Poikiloderma of Civatte, Slapped Neck Solar Melanosis, Basal Melanin Stores
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Melanocytes and Their Diseases
Downloaded from http://perspectivesinmedicine.cshlp.org/ on October 2, 2021 - Published by Cold Spring Harbor Laboratory Press Melanocytes and Their Diseases Yuji Yamaguchi1 and Vincent J. Hearing2 1Medical, AbbVie GK, Mita, Tokyo 108-6302, Japan 2Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 Correspondence: [email protected] Human melanocytes are distributed not only in the epidermis and in hair follicles but also in mucosa, cochlea (ear), iris (eye), and mesencephalon (brain) among other tissues. Melano- cytes, which are derived from the neural crest, are unique in that they produce eu-/pheo- melanin pigments in unique membrane-bound organelles termed melanosomes, which can be divided into four stages depending on their degree of maturation. Pigmentation production is determined by three distinct elements: enzymes involved in melanin synthesis, proteins required for melanosome structure, and proteins required for their trafficking and distribution. Many genes are involved in regulating pigmentation at various levels, and mutations in many of them cause pigmentary disorders, which can be classified into three types: hyperpigmen- tation (including melasma), hypopigmentation (including oculocutaneous albinism [OCA]), and mixed hyper-/hypopigmentation (including dyschromatosis symmetrica hereditaria). We briefly review vitiligo as a representative of an acquired hypopigmentation disorder. igments that determine human skin colors somes can be divided into four stages depend- Pinclude melanin, hemoglobin (red), hemo- ing on their degree of maturation. Early mela- siderin (brown), carotene (yellow), and bilin nosomes, especially stage I melanosomes, are (yellow). Among those, melanins play key roles similar to lysosomes whereas late melanosomes in determining human skin (and hair) pigmen- contain a structured matrix and highly dense tation. -
Melasma on the Nape of the Neck in a Man
Letters to the Editor 181 Melasma on the Nape of the Neck in a Man Ann A. Lonsdale-Eccles and J. A. A. Langtry Sunderland Royal Hospital, Kayll Road, Sunderland SR4 7TP, UK. E-mail: [email protected] Accepted July 19, 2004. Sir, sunlight and photosensitizing agents may be more We report a 47-year-old man with light brown macular relevant. pigmentation on the nape of his neck (Fig. 1). It was The differential diagnosis for pigmentation at this site asymptomatic and had developed gradually over 2 years. includes Riehl’s melanosis, Berloque dermatitis and He worked outdoors as a pipe fitter on an oilrig module; poikiloderma of Civatte. Riehl’s melanosis typically however, he denied exposure at this site because he involves the face with a brownish-grey pigmentation; always wore a shirt with a collar that covered the biopsy might be expected to show interface change and affected area. However, on further questioning it liquefaction basal cell degeneration with a moderate transpired that he spent most of the day with his head lymphohistiocytic infiltrate, melanophages and pigmen- bent forward. This reproducibly exposed the area of tary incontinence in the upper dermis. It is usually pigmentation with a sharp cut off inferiorly at the level associated with cosmetic use and may be considered of his collar. He used various shampoos, aftershaves and synonymous with pigmented allergic contact dermatitis shower gels, but none was applied directly to that area. of the face (6, 7). Berloque dermatitis is considered to be His skin was otherwise normal and there was no family caused by a photoirritant reaction to bergapentin; it history of abnormal pigmentation. -
An Unusual Presentation of a Unilateral Asymptomatic Riehl's
