DOCSLIB.ORG

Atopic Dermatitis  Sebum Production by the Sebaceous Gland  Infections: Zoster  P

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Atopic Dermatitis  Sebum Production by the Sebaceous Gland  Infections: Zoster  P Overview Pathogenesis of Acne Vulgaris Inflammatory Diseases of the skin: Acne, Rosacea, Psoriasis, Atopic Dermatitis Sebum production by the sebaceous gland Infections: Zoster P. acnes follicular colonization Pre-malignant and malignant neoplasms: Actinic Alteration in the keratinization process Keratoses, Basal Cell Carcinoma, Squamous Cell Carcinoma, Melanoma Release of inflammatory mediators into the skin, i.e. role of sebaceous lipids and inflammatory mediators including MMPs. Inflammatory Acne Papules Comedones Pustules Open (Blackheads) Closed (Whiteheads) Acne Scarring Nodules Cysts Strategic Approach to Acne Therapy Role of retinoids Topical/Systemic antibiotics have no role as monotherapy Treatment of Acne Oral isotretinoin should be considered as first line in severe acne Azeleic acid is useful in pregnancy and patients with hyperpigmentation Moderate Inflammatory Acne Oral Contraceptives and Acne Treatment Hormonal Therapy Norgestimate-ethinyl estradiol Oral contraceptives may be helpful in some women Norethindrone acetate-ethinyl estradiol May take 3 months to see improvement. Drospirenone-ethinyl estradiol Spiranolactone useful in some. If acne is accompanied by irregular menses, female Use with topicals patterned hair loss or hirsutism, consider endocrine workup. As effective as oral antibiotics at 6 months Severe Nodulocystic, Scarring Isotretinoin-Before and After or Resistant Acne Isotretinoin Synthetic oral retinoid 16-20 week course Regular laboratory evaluation and contraceptive counseling for females Registration with iPledge Program required Acne and Diet Rosacea Powell NEJM 352;8 Feb 2005 High Glycemic index diet causes hyperinsulinemia leading to increase in IGF-1 Causes keratinocyte and sebocyte proliferation, lipogenesis Cascade of events activates androgens Subtype 1 Subtype 3 Observational studies suggest milk consumption imparts increased risk for acne Subtype 2 Subtype 4 Rosacea Rosacea Rosacea Rosacea Variants Papule and pustules Opthalmic Rosacea- treatment of choice: oral antibiotics Telangiectasias Steroid Rosacea- resulting from long term topical or systemic Flushing and blushing steroid use Sebaceous hyperplasia Perioral Dermatitis- triggered or aggravated by steroid use Triggers: cold, heat, UV, irritation, emotions, alcoholic beverages, spicy foods, hot beverages Rosacea Treatments Rosacea Topical: clindamycin, erythromycin, metronidazole, sulfur-based lotions, azelaic acid, sunscreens, ivermectin oxymetazoline hydrochloride cream 1%, brimonidine- facial erythema Systemic: tetracyclines, erythromycin, isotretinoin Psoriasis Psoriasis An immune dysregulatory disease secondary to T-cell activation, release of TH1 based cytokines. Cytokines cause keratinocytic proliferation and recruitment of inflammatory cells into the skin 2% of the U.S. population Bimodal incidence: peaks at ages 29 and 55 Early onset associated with increased severity and family history Generalized plaque psoriasis Guttate psoriasis . scattered scaly papules . trunk and proximal extremities . can be associated with streptococcal infection . can be seen as first sign of disease in children or acute exacerbation in adults Inverse psoriasis Nail Findings . nail pits . yellowish discoloration . commonly involves axilla, groin, umbilicus beneath nail plate . may not see much scaling . higher risk of secondary infection National Psoriasis Foundation Recommends: Triggers BP, pulse, BMI every 2 years Streptococcal infection (Guttate) HIV Fasting blood