Supplementary Material for: Late-Onset Alopecia Areata: A Retrospective Cohort Study

<p><b><i>Background:</i></b> Alopecia areata is an immune-mediated disease presenting with sudden onset of nonscarring hair loss. Onset is more common earlier in life, and little is known regarding late-onset alopecia areata. <b><i>Objectives:</i></b> To describe the epidemiology, clinical patterns, disease course, and outcome of late-onset alopecia areata in Israeli patients referred to a tertiary medical center. <b><i>Materials and Methods:</i></b> This retrospective cohort study considered patients whose disease onset occurred at age ≥50 years. Patients were recruited from among all alopecia areata patients visiting a tertiary center between January 2009 and April 2015. <b><i>Results:</i></b> Of the 29 people included, 25 (86.2%) were female (female-to-male ratio, 6.2:1). There was a family history of alopecia areata in 17.2%, thyroid disease in 31%, atopic background in 6.9%, and 17/29 (58.6%) reported a significant stressful event. The most common disease pattern was patchy, and disease was mild in the majority of participants. Complete hair regrowth was observed in 82.8% of participants, and 37.9% relapsed. <b><i>Conclusion:</i></b> Late-onset alopecia areata is characterized by marked female predominance, less extensive disease, and a high incidence of complete hair regrowth.</p

Clinical significance of Candida isolation from dystrophic fingernails

Background: Candida onychomycosis mostly involves fingernails. Yet, in contrast to dermatophytes, Candida isolation from dystrophic fingernails does not prove casualty, as sample contamination and non-pathogenic Candida growth occur. Characterising treatment outcome of Candida-positive dystrophic nails is crucial to avoid unnecessary treatment. Objective: To investigate predicators associated with treatment outcome among Candida-positive dystrophic fingernails. Patients and methods: A retrospective cohort study was carried out among 108 adults with Candida-positive dystrophic fingernails not cured with adequate systemic anti-fungal course. Diagnosis was based on a single mycological culture. Patients with treatment failure (n = 85; 78.7% of the cases) were compared to patients with partial response (mild to almost cure; n = 23; 21.3% of the cases) at 9 to 12 months following treatment initiation. Results: Treatment failure was significantly associated with primary onycholysis (odds ratio [OR] 2.8; 95% confidence interval [CI] 1.1-7.4) and prolonged dystrophy (12.8 vs. 3.7 years in average), compared to partial treatment response. Non-responders had lower odds to present with distal lateral subungual onychomycosis, compared to partial responders (OR 0.3; 95% CI 0.1-0.7). Demographic and mycological characteristics, as well as number of nails affected, co-presence of paronychia, and treatment regime were not found to be associated with treatment response. Conclusion: Candida-positive primary onycholysis was shown to be non-responsive to systemic anti-fungal treatment, suggesting that anti-fungal treatment is not indicated. For other clinical scenarios, high proportions of treatment non-response suggest that determining causality of Candida should not be based on a single positive mycological culture. © 2020 Blackwell Verlag Gmb

Irradiation of austenitic steel 10Cr12Mn14Ni4AlMo and titanium alloy Ti-Al-V by pulsed streams of fast nitrogen ions and plasma in a dense plasma focus

Austenitic steel 10Cr12Mn14Ni4AlMo and Ti-4Al-3V alloy were irradiated with nanosecond pulsed nitrogen ion and plasma streams in plasma focus devices. The two different modes of the treatment were applied: high power density (greater-than or equal to 10 8 W/cm2) irradiation with melting of the surface layer and irradiation with power density similar to 10 7 W/cm2 below the melting threshold. Structure and phase changes as well as the mechanisms of modification and hardening of the surface layers of the steel and titanium alloy upon applied irradiation are discussed

