Alopecias in Lupus Erythematosus
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Dissecting Cellulitis
Patient Information Leaflet Dr Paul Farrant FRCP Consultant Dermatologist Janet Dix (Secretary to Dr Paul Farrant) Tel 01444 412273 Fax 01444 657397 Email [email protected] Web drpaulfarrant.co.uk Dissecting Cellulitis What is dissecting cellulitis? Dissecting cellulitis is a type of scarring hair loss that presents with pustules, boggy swellings, and sinuses within the scalp. What causes dissecting cellulitis? The cause of dissecting cellulitis is not known. It is associated with severe cystic acne known as acne conglobata, and hidradenitis suppurativa, which causes cystic swellings in the armpits and groin. In all of these conditions the hair follicle becomes blocked, dilates and ruptures. This causes an inflammatory response in the skin, which leads to pus formation, swellings and sinus formation. It is not uncommon for bacteria to be isolated from the skin but this is likely to be secondary to the inflammatory process. Is dissecting cellulitis inherited? Dissecting cellulitis is most commonly seen in Afro-Caribbean men but the racial predilection is more likely to be due to the shape and structural differences of Afro-Caribbean hair than a genetic predisposition to the condition. Hair care practices, such as clipping, may also play a role. It is not thought to be an inherited condition. What are the symptoms? Patients with dissecting cellulitis often complain of pain, tenderness and fluid discharge from the affected area. It is associated with hair loss. What does dissecting cellulitis look like? Dissecting Cellulitis is characterised by a localised area of hair loss, pustules, boggy swellings and sinus formation. Gentle pressure on the boggy areas may lead to expression of pus or serous fluid. -
Guidelines of Care for the 10 Most Common Dermatologic Diseases
1 Guidelines of Care for the 10 most common dermatologic diseases: Copyright by the American Academy of Dermatology, Inc. Disclaimer Adherence to these guidelines will not ensure successful treatment in every situation. Further, these guidelines should not be deemed inclusive of all proper methods of care or exclusive of other methods of care reasonably directed to obtaining the same results. The ultimate judgment regarding the propriety of any specific procedure must be made by the physician in light of all the circumstances presented by the individual patient. For the benefit of members of the American Academy of Dermatology who practice in countries outside the jurisdiction of the United States, the listed treatments may include agents that not currently approved by the U.S. Food and Drug Administration. 1. Acne Vulgaris 2. Alopecia Areata 3. Atopic Dermatitis 4. Contact Dermatitis 5. Cutaneous Adverse Drug Reactions 6. Nail Disorders 7. Psoriasis 8. Superficial Mycotic Infections of the Skin: Mucocutaneous Candidiasis, Onychomycosis, Piedra, Pityriasis, Tinea Capitis , Tinea Barbae, Tinea Corporis, Tinea Cruris, Tinea Faciei, Tinea Manuum, and Tinea Pedis. 9. Vitiligo 10. Warts: Human Papillomavirus 1 2 1- Guidelines of Care for Acne Vulgaris* Reference: 1990 by the American Academy of Dermatology, Inc. I. Introduction The American Academy of Dermatology’s Committee on Guidelines of Care is developing guidelines of care for our profession. The development of guidelines will promote the continued delivery of quality care and assist those outside our profession in understanding the complexities and boundaries of care provided by dermatologists. II. Definition Acne vulgaris is a follicular disorder that affects susceptible pilosebaceous follicles, primarily of the face, neck, and upper trunk, and is characterized by both noninflammatory and inflammatory lesions. -
Negative Emotions in Skin Disorders: a Systematic Review