glucose, lipid levels every 5 years if no additional Drugs: Lithium, steroids, Beta-blockers, Interferons, ACE risk factors, every 2 years with risk factors inhibitors, G-CSF Joint status every visit- 5-8% of patients with psoriasis also suffer from PsA Psoriasis Treatment-Topical Systemic Therapy Anthralin PUVA Vitamin D3 Analogues Methotrexate Tazarotene Cyclosporine Tar Retinoids- Acitretin Topical glucocorticoids Biologic Agents- Etanercept, Efaluzimab, Adalumimab, Alefacept, Infliximab, Secukinumab Apremilast Biologics and Psoriasis TNF-alpha Safety Warnings • 8 FDA approved biologics for psoriasis • Serious infections • New targets in development in response to advancements in basic • Malignancies science • Demyelinating disease • Therapies targeting IL-17 and IL-23 exhibit promising potential • Congestive heart failure thus far • Hepatitis B • Further study is necessary to elucidate the long term efficacy and • Hematologic safety characteristics of these categories of drugs • Autoimmunity Rubbert-Roth A. Rheumatology. • Live vaccines 2012;51:v38-47 Bioloigics-Clinical Pearls Biologics -Psoriasis • Adalimumab • Guselkumab –-q8-12 weeks • Etanercept • Brodalumab • Apremilast • Ixekizumab • Certolizumab - doesn’t cross placenta • Secukinumab – not associated with TB reactivation • Tildrakizumab- takes time to work (several mos) • Ustekinumab – safe in adolescents • Tofacitinib –JAK1 inhibitor for vitiligo, concomitant with light • Risankizumab/Mirikizumab Atopic Dermatitis Atopic Dermatitis Pruritus Facial/ Extensor involvement in pediatrics Flexural lichenification in adults Personal/ Family History of atopy Atopic Dermatitis- Associated Features Atopic Dermatitis and Food Xerosis Prenatal and postnatal probiotic supplementation decreases risk Cutaneous infections- S. aureus, Herpes, Molluscum Restriction diets helpful only if oral food challenge is positive Keratosis Pilaris Pityriasis Alba Nipple Eczema Elevated Serum IgE Orbital darkening Fig 2 Atopic Dermatitis- Management Crisaborole ointment Emollients are key part of treatment Topical glucocorticoids Topical calcineurin inhibitors Antihistamines Phototherapy Systemic immunosuppression in severe disease Novel therapy: Crisaborole ointment (PDE4 inhibitor) Dupilumab acetyl dipeptide cream Journal of the American Academy of Dermatology 2016 75, 494-503.e4DOI: (10.1016/j.jaad.2016.05.046) Copyright © 2016 American Academy of Dermatology, Inc. Terms and Conditions Novel Therapy- Atopic Dermatitis Atopic Dermatitis: Advances in Therapy Dupilumab-a monoclonal antibody that targets both interleukin-4 and interleukin-13 Dupilumab Dupilumab therapy provides clinically meaningful improvement in patient-reported outcomes (PROs): A phase IIb, randomized, placebo-controlled, clinical trial in adult patients with moderate to Phosphodiesterase 4 inhibitors severe atopic dermatitis (AD) Crisaborole ointment 2% Eric L. Simpson, MD, MCR et al JAK inhibitors Journal of the American Academy of Dermatology Emerging therapies Volume 75, Issue 3, Pages 506-515 (September 2016) DOI: 10.1016/j.jaad.2016.04.054 Monoclonal Ab against IL 13 and IL 31 RA TRPV1 antagonists T-cell inhibitors Copyright © 2016 American Academy of Dermatology, Inc. Terms and Conditions Zoster/ Shingles •May involve multiple dermatomes or may be generalized in immunosuppressed patients Zoster/ Shingles Zoster Varicella-zoster Virus 5% with non-specific prodromal symptoms 2/3 of patients are over 50 years of age Preceded by pain, paresthesia in the involved dermatome Risk factors: advanced age, malignancy, immunosuppression, xrt, Pain may mimic acute abdomen or MI HIV May involve multiple dermatomes or may be generalized in Reactivation of the virus in the sensory ganglia