Journal of Clinical and Aesthetic Dermatology

Updates on Psoriasis & Cutaneou Oncology

An evidence-based, peer-reviewed journal for practicing clinicians in the field of dermatology

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S23 P r o c e e D i n G s JCAD jOUrnAl Of ClInICAl And AEsthEtIC dErMAtOlOgy september 2017 • volume 10 • number 9 • supplement lymphocyte activation gene 3 (laG3), cytotoxic t lymphocyte-associated 4 (ctla4), indoleamine 2,3 dioxygenase (iDo1), apoptosis, programmed cell death 1 ligand (PDl1), programmed cell death 1 ligand 2 (PDl2), and il-10. a study recently reported decreased expression of these in immunochemistry studies of psoriatic skin. 118 thus, psoriasis chronicity may be related to the absence of negative immune regulatory pathways, and these negative pathways may be potential therapeutic targets. furthermore, the researchers hypothesize that negative immune regulation limits disease progression in mild forms of psoriasis vulgaris and in the small-plaque asian variant of psoriasis. When psoriasis is described as "mild," it typically refers to a reduced Bsa adected rather than specifc skin pathology. in general, mild psoriasis adects less than 10 percent of the body surface, accounts for about 80 percent of all psoriasis cases, and responds to topical treatment. Moderate-to-severe psoriasis adects over 10 percent of the Bsa, accounts for 20 percent of psoriasis cases, and may require systemic therapy. However, even patients with mild psoriasis are still at greater risk for cardiovascular disease than normal controls. the comorbidities associated with severe psoriasis also occur in mild psoriasis. While systemic treatment is not always appropriate for mild psoriasis, a case-by-case evaluation may be warranted, weighing the potential risks (comorbidities) and benefts for the individual patient. the high expression of negative immune regulators creates the potential to modify disease if, for example, systemic treatments targeting il-17a/f are employed. this leaves an important and as-yet unanswered questions about psoriasis: if one could deplete or substantially reduce edector t- cell clones in mild plaques, would there be enough checkpoint inhibition or treg function to prevent reactivation of disease-causing clones? our current understanding of mild psoriasis includes some important points. first, it is not always "mild" in terms of the skin reactions to underlying t-cells. topical products are the frst- line approach to mild psoriasis, but their edectiveness can be limited particularly in comparison to systemic agents. also, patients with mild psoriasis are at increased risk for comorbidities. Given these facts, we might ask if there is a subset of mild psoriasis patients who ought to be treated with relatively safe biologics or other systemic agents. the answers to these questions are not yet clear but pose some important ideas that may potentially alter how we treat patients with mild psoriasis. frOM UV tO sCC skin cancer remains by far the most common malignancy in humans in the world, including in europe. 119 in terms of tumor etiology, nonmelanoma skin cancer (nMsc) should be included, as it encompasses basal cell carcinoma (Bcc), Bowen's disease, cutaneous squamous cell carcinoma (scc), and its early antecedent, actinic keratosis (aK). 120 Bcc is the most frequent form of invasive cancer around the world; in Germany, individuals approximately have a 30-percent lifetime risk of developing a Bcc. 121 the risk factors for skin cancer are well known and include ultraviolet (uv) radiation, the human papillomavirus (HPv), and immunosuppression. 120 HPv has been implicated in benign and malignant cutaneous lesions and plays what seems to be an active role in the pathogenesis of certain cutaneous cancers. 120 Papillomaviruses are small Dna viruses found in more than 20 mammalian and avian species; the genome is composed of nearly 8,000 base pairs. HPv may infect keratinocytes of the skin and mucosa. 122 the genital types of HPv are distinct from cutaneous HPv in that the virus does not integrate with the host genome in the skin. integrated e6 and e7 genes can be observed in genital forms of the HPv. HPv23 and HPv38 may be a cofactor in certain cutaneous cancers, particularly in immunosuppressed patients, such as transplant patients, Hiv patients, or patients with other autoimmune disorders under pharmacological immunosuppressive therapy. While Bcc typically presents as a single tumor, aK is best described as a feld cancerization, which is described as a continuum in which precancerous and cancerous cells reside in an area of skin that may be adjacent or near skin that does not appear to be involved in the cancer. 123 using the continuum paradigm, aK commences with photodamage and culminates in invasive scc. similar but diderentially expressed genes found present in both aK and scc suggests that aK may be a precursor lesion of scc. 124 Gene expression has been studied in photodamaged and photoaged skin. sun exposure can prompt the down- regulation of specifc genes, which starts very early with photodamage and photoaging and precedes to more overt signs of aK over time. this raises two important questions: 1) Where CUtAnEOUs OnCOlOgy

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