Secondary Comedones in a Case of Acne Conglobata Correlate with Double-ended Pseudocomedones in Hidradenitis Suppurativa

Lacarrubba, Francesco; Dall’Oglio, Federica; Musumeci, Maria Letizia; Nasca, Maria Rita; Micali, Giuseppe

doi:10.2340/00015555-2664

Cited by 8 publications

(4 citation statements)

References 2 publications

(3 reference statements)

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“… 9 , 10 , 11 Comedones are present in flexural and nonflexural inflamed and scarred tissues, as well as noninflamed tissues. 9 , 10 , 11 Subclinical inflammation (observed in hidradenitis suppurativa) 12 , 13 precedes comedogenesis in acne-prone skin, 14 , 15 , 16 , 17 , 18 , 19 , 20 involving keratinocyte-derived proinflammatory mediators (lipoteichoic acid, CCL20, and interleukin [IL] 1α). 18 , 19 , 20 , 21 , 22 , 23 , 24 Ex vivo studies of the follicular infundibum 25 isolated in vitro are able to recapitulate the formation of comedones with addition of IL-1α and prevent formation with the addition of IL-1 receptor antagonist.…”

Section: Follicular Occlusion Is Clinically and Experimentally A Product Of Inflammation Rather Than A Causementioning

confidence: 99%

Hidradenitis suppurativa is an autoinflammatory keratinization disease: A review of the clinical, histologic, and molecular evidence

Frew

2020

JAAD International

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The pathogenic model of hidradenitis suppurativa is in the midst of a paradigm shift away from a disorder of primary follicular occlusion to an autoinflammatory keratinization disease. Observational, experimental, and therapeutic evidence supports the concept of hidradenitis suppurativa as a primarily inflammatory disorder, a disorder of autoimmunity, or both, in contrast to the current prevailing paradigm of primary follicular occlusion. The lack of reliable and high-fidelity disease models has limited the available experimental and mechanistic evidence to support or refute one pathogenic model over another. This scholarly review synthesizes the existing clinical, histologic, and molecular data to evaluate the extant evidence supporting the autoinflammatory paradigm and further informing the molecular mechanisms of hidradenitis suppurativa pathogenesis. Follicular hyperkeratosis/occlusion and perifollicular inflammation coexist in histologic specimens, with interleukin 1a demonstrated to stimulate comedogenesis in the infundibulum. pH elevation in occluded body sites alters the microbiome and amplifies existing T-helper cell type 17 immunoresponses. Known metabolic comorbidities and smoking are known to upregulate interleukin 1a in follicular keratinocytes. Identified genetic variants may alter epidermal growth factor receptor signaling, leading to upregulated keratinocyte inflammatory responses. The process of follicular rupture and dermal tunnel formation can be explained as secondary responses to inflammatory activation of fibroblasts and epithelial-mesenchymal transition, with antibody production associated with inflammatory amplification in advanced disease. This review aims to reevaluate and integrate the current clinical, histologic, and molecular data into a pathogenic model of hidradenitis suppurativa. This is essential to advance our understanding of the disease and identify novel therapeutic targets and approaches.

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Section: Follicular Occlusion Is Clinically and Experimentally A Product Of Inflammation Rather Than A Causementioning

confidence: 99%

Hidradenitis suppurativa is an autoinflammatory keratinization disease: A review of the clinical, histologic, and molecular evidence

Frew

2020

JAAD International

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“…Early lesions: follicular plugging (yellow clods) perifollicular whitish halo, and white scales Mature lesions: blurred, telangiectatic, arborizing vessels; white structureless areas; and hyperpigmentation [29] Acne vulgaris Comedones: Erythematous periphery; dilated, roundish, central pore filled with a brown-yellow plug [30] Inflammatory lesions: erythematous roundish areas with central white-yellowish structure [31] Lupus vulgaris Yellow to golden-colored background, fine focused telangiectasias, milia-like cysts, and whitish reticular streaks [32] Malar lesion of SLE Reddish/salmon-colored follicular dots surrounded by white halos, branched vessels, white scaling, dotted and network-like vessels [18]…”

Section: Fundingmentioning

confidence: 99%

Summarization and comparison of dermoscopic features on different subtypes of rosacea