immunosuppressed patients Consider if pt complains of pain in dermatomal distribution for more than 24-48 hrs even in the absence of skin lesions Zoster Zoster- Therapy Diagnosis may be confirmed by: Treatment Tzanck smear –most rapid, non-specific Ideally initiate within 48-72 hours of rash Direct antigen detection – rapid, specific Oral antiviral agents: Viral culture Acyclovir 800mg five times/day x 7-10 days Valacyclovir 1gm TID x 7d Famciclovir 500mg TID x 7d IV Acyclovir for immunosuppressed patients Zoster- Pain Management Zoster Prevention Treatment of Acute Pain: Treatment of Post-Herpetic Decrease number of new cases of Zoster NSAIDs Neuralgia: Decrease severity of Zoster outbreaks Short course of Opiates Oral Tricyclics +/- Systemic corticosteroids Capsaicin cream Decrease long-term consequences i.e. post-herpetic neuralgia Pain usually improves over weeks to Topical Anesthetics Acceptable cost/benefit ratio months Nerve blocks Gabapentin 1800mg-3600 mg/d Pregabalin 150-600 mg Shingles Prevention Study Contraindications Conclusions: Risk of Zoster reduced by 51% compared to Any patient with a history of acquired or primary immunodeficiency states placebo such as: Leukemia/lymphoma Effect greatest in 60-69 y/o AIDS FDA approved for people aged 50 years and older High dose corticosteroids Active unrelated tuberculosis Reduced burden of illness by 61% Pregnancy Reduced incidence of PHN by 66.5% Active Zoster Reduced incidence of HZ by 51% History of anaphylactic reaction to gelatin, neomycin, or other vaccine component Actinic Actinic Keratoses Keratoses Actinic Keratosis Actinic Keratosis- Therapy Common, pre-cursors to Squamous Cell Carcinoma- .025%- Cryotherapy 16%/yr progress to SCC Topical 5-Fluorouracil Risk factors: age, male gender, fair skin, immunosuppression, Imiquimod lifetime sun exposure, albinism/ xeroderma pigmentosum Diclofenac- NSAID UVB triggers genetic mutations in keratinocytes Ingenol Mebutate P53 most altered tumor suppressor gene in AK/ SCC Photodynamic therapy Clinical: sun exposed areas, flat, erythematous, rough scale (better Dermabrasion/ chemical peels/ laser felt than seen) Systemic retinoids- transplant Actinic
Load more

Recommended publications
  • What Are Basal and Squamous Cell Skin Cancers?
    cancer.org | 1.800.227.2345 About Basal and Squamous Cell Skin Cancer Overview If you have been diagnosed with basal or squamous cell skin cancer or are worried about it, you likely have a lot of questions. Learning some basics is a good place to start. ● What Are Basal and Squamous Cell Skin Cancers? Research and Statistics See the latest estimates for new cases of basal and squamous cell skin cancer and deaths in the US and what research is currently being done. ● Key Statistics for Basal and Squamous Cell Skin Cancers ● What’s New in Basal and Squamous Cell Skin Cancer Research? What Are Basal and Squamous Cell Skin Cancers? Basal and squamous cell skin cancers are the most common types of skin cancer. They start in the top layer of skin (the epidermis), and are often related to sun exposure. 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 Cancer starts when cells in the body begin to grow out of control. Cells in nearly any part of the body can become cancer cells. To learn more about cancer and how it starts and spreads, see What Is Cancer?1 Where do skin cancers start? Most skin cancers start in the top layer of skin, called the epidermis. There are 3 main types of cells in this layer: ● Squamous cells: These are flat cells in the upper (outer) part of the epidermis, which are constantly shed as new ones form. When these cells grow out of control, they can develop into squamous cell skin cancer (also called squamous cell carcinoma).
