Acanthosis Nigricans 4 (Table) Benign Type 5 (Table) Acne Rosacea 40--3

Total Page:16

File Type:pdf, Size:1020Kb

Acanthosis Nigricans 4 (Table) Benign Type 5 (Table) Acne Rosacea 40--3 Index acanthosis nigricans 4 (table) benign migratory glossitis (erythema benign type 5 (table) migrans; geographic tongue) 2 acne rosacea 40--3 blastomycosis 7 (table) sclerokeratitis 41 blepharitis 35--40 treatment 42-3 anergic 43 acrodermatitis enteropathica (Danbolt- classification 35 (table) Closs syndrome) 5 (table) rosacea 40--3 acromegaly 55 treatment 42-3 actinic granuloma of O'Brien 75 seborrhoeic 36 Addison's disease 4 (table) staphylococcal 36 agammaglobulinaemia, sex-linked 24 treatment 39--40 (table) Bloch-Sulzberger syndrome allergic eye disease 43-9 (il1lcontinentia pigmenti) 5 (table), hypertrophic papillae 54 (table) (cobblestones) 45-6 Bloom syndrome 4 alopecia, granulomatous 72 bull om. dermatoses 49-53 5-amino-laevulinate synthase 87 bullou~. disease of childhood, amyloidosis 4 (table) chronic 50 anaemia 7 (table) bullous pemphigoid 15 angioedema of lips 25 (table) angioid streaks 55-6 calcinosis cutis 75 angular cheilitis (angular cheilosis; candidosis, chronic mucocutaneous angular stomatitis; perleche) 26- candidosis endocrinopathy 8 syndrome 24 (table) ataxia telangiectasia 24 (table) cataract 54 atopic dermatitis 54 (table) steroid 56 atypical facial necrobiosis of Dowling chalazion (meibomian cyst) 37,38 and Wilson-Jones 75, 76-7 (fig.), 40 chalazoderma 72 Chediak-Higashi syndrome 25 (table) Beh~et's syndrome 4 (table), 7 cheilitis glandularis 25 (table) (table), 21-3 cheilitis granulomatosa 25 (table), 29 109 INDEX chickenpox 4 (table) Ehlers-Danlos syndrome chloroquine 58-9 (fibrodysplasia hyperelastica) 5 chondroectocermal dysplasia (Ellis-van (table), 55 Creveld syndrome) 5 (table) Ellis-van Creveld syndrome coeliac disease 7 (table) (chondroectodermal dysplasia) 5 congenital dyskeratosis (Schiifer's (table) syndrome) 54 (table) epidermolysis bullosa 5 (table), 7 congenital ichthyosiform (table) erythroderma 54 (table) erythema migrans (benign migrator)' congenital skin atrophy (Siemen's glossitis; geographic tongue) 2 syndrome) 54 (table) erythema multiforme 7 (table), 13-15, conjunctivitis 23 (table), 72 allergic, acute/chronic 44 erythema multi forme-like lesions 72 vernal 44-5 erythema nodosum 62-3, 64 (fig.) bulbar 46 erythroplasia 9 limbal 46-7 eyelids, contact sensitivity 53--4 palpebral 46-7 treatment 47-8 contact sensitivity 53--4 Fabry syndrome 5 (table) Cowden syndrome (multiple hamartoma Felty's syndrome 7 (table) and neoplasia syndrome) 5 (table) fibrodysplasia hyperelastica (Ehlers- Coxsackie viruses 7 (table) Danlos syndrome) 5 (table), 55 Crohn's disease focal dermal hypoplasia (Goltz cutaneous 77 syndrome) 5 (table) lips 25 (table) Fordyce spots (ectopic sebaceous oral 7 (table), 29-31 glands) 2 cytotoxic agents 7 (table) Danbolt--Closs syndrome Gardner's syndrome 5 (table) (acrodermatitis enteropathica) 5 geographic tongue (erythema migrans; (table) benign migratory glossitis) 2 Darier-Roussy sarcoids (subcutaneous gingivitis sarcoidosis) 68,69 (fig.) acute ulcerative 7 (table) Darier-White disease 5 (table) desquamative 9 (fig.) deficiency states 7 ( table) Goltz syndrome (focal dermal dermatitis herpetiformis 7 (table), 16, hypoplasia) 5 (table) 23 (table) Gorlin-Goltt syndrome (multiple basal desquamative gingivitis 9 (fig.) cell naevi syndrome) 5 Di George syndrome 24 (table) graft-versus-host disease 