Compensation for Occupational Skin Diseases
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Contact Vitiligo Following Allergic Contact Dermatitis *Ricardo Ruiz-Villaverde, Francisco J Navarro-Triviño
SUBMITTED 19 JAN 21 REVISION REQ. 17 MAR 21; REVISION 5 APR 21 ACCEPTED 21 APR 21 ONLINE-FIRST: MAY 2021 DOI: https://doi.org/10.18295/squmj.5.2021.078 Contact Vitiligo Following Allergic Contact Dermatitis *Ricardo Ruiz-Villaverde, Francisco J Navarro-Triviño Department of Dermatology, Hospital Universitario San Cecilio, Granada, Spain *Corresponding Author’s e-mail: [email protected] Introduction A 45-year-old man, construction worker, with no personal history of psoriasis, atopic dermatitis, and vitiligo, was referred to our Contact Eczema Department with a chronic hand eczema and skin depigmentation over a period of 12 months. Skin depigmentation appeared few months later regarding the primary eczema. The patient reported the use of rubber gloves for many years. He had noticed itching and mild erythema over both hands. Currently, he wears nitrile gloves at work. Physical examination showed symmetric erythematous-squamous, hyperkeratotic and fissured plaques on both hands (Fig. 1A), and ventral aspect of wrists (Fig. 1B). Skin depigmentation areas showed irregular edges (Fig. 1C). Wood´s lamp examination accentuated the depigmentation areas overlap the eczema (Fig. 2A-B), without vitiligo pattern. No other anatomical sites were involved. Blood test showed no significant alterations, including data from autoimmune thyroiditis, celiac disease, and pernicious anaemia. Patch tests were performed with the European Comprehensive Baseline Series (Chemotechnique Diagnostics, Vellinge, Sweden), rubber additives series (Chemotechnique Diagnostics), and hydroquinone monobenzylether 1% pet (Shoe series, Chemotechnique Diagnosis). The results were interpreted according to the criteria of the International Contact Dermatitis Research Group. Patch tests were read on day (D) 2 and D4. -
Chloracne: from Clinic to Research
DERMATOLOGICA SINICA 30 (2012) 2e6 Contents lists available at SciVerse ScienceDirect Dermatologica Sinica journal homepage: http://www.derm-sinica.com REVIEW ARTICLE Chloracne: From clinic to research Qiang Ju 1, Kuochia Yang 2, Christos C. Zouboulis 3, Johannes Ring 4, Wenchieh Chen 4,* 1 Department of Dermatology, Shanghai Skin Disease and STD Hospital, Shanghai, People’s Republic of China 2 Department of Dermatology, Changhua Christian Hospital, Changhua, Taiwan 3 Departments of Dermatology, Venereology, Allergology and Immunology, Dessau Medical Center, Dessau, Germany 4 Department of Dermatology and Allergy, Technische Universität München, Munich, Germany article info abstract Article history: Chloracne is the most sensitive and specific marker for a possible dioxin (2,3,7,8-tetrachlorodibenzo-p- Received: Oct 31, 2011 dioxin) intoxication. It is clinically characterized by multiple acneiform comedone-like cystic eruptions Revised: Nov 9, 2011 mainly involving face in the malar, temporal, mandibular, auricular/retroauricular regions, and the Accepted: Nov 9, 2011 genitalia, often occurring in age groups not typical for acne vulgaris. Histopathology is essential for adefinite diagnosis, which exhibits atrophy or absence of sebaceous glands as well as infundibular Keywords: dilatation or cystic formation of hair follicles, hyperplasia of epidermis, and hyperpigmentation of aryl hydrocarbon receptor stratum corneum. The appearance of chloracne and its clinical severity does not correlate with the blood chloracne “ ” 2,3,7,8-tetrachlorodibenzo-p-dioxin levels of dioxins. Pathogenesis of chloracne remains largely unclear. An aryl hydrocarbon receptor - polyhalogenated aromatic hydrocarbons mediated signaling pathway affecting the multipotent stem cells in the pilosebaceous units is probably sebaceous gland the major molecular mechanism inducing chloracne. -
Scalp Eczema Factsheet the Scalp Is an Area of the Body That Can Be Affected by Several Types of Eczema