Fei

Han

et al. 2022

Chinese Medical Journal

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Background: The dermoscopic features of rosacea have already been reported. However, the current findings are incomplete, and little is known about phymatous rosacea. Hence, this study aimed to summarize and compare the dermoscopic features and patterns of three rosacea subtypes (erythematotelangiectatic [ETR], papulopustular [PPR], and phymatous [PHR]) in the Chinese Han population and to evaluate whether these features differ with patients’ genders, ages, and durations. Methods: Dermoscopic images of 87 rosacea patients were collected in non-polarized and polarized dermoscopy contact modes at 20-fold magnification. Dermoscopic features, including vessels, scales, follicular findings, and other structures, were summarized and evaluated. Results: The reticular linear vessels and red diffuse structureless areas of ETR were distinctive. For PPR, red diffuse structureless areas, reticular linear vessels, yellow scales, follicular plugs, and follicular pustules were typical dermoscopic criteria. The common dermoscopic features of PHR were: orange diffuse structureless areas, linear vessels with branches, perifollicular white color, orange focal structureless areas, and white lines. The following features statistically differed among the three rosacea subtypes: reticular linear vessels ( P < 0.001), unspecific linear vessels ( P = 0.005), linear vessels with branches ( P < 0.001), yellow scales ( P = 0.001), follicular plugs ( P < 0.001), perifollicular white color ( P < 0.001), red diffuse structureless areas ( P = 0.022), orange diffuse structureless areas ( P < 0.001), red focal structureless areas ( P = 0.002), orange focal structureless areas ( P = 0.003), white lines ( P < 0.001), follicular pustules ( P < 0.001), and black vellus hairs ( P < 0.001). Conclusions: The dermoscopic patterns of ETR are red diffuse structureless areas and reticular linear vessels. For PPR, the pattern comprehends combinations of red diffuse structureless areas, reticular linear vessels, yellow scales, follicular plugs, and follicular pustules. Meanwhile, PHR is characterized by remarkable orange diffuse structureless areas, linear vessels with branches, perifollicular white color, orange focal structureless areas, and white lines.

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“…However, in each instance, the coexistence of perifollicular inflammation is comparably prominent 10,13,14 . Clinically, comedones (both open and closed) as well as typical double‐sided comedones 40 are present in diseased areas, inflamed tissues, and also in scarred, noninflamed tissues 13,14,40–42 . They are also present in areas not exposed to flexural occlusion 43 …”

Section: Follicular Occlusionmentioning

confidence: 99%

“…10,13,14 Clinically, comedones (both open and closed) as well as typical double-sided comedones 40 are present in diseased areas, inflamed tissues, and also in scarred, noninflamed tissues. 13,14,[40][41][42] They are also present in areas not exposed to flexural occlusion. 43 Von Laffert et al 13,14 report comedones as more common in endstage fibrotic and scarred lesions and independent of the follicular unit.…”

Section: Follicular Occlusionmentioning

confidence: 99%

The pathogenesis of hidradenitis suppurativa: Evolving paradigms in a complex disease

Kozera

Frew

2022

Dermatological Reviews

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Hidradenitis suppurativa is a complex inflammatory skin disease with the molecular pathogenesis of disease incompletely understood. Recent observational and experimental insights into disease pathogenesis are challenging long-held beliefs regarding the causes and mechanisms of disease. The most effective treatments to date are anti-inflammatory in nature suggesting inflammation is the major driver of disease activity. This study critically evaluates the existing literature regarding the mechanisms of disease pathogenesis. Specifically, it questions the role of follicular occlusion as the central driver of disease activity and reframes hidradenitis suppurativa as a complex autoinflammatory and autoimmune disorder. Ongoing efforts to understand the mechanisms of disease will no doubt lead to more efficacious therapeutics to control this burdensome disabling disease.

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Secondary Comedones in a Case of Acne Conglobata Correlate with Double-ended Pseudocomedones in Hidradenitis Suppurativa

Cited by 8 publications

References 2 publications

Hidradenitis suppurativa is an autoinflammatory keratinization disease: A review of the clinical, histologic, and molecular evidence

Hidradenitis suppurativa is an autoinflammatory keratinization disease: A review of the clinical, histologic, and molecular evidence

Summarization and comparison of dermoscopic features on different subtypes of rosacea

The pathogenesis of hidradenitis suppurativa: Evolving paradigms in a complex disease

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