REVIEW ARTICLE Negative Emotions in Skin Disorders: A Systematic Review Emociones negativas en enfermedades de la piel: una revisión sistemática Carmela Mento1, Amelia Rizzo2?, Maria Rosaria Anna Muscatello2, Rocco Antonio Zoccali2, Antonio Bruno2 1Department of Cognitive Sciences, Psychological, Educational and Cultural Studies, ◦ University of Messina, Italy. Vol 13, N 1 2Department of Biomedical and Dental Sciences and Morphofunctional Imaging, https://revistas.usb.edu.co/index.php/IJPR University of Messina, Italy. ISSN 2011-2084 E-ISSN 2011-7922 Abstract. The main purpose of this study is to describe how negative emotions were investigated in the sphere of dermatological diseases, in order (1) to summarize literature trends about skin disorders and emotions, (2) to highlight any imbalances between the most studied and neglected emotions, (3) and to offer directions for future research. A computerized literature search provided 41 relevant and potentially eligible studies. Results showed that the study of emotions in skin disease is limited to Sadness/depression and Fear/anxiety. The emotions of Anger and Disgust have been poorly explored in empirical studies, despite they could be theoretically considered a vulnerability factor for OPEN ACCESS the development of skin disorders and the dermatological extreme consequences, as negative emotionality toward self and the pathological skin condition. The Editor: Jorge Mauricio Cuartas Arias, bibliometric qualitative analysis with VOSViewer software revealed that the Universidad de San Buenaventura, majority of the studies have been focused on the relationships between vitiligo Medellín, Colombia and Sadness/depression, dermatitis and Fear/anxiety, psoriasis, and Anger, suggesting the need of future research exploring Disgust and, in general, a wider Manuscript received: 30–04–2019 Revised:15–08–2019 emotional spectrum. -
Pediatric and Adolescent Dermatology
Pediatric and adolescent dermatology Management and referral guidelines ICD-10 guide • Acne: L70.0 acne vulgaris; L70.1 acne conglobata; • Molluscum contagiosum: B08.1 L70.4 infantile acne; L70.5 acne excoriae; L70.8 • Nevi (moles): Start with D22 and rest depends other acne; or L70.9 acne unspecified on site • Alopecia areata: L63 alopecia; L63.0 alopecia • Onychomycosis (nail fungus): B35.1 (capitis) totalis; L63.1 alopecia universalis; L63.8 other alopecia areata; or L63.9 alopecia areata • Psoriasis: L40.0 plaque; L40.1 generalized unspecified pustular psoriasis; L40.3 palmoplantar pustulosis; L40.4 guttate; L40.54 psoriatic juvenile • Atopic dermatitis (eczema): L20.82 flexural; arthropathy; L40.8 other psoriasis; or L40.9 L20.83 infantile; L20.89 other atopic dermatitis; or psoriasis unspecified L20.9 atopic dermatitis unspecified • Scabies: B86 • Hemangioma of infancy: D18 hemangioma and lymphangioma any site; D18.0 hemangioma; • Seborrheic dermatitis: L21.0 capitis; L21.1 infantile; D18.00 hemangioma unspecified site; D18.01 L21.8 other seborrheic dermatitis; or L21.9 hemangioma of skin and subcutaneous tissue; seborrheic dermatitis unspecified D18.02 hemangioma of intracranial structures; • Tinea capitis: B35.0 D18.03 hemangioma of intraabdominal structures; or D18.09 hemangioma of other sites • Tinea versicolor: B36.0 • Hyperhidrosis: R61 generalized hyperhidrosis; • Vitiligo: L80 L74.5 focal hyperhidrosis; L74.51 primary focal • Warts: B07.0 verruca plantaris; B07.8 verruca hyperhidrosis, rest depends on site; L74.52 vulgaris (common warts); B07.9 viral wart secondary focal hyperhidrosis unspecified; or A63.0 anogenital warts • Keratosis pilaris: L85.8 other specified epidermal thickening 1 Acne Treatment basics • Tretinoin 0.025% or 0.05% cream • Education: Medications often take weeks to work AND and the patient’s skin may get “worse” (dry and red) • Clindamycin-benzoyl peroxide 1%-5% gel in the before it gets better. -
A Review of the Evidence for and Against a Role for Mast Cells in Cutaneous Scarring and Fibrosis
