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Background The European hidradenitis suppurativa (HS) guidelines recommend a multidisciplinary approach for patients with HS and management of comorbidities. Objective We aimed to describe the organization of a multidisciplinary HS program and characterize the patient population. Methods We conducted a retrospective study of patients with HS undergoing prospectively defined multidisciplinary work-up including examinations by a dermatologist, plastic surgeon, smoking specialist, and nutritionist in our outpatient unit between October 2015 and January 2017. Results The study included 49 patients with a sex ratio of 1:1. A total of 73.4% of patients were smokers, 20.4% were overweight, 48.9% were obese, and 30.6% had symptoms of depression. The mean Sartorius score was 30.4 (±17.6). The outcome of plastic surgery consultation was as follows: 16 patients had operations, 5 were excluded based on medical history, 9 refused surgery, and 16 remained undecided. The refusal rates for consulting with the smoking cessation and nutrition specialists were 55.8% and 69.5%, respectively. Twelve patients received antibiotics, 9 received biologics, 9 underwent medico-surgical treatment, 9 underwent surgery, and 10 were lost to follow-up. The mean visual analogue scale score for satisfaction was 8.3 (±1.6; n = 28). Conclusion An integrated multidisciplinary care model for HS is associated with high patient satisfaction. Adherence to the proposed comorbidity management was higher in female patients and related to empathetic interactions with physicians.

In this study, we compared the effects of sunscreens and antioxidants on reconstructed epidermis made with or without melanocytes 24 h after UVB, UVA or UVA+B irradiation. For this purpose, we studied sunburn cells and cyclobutane pyrimidine dimer formation, protein and lipid oxidation, catalase and superoxide dismutase activities and vitamin E levels. Topical sunscreens protected against direct cell death and thymine dimer formation whereas their protective effect against protein and lipid oxidation and antioxidant depletion was less marked partly due to the difficulty of spreading the cream. Antioxidant molecules protected against direct cell death and protein oxidation but not against thymine dimer formation. Since topical sunscreens and systemic antioxidant protected the skin differently, we speculate that their association might protect more efficiently against UV-induced damage. This model is relevant to study systemic molecules but is less practical, due to the technical limitations of studying topical molecules.

Background. Nonablative remodeling has been recently proposed as an alternative to CO2 and Er:YAG resurfacing. Objective. To evaluate the efficacy and safety of a 1540 nm Er:glass laser with contact cooling in nonablative skin remodeling, focused on perioral and periorbital rhytides. Methods. Sixty patients (mean age 47 years), Fitzpatrick skin types I–IV were treated four times over 6-week intervals. Patients were evaluated using digital photographs, histology, ultrasound imaging, and profilometry with silicone imprints in order to quantitate the degree of clinical improvement. Results. All subjects reported subjective improvement in the quality and visual aspect of their skin. This was confirmed by a 40.2% reduction of anisotropy (P < .001) 6 weeks after the fourth treatment. Ultrasound imaging demonstrated a 17% increase of dermis thickness (P < .005). Biopsy specimens showed evidence of new collagen formation. Conclusion. This study has clearly demonstrated that irradiation with 1540 nm Er:glass laser can lead to new collagen formation, dermis thickening, reduction of anisotropy of the skin, and clinical improvements. The lack of adverse effects confirmed that this 1540 nm laser emitting in a pulsed mode coupled with an efficient cooling system is safe.

Cutaneous parameters such as dermal thickness, stiffness, elasticity, skin surface lipid and hydration were evaluated using noninvasive methods in 77 growth hormone-deficient (GHD) children before replacement therapy and in 70 non-GHD children. We showed that in GHD children, dermis was thinner (0.70 ± 0.10 vs. 0.80 ± 0.10 mm, p < 0.0001 for prepubertal children and 0.81 ± 0.10 vs. 0.94 ± 0.11 mm, p < 0.0001 for pubertal children), stiffer (178.5 ± 57.3 vs. 113.09 ± 37 kPa, p < 0.0001 for prepubertal children and 172.5 ± 61.7 vs. 117.3 ± 42.5 kPa for pubertal children, p < 0.001) and less elastic (0.44 ± 0.09 vs. 0.39 ± 0.06 (nonelasticity index), p < 0.01 for prepubertal children and 0.39 ± 0.05 vs. 0.33 ± 0.04, p < 0.001 for pubertal children) compared to controls. Fourteen GHD children were re-evaluated after 1 year of GH treatment: dermal thickness and skin stiffness were significantly improved (p < 0.001 and p < 0.05 respectively) while elasticity was not modified. During the same period, 11 controls did not show any significant cutaneous modification. IGF-1 values, but not IGFBP-3 values, correlated positively with dermal thickness in GHD children, before and after 1 year of GH treatment. To conclude, GHD children exhibited specific cutaneous modifications. In a subset of GHD children, we showed that these modifications were influenced by GH treatment. More extensive studies are needed to see if these changes correlated with other GH effects.