ts & C por a e se R S l Michael, Med Rep Case Stud 2018, 3:1 t a u c d i i DOI: 10.4172/2572-5130.1000152 d e s e M + Medical Reports and Case Studies ISSN: 2572-5130 Case Report Open Access An Unusual Presentation of a Unilateral Asymptomatic Riehl’s Melanosis in a 45 Year Old Male Chan Kam Tim Michael* Department of Dermatology, Hong Kong Academy of Medicine, Hong Kong *Corresponding author: Chan Kam Tim Michael, Department of Dermatology, Hong Kong Academy of Medicine, Hong Kong, Tel: +85221282129; E-mail: [email protected] Received Date: Feb 12, 2018; Accepted Date: Mar 12, 2018; Published Date: Mar 21, 2018 Copyright: © 2018 Michael CKT. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Introduction but of post-inflammatory hyperpigmentation, Acquired unilateral Nevus (Hori’s Nevus), Riehl’s melanosis, Drug-induced Pigmented contact dermatitis (PCD), also known as Riehl’s hyperpigmentation, Lichenoid dermatitis; as well as Melasma and melanosis, is a rare facial hyperpigmentation usually secondary to Ochronosis. cosmetics. There are few documented reports in the literature, and many cases without proven diagnosis may have been treated with pigment lasers, especially in beauty parlour settings. We report a case referred from a private practitioner who has a special interest in dermatology. The patient was diagnosed subsequently as having Riehl’s melanosis and treated with non-tyrosinase inhibitor bleaching agents, sun avoidance and mandatory abstinence from over-the-counter cosmetic products. -
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 . -
Hereditary Hearing Impairment with Cutaneous Abnormalities
G C A T T A C G G C A T genes Review Hereditary Hearing Impairment with Cutaneous Abnormalities Tung-Lin Lee 1 , Pei-Hsuan Lin 2,3, Pei-Lung Chen 3,4,5,6 , Jin-Bon Hong 4,7,* and Chen-Chi Wu 2,3,5,8,* 1 Department of Medical Education, National Taiwan University Hospital, Taipei City 100, Taiwan; [email protected] 2 Department of Otolaryngology, National Taiwan University Hospital, Taipei 11556, Taiwan; [email protected] 3 Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei City 100, Taiwan; [email protected] 4 Graduate Institute of Medical Genomics and Proteomics, National Taiwan University College of Medicine, Taipei City 100, Taiwan 5 Department of Medical Genetics, National Taiwan University Hospital, Taipei 10041, Taiwan 6 Department of Internal Medicine, National Taiwan University Hospital, Taipei 10041, Taiwan 7 Department of Dermatology, National Taiwan University Hospital, Taipei City 100, Taiwan 8 Department of Medical Research, National Taiwan University Biomedical Park Hospital, Hsinchu City 300, Taiwan * Correspondence: [email protected] (J.-B.H.); [email protected] (C.-C.W.) Abstract: Syndromic hereditary hearing impairment (HHI) is a clinically and etiologically diverse condition that has a profound influence on affected individuals and their families. As cutaneous findings are more apparent than hearing-related symptoms to clinicians and, more importantly, to caregivers of affected infants and young individuals, establishing a correlation map of skin manifestations and their underlying genetic causes is key to early identification and diagnosis of syndromic HHI. In this article, we performed a comprehensive PubMed database search on syndromic HHI with cutaneous abnormalities, and reviewed a total of 260 relevant publications. -
Treatment of Poikiloderma of Civatte with Ablative Fractional Laser Resurfacing: Prospective Study and Review of the Literature Emily P
JUNE 2009 527 Vo l u m e 8 • Is s u e 6 CO P YR IGHT © 2009 ORIGINAL ARTICLES JOURN A L OF DRUGS IN DER MA TOLOGY Treatment of Poikiloderma of Civatte With Ablative Fractional Laser Resurfacing: Prospective Study and Review of the Literature emily P. Tierney MD and C. William Hanke MD MPH Laser and Skin Surgery Center of Indiana, Carmel, IN ABSTRACT Background: Previous laser treatments for Poikiloderma of Civatte (PC) (i.e., Pulsed dye, Intense Pulsed Light, KTP and Argon) are limited by side effect profiles and/or efficacy. Given the high degree of safety and efficacy of ablative fractional photothermolysis (AFP) for photoaging, we set out to assess the efficacy of PC with AFP. Design: A prospective pilot study for PC in 10 subjects with a series of 1−3 treatment sessions. Treatment sessions were adminis- tered at 6−8 week intervals with blinded physician photographic analysis of improvement at 2 months post-treatment. Evaluation was performed of five clinical indicators, erythema/telangiecatasia, dyschromia, skin texture, skin laxity and cosmetic outcome. Results: The number of treatments required for improvement of PC ranged from 1 to 3, with an average of 1.4. For erythema/te- langiecatasia, the mean score improved 65.0% (95% CI: 60.7%, 69.3%) dyschromia, 66.7% (95% CI: 61.8%, 71.6%), skin texture, 51.7% (95% CI: 48.3%, 55.1%) and skin laxity, 52.5% (95% CI: 49.6%, 55.4%). For cosmetic outcome, the mean score improved 66.7% (95% CI: 62.6%, 70.8%) at 2 months post treatment. -