24 (table) Dowling-Wilson Jones syndrome 75, granuloma annulare 75, 77 (fig.) 76-7 granulomatosis 25 (table), 29 dyskeratosis congenita (Zinsser­ granulomatous disease, chronic 25 Engmann--Cole syndrome) 5 (table) (table) Gronblad-Strandberg syndrome (pseudoxanthoma e1asticum) 6 ectodermal dysplasia 5 (table), 54 (table), 55 (table) Gunther's disease (congenital ectopic sebaceous glands (Fordyce erythropoietic porphyria) 86 spots) 2 (table), 88 (table), 89 (table), 96-7 110 INDEX harderoporphyria 90 (table) lead poisoning 55 haem leukoedema 2 biosynthesis 84 (fig.), 87 leukopenia 7 (table) precursor overproduction 84 (fig.), leukaemia 7 (table) 87 Jichen planus 6-11,23 (table) hairy tongue 2 aetiology 9-10 hand, foot and mouth disease 4 (table) clinical appearance 8-9 hereditary angioedema 24 (table) diagnosis 10-11 hereditary benign intraepithelial management 11 dyskeratosis 5 (table) prognosis 9 hereditary coproporphyria 86 (table), linear 19A disease 88 (table), 100 ocular lesions 50, 52 homozygous 90 oral lesions 7 (table), 16,23 (table) inheritance 89 (table) lip hereditary haemorrhagic diseases involving 23-31 telangiectasia 5 (table) swellings 25 (table) herpes labialis, recurrent 28-9 tumours 25 (table) herpesviruses 7 (table) lipoid proteinosis (hyalinosis cutis et histoplasmosis 7 (table) mucosae; Urbach-Wiethe human immune deficiency virus 7 syndrome) 5 (table) (table), 24 (table) Lofgren's syndrome 63 hyalinosis cutis et mucosae (lipoid lupus erythematosis 4 (table), 7 (table). proteinosis; Urbach-Wiethe 19-21,23 (table) syndrome) 5 (table) lupus pernio 62, 69-70 hydroxychloroquine 58 lupus vulgaris 65, 66 (fig.) hyper-IgE syndrome (Job's syndrome) 25 hypertrichosis McCune-Albright syndrome 4 (table) gingival hyperplasia associated Maffucci syndrome 6 (table) porphyrial 92 measles 4 (table) meibomian cyst (chalazion) 37,38 immunodeficiency, common (fig.),40 variable 24 (table) meibomian gland disease 36-9 incontinentia pigmenti (Bloch­ meibomian keratoconjunctivitis 37-8, Sulzberger syndrome) 5 (table), 40 54 (table) meibomian seborrhoea 39 infantile poikiloderma (Rothmund's meibomitis 37-9 syndrome) 54 treatment 39-40 Jadassohn-Lewandowski syndrome Melkersson-Rosenthal syndrome 25 (pachyonychia congenital 5 (table), 29, 77 (table) mepacrine 59 Job's syndrome (hyper-IgE 8-metboxypsoralen 57 syndrome 25 (table) Mibelli's disease (porokeratosis) 6 (table) Kawasaki's disease (mucocutaneous Miescher's granulomatous cheilitis 77, lymph node syndroine) 4 (table) 78 kerato-conjunctivitis, adult atopic 48- mouth 9 disease relationships 3--6 K viem-Siltzbach test 70-1 normal/benign variants 2 111 INDEX mucocutaneous lymph node syndrome porphobilinogen synthase (Kawasaki's disease) 4 (table) deficiency 85, 86 (table), 88 (table) mucous membrane pemphigoid 11-13 porphyria 83-107 multiple basal cell naevi syndrome acute hepatic 86 (table), 88, 99-100 (Gorlin-Goltz syndrome) 5 management 107 (table) acute intermittent 85, 86 (table), 88 multiple hamartoma and neoplasia (table) syndrome (Cowden syndrome) 5 inheritance 89 (table) (table) autosomal dominant homozygous mycobacterial infection 7 (table) forms 90 (table) myeloperoxidase deficiency 25 (table) biochemical genetics 89-90 classification 85 necrobiosis lipoidica 75 congenital (Gunther's disease) 4 neurofibromatosis 6 (table) (table), 86 (table), 89 (table), 96-7 neutropenia diagnosis 101-4 chronic benign 25 (table) latent porphyria 104-5 cyclic 24 (table) hepatoerythropoietic 90 (table) hereditary coproporphyria 86 (table) histopathology 94 oral mucosa I hypertrichosis 92 oral ulceration 7 (table) inherited 89 (table) management 105-7 pachyonychia congenita (Jadassohn­ metabolic abnormalities 86-8 Lewandowski syndrome) 5 porphobilinogen (PBG)-synthase (table) deficiency 85 Paget's disease 55 prevalence 85-6 papillomavirus infections 4 (table) prevention of light-induced skin Papillon-Lefevre syndrome 6 (table) damage 105 pemphigoid types 86 (table) bullous 23 (table) variegate 86 (table), 88 (table), 100 mucous membrane 23 (table), 50,52 homozygous 90 ocular lesions 50-3 inheritance 89 (table) oral ulceration 7 (table) porphyria cutanea tarda 86,87,88 pemphigus foliaceus 50 (table), 93 (fig.), 97-9 pemphigus vulgaris inheritance 89 (table) conjunctivitis 49-50 treatment 106-7 oral lesions 7 (table), 17-19,23 porphyria cutanea tarda-type skin (table) lesions perleche (angular cheilitis) 26-8 adults 102-4 Peutz-Jeghers syndrome 6 (table) children 104 phenytoin 7 (table) porphyrins photo-onycholysis 91 mechanism of skin damage 95-6 pityriasis rosea 4 (table) photosensitization 87 pityriasis rubra pilaris 6 (table) clinical features 90-4 poliosis 56 protoporphyria (erythropoietic polyarteritis nodosa 4 (table), 23 protoporphyria; erythrohepatic (table) protoporphyria) 86 (table), 89, 91 porokeratosis (Mibelli's disease) 6 100-1 (table) homozygous 90 112 INDEX inheritance 89 (table) reactive lesions 62-3 liver disease 106 scar 68 prurigo 72 subcutaneous (Darier-Roussy nodular 72 sarcoids) 68,69 (fig.) pseudoxanthoma elasticum (Gronblad­ thrombophlebitis 72, 73 (fig.) Strandberg syndrome) 6 (table), vasculitis 72 55 vulval 75 psoralen/UVA (PUV A) therapy 57-8 Schafer's syndrome (congenital psoriasiform lesions 78 dyskeratosis) 54 (table) psoriasis 23 (table) scleroderma 4 (table) scleropoikiloderma (Werner's Reiter's syndrome 4 (table), 7 (table) syndrome) 54 (table) retinal disorders 54-6 selective IgA deficiency 24 (table) angioid streaks 55--6 severe combined immunodeficiency 24 rheumatoid nodules 77 (table) Rothmund's syndrome (infantile sicca syndrome 72 poikiloderma) 54 (table) sickle cell anaemia 55 Siemen's syndrome (congenital skin atrophy) 54 (table) sarcoidosis 61-2 Sjogren-Larsson syndrome 6 (table) actinic 75 staphylococcal hypersensitivity aestival 75 syndrome 40 alopecia 72 steroids 56 angiolupoid nodules 68 Sturge---Weber syndrome 6 (table) associated diseases 78--9 syphilis 7 (table) autoimmune disease? 78-9 conjunctival 72 dactylitis 74 teeth 1 elephantine 73 thiomersal 53 eruptive 74-5 tongue erythema multiforme see erythema fissured (scrotal) 2 multi forme geographic (erythema migrans; benign migratory glossitis) 2 formes sphace/iques 73 fulminant 72 hairy 2 granulomatous lesions 63-71 tuberose sclerosis 6 (table) hypopigmented 72-3, 74 (fig.) Trantas' spots 46 ichthyosis 72 tylosis 6 (table) K viem-Siltzbach test 70--1 lips 25 (table) ulcerative colitis 7 (table) micropapular 67,68 (fig.) Urbach-Wiethe syndrome (lipoid mucosal 72 proteinosis; hyalinosis cutis et nail 74 mucosae) 5 (table) 'naked granulomas' 65 uroporphyrin 96 nodules 67 oral lesions 4 (table) palmoplantar 74 Werner's syndrome papules 67 (scleropoikiloderma) 54 (table) perianal 75 white sponge naevus 6 (table) plaques 69--70 Wickham's striae 8 113 INDEX Wiskott-Aldrich syndrome 24 (table) Zinsser-Engmann-Cole syndrome (dyskeratosis congenita) 5 (table) xanthomatosis 6 (table) zoster 4 (table) xeroderma pigmentosum 6 (table) 114 .
