enzyme in mitochondria.
Results: The CYGB gene and protein were downregulated after treatment with CYGB siRNA. Inhibition of CYGB expression with siRNA also tended to decrease the levels of PGC-1α messenger ribonucleic acid (mRNA) and protein, as well as SDH enzyme activity.
Conclusion: Inhibition of CYGB expression with siRNA tended to decrease mitochondrial biogenesis and function. This may be useful for understanding the excessive proliferation of fibroblasts in keloids and for development of treatment for keloids.

Matched MeSH terms: Keloid
Keloid pathogenesis via Drosophila similar to mothers against decapentaplegic (SMAD) signaling in a primary epithelial-mesenchymal in vitro model treated with biomedical-grade chitosan porous skin regenerating template

Lim CK, Halim AS, Yaacob NS, Zainol I, Noorsal K

J Biosci Bioeng, 2013 Apr;115(4):453-8.
PMID: 23177217 DOI: 10.1016/j.jbiosc.2012.10.010

The effects of locally produced chitosan (CPSRT-NC-bicarbonate) in the intervention of keloid pathogenesis were investigated in vitro. A human keratinocyte-fibroblast co-culture model was established to investigate the protein levels of human collagen type-I, III and V in a western blotting analysis, the secreted transforming growth factor-β1 (TGF-β1) in an enzyme-linked immunosorbent assay (ELISA) and the mRNA levels of TGF-β1's intracellular signaling molecules (SMAD2, 3, 4 and 7) in a real-time PCR analysis. Keratinocyte-fibroblast co-cultures were maintained in DKSFM:DMEM:F12 (2:2:1) medium. Collagen type-I was found to be the dominant form in primary normal human dermal fibroblast (pNHDF) co-cultures, whereas collagen type-III was more abundant in primary keloid-derived human dermal fibroblast (pKHDF) co-cultures. Collagen type-V was present as a minor component in the skin. TGF-β1, SMAD2 and SMAD4 were expressed more in the pKHDF than the pNHDF co-cultures. Co-cultures with normal keratinocytes suppressed collagen type-III, SMAD2, SMAD4 and TGF-β1 expressions and CPSRT-NC-bicarbonate enhanced this effect. In conclusion, the CPSRT-NC-bicarbonate in association with normal-derived keratinocytes demonstrated an ability to reduce TGF-β1, SMAD2 and SMAD4 expressions in keloid-derived fibroblast cultures, which may be useful in keloid intervention.

Matched MeSH terms: Keloid/metabolism*