    [Show full text]
  • Thrombotic Thrombocytopenic Purpura Due to Checkpoint Inhibitors
    Hindawi Case Reports in Hematology Volume 2018, Article ID 2464619, 4 pages https://doi.org/10.1155/2018/2464619 Case Report Thrombotic Thrombocytopenic Purpura due to Checkpoint Inhibitors Alexey Youssef,1 Nawara Kasso,2 Antonio Sergio Torloni,3 Michael Stanek,4 Tomislav Dragovich,5 Mark Gimbel,6 and Fade Mahmoud 6 1Centre for Tropical Medicine and Global Health, Nuffield Department of Medicine, University of Oxford, Oxford, UK 2Faculty of Medicine, Tishreen University, Lattakia, Syria 3Medical Director, Stem Cell )erapy, Apheresis, and Transfusion Medicine, Banner MD Anderson Cancer Center, Gilbert, AZ, USA 4Division of Hematology, Banner MD Anderson Cancer Center, Gilbert, AZ, USA 5Chief, Division of Medical Oncology and Hematology, Banner MD Anderson Cancer Center, Gilbert, AZ, USA 6)e T.W. Lewis Melanoma Center of Excellence, Banner MD Anderson Cancer Center, Gilbert, AZ, USA Correspondence should be addressed to Fade Mahmoud; [email protected] Received 16 September 2018; Revised 23 November 2018; Accepted 28 November 2018; Published 20 December 2018 Academic Editor: Akimichi Ohsaka Copyright © 2018 Alexey Youssef et al. ,is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Ipilimumab is a monoclonal antibody that enhances the efficacy of the immune system by targeting a cytotoxic T-lymphocyte- associated protein 4 (CTLA-4), which is a protein receptor that downregulates the immune system. Nivolumab is also a hu- manized monoclonal antibody that targets another protein receptor that prevents activated T cells from attacking the cancer; this receptor is called programmed cell death 1 (PD-1).
    [Show full text]
  • An Uncommon but Often Lethal Skin Cancer Could Be That Individual Melanoma Patients Cancers Can Be Assessed by Gene Expression to Answer These Questions
    HEALTH in the US and Australia are successfully actions of vitamin D, genetic alterations CONCLUSION treated by early surgery. However, 10 in the gene that controls the vitamin D At this point, the role of genetics in percent of melanomas have been highly receptor or related genes might reasonably melanoma is still unclear. While intense, recalcitrant to treatment. In the quest for be associated with poorer survival from intermittent sun exposure is clearly better understanding, multiple investiga- melanoma. It may be that individuals who important in the etiology of melanoma, tors are evaluating the role of genetic factors have aggressive melanoma have a different its importance for survival is not known. in survival. While excessive, intermittent set of genetic mutations from those com- Therefore, one cannot reliably say whether sun exposure is an important risk factor mon in more indolent melanomas. nature or nurture (i.e., behavior) is more Merkel Cell Carcinoma: for melanoma, it does not appear to be as- The genetic factors associated with important in either the etiology or the sociated with poorer melanoma survival. melanoma progression and survival are progression of melanoma. Hopefully, this Thus, genetic factors may be the culprit; it still being explored. While genetics in other uncertainty will continue to spur research An Uncommon But Often Lethal Skin Cancer could be that individual melanoma patients cancers can be assessed by gene expression to answer these questions. JAYASRI IYER, MD, AND PAUL NGHIEM, MD, PHD with a particular constellation of inherited analyses from fresh tumor tissue, this is ex- genetic mutations are those who have tremely difficult in melanoma, as primary DR.