Recommended publications
  • PGD: a Celebration of 20 Years
    PGD: A Celebration of 20 years: What is Reality and What is Not? Roma June 30, 2010 Mark Hughes, M.D., Ph.D . Professor of Genetics, Internal Medicine, Pathology Director, Genesis Genetics Institute Director, State of Michigan Genomic Technology Center Reality – (Three obvious ones) PGD • Has led to the birth of thousands of healthy children to very desperate, genetically at-risk couples. • Remains at the very limit of medical diagnostic testing • The technology continues to improve - – but it is not reality to think PGD will ever have a 0% false positive or false negative rate Reality: We still do not know What is best to biopsy, and when? Polar Body Blastomere Trophoectoderm Variation in Biopsy Skill Clinic Biopsies +HCG / ET 1 314 17% 2 427 26% 3 181 12% 4 712 31% Reality: We all are controversial • PGD has raised international controversy – How is it bioethically different from Prenatal Testing? – Who should control the use of these technologies? – Should there be government PGD testing standards? • What is the difference between a Disease and a Trait - and who decides? PGD Disorders (A, B, C) • ACHONDROPLASIA (FGFR) • BARTH DILIATED CARDIOMYOPATHY • ACTIN-NEMALIN MYOPATHY (ACTA) • BETA THALASSEMIA (HBB) • ADRENOLEUKODYSTROPHY (ABCD) • BLOOM SYNDROME • AGAMMAGLOBULINEMIA-BRUTON (TYKNS) • BREAST CANCER (BRCA1 & 2) • ALAGILLE SYNDROME (JAG) • CACH-ATAXIA (EIFB) • ALDOLASE A, FRUCTOSE-BISPHOSPHATE • CADASIL (NOTCH) • ALPHA THALASSEMIA (HBA) • CANAVAN DISEASE (ASPA) • ALPHA-ANTITRYPSIN (AAT) • CARNITINE-ACYLCARN TRANSLOCASE • ALPORT SYNDROME
    [Show full text]
  • Associated Palmoplantar Keratoderma
    DR ABIGAIL ZIEMAN (Orcid ID : 0000-0001-8236-207X) Article type : Review Article Pathophysiology of pachyonychia congenita-associated palmoplantar keratoderma: New insight into skin epithelial homeostasis and avenues for treatment Authors: A. G. Zieman1 and P. A. Coulombe1,2 # Affiliations: 1Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109, USA; 2Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI 48109, USA #Corresponding author: Pierre A. Coulombe, PhD, 3071 Biomedical Sciences Research Building, 109 Zina Pitcher Place, Ann Arbor, MI 48109, USA. Tel: 734-615-7509. Email: [email protected]. Funding Sources: These studies were supported by grant AR044232 issued to P.A.C. from the National Institute of Arthritis, Musculoskeletal and Skin Disease (NIAMS). A.G.Z. received support from grant T32 CA009110 from the National Cancer Institute. Author Manuscript This is the author manuscript accepted for publication and has undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/BJD.18033 This article is protected by copyright. All rights reserved Conflict of interest disclosures: None declared. Bulleted statements: What’s already known about this topic? Pachyonychia congenita is a rare genodermatosis caused by mutations in KRT6A, KRT6B, KRT6C, KRT16, KRT17, which are normally expressed in skin appendages and induced following injury. Individuals with PC present with multiple clinical symptoms that usually include thickened and dystrophic nails, palmoplantar keratoderma (PPK), glandular cysts, and oral leukokeratosis.