12 Scalp eczema factsheet The scalp is an area of the body that can be affected by several types of eczema. The scalp may be dry, itchy and scaly in a chronic phase and inflamed (red), weepy and painful in an acute (eczema flare) phase. Aside from eczema, there are a number of reasons why the scalp can become dry and itchy (e.g. psoriasis, fungal infection, ringworm, head lice etc.), so it is wise to get a firm diagnosis if there is uncertainty. Types of eczema • Hair clips and headgear – especially those containing that affect the scalp rubber or nickel. Seborrhoeic eczema (dermatitis) is one of the most See the NES booklet on Contact Dermatitis for more common types of eczema seen on the scalp and hairline. details. It can affect babies (cradle cap), children and adults. The Irritant contact dermatitis is a type of eczema that skin appears red and scaly and there is often dandruff as occurs when the skin’s surface is irritated by a substance well, which can vary in severity. There may also be a rash that causes the skin to become dry, red and itchy. on other parts of the face, such as around the eyebrows, For example, shampoos, mousses, hair gels, hair spray, eyelids and sides of the nose. Seborrhoeic eczema can perm solution and fragrance can all cause irritant contact become infected. See the NES factsheets on Adult dermatitis. See the NES booklet on Contact Dermatitis for Seborrhoeic Dermatitis and Infantile Seborrhoeic more details. Dermatitis and Cradle Cap for more details. -
General Dermatology an Atlas of Diagnosis and Management 2007
An Atlas of Diagnosis and Management GENERAL DERMATOLOGY John SC English, FRCP Department of Dermatology Queen's Medical Centre Nottingham University Hospitals NHS Trust Nottingham, UK CLINICAL PUBLISHING OXFORD Clinical Publishing An imprint of Atlas Medical Publishing Ltd Oxford Centre for Innovation Mill Street, Oxford OX2 0JX, UK tel: +44 1865 811116 fax: +44 1865 251550 email: [email protected] web: www.clinicalpublishing.co.uk Distributed in USA and Canada by: Clinical Publishing 30 Amberwood Parkway Ashland OH 44805 USA tel: 800-247-6553 (toll free within US and Canada) fax: 419-281-6883 email: [email protected] Distributed in UK and Rest of World by: Marston Book Services Ltd PO Box 269 Abingdon Oxon OX14 4YN UK tel: +44 1235 465500 fax: +44 1235 465555 email: [email protected] © Atlas Medical Publishing Ltd 2007 First published 2007 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, without the prior permission in writing of Clinical Publishing or Atlas Medical Publishing Ltd. Although every effort has been made to ensure that all owners of copyright material have been acknowledged in this publication, we would be glad to acknowledge in subsequent reprints or editions any omissions brought to our attention. A catalogue record of this book is available from the British Library ISBN-13 978 1 904392 76 7 Electronic ISBN 978 1 84692 568 9 The publisher makes no representation, express or implied, that the dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up-to-date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. -
Allergic Contact Rashes Allergic Contact Dermatitis Is Caused by the Body’S Reaction to Something That It Comes in Direct Skin Contact with It
1812 W. Burbank Blvd. #1046 | Burbank, CA 91506 Tel: (877) 822-2223 | Fax: (323) 935-8804 DermLA.com Allergic Contact Rashes Allergic contact dermatitis is caused by the body’s reaction to something that it comes in direct skin contact with it. Many different substances can cause allergic contact dermatitis, and we call these substances “allergens”. Usually this substance causes no trouble for most people, and may not even be noticed the first time the person is exposed. But once the skin becomes sensitive or allergic to the substance, any exposure will produce a rash. The rash usually doesn’t start until a day or two later, but can start a soon as hours or as late as weeks. You can become allergic or sensitive to anything at anytime, even a product you have used for years. Allergic contact dermatitis is not usually caused by things like acid, alkali, solvent, strong soap or detergent. These harsh compounds, which can produce a reaction on anyone’s skin, are known as “irritants.” Although some chemicals are both irritants and allergens, allergic contact dermatitis results from brief contact with substances that don’t usually provoke a reaction in most people. The dermatitis usually shows redness, swelling and water blisters, from tiny to large. The blisters may break,forming crusts and scales. Untreated, the skin may darken and become leathery and cracked. Allergic contact dermatitis can be difficult to distinguish from other rashes, especially after it been present for a while. The dermatologist and patient will discuss the materials that touch the person’s skin at work and home, and try to identify the allergen. -