    [Show full text]
  • A Brighter Future for Psoriasis Patients Melanoma and Skin Cancer Center
    Skin Health FROM THE MOUNT SINAI DEPARTMENT OF DERMATOLOGY FALL 2013 MESSAGE FROM THE CHAIR A Brighter Future for Psoriasis Patients By Mark G. Lebwohl, MD, Sol and Clara Kest Professor and Chair ount Sinai has been at the forefront of psoriasis research since Mthe 1980’s, when we introduced a topical combination regimen that remains the standard of care around the world even today. This consists of both a superpotent corticosteroid and a vitamin-D analog such as calcipotriene (Dovonex®) or calcitriol (Vectical®). The use of combination therapy led to the invention of Taclonex®, a popular and effective psoriasis formula that contains two topical agents. While refining the concept of combination therapy, we discovered that some topical preparations inactivate others, and subsequently we fostered the understanding that two or more ingredients, when applied together, must be shown to be compatible. In recent years this rule has been Dr. Mark G. Lebwohl embraced for all topical medicines, not just for psoriasis drugs. continued on page 4 BREAKING NEWS In This Issue Melanoma and Skin Cancer Center By Philip Friedlander, MD, PhD LASER HAIR REMOVAL Alan Kling, MD Page 2 he Tisch Cancer Institute is pleased to announce the creation of the Melanoma and TSkin Cancer Center, a virtual gathering place designed to provide a full array of medical LOOKING FAB THIS FALL resources to skin cancer patients. As part of its mission to deliver the highest quality of care, David S. Orentreich, MD the Center has assembled a team of leading specialists representing the fields of dermatology, Marina I. Peredo, MD medical oncology, surgery, dermatopathology, podiatry, and social work.
    [Show full text]
  • Merkel Cell Carcinoma: Update and Review Timothy S
    Merkel Cell Carcinoma: Update and Review Timothy S. Wang, MD,* Patrick J. Byrne, MD, FACS,† Lisa K. Jacobs, MD,‡ and Janis M. Taube, MD§ Merkel cell carcinoma (MCC) is a rare, aggressive, and often fatal cutaneous malignancy that is not usually suspected at the time of biopsy. Because of its increasing incidence and the discovery of a possible viral association, interest in MCC has escalated. Recent effort has broadened our breadth of knowledge regarding MCC and developed instruments to improve data collection and future study. This article provides an update on current thinking about the Merkel cell and MCC. Semin Cutan Med Surg 30:48-56 © 2011 Elsevier Inc. All rights reserved. erkel cell carcinoma (MCC) is a rare, aggressive, and current thinking, including novel insights into the Merkel Moften fatal cutaneous malignancy. It usually presents as cell; a review of the 2010 National Comprehensive Cancer a banal-appearing lesion and the diagnosis is rarely suspected Network (NCCN) therapeutic guidelines and new American at the time of biopsy. Because of increasing incidence and the Joint Committee on Cancer (AJCC) staging system; recom- discovery of a possible viral association, interest in MCC has mendations for pathologic reporting and new diagnostic escalated rapidly. codes; and the recently described Merkel cell polyoma virus From 1986 to 2001, the incidence of MCC in the United (MCPyV). States has tripled, and approximately 1500 new cases are diagnosed each year.1,2 MCC occurs most frequently among elderly white patients and perhaps slightly more commonly History in men. MCCs tend to occur on sun-exposed areas, with Merkel cells (MCs) were first described by Friedrich Merkel 3 nearly 80% presenting on the head, neck, and extremities.