    [Show full text]
  • Prevalence of Developmental Oral Mucosal Lesions Among a Sample of Denture Wearing Patients Attending College of Dentistry Clinics in Aljouf University
    European Scientific Journal August 2016 edition vol.12, No.24 ISSN: 1857 – 7881 (Print) e - ISSN 1857- 7431 Prevalence Of Developmental Oral Mucosal Lesions Among A Sample Of Denture Wearing Patients Attending College Of Dentistry Clinics In Aljouf University Abdalwhab M.A .Zwiri Assistant professor of oral medicine, Aljouf University, Sakaka, Aljouf , Saudi Arabia Santosh Patil Assistant professor of Radiology, Aljouf University, Sakaka, Aljouf , Saudi Arabia Fadi AL- Omair Intern dentist, Aljouf University, Sakaka, Aljouf , Saudi Arabia Mohammed Assayed Mousa Lecturer of prosthodontics, Aljouf University, Sakaka, Aljouf , Saudi Arabia Ibrahim Ali Ahmad Department of Dentistry, AlWakra Hospital, Hamad Medical Corporation, AlWakra, Qatar doi: 10.19044/esj.2016.v12n24p352 URL:http://dx.doi.org/10.19044/esj.2016.v12n24p352 Abstract Introduction: developmental oral lesions represent a group of normal lesions that can be found at birth or evident in later life. These lesions include fissured and geographic tongue, Fordyce’s granules and leukoedema. Study aims: to investigate the prevalence of some developmental oral mucosal lesions among dental patients wearing dentures who were attending college of dentistry clinics in Aljouf University, and specialized dental center of ministry of health. Methods and subjects: a retrospective design was conducted to collect data from 344 wearing denture dental patients who were attending college of dentistry clinics in Aljouf University, and specialized dental center of ministry of health. A working excel sheet was created for patients and included data related to personal information such as age and gender; and oral developmental lesions. The software SPSS version 20 was used to analyze data. Statistical tests including frequency, percentages, and One way Anova were used to describe data.
    [Show full text]
  • Update on Genital Dermatoses
    UPDATE ON GENITAL DERMATOSES Sangeetha Sundaram Consultant GUM/HIV Southampton 07/11/2018 Normal variants • Fordyce spots • Vestibular papillae • Pearly penile papules • Angiokeratoma • Epidermal cysts • Skin tags Inflammatory dermatoses • Irritant dermatitis • Lichen sclerosus • Lichen simplex chronicus • Lichen planus • Seborrhoeic dermatitis • Psoriasis History • Itching? Where exactly? Waking up at night scratching? • Soreness/burning/raw? Where exactly? When? • Pain with sex? Where exactly? When exactly? • Discharge? • Skin trouble elsewhere? • Mouth ulcers? • Irritants in lifestyle Examination Irritants • Soap and shower gel (even Dove, Simple and Sanex…) • Sanitary pads and panty liners (especially when worn daily) • Moistened wipes • Synthetic underwear • Tight clothing • Feminine washes • Topical medication (creams and gels) • Urine, faeces, excessive vaginal discharge • Lubricants • Spermicides Basic vulval toolkit • Stop soap/shower gel (even Dove and Simple and Sanex!) • Stop pads/ panty liners (except during menses) • Loose cotton pants • Emollient soap substitute and barrier ointment Lichen simplex chronicus • Itching wakes her at night • Scratches in her sleep • Always same place(s) Lichen simplex chronicus - management • Stop soap/shower gel • Stop pads/ panty liners (except during menses) • Loose cotton pants • Emollient soap substitute and barrier ointment • Identify underlying condition(s), if any • Dermovate ointment every night for 2 weeks, then alternate nights for 2 weeks, then twice weekly for 2 weeks, then stop
    [Show full text]
  • WES Gene Package Multiple Congenital Anomalie.Xlsx