Allergic Contact Dermatitis with Sparing of Exposed Psoriasis Plaques
CASE LETTER Allergic Contact Dermatitis With Sparing of Exposed Psoriasis Plaques Eric Sorenson, MD; Kourosh Beroukhim, MD; Catherine Nguyen, MD; Melissa Danesh, MD; John Koo, MD; Argentina Leon, MD were noted on the face, trunk, arms, and legs, sparing the PRACTICE POINTS well-demarcated scaly psoriatic plaques on the arms and • Patients with plaque-type psoriasis who experience legs (Figure). The patient was given intravenous fluids allergic contact dermatitis (ACD) may present with and intravenous diphenhydramine. After responding to sparing of exposed psoriatic plaques. initial treatment, the patient was discharged with ibupro- • The divergent immunologic milieus present in ACD fen and a taperingcopy dose of oral prednisone from 60 mg and psoriasis likely underly the decreased incidence 5 times daily, to 40 mg 5 times daily, to 20 mg 5 times of ACD in patients with psoriasis. daily over 15 days. Allergic contact dermatitis occurs after sensitization to environmental allergens or haptens. Clinically, ACD is characterizednot by pruritic, erythematous, vesicular papules To the Editor: and plaques. The predominant effector cells in ACD are Allergic contact dermatitis (ACD) is a delayed-type hypersensitivity reaction against antigens to whichDo the skin’s immune system was previously sensitized. The initial sensitization requires penetration of the antigen through the stratum corneum. Thus, the ability of a par- ticle to cause ACD is related to its molecular structure and size, lipophilicity, and protein-binding affinity, as well as the dose and duration of exposure.1 Psoriasis typically presents as well-demarcated areas of skin that may be erythematous, indurated, and scaly to variable degrees. Histologically, psoriasis plaquesCUTIS are characterized by epidermal hyperplasia in the presence of a T-cell infiltrate and neutrophilic microabscesses. -
Pigmented Contact Dermatitis and Chemical Depigmentation
18_319_334* 05.11.2005 10:30 Uhr Seite 319 Chapter 18 Pigmented Contact Dermatitis 18 and Chemical Depigmentation Hideo Nakayama Contents ca, often occurs without showing any positive mani- 18.1 Hyperpigmentation Associated festations of dermatitis such as marked erythema, with Contact Dermatitis . 319 vesiculation, swelling, papules, rough skin or scaling. 18.1.1 Classification . 319 Therefore, patients may complain only of a pigmen- 18.1.2 Pigmented Contact Dermatitis . 320 tary disorder, even though the disease is entirely the 18.1.2.1 History and Causative Agents . 320 result of allergic contact dermatitis. Hyperpigmenta- 18.1.2.2 Differential Diagnosis . 323 tion caused by incontinentia pigmenti histologica 18.1.2.3 Prevention and Treatment . 323 has often been called a lichenoid reaction, since the 18.1.3 Pigmented Cosmetic Dermatitis . 324 presence of basal liquefaction degeneration, the ac- 18.1.3.1 Signs . 324 cumulation of melanin pigment, and the mononucle- 18.1.3.2 Causative Allergens . 325 ar cell infiltrate in the upper dermis are very similar 18.1.3.3 Treatment . 326 to the histopathological manifestations of lichen pla- 18.1.4 Purpuric Dermatitis . 328 nus. However, compared with typical lichen planus, 18.1.5 “Dirty Neck” of Atopic Eczema . 329 hyperkeratosis is usually milder, hypergranulosis 18.2 Depigmentation from Contact and saw-tooth-shape acanthosis are lacking, hyaline with Chemicals . 330 bodies are hardly seen, and the band-like massive in- 18.2.1 Mechanism of Leukoderma filtration with lymphocytes and histiocytes is lack- due to Chemicals . 330 ing. 18.2.2 Contact Leukoderma Caused Mainly by Contact Sensitization . -
Abstracts from the 9Th World Congress on Itch October 15–17, 2017