Erosive pustular dermatosis of the scalp: a multicentre study

Background: Erosive pustular dermatosis of the scalp (EPDS) is characterized by crusted erosions or superficial ulcerations that lead to scarring alopecia. Objectives and Methods: We performed a multicentre retrospective clinical study including 56 patients (29 females and 27 males, mean age 62.7) with a confirmed EPDS in order to describe epidemiology, clinical findings and therapeutic choices of this disease. Results: Mechanical/chemical trauma was reported in 28.6%, a previous infection in 10.7%, a previous cryotherapy in 5.4% androgenetic alopecia in 48.2% and severe actinic damage in 25%. Trichoscopy showed absence of follicular ostia, tufted and broken hair, crusts, serous exudate, dilated vessels, pustules and hyperkeratosis. Histopathology revealed three different features, depending on the disease duration. The most prescribed therapy was topical steroids (62.5%), followed by the combination of topical steroids and topical tacrolimus (8.9%), systemic steroids (7.1%) and topical tacrolimus (5.4%). A reduction of inflammatory signs was observed in 28 patients (50%) treated with topical steroids and in all three patients treated with topical tacrolimus. Conclusion: The relatively high number of patients collected allowed us to identify a better diagnostic approach, using trichoscopy and a more effective therapeutic strategy, with high-potency steroids or tacrolimus, which should be considered as first-line treatment

How to Evaluate Treatment Response in Hair Diseases

When treating patients with scalp diseases, it is essential to be able to evaluate treatment response. Treatment response will allow further decision-making such as increasing or decreasing treatment dose, changing the treatment vehicle, changing therapy, or adding adjuvant treatments. Sometimes, hair disorders have multifactorial causes, so response to treatment may be affected not only by the prescribed therapy but also by other factors. Follow-up must include photographic and trichoscopic documentation, as well as inquiring about patient coping and expectations. Treatment goals must be clear to the patient. We should consider that a patient might have more than one disease or a new disease can appear such as contact dermatitis, impetigo, or tinea. If there is no response after 3–6 months of therapy with good patient compliance, a trichoscopy-guided biopsy might reveal valuable information. Another important challenge to be considered is cicatricial alopecia; even to the most trained eye, cicatricial diseases can mimic noncicatricial pathologies, and cicatricial alopecias tend to have an initial inflammatory phase in which no cicatricial findings are found. Dynamic trichoscopy is the best way to evaluate treatment response since it allows the assessment of trichoscopic signs of active disease. This assessment will benefit therapeutic decision and selection of a biopsy area. Knowledge of trichoscopic signs of active inflammation and signs of fibrosis in each disease will enable the clinician to understand that trichoscopy allows to identify the mechanisms of the disease rather than pathognomonic and unchanging signs. In this chapter, we will describe every step to be taken in all the possible presentations that a physician could face during treatment of hair disorders. The authors have tried to summarize and explain step by step what to expect, how to evaluate, and what to do when treatment is not working, trying to offer a guidance for all those who help patients with hair disorders

T-Cadherin is an auxiliary negative regulator of EGFR pathway activity in cutaneous squamous cell carcinoma: impact on cell motility

Genetic and epigenetic studies in different cancers, including cutaneous carcinomas, have implicated T-cadherin (T-cad) as a tumor suppressor. Immunohistochemical and in vitro studies have suggested that T-cad loss promotes incipient invasiveness in cutaneous squamous cell carcinoma (SCC). Molecular mechanisms are unknown. This study found that the main consequence of T-cad silencing in SCC is facilitation of ligand-dependent EGFR activation, whereas T-cad overexpression impedes EGFR activation. Gain- and loss-of-function studies in A431 SCC cells demonstrate T-cad-controlled responsiveness to EGF with respect to pharmacological inhibition of EGFR and to diverse signaling and functional events of the EGFR activation cascade (EGFR phosphorylation, internalization, nuclear translocation, cell retraction/de-adhesion, motility, invasion, integrin β1, and Rho small GTPases such as RhoA, Rac1, and Cdc42 activation). Further, T-cad modulates the EGFR pathway activity by influencing membrane compartmentalization of EGFR; T-cad upregulation promotes retention of EGFR in lipid rafts, whereas T-cad silencing releases EGFR from this compartment, rendering EGFR more accessible to ligand stimulation. This study reveals a mechanism for fine-tuning of EGFR activity in SCC, whereby T-cad represents an auxiliary "negative" regulator of the EGFR pathway, which impacts invasion-associated behavioral responses of SCC to EGF. This action of T-cad in SCC may serve as a paradigm explaining other malignancies displaying concomitant T-cad loss and enhanced EGFR activity