    Whole Exome Sequencing Gene package Multiple congenital anomalie, version 5, 1‐2‐2018 Technical information DNA was enriched using Agilent SureSelect Clinical Research Exome V2 capture and paired‐end sequenced on the Illumina platform (outsourced). The aim is to obtain 8.1 Giga base pairs per exome with a mapped fraction of 0.99. The average coverage of the exome is ~50x. Duplicate reads are excluded. Data are demultiplexed with bcl2fastq Conversion Software from Illumina. Reads are mapped to the genome using the BWA‐MEM algorithm (reference: http://bio‐bwa.sourceforge.net/). Variant detection is performed by the Genome Analysis Toolkit HaplotypeCaller (reference: http://www.broadinstitute.org/gatk/). The detected variants are filtered and annotated with Cartagenia software and classified with Alamut Visual. It is not excluded that pathogenic mutations are being missed using this technology. At this moment, there is not enough information about the sensitivity of this technique with respect to the detection of deletions and duplications of more than 5 nucleotides and of somatic mosaic mutations (all types of sequence changes). HGNC approved Phenotype description including OMIM phenotype ID(s) OMIM median depth % covered % covered % covered gene symbol gene ID >10x >20x >30x A4GALT [Blood group, P1Pk system, P(2) phenotype], 111400 607922 101 100 100 99 [Blood group, P1Pk system, p phenotype], 111400 NOR polyagglutination syndrome, 111400 AAAS Achalasia‐addisonianism‐alacrimia syndrome, 231550 605378 73 100 100 100 AAGAB Keratoderma, palmoplantar,
    [Show full text]
  • BIMJ April 2013
    Original Article Brunei Int Med J. 2013; 9 (5): 290-301 Yellow lesions of the oral cavity: diagnostic appraisal and management strategies Faraz MOHAMMED 1, Arishiya THAPASUM 2, Shamaz MOHAMED 3, Halima SHAMAZ 4, Ramesh KUMARASAN 5 1 Department of Oral & Maxillofacial Pathology, Dr Syamala Reddy Dental College Hospital & Research Centre, Bangalore, India 2 Department of Oral Medicine & Radiology, Dr Syamala Reddy Dental College Hospital & Research Centre, Bangalore, India 3 Department of Community & Public Health Dentistry, Faculty of Dentistry, Amrita University, Cochin, India 4 Amrita center of Nanosciences, Amrita University, Cochin, India 5 Oral and Maxillofacial Surgery, Faculty of Dentistry, AIMST University, Kedah, Malaysia ABSTRACT Yellow lesions of the oral cavity constitute a rather common group of lesions that are encountered during routine clinical dental practice. The process of clinical diagnosis and treatment planning is of great concern to the patient as it determines the nature of future follow up care. There is a strong need for a rational and functional classification which will enable better understanding of the basic disease process, as well as in formulating a differential diagnosis. Clinical diagnostic skills and good judgment forms the key to successful management of yellow lesions of the oral cavity. Keywords: Yellow lesions, oral cavity, diagnosis, management INTRODUCTION INTRODUCTI Changes in colour have been traditionally low lesions have a varied prognostic spec- used to register and classify mucosal and soft trum. The yellowish colouration may be tissue pathology of the oral cavity. Thus, the- caused by lipofuscin (the pigment of fat). It se lesions have been categorised as white, may also be the result of other causes such red, white and red, blue and/or purple, as accumulation of pus, aggregation of lym- brown, grey and/or black and yellow.
    [Show full text]
  • Fordyce's Granules Or Heterotopic/Ectopic Sebaceous Gland (Neville Et Al, 2009)
    Republic of Iraq Ministry of Higher Education And scientific Research University of Baghdad College of Dentistry Fordyce’s granules A project submitted to the Council of the College of Dentistry at the University of Baghdad, Department of Oral Medicine, in partial fulfillment of the requirement for B.D.S. degree Done by: Zahraa Fakher Abd_Algany Supervisor RanaMurtadha Hassan )B.D.S., M.Sc( 2017-2018 List of content Subject Page NO. List of content I List of figures II List of table II Introduction 1 Aim of study 2 Chapter one: Review of literature 3 1.1 oral cavity 3 1.2 Definition 4 1.3 Epidemiology 4 1.4 etiology 5 1.5 Classification 5 1.6 clinical 6 1.7 Histology 8 1.8 Complications 10 1.9 Prognosis 10 1.10 Diagnosis and Treatment 11 1.10.1 Treatment of Fordyce Spots With CO2 Laser 11 1.10.2 bichloracetic acid 13 1.10.2.1 The Advantages of bichloracetic acid 13 treatment 1.10.2.2 Risk of bichloracetic acid treatment 14 1.10.3 5-aminolevulinic acid photodynamic therapy 15 1.10.3.1 Low cure rate in Fordyce spots by 5- 16 aminolevulinic acid photodynamic therapy is caused by Chapter two: Materials and methods 18 Chapter Three: RESULTS 19 3.1 Age 19 3.2 Gender 21 3.3 site 22 3.4 Geographic: 23 Chapter Four: Discussion 25 4.1 Age 25 4.2 site 25 4.3 Geographic 25 Chapter five :Conclusion 26 References 27 List of figure Fig. no. subject Page no.