To assess the photoprotective role of melanocytes in the epidermis, we studied the effects of ultraviolet B on an epidermis reconstructed with and without melanocytes. To address more specifically the role of melanin in fair-skinned individuals, experiments were done with cells obtained from human skin of low phototypes (II-III). To study the effect of constitutive melanin and possibly that of newly synthesized melanin precursors, a single dose of ultraviolet B (0.10 or 0.15 J per cm2, corresponding to a 4-5 minimal erythema dose in vivo) was administered to reconstructs and the effects were monitored over the first 24 h. When reconstructs with and without melanocytes were compared, no difference was found for DNA damage/repair assessed with antibodies to cyclobutane pyrimidine dimers and 6-4 photoproducts. More necrotic/apoptotic cells, however, were noted 24 h following ultraviolet B irradiation in reconstructs lacking melanocytes. Twenty-four hours following ultraviolet B irradiation the number of necrotic/apoptotic cells and the number of cyclobutane pyrimidine dimer positive cells was coarsely concentration-dependent. The number of cyclobutane pyrimidine dimer positive cells, however, was independent of the type of reconstruct used (with/without melanocytes). In conclusion, low phototype melanocytes seem to protect epidermal basal cells against ultraviolet B-induced apoptosis/necrosis and may preserve the overall integrity of the epidermis after ultraviolet B irradiation. On the contrary, such melanocytes do not seem to have a protective role against DNA damage and may not prevent cancer.

The known role of steroids on the hair follicle leads us to investigate their effects on hair follicle cell angiogenic responses in vitro. We verified, using the immunohistochemical technique, whether human occipital scalp follicle cells express steroid receptors in vitro. We showed that androgen and estrogen receptors were expressed by dermal papilla cells (DPC) and keratinocytes from the outer root sheath in vitro. With regard to steroidal enzymes (type I and II 5alpha-reductases and Cytochrome-p-450-aromatase), the type I 5alpha-reductase gene is much more expressed in DPC than in dermal fibroblasts; however, the type II 5a-reductase gene is transcribed more in dermal fibroblasts than in DPC. The transcription of the two 5alpha-reductase isoform genes in cultured DPC is regulated by a 5alpha-reductase inhibitor. We also demonstrated that DPC, dermal fibroblasts, and outer root shealth keratinocytes expressed cytochrome-p-450-aromatase. Using ELISA and reverse transcriptase-polymerase chain reaction, we investigated the role played by some steroids (estrogens, androgens, antiandrogens) in the modulation of vascular endothelial growth factor (VEGF) expression by DPC. The association of different treatments of DPC (5alpha-reductase inhibitor and androgen receptor antagonist) shows a great stimulation of VEGF and aromatase expression. Strong stimulation of VEGF protein and gene expression is observed in the presence of 17beta-estradiol. Also, the concentration-dependent inhibition of VEGF expression by DPC using the cytochrome-p-450-aromatase inhibitor, confirms the involvement of this estrogenic pathway in the regulation of VEGF expression in vitro.

The transition of the late anagen to the catagen phase is concomitant with the disappearance of perifollicular capillaries, and therefore cyclical hair growth might depend on the ability of the dermal papilla to synthesize and release soluble growth and differentiation factors toward pre-existing capillaries. We characterized an angiogenic growth factor in the conditioned medium of dermal papilla cells indistinguishable from vascular endothelial growth factor as judged by biochemical and immunologic criteria. In addition, these cells bind vascular endothelial, growth factor on two binding sites and proliferate or migrate in the presence of this growth factor. Moreover, neutralizing antibodies inhibit these biologic effects, confirming that vascular endothelial growth factor might contribute to hair growth either by acting directly on papilla cells or by stimulating the local vascularization.