    [Show full text]
  • Treatment of Psoriasis After Initiation of Nivolumab Therapy for Metastatic Malignant Melanoma: an Ancient Drug Revisited
    LETTER TO THE EDITOR DOI: 10.4274/jtad.galenos.2020.13007 J Turk Acad Dermatol 2020;14(3):93-94 Treatment of Psoriasis After Initiation of Nivolumab Therapy for Metastatic Malignant Melanoma: An Ancient Drug Revisited Gökhan Okan1, Kezban Nur Pilancı2, Cuyan Demirkesen3 1Private Dermatologist, Istanbul, Turkey 2Memorial Bahcelievler Hospital, Clinic of Oncology, Istanbul, Turkey 3Acibadem University Faculty of Medicine, Department of Pathology, Istanbul, Turkey Keywords: Checkpoint inhibitors, Nivolumab, Psoriasis, Melanoma, Sulfasalazine Dear Editor, Checkpoint inhibition can cause various immune-related adverse events in any organ but skin toxicity occurs most frequently [1]. We report de novo development of psoriasis vulgaris in a patient receiving nivolumab for treatment of metastatic melanoma which was controlled with sulfasalazine (SSZ). A 69-year-old male was initiated with nivolumab 3 mg/kg every two weeks for metastatic BRAF-negative melanoma of the back. The patient’s medical history was notable for arterial hypertension and dyslipidemia for which he has been medically treated. There was no personal or family history of psoriasis. One week after the fourth cycle of nivolumab, asymptomatic, sharply bordered, erythematous and scaly plaques were seen on the the anterolateral aspects of shins, dorsa of hands, feet, scalp, and trunk (Figure 1a). A skin biopsy revealed psoriasiform epidermal hyperplasia with prominent orthohyperkeratosis, and mounds of parakeratosis, containing neutrophils. The suprapapillary epidermis was thinned, and there were collections of neutrophils in the spinous layers which were consistent with psoriasis (Figure 1b, 1c). The patient had psoriasis area and severity index score of 12. He did not have psoriatic arthritis. The patient’s melanoma improved with nivolumab therapy but the skin lesions increased.
    [Show full text]
  • MAGE-A Expression in Oral and Laryngeal Leukoplakia Predicts Malignant Transformation
    Modern Pathology (2019) 32:1068–1081 https://doi.org/10.1038/s41379-019-0253-5 ARTICLE MAGE-A expression in oral and laryngeal leukoplakia predicts malignant transformation 1 2 1 1 1 5 Christoph A. Baran ● Abbas Agaimy ● Falk Wehrhan ● Manuel Weber ● Verena Hille ● Kathrin Brunner ● 3 3 4 1 1 Claudia Wickenhauser ● Udo Siebolts ● Emeka Nkenke ● Marco Kesting ● Jutta Ries Received: 15 October 2018 / Revised: 17 February 2019 / Accepted: 27 February 2019 / Published online: 1 April 2019 © United States & Canadian Academy of Pathology 2019 Abstract Leukoplakia is a potential precursor of oral as well as laryngeal squamous cell carcinoma. Risk assessment of malignant transformation based on the grade of dysplasia of leukoplakia often does not lead to reliable results. However, oral squamous cell carcinoma, laryngeal squamous cell carcinoma, and leukoplakia express single or multiple members of the melanoma- associated antigens A (MAGE-A) family, while MAGE-A are absent in healthy mucosal tissue. The present study aimed at determining if there is an association between the expression of MAGE-A in leukoplakia and malignant transformation to oral or laryngeal squamous cell carcinoma. Paraffin-embedded tissues of 205 oral and laryngeal leukoplakia, 90 1234567890();,: 1234567890();,: corresponding tumors, and 40 healthy oral mucosal samples were included in the study. The grade of dysplasia of the leukoplakia samples was determined histopathologically. The leukoplakia samples were divided into lesions that transformed to oral and laryngeal squamous cell carcinoma (n = 91) and lesions that did not (n = 114) during a 5 years follow-up. The expression of MAGE-A3/6 and MAGE-A4 was analyzed by real-time RT-PCR.