ISSN 0001-5555 ActaDV Volume 97 2017 SEPTEMBER, No. 8 ADVANCES IN DERMATOLOGY AND VENEREOLOGY A Non-profit International Journal for Interdisciplinary Skin Research, Clinical and Experimental Dermatology and Sexually Transmitted Diseases Abstracts from the 9th World Congress on Itch October 15–17, 2017 Official Journal of - European Society for Dermatology and Wroclaw, Poland Psychiatry Affiliated with - The International Forum for the Study of Itch Immediate Open Access Acta Dermato-Venereologica www.medicaljournals.se/adv Abstracts from the 9th World Congress on Itch DV cta A enereologica V Organizing Committee Scientific Committee ermato- Congress President: Jacek C Szepietowski (Wroclaw, Poland) Jeffrey D. Bernhard (Massachusetts, USA) D Congress Secretary General: Adam Reich (Rzeszów, Poland) Earl Carstens (Davis, USA) Congress Secretary: Edyta Lelonek (Wroclaw, Poland) Toshiya Ebata (Tokyo, Japan) cta Alan Fleischer (Lexington, USA) A IFSI President: Earl Carstens (Davis, USA) IFSI Vice President: Elke Weisshaar (Heidelberg, Germany) Ichiro Katayama (Osaka, Japan) Ethan Lerner (Boston, USA) Staff members of the Department of Dermatology, Venereology and Allergology, Wroclaw Medical University, Wroclaw, Poland Thomas Mettang (Wiesbaden, Germany) Martin Schmelz (Mannheim, Germany) Sonja Ständer (Münster, Germany) DV Jacek C. Szepietowski (Wroclaw, Poland) cta Kenji Takamori (Tokyo, Japan) A Elke Weisshaar (Heidelberg, Germany) Gil Yosipovitch (Miami, USA) Contents of this Abstract book Program 1000 Abstracts: Lecture Abstracts 1008 Poster Abstracts 1035 Author Index 1059 dvances in dermatology and venereology A www.medicaljournals.se/acta doi: 10.2340/00015555-2773 Journal Compilation © 2017 Acta Dermato-Venereologica. Acta Derm Venereol 2017; 97: 999–1060 1000 9th World Congress of Itch Sunday, October 15, 2017 Abstract # 1:30-3:30 PM IFSI Board meeting DV 5:00-5:20 PM OPENING CEREMONY 5:00-5:10 PM Opening remarks cta Jacek C. -
Copyrighted Material
1 Index Note: Page numbers in italics refer to figures, those in bold refer to tables and boxes. References are to pages within chapters, thus 58.10 is page 10 of Chapter 58. A definition 87.2 congenital ichthyoses 65.38–9 differential diagnosis 90.62 A fibres 85.1, 85.2 dermatomyositis association 88.21 discoid lupus erythematosus occupational 90.56–9 α-adrenoceptor agonists 106.8 differential diagnosis 87.5 treatment 89.41 chemical origin 130.10–12 abacavir disease course 87.5 hand eczema treatment 39.18 clinical features 90.58 drug eruptions 31.18 drug-induced 87.4 hidradenitis suppurativa management definition 90.56 HLA allele association 12.5 endocrine disorder skin signs 149.10, 92.10 differential diagnosis 90.57 hypersensitivity 119.6 149.11 keratitis–ichthyosis–deafness syndrome epidemiology 90.58 pharmacological hypersensitivity 31.10– epidemiology 87.3 treatment 65.32 investigations 90.58–9 11 familial 87.4 keratoacanthoma treatment 142.36 management 90.59 ABCA12 gene mutations 65.7 familial partial lipodystrophy neutral lipid storage disease with papular elastorrhexis differential ABCC6 gene mutations 72.27, 72.30 association 74.2 ichthyosis treatment 65.33 diagnosis 96.30 ABCC11 gene mutations 94.16 generalized 87.4 pityriasis rubra pilaris treatment 36.5, penile 111.19 abdominal wall, lymphoedema 105.20–1 genital 111.27 36.6 photodynamic therapy 22.7 ABHD5 gene mutations 65.32 HIV infection 31.12 psoriasis pomade 90.17 abrasions, sports injuries 123.16 investigations 87.5 generalized pustular 35.37 prepubertal 90.59–64 Abrikossoff -
Pili Torti: a Feature of Numerous Congenital and Acquired Conditions
Journal of Clinical Medicine Review Pili Torti: A Feature of Numerous Congenital and Acquired Conditions Aleksandra Hoffmann 1 , Anna Wa´skiel-Burnat 1,*, Jakub Z˙ ółkiewicz 1 , Leszek Blicharz 1, Adriana Rakowska 1, Mohamad Goldust 2 , Małgorzata Olszewska 1 and Lidia Rudnicka 1 1 Department of Dermatology, Medical University of Warsaw, Koszykowa 82A, 02-008 Warsaw, Poland; [email protected] (A.H.); [email protected] (J.Z.);˙ [email protected] (L.B.); [email protected] (A.R.); [email protected] (M.O.); [email protected] (L.R.) 2 Department of Dermatology, University Medical Center of the Johannes Gutenberg University, 55122 Mainz, Germany; [email protected] * Correspondence: [email protected]; Tel.: +48-22-5021-324; Fax: +48-22-824-2200 Abstract: Pili torti is a rare condition characterized by the presence of the hair shaft, which is flattened at irregular intervals and twisted 180◦ along its long axis. It is a form of hair shaft disorder with increased fragility. The condition is classified