International Journal of Molecular Sciences Review A Review of the Evidence for and against a Role for Mast Cells in Cutaneous Scarring and Fibrosis Traci A. Wilgus 1,*, Sara Ud-Din 2 and Ardeshir Bayat 2,3 1 Department of Pathology, Ohio State University, Columbus, OH 43210, USA 2 Centre for Dermatology Research, NIHR Manchester Biomedical Research Centre, Plastic and Reconstructive Surgery Research, University of Manchester, Manchester M13 9PT, UK; [email protected] (S.U.-D.); [email protected] (A.B.) 3 MRC-SA Wound Healing Unit, Division of Dermatology, University of Cape Town, Observatory, Cape Town 7945, South Africa * Correspondence: [email protected]; Tel.: +1-614-366-8526 Received: 1 October 2020; Accepted: 12 December 2020; Published: 18 December 2020 Abstract: Scars are generated in mature skin as a result of the normal repair process, but the replacement of normal tissue with scar tissue can lead to biomechanical and functional deficiencies in the skin as well as psychological and social issues for patients that negatively affect quality of life. Abnormal scars, such as hypertrophic scars and keloids, and cutaneous fibrosis that develops in diseases such as systemic sclerosis and graft-versus-host disease can be even more challenging for patients. There is a large body of literature suggesting that inflammation promotes the deposition of scar tissue by fibroblasts. Mast cells represent one inflammatory cell type in particular that has been implicated in skin scarring and fibrosis. Most published studies in this area support a pro-fibrotic role for mast cells in the skin, as many mast cell-derived mediators stimulate fibroblast activity and studies generally indicate higher numbers of mast cells and/or mast cell activation in scars and fibrotic skin. -
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. -
Alopecia Areata Part 1: Pathogenesis, Diagnosis, and Prognosis
Clinical Review Alopecia areata Part 1: pathogenesis, diagnosis, and prognosis Frank Spano MD CCFP Jeff C. Donovan MD PhD FRCPC Abstract Objective To provide family physicians with a background understanding of the epidemiology, pathogenesis, histology, and clinical approach to the diagnosis of alopecia areata (AA). Sources of information PubMed was searched for relevant articles regarding the pathogenesis, diagnosis, and prognosis of AA. Main message Alopecia areata is a form of autoimmune hair loss with a lifetime prevalence of approximately 2%. A personal or family history of concomitant autoimmune disorders, such as vitiligo or thyroid disease, might be noted in a small subset of patients. Diagnosis can often be made clinically, based on the characteristic nonscarring, circular areas of hair loss, with small “exclamation mark” hairs at the periphery in those with early stages of the condition. The diagnosis of more complex cases or unusual presentations can be facilitated by biopsy and histologic examination. The prognosis varies widely, and poor outcomes are associated with an early age of onset, extensive loss, the ophiasis variant, nail changes, a family history, or comorbid autoimmune disorders. Conclusion Alopecia areata is an autoimmune form of hair loss seen regularly in primary care. Family physicians are well placed to identify AA, characterize the severity of disease, and form an appropriate differential diagnosis. Further, they are able educate their patients about the clinical course of AA, as well as the overall prognosis, depending on the patient subtype. Case A 25-year-old man was getting his regular haircut when his EDITor’s KEY POINTS • Alopecia areata is an autoimmune form of barber pointed out several areas of hair loss. -
Alopecia, Particularly: Alopecia Areata Androgenetic Alopecia Telogen Effluvium Anagen Effluvium