    [Show full text]
  • Actinic Keratosis
    ACTINIC KERATOSIS http://www.aocd.org An actinic keratosis is a scaly or crusty bump that forms on the skin surface. They are also called solar keratosis, sun spots, or precancerous spots. Dermatologists call them "AK's" for short. They range in size from as small as a pinhead to over an inch across. They may be light or dark, tan, pink, red, a combination of these, or the same color as ones skin. The scale or crust is horn-like, dry, and rough, and is often recognized easier by touch rather than sight. Occasionally they itch or produce a pricking or tender sensation, especially after being in the sun. They may disappear only to reappear later. Half of the keratosis will go away on their own if one avoid all sun for a few years. One often sees several actinic keratoses show up at the same time. Keratoses are most likely to appear on sun exposed areas: face, ears, bald scalp, neck, backs of hands and forearms, and lips. They may be flat or raised on appearance. Why is it dangerous? Actinic keratosis can be the first step in the development of skin cancer, and, therefore, is a precursor of cancer or a precancer. It is estimated that 10 to 15 percent of active lesions, which are redder and more tender than the rest will take the next step and progress to squamous cell carcinomas. These cancers are usually not life threatening, provided they are detected and treated in the early stages. However, if this is not done, they can bleed, ulcerate, become infected, or grow large and invade the surrounding tissues and, 3% of the time, will metastasize or spread to the internal organs.
    [Show full text]
  • Melanoma in a Psoriatic Plaque Nancy Tran, Plantation, Florida Harold S
    Melanoma in a Psoriatic Plaque Nancy Tran, Plantation, Florida Harold S. Rabinovitz, MD, Plantation, Florida Margaret Oliviero, RN, MSN, Plantation, Florida Alfred Kopf, MD, New York, New York This is the first reported case of a melanoma in a psoriatic plaque. The clinical, dermoscopic, and histologic features of this case are detailed. A re- view of the risk of melanoma among patients treated with psoralen-ultraviolet A is presented. his report details the case of a 45-year-old man diagnosed with melanoma within a psoriatic T plaque. The patient had no history of psoralen- ultraviolet A (PUVA) treatment. This is the first such reported case. Case Report A 45-year-old man was referred for evaluation of his long history of psoriasis for which he had never sought treatment. He noted that the psoriasis had worsened over the past several months. He also reported hav- ing a “mole” on his left upper back since birth. Over the past 2 years, he noticed that the mole had slowly increased in size, and over the past few weeks, it had gradually darkened. The patient believed this was due to the fact that he had banged his shoulder and trau- matized the lesion. He had no personal history of skin cancer. His father had a non-melanoma skin cancer, however, there was no family history of melanoma. Physical examination revealed extensive psoriatic plaques on his chest, arms, and legs. On his left up- per back, he had a psoriatic plaque, which measured FIGURE 1. A psoriatic plaque on the left, upper back.
    [Show full text]
  • Melanoma Detection: Different Tools for Different Populations
    Melanoma detection: Different tools for different populations Sancy Leachman, MD, PhD Internal Medicine Review - Breakout 2/5/2020 No Relevant Conflicts of Interest MoleMapper (iPhone App) free & open source Non-topic related COI: Myriad Genetic Laboratories (early access) Castle BioSciences (early access) Palvella Therapeutics (advisory board) DermDetect (Business Associate Agreement) Merck (advisory board) Orlucent (advisory board Today’s Objectives • Evaluate the Lesion: Practice visual identification • Biopsy: Identify melanoma biopsy guidelines • Resources: Identify where to find further CME and un- branded patient education materials How to perform a total body skin examination Opportunistic exam: • Exam areas of skin that are readily available without having the patient change into a gown Rapid total body skin examination: • 5 minutes or less • Start with the scalp/face, then work your way down • Do it in the same order every time Thorough skin examination +/- dermoscopy: • Necessary for patients with numerous nevi • Consider referral to derm Self-Exams: Empowering Patients • Performance of a monthly Total Self-Skin Exam (TSSE) is associated with thinner melanomas and reduced mortality • Roughly 75% of melanomas are first detected by the patient, not the provider • Patients should conduct a TSSE once a month to look for new, changing, or non-healing lesions 5 Self Exams and Partner Exams • Use mirrors (ideally full-length and hand mirror) to examine skin from head to toe • If available, a partner can assist in monitoring difficult-to-see