    [Show full text]
  • Indian Journal of Dermatology, Venereology & Leprology
    ISSN 0378-6323 E-ISSN 0973-3930 Indian Journal of Dermatology, Venereology & Leprology VVolol 7744 | IIssuessue 1 | JJan-Feba n -F e b 22008008 The Indian Journal of Dermatology, Venereology and Leprology (IJDVL) EDITOR is a bimonthly publication of the Uday Khopkar Indian Association of Dermatologists, Venereologists and Leprologists (IADVL) ASSOCIATE EDITORS and is published for IADVL by Medknow Ameet Valia Sangeeta Amladi Publications. The Journal is indexed/listed with ASSISTANT EDITORS Science Citation Index Expanded, K. C. Nischal Sushil Pande Vishalakshi Viswanath PUBMED, EMBASE, Bioline International, CAB Abstracts, Global Health, DOAJ, Health and Wellness EDITORIAL BOARD Research Center, SCOPUS, Health Reference Center Academic, InfoTrac Chetan Oberai (Ex-ofÞ cio) Koushik Lahiri (Ex-ofÞ cio) Sanjeev Handa One File, Expanded Academic ASAP, Arun Inamdar Joseph Sundharam S. L. Wadhwa NIWI, INIST, Uncover, JADE (Journal Binod Khaitan Kanthraj GR Sharad Mutalik Article Database), IndMed, Indian D. A. Satish M. Ramam Shruthakirti Shenoi Science Abstract’s and PubList. D. M. Thappa Manas Chatterjee Susmit Haldar H. R. Jerajani Rajeev Sharma Venkatram Mysore All the rights are reserved. Apart from any Sandipan Dhar fair dealing for the purposes of research or private study, or criticism or review, no EDITORIAL ADVISORY BOARD part of the publication can be reproduced, Aditya Gupta, Canada Jag Bhawan, USA stored, or transmitted, in any form or by C. R. Srinivas, India John McGrath, UK any means, without the prior permission of Celia Moss, UK K. Pavithran, India the Editor, IJDVL. Giam Yoke Chin, Singapore R. G. Valia, India The information and opinions presented in Gurmohan Singh, India Robert A.
    [Show full text]
  • Innovations and Transformations
    International Pachyonychia Congenita Consortium (IPCC) Symposium Innovations and Transformations June 28-29, 2021 A virtual meeting 1 Sponsored by About Pachyonychia Congenita Project PC Project connects patients, researchers, medical professionals, and industry partners in a united and global effort to help those who suffer from the painful and debilitating effects of Pachyonychia Congenita (PC), a rare genetic skin disease. The International Pachyonychia Congenita Research Registry (IPCRR) gathers data from pa- tients through an online registry and provides free genetic testing to those who join. Patients in the registry are offered individualized support and are notified of studies for PC treatments, advances in research, and activities such as online forums and patient support meetings. Please refer your patients with severe PPKs to PC Project for a definitive diagnosis: https:// www.pachyonychia.org/patient-registry/ PC Project sponsors the International PC Consortium (IPCC) which facilitates collaboration among scientists, physicians, and other professionals interested in advancing research and translational therapeutics for PC. De-identified data from the registry is freely shared and available for research. PC Project invites all interested physicians, scientists and industry part- ners to join the IPCC, a special group, founded and fueled by love for these patients with se- vere unmet needs. Thank you for helping us achieve our vision: A day when those who suffer from PC will live without excruciating pain, isolation, and embarrassment.
    [Show full text]
  • 1 Introduction 1
    1 Introduction 1 Part I The Mechanisms of Cutaneous Mosaicism 2 Mosaicism as a Biological Concept 5 2.1 Historical Beginnings 5 2.2 Mosaicism in Plants 6 2.3 Mosaicism in Animals 7 2.4 Mosaicism in Human Skin 9 2.5 Mosaicism Versus Chimerism 10 References 11 3 Two Major Categories of Mosaicism 13 3.1 Genomic Mosaicism 13 3.1.1 Genomic Mosaicism of Autosomes 13 3.1.2 Genomic X-Chromosome Mosaicism in Male Patients 24 3.1.3 Superimposed Segmental Manifestation of Polygenic Skin Disorders 24 3.2 Epigenetic Mosaicism 26 3.2.1 Epigenetic Mosaicism of Autosomal Genes 26 3.2.2 Epigenetic Mosaicism of X Chromosomes 27 References 31 4 Relationship Between Hypomorphic Alleles and Mosaicism of Lethal Mutations 39 References 41 Part II The Patterns of Cutaneous Mosaicism 5 Six Archetypical Patterns 45 5.1 Lines of Blaschko 45 5.1.1 Lines of Blaschko, Narrow Bands 52 5.1.2 Lines of Blaschko, Broad Bands 52 5.1.3 Analogy of Blaschko's Lines in Other Organs. ... 53 5.1.4 Blaschko's Lines in Animals 54 5.1.5 Analogy of Blaschko's Lines in the Murine Brain. 54 http://d-nb.info/1034513591 X 5.2 Checkerboard Pattern 56 5.3 Phylloid Pattern 57 5.4 Large Patches Without Midline Separation 57 5.5 Lateralization Pattern 57 5.6 Sash-Like Pattern 58 References 59 6 Less Well Defined or So Far Unclassifiable Patterns 63 6.1 The Pallister-Killian Pattern 63 6.2 The Mesotropic Facial Pattern 64 References 65 Part III Mosaic Skin Disorders 7 Nevi 69 7.1 The Theory of Lethal Genes Surviving by Mosaicism 70 7.2 Pigmentary Nevi 70 7.2.1 Melanocytic Nevi 70 7.2.2 Other Nevi Reflecting Pigmentary Mosaicism.
