RESULTS
All 8 post-meeting statements received a mean score of ≥4 (Table 1). The authors emphasized that, although potentially limited by temporal or logistic constraints, dermatologists should endeavor to discuss skin care during every AV/rosacea visit. Optimal skin care may improve both diseases, potentially with minimal pharmacotherapy. Furthermore, poor choices made by an uninformed patient may derail an otherwise ideal therapeutic approach.
Acne Vulgaris
Barrier Dysfunction
Epidermal barrier dysfunction (EBD) is well-known in AV as adverse effects of over-the-counter (OTC) products, and prescription and adjunctive procedural therapies.16 These effects, clinically noted as xerosis, abnormal sensations (eg, stinging, burning, tingling, pruritus), pain, tightness, and/or an irritant dermatitis, are all signs of increased transepidermal water loss (TEWL) and may be partially mitigated with concurrent use of appropriate moisturizers.16-21
Data suggest AV patients may have pre-existing EBD.22-25 Untreated Japanese male AV patients ages 14-26 (moderate, n=11; mild, n=25) had significantly greater TEWL that correlated with AV severity than age/gender-matched controls (n=29) (TEWL g/m2/h±SD: Control 10.3±2.4; Mild, 14.4±2.5; Moderate, 16.8±3.8, P<.01).22
TEWL may worsen as patients approach puberty, regardless of AV, with one study finding among 132 healthy children (boys, n=67; girls, n=65) ages 6-13 that TEWL was significantly greater by age 9 for girls and 11 for boys vs their 6-year-old counterparts (P<.05).25
Compared against an internal ceramide standard, a decrease in total stratum corneum (SC) ceramides in AV (μg±SD: moderate 3.4±0.45; mild 4.07±.87) vs control (6.49±0.98) (P<.05) had a significant negative correlation with increased TEWL.23 After isolating total ceramide and sphingosine from other SC lipids, there was also a significant negative correlation with decreasing total ceramide (P<0.1) and free sphingosine (P<0.1) with worsening AV severity.23 Of note, similar ceramide derangements have been found in and are thought to pathologically contribute to EBD in psoriasis and AD.26
Together these data suggest increases in TEWL may be a result of ceramide imbalances due to adrenarche-induced ceramide synthetic dysfunction. Although these changes may not be specific to AV, EBD may be associated with, and potentially precede and/or exacerbate, clinically-evident AV.
Microbiome Dysbiosis
In AV, there are two broadly distinct CMs: superficial and follicular.27 Superficial facial and truncal CM are dominated by Staphylococci spp. (eg, S. epidermidis) which account for >27% of bacteria, while anaerobic Propionibacteria (including Cutibacterium acnes) account for <2%.28 Conversely, the physiologically-healthy follicular CM is more homogenous, with C. acnes comprising 89% to 94% of the bacterial population, functioning as a commensal organism in healthy skin.14,29 This disparity may suggest that, unlike in the superficial CM, the sebum-abundant follicular milieu may self-select for lipophilic organisms and that the absence of microbiota species diversity could be the norm.14
Counterintuitively, C. acnes follicular colonization is one of the 4 dogmatic factors of AV pathogenesis and may correlate with severity.25,30-32 During puberty there is a significant increase in absolute abundances of organisms25 and relative abundance of C. acnes that parallels increase in sebum production.33-35 Conversely, the decreased incidence and prevalence of AV (~3- 5% of individuals) by the fifth decade of life coincides with up to a 49.9% of the reduction in Propionibacterium spp. and may be due to age/age-related changes, a significant decrease in sebum production, and increase in overall CM diversity.36-38 C. acnes phylotypes are distinct between individuals with and without AV (Figure 3).27,29,39-42
C. acnes phylotype IA1 (and to a lesser degree IA2) represents 55-67% of all C. acnes in mild and severe AV (respectively), whereas, in healthy skin, IA1 exists alongside other phylotypes including IA2, II, and III.42 This homogenization of C. acnes phylotypes may correlate with increasing AV severity, as one study found phylotype IA1 comprised 84.4% and 95.6% of all C. acnes on the face and back (respectively) of individuals with severe AV compared with healthy individuals who had ~39% phylotype IA1 and ~43% phylotype II.43
Compared with C. acnes phylotype II, a commensal strain, phylotype IA1 (Figure 3) has pro-inflammatory capabilities via increased activation of toll-like receptor 2 (TLR2) Th1/Th17 axis, decreased interleukin-10 (IL-10) response,29,44 and a combination of virulence factors including: increased triacylglyceride lipase activity generating short-chain fatty acids,45,46 β-hemolytic,