    [Show full text]
  • Skin Cancer for Dental Professionals
    ARTICLE CPD: ONE HOUR Skin cancer for dental professionals ©iStockphoto/Thinkstock Visiting the dental practice is a valuable opportunity for skin cancer screening, says Ben J. Steel.1 kin cancer is the commonest Examination of the oral mucosa for signs of ad hoc screening for head and neck skin form of cancer in the UK. In of oral squamous cell carcinoma and other malignancy. Patients with suspicious lesions 2010, 112,367 skin cancers were mucosal conditions is an accepted part of could be referred to their general medical registered in the UK out of a the normal dental check-up, as is an extra- practitioner (GP) or an oral and maxillofacial total of 424,128 cancers of all oral examination to check the facial hard surgeon for further management. types.1 Three main types are and soft tissues, jaw joints and cervicofacial This article will present an overview of the Srecognised: basal cell carcinoma (BCC) lymph nodes.2 A brief look at the head three forms of skin cancer most likely to be and squamous cell carcinoma (SCC), and neck skin for suspicious lesions could seen among dental patients in the UK. which collectively comprise non-melanoma easily be incorporated into this structure. skin cancer (NMSC), and malignant In the two years leading to September 2012, BASAL CELL CARCINOMA melanoma (MM). 29.6 million people in the UK attended a Epidemiology dentist, representing some 52.1% of the This is the commonest type of skin cancer, 1Medical student, Hull York Medical adult population.3 With such a considerable and indeed any cancer, in the UK, with at School; general dental practitioner, proportion of the population passing through, least 48,000 cases registered in England each Hull Royal Infirmary there exists a valuable opportunity for a form year between 2004 and 2006.4 This is believed 09 BDJ Team www.nature.com/BDJTeam © 2014 Macmillan Publishers Limited.
    [Show full text]
  • Cutaneous Events Associated with Immunotherapy of Melanoma: a Review
    Journal of Clinical Medicine Review Cutaneous Events Associated with Immunotherapy of Melanoma: A Review Lorenza Burzi 1,†, Aurora Maria Alessandrini 2,3,†, Pietro Quaglino 1, Bianca Maria Piraccini 2,3, Emi Dika 2,3,† and Simone Ribero 1,*,† 1 Department of Medical Sciences, Dermatology Clinic, University of Turin, 10126 Turin, Italy; [email protected] (L.B.); [email protected] (P.Q.) 2 Dermatology, Department of Experimental Diagnostic and Specialty Medicine (DIMES), University of Bologna, 40138 Bologna, Italy; [email protected] (A.M.A.); [email protected] (B.M.P.); [email protected] (E.D.) 3 Dermatology, IRCCS Sant’Orsola Hospital, 40138 Bologna, Italy * Correspondence: [email protected] † Equal Contribution. Abstract: Immunotherapy with checkpoint inhibitors significantly improves the outcome for stage III and IV melanoma. Cutaneous adverse events during treatment are often reported. We herein aim to review the principal pigmentation changes induced by immune check-point inhibitors: the appear- ance of vitiligo, the Sutton phenomenon, melanosis and hair and nail toxicities. Keywords: melanoma; immunotherapy; pigmentation disorders; vitiligo; melanosis; halo nevus; alopecia; poliosis Citation: Burzi, L.; Alessandrini, A.M.; Quaglino, P.; Piraccini, B.M.; 1. Introduction Dika, E.; Ribero, S. Cutaneous Events The function of the immune system in melanoma disease course is well established. Associated with Immunotherapy of Immune checkpoint inhibitors have shown promise in enhancing the immune system to Melanoma: A Review. J. Clin. Med. fight against cancer cells and in providing a higher response rates than chemotherapies 2021, 10, 3047. https://doi.org/ used in the past [1,2]. 10.3390/jcm10143047 Tumor cells inactivate the process of immunosurveillance by expressing ligands Academic Editor: Masutaka Furue of immune checkpoint pathways.
    [Show full text]