    [Show full text]
  • Fordyce's Disease Treated with Pimacrolimus: a Rare Case Report
    CASE REPORT Fordyce's Disease Treated with Pimacrolimus: A Rare Case Report *T Hoque1, AZMM Islam2 ABSTRACT Fordyce's disease, a rarely found disease of lips has been reported recently in department of Skin and VD, Gonosashthaya Somaj Vittic Medical College Hospital, Savar, Dhaka. Occasionally it may not be possible to identify the cause. The patient presented with identical features of Fordyce's disease and lip biopsy for histopathology showed the features of Fordyce's disease. Then patient was treated with Pimecrolimus cream and improved. Fordyce's disease is an extremely rare disorder. So its cutaneous findings, histopathology and treatments are highlighted here. Key Words: Fordyce's disease, histopathology, Pimacrolimus. Introduction Fordyce's disease is ectopically located sebaceous common cause behind the condition. The glands, over mucous membrane of the mouth and development of yellowish papules and their location lips1,14, characterized by the presence of whitish or may indicate actopic sebaceous glands due to yellowish, scanty or abundant, discrete, aggravated abnormal disposition during embroyonic and often coalescent milium like bodies.2 It occurs development.5 Sometimes warts are mistakenly commonly inside of the mouth laterally along the diagnosed as Fordyce's condition, because of line of the teeth as far back as the last molar and similarity in involvement of vermilion border in both possibly somewhat less frequently on the vermilion cases.6 In cases the Fordyce's condition affected or mucous and inner surface of the lips, cheeks, less genital area that need for biopsy or blood often glans penis, labia mejora and minora.1,15 The examination considering the similarity in appearance lesions are from 1mm to 3 mm in size and usually of with some of Sexually transmitted diseases.
    [Show full text]
  • Hereditary Palmoplantar Keratoderma "Clinical and Genetic Differential Diagnosis"
    doi: 10.1111/1346-8138.13219 Journal of Dermatology 2016; 43: 264–274 REVIEW ARTICLE Hereditary palmoplantar keratoderma “clinical and genetic differential diagnosis” Tomo SAKIYAMA, Akiharu KUBO Department of Dermatology, Keio University School of Medicine, Tokyo, Japan ABSTRACT Hereditary palmoplantar keratoderma (PPK) is a heterogeneous group of disorders characterized by hyperkerato- sis of the palm and the sole skin. Hereditary PPK are divided into four groups – diffuse, focal, striate and punctate PPK – according to the clinical patterns of the hyperkeratotic lesions. Each group includes simple PPK, without associated features, and PPK with associated features, such as involvement of nails, teeth and other organs. PPK have been classified by a clinically based descriptive system. In recent years, many causative genes of PPK have been identified, which has confirmed and/or rearranged the traditional classifications. It is now important to diag- nose PPK by a combination of the traditional morphological classification and genetic testing. In this review, we focus on PPK without associated features and introduce their morphological features, genetic backgrounds and new findings from the last decade. Key words: diffuse, focal, punctate, striate, transgrediens. INTRODUCTION psoriasis vulgaris confined to the palmoplantar area (Fig. 1b) are comparatively common and are sometimes difficult to Palmoplantar keratoderma (PPK) is a heritable or acquired dis- distinguish from hereditary PPK. A skin biopsy is essential in order characterized by abnormal hyperkeratotic thickening of diagnosing these cases. Lack of a family history is not neces- the palm and sole skin. In a narrow sense, PPK implies heredi- sarily evidence of an acquired PPK, because autosomal reces- tary PPK, the phenotype of which usually appears at an early sive PPK can appear sporadically from parent carriers and age.
    [Show full text]