Erythema Migrans-like COVID Vaccine Arm: A Literature Review

COVID Vaccine Arm (CVA) is an adverse drug reaction from mRNA vaccine for SARS-CoV-2. CVA is characterized by erythema and edema on the vaccination site (usually deltoid area) that appears from 5 to 10 days after vaccination and is sometimes associated with itching or pain. The exact etiology of CVA is still unclear, but delayed hypersensitivity against an excipient seems to play an essential role in the pathogenesis of the disease. This work performs a systematic literature review on CVA using three different databases containing articles published until 10 November 2021. The literature review includes eight papers reporting single cases or case series of CVA. Moreover, it also addresses, other cutaneous reactions following COVID 19 vaccinations as well as possible differential diagnosis. CVA migrans-like erythema is characterized by a ring-shaped rash in the injection area, which appears some days after the injection and disappears in about 10 days. This reaction may appear more rapidly in subsequent doses

Sequential Use of CO2 Laser Prior to Nd:YAG and Dye Laser in the Management of Non-Facial Warts: A Retrospective Study

Background and Objectives: Warts are benign lesions of viral etiology characterized by a hyperkeratotic appearance tending to spread across the skin surface. Various treatments have been proposed to manage this condition, such as acids, imiquimod, photodynamic therapy, cryotherapy, and various lasers. Materials and Methods: In this paper, we describe a combination protocol using CO2 laser prior to Nd:YAG laser for lesions interesting the palmoplantar areas or dye laser for lesions on other skin surfaces in the management of non-facial warts resistant to traditional therapies. In total, 34 patients with 103 warts suffering from wart infection resistant to traditional therapies treated from 1 January 2019 to 1 June 2020 were retrospectively enrolled at the Dermatological Unit of Magna Graecia University (Catanzaro, Italy). Two dermatologists measured clinical results, classifying lesions with complete resolution, partial resolution, or non-responding. Patients at four months follow-up were asked to evaluate their degree of satisfaction with a visual analog scale (VAS). Results: Almost all patients reported the complete resolution of lesions, with no patient reporting scarring. Five patients reported hypopigmentation in the treated areas. The mean satisfaction level was high. Only three patients experienced a relapse of the condition. Conclusions: Using a vascular laser following a CO2 superficial ablation of warts may help reduce the risk of scarring and decrease the incidence of relapses for lesions resistant to traditional therapies. Therefore, more extensive studies will be necessary to confirm the obtained results

Fractional Q-Switched 1064 nm Laser for Treatment of Atrophic Scars in Asian Skin

Background and Objectives: Asian patients with Fitzpatrick skin type III–IV are a less studied subtype of patients in the medical literature. Q-Switched, 1064 nm neodymium-doped yttrium aluminum garnet (Nd: YAG) laser with a fractionated beam profile (QSF) is a new modality that was reported to be effective in the treatment of scars. This study aims to evaluate the efficacy and safety of QSF Nd: YAG laser in treating scars in Asian patients. Materials and Methods: A total of 29 Subjects were treated with 1064 nm QSF laser. Each patients had three treatments with a fractionated microlens array handpiece every 8 weeks). Efficacy of treatment was evaluated using the Goodman and Baron’s quantitative grading scale before and 3 months after the last treatment. Results: All 29 patients treated had significant improvement of acne scars according to Goodman and Baron’s Quantitative Global Acne Scarring Grading System. No side effect has been observed except some minor erythematous reactions in three patients. Conclusions: Our results confirm that the 1064 nm QSF Nd: YAG laser is a safe and effective technique for treating scars in Asians

High mobility group A1 protein modulates autophagy in cancer cells.

High Mobility Group A1 (HMGA1) is an architectural chromatin protein whose overexpression is a feature of malignant neoplasias with a causal role in cancer initiation and progression. HMGA1 promotes tumor growth by several mechanisms, including increase of cell proliferation and survival, impairment of DNA repair and induction of chromosome instability. Autophagy is a self-degradative process that, by providing energy sources and removing damaged organelles and misfolded proteins, allows cell survival under stress conditions. On the other hand, hyper-activated autophagy can lead to non-apoptotic programmed cell death. Autophagy deregulation is a common feature of cancer cells in which has a complex role, showing either an oncogenic or tumor suppressor activity, depending on cellular context and tumor stage. Here, we report that depletion of HMGA1 perturbs autophagy by different mechanisms. HMGA1-knockdown increases autophagosome formation by constraining the activity of the mTOR pathway, a major regulator of autophagy, and transcriptionally upregulating the autophagy-initiating kinase Unc-51-like kinase 1 (ULK1). Consistently, functional experiments demonstrate that HMGA1 binds ULK1 promoter region and negatively regulates its transcription. On the other hand, the increase in autophagosomes is not associated to a proportionate increase in their maturation. Overall, the effects of HMGA1 depletion on autophagy are associated to a decrease in cell proliferation and ultimately impact on cancer cells viability. Importantly, silencing of ULK1 prevents the effects of HMGA1-knockdown on cellular proliferation, viability and autophagic activity, highlighting how these effects are, at least in part, mediated by ULK1. Interestingly, this phenomenon is not restricted to skin cancer cells, as similar results have been observed also in HeLa cells silenced for HMGA1. Taken together, these results clearly indicate HMGA1 as a key regulator of the autophagic pathway in cancer cells, thus suggesting a novel mechanism through which HMGA1 can contribute to cancer progression