into inherited and acquired. Inherited forms may be either isolated or associated with numerous genetic diseases or syndromes (e.g., Menkes disease, Björnstad syndrome, Netherton syndrome, and Bazex-Dupré-Christol syndrome). Moreover, pili torti may be a feature of various ectodermal dysplasias (such as Rapp-Hodgkin syndrome and Ankyloblepharon-ectodermal defects-cleft lip/palate syndrome). Acquired pili torti was described in numerous forms of alopecia (e.g., lichen planopilaris, discoid lupus erythematosus, dissecting Citation: Hoffmann, A.; cellulitis, folliculitis decalvans, alopecia areata) as well as neoplastic and systemic diseases (such Wa´skiel-Burnat,A.; Zółkiewicz,˙ J.; as cutaneous T-cell lymphoma, scalp metastasis of breast cancer, anorexia nervosa, malnutrition, Blicharz, L.; Rakowska, A.; Goldust, M.; Olszewska, M.; Rudnicka, L. -
Occupational Skin Disease C.J
Postgraduate Medical Journal (1989) 65, 374- 380 Postgrad Med J: first published as 10.1136/pgmj.65.764.374 on 1 June 1989. Downloaded from Occupational Medicine Occupational skin disease C.J. Stevenson Department ofOccupational Health and Hygiene, University ofNewcastle upon Tyne, Newcastle upon Tyne, UK. Introduction Diagnosis ofoccupational skin disease It is opportune to discuss occupational skin disorders Early diagnosis depends upon awareness of the pos- since recently a 'Save your Skin' Campaign has been sibility that a presenting dermatosis can be occupa- undertaken in the United Kingdom by the Employ- tional in origin. Sometimes the dermatosis is quite ment Advisory Service of the Health and Safety specific for exposure to a chemical, for example the Executive to increase the awareness of employers and lichenoid dermatosis seen in persons working with employees of the need to prevent skin problems in colour developers.3 Sometimes the dermatosis is a industry.' This was justified because skin disorders lookalike of a non-occupational disorder, such as caused by substances at work are the most common vitiligo, and sometimes we are faced with contact occupational health problem. dermatitis which could equally well be due to an Contact dermatitis (eczematous dermatitis of offending substance in the domestic environment. It is predominantly exogenous aetiology) is the com- important to realise that the environment is constantly monest form of occupational skin disease. However, changing and new processes are being introduced. For other occupational skin disorders occur, often presen- example, grass cutting by strimmers is now known to ting to physicians of different disciplines, for example cause a distinctive phytophotodermatosis in some infectious conditions, occupational skin cancer, individuals.4 copyright. -
Acne and Related Conditions
Rosanne Paul, DO Madeline Tarrillion, DO Miesha Merati, DO Gregory Delost, DO Emily Shelley, DO Jenifer R. Lloyd, DO, FAAD American Osteopathic College of Dermatology Disclosures • We do not have any relevant disclosures. Cleveland before June 2016 Cleveland after June 2016 Overview • Acne Vulgaris • Folliculitis & other – Pathogenesis follicular disorders – Clinical Features • Variants – Treatments • Rosacea – Pathogenesis – Classification & clinical features • Rosacea-like disorders – Treatment Acne vulgaris • Pathogenesis • Multifactorial • Genetics – role remains uncertain • Sebum – hormonal stimulation • Comedo • Inflammatory response • Propionibacterium acnes • Hormonal influences • Diet Bolognia et al. Dermatology. 2012. Acne vulgaris • Clinical Features • Face & upper trunk • Non-inflammatory lesions • Open & closed comedones • Inflammatory lesions • Pustules, nodules & cysts • Post-inflammatory hyperpigmentation • Scarring • Pitted or hypertrophic Bolognia et al. Dermatology. 2012. Bolognia et al. Dermatology. 2012. Acne variants • Acne fulminans • Acne conglobata • PAPA syndrome • Solid facial edema • Acne mechanica • Acne excoriée • Drug-induced Bolognia et al. Dermatology. 2012. Bolognia et al. Dermatology. 2012. Bolognia et al. Dermatology. 2012. Bolognia et al. Dermatology. 2012. Acne variants • Occupational • Chloracne • Neonatal acne (neonatal cephalic pustulosis) • Infantile acne • Endocrinological abnormalities • Apert syndrome Bolognia et al. Dermatology. 2012. Bolognia et al. Dermatology. 2012. Acne variants • Acneiform