432 Teams Dermatology Hair disorders Color Code: Original, Team’s note, Important, Doctor’s note, Not important, Old teamwork Done by: Shaikha Aldossari Reviewer: Lama AlTawil 8 Team Leader: Basil Al Suwaine&Lama Al Tawil 432 Dermatology Team Lecture 8: Hair Disorders Objectives 1- Normal anatomy of hair follicle and hair cycle. 2- Causes, features and management of non scarring alopecia, particularly: Alopecia areata Androgenetic alopecia Telogen effluvium Anagen effluvium 3- Causes and features of scarring alopecia. 4- Causes and features of Excessive hair growth. hair disorder Excessive hair Alopecia growth non scarring Hirsutism Hypertrichosis scarring Anagen Telogen Androgenetic Alopecia effluvium effluvium Alopecia Areata P a g e | 1 432 Dermatology Team Lecture 8: Hair Disorders Anatomy of hair follicle: The Arrector piliResponsible for piloerection (goose bumps ) that happens when one is cold (produces energy and therefor warmth) . hair follicle becomes vertical instead of oblique Cuticle is the last layer here . what we can see outside . it has 7 layers of keratinocytes How many hairs in the body? 5 millions hairs in the body, 100,000 in the scalp. Growth rate: 0.3mm/day for scalp hair i.e.1cm/month Hair follicle bulge: -Very important part since it has stem cells .its the inertion of the arrector pili Hair follicle on vertical section: -So any pathological process affecting any part other Initially the shaft and the follicle are one than this, hair would still be able to regrow. organ then when you reach 1/3 the follicle -If we want to destroy a hair follicle, we’d target the bulge. -
Fundamentals of Dermatology Describing Rashes and Lesions
Dermatology for the Non-Dermatologist May 30 – June 3, 2018 - 1 - Fundamentals of Dermatology Describing Rashes and Lesions History remains ESSENTIAL to establish diagnosis – duration, treatments, prior history of skin conditions, drug use, systemic illness, etc., etc. Historical characteristics of lesions and rashes are also key elements of the description. Painful vs. painless? Pruritic? Burning sensation? Key descriptive elements – 1- definition and morphology of the lesion, 2- location and the extent of the disease. DEFINITIONS: Atrophy: Thinning of the epidermis and/or dermis causing a shiny appearance or fine wrinkling and/or depression of the skin (common causes: steroids, sudden weight gain, “stretch marks”) Bulla: Circumscribed superficial collection of fluid below or within the epidermis > 5mm (if <5mm vesicle), may be formed by the coalescence of vesicles (blister) Burrow: A linear, “threadlike” elevation of the skin, typically a few millimeters long. (scabies) Comedo: A plugged sebaceous follicle, such as closed (whitehead) & open comedones (blackhead) in acne Crust: Dried residue of serum, blood or pus (scab) Cyst: A circumscribed, usually slightly compressible, round, walled lesion, below the epidermis, may be filled with fluid or semi-solid material (sebaceous cyst, cystic acne) Dermatitis: nonspecific term for inflammation of the skin (many possible causes); may be a specific condition, e.g. atopic dermatitis Eczema: a generic term for acute or chronic inflammatory conditions of the skin. Typically appears erythematous, -
Advances in Seborrheic Keratosis
A CME/CE-Certified Supplement to Original Release Date: December 2018 Advances in Seborrheic Expiration Date: December 31, 2020 Estimated Time To Complete Activity: 1 hour Participants should read the activity information, Keratosis review the activity in its entirety, and complete the online post-test and evaluation. Upon completing this activity as designed and achieving a passing score on FACULTY the post-test, you will be directed to a Web page that will Joseph F. Fowler Jr, MD Michael S. Kaminer, MD allow you to receive your certificate of credit via e-mail Clinical Professor and Director Associate Clinical Professor of Dermatology or you may print it out at that time. Contact and Occupational Yale Medical School The online post-test and evaluation can be accessed Dermatology New Haven, Connecticut at http://tinyurl.com/SebK2018. University of Louisville School of Adjunct Assistant Professor of Medicine Medicine (Dermatology), Warren Alpert Medical School Inquiries about continuing medical education (CME) Louisville, Kentucky of Brown University accreditation may be directed to the University of Providence, Rhode Island Louisville Office of Continuing Medical Education & Professional Development (CME & PD) at cmepd@ louisville.edu or (502) 852-5329. Designation Statement eborrheic keratosis (SK) has been called keratinizing surface.12 They can develop virtually The University of Louisville School of Medicine the “Rodney Dangerfield of skin lesions”— anywhere except for the palms, soles, and mucous designates this Enduring material for a maximum of 9 1.0 AMA PRA Category 1 Credit(s)™. Physicians should it earns little respect (as a clinical concern) membranes, but are most commonly observed claim only the credit commensurate with the extent of Sbecause of its benignity, commonality, usual on the trunk and face.6,13 The tendency to develop their participation in the activity. -
Linear Scleroderma “En Coup De Sabre” Coexisting with Plaque-Morphea
661 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.74.5.661 on 1 May 2003. Downloaded from SHORT REPORT Linear scleroderma “en coup de sabre” coexisting with plaque-morphea: neuroradiological manifestation and response to corticosteroids I Unterberger, E Trinka, K Engelhardt, A Muigg, P Eller, M Wagner, N Sepp, G Bauer ............................................................................................................................. J Neurol Neurosurg Psychiatry 2003;74:661–664 progression of skin lesions or any neurological abnormalities A 24 year old woman in the 33rd week of pregnancy during follow up. developed progressive neurological complications with On admission the patient was in the 33rd week of right sided hemiparesis in association with the occurrence pregnancy. She was fully oriented, had normal speech, and of linear scleroderma “en coup de sabre” (LSCS) and pre- presented with a right sided hemiparesis (grade 3/5, MRC existing plaque-morphea, already being treated by scale) with a positive Babinski sign on the right. There was no balneophototherapy. Further progression of neurological history of head trauma. symptoms led to a caesarean section with the delivery of a Routine laboratory testing and comprehensive serological healthy child. Brain magnetic resonance imaging (MRI) screening including antineutrophilic cytoplasmic antibodies showed focal T2 signal increases in the left frontoparietal (ANCA), anticardiolipin antibodies, and antibodies against region directly adjacent to the area of LSCS. -
Keratitis-Ichthyosis-Deafness Syndrome in Association With
Genes and skin Eur J Dermatol 2005; 15 (5): 347-52 Laura MAINTZ1 Regina C. BETZ2 Keratitis-ichthyosis-deafness syndrome Jean-Pierre ALLAM1 in association with follicular occlusion triad Jörg WENZEL1 Axel JAKSCHE3 Nicolaus FRIEDRICHS4 Thomas BIEBER1 Keratitis-Ichthyosis-Deafness syndrome is a rare congenital disorder of Natalija NOVAK1 the ectoderm caused by mutations in the connexin-26 gene (GJB2) on 1 chromosome 13q11-q12, giving rise to keratitis, erythrokeratoderma Department of Dermatology, University of and neurosensory deafness. We report the case of a 31-year-old black Bonn, Sigmund-Freud-Str. 25, 53105 Bonn, Germany male diagnosed as having KID syndrome. Sequencing analysis showed 2 Institute of Human Genetics, University of a heterozygous missense mutation D50N (148G > A) in the GJB2 gene. Bonn, Wilhelmstr. 31, 53115 Bonn, In addition to the classical features of vascularizing keratitis, erythro- Germany 3 Department of Ophthalmology, University keratoderma and congenital deafness, our patient presented a follicular of Bonn, Sigmund-Freud-Str. 25, 53105 occlusion triad with hidradenitis suppurativa (HS, alias acne inversa), Bonn, Germany acne conglobata and dissecting cellulitis of the scalp, leading to cicatri- 4 Institute of Pathology, University of Bonn, Sigmund-Freud-Str. 25, 53105 Bonn, cial alopecia and disfiguring, inflammatory vegetations of his scalp. Germany Conservative therapy such as a keratolytic, rehydrating and antiseptic external therapy, antibiotic, antimycotic and retinoids were only of Reprints: N. Novak moderate benefit, so we finally chose the curative possibility of surgery Fax: (+49) 228 287 4883 <[email protected]> therapy of the axillar papillomas and of the scalp. The inflammatory papillomatous regions of the axillae and of the scalp were radically debrided.