Xeroderma Pigmentosum: an Insight Into DNA Repair Processes
ACCME/Disclosures The USCAP requires that anyone in a position to influence or control the content of CME disclose any relevant financial relationship WITH COMMERCIAL INTERESTS which they or their spouse/partner have, or have had, within the past 12 months, which relates to the content of this educational activity and creates a conflict of interest. Dr. Jennifer O. Black declares she has no conflict(s) of interest to disclose. Xeroderma Pigmentosum: An Insight into DNA Repair Processes Jennifer O. Black, MD Assistant Professor Division of Pediatric Pathology and Laboratory Medicine Children’s Hospital Colorado University of Colorado Anschutz Medical Campus Aurora, Colorado Introduction: Xeroderma Pigmentosum Xeroderma Pigmentosum (XP): • Initially described 1874 • Rare autosomal recessive disorder • Prevalence: 1-45/million, variable ethnic frequency • UV radiation sensitivity disorder characterized by: • Severe skin burning following minimal sun exposure • Early freckling (before 2 years of age) • Skin cancer at an early age Kraemer KH, DiGiovann JJ. Photochemistry and Photobiology 91:452-459, 2015 Introduction: Xeroderma Pigmentosum XP Clinical Spectrum: • Skin Changes: o Early freckling and subsequent checkered pigmentation o Thin, dry, contracted skin o Telangiectasias o Skin cancers: o Squamous cell carcinoma o Basal cell carcinoma o Melanoma Courtesy Dr. Bahig M. Shehata, Children’s Healthcare of Atlanta Introduction: Xeroderma Pigmentosum Squamous Cell Carcinoma Robbins and Cotran Pathologic Basis of Disease. Lazar, Alexander J.F.; -
Journal of Pigmentary Disorders Yayli, Pigmentary Disorders 2015, 2:1 DOI: 10.4172/2376-0427.1000158
igmentar f P y D l o i a so n r r d u e r o J s Journal of Pigmentary Disorders Yayli, Pigmentary Disorders 2015, 2:1 DOI: 10.4172/2376-0427.1000158 ISSN: 2376-0427 Review Open Access Treatment of Hyperpigmentation in Darker Skins Savas Yayli* Department of Dermatology, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkey *Corresponding author: Savas Yayli, Department of Dermatology, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkey, Tel: 90 462 377 53 88; E- mail: [email protected] Rec date: Dec 14, 2014; Acc date: Dec 28, 2014; Pub date: Jan 02, 2015 Copyright: © 2015 Yayli S, This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Introduction many newer agents are in the market [6]. Beside those newers, fixed TC including hydroquinone 4%, tretinoine 0.05%, flucinolon Darker skin or skin of colour means higher Fitzpatrick skin types in acetonide 0.01% is shown as the therapy with highest evidence – still a wide range of racial and ethnic groups referring to persons from little controlled studies - in Latin guide of melasma or recent reviews. African, Asian, Native American, Middle Eastern and Hispanic If there is an irritation or allergy to one of compounds of this TC, one backgrounds. Darker skin types are characterized by higher content of may use it as dual combinations. In Latin guide for treatment of melanin, higher eumelanin to pheomelanin ratio. This is an advantage melasma, second line therapies are TC plus peels or for protection against ultraviolet (UV) radiation, however it also microdermabrasion, and lastly lasers and light sources [4,7]. -
Congenital Horner Syndrome with Heterochromia Iridis Associated with Ipsilateral Internal Carotid Artery Hypoplasia
CASE REPORT Print ISSN 1738-6586 / On-line ISSN 2005-5013 J Clin Neurol 2014 Open Access Congenital Horner Syndrome with Heterochromia Iridis Associated with Ipsilateral Internal Carotid Artery Hypoplasia Fabrice C. Deprez,a Julie Coulier,b Denis Rommel,a Antonella Boschib aDepartments of Radiology and bOphthalmology, Cliniques Universitaires Saint-Luc, UCL, Brussels, Belgium BackgroundzzHorner syndrome (HS), also known as Claude-Bernard-Horner syndrome or Received August 5, 2013 oculosympathetic palsy, comprises ipsilateral ptosis, miosis, and facial anhidrosis. Revised April 15, 2014 Accepted April 21, 2014 Case ReportzzWe report herein the case of a 67-year-old man who presented with congenital HS associated with ipsilateral hypoplasia of the internal carotid artery (ICA), as revealed by Correspondence heterochromia iridis and confirmed by computed tomography (CT). Fabrice C. Deprez, MD Department of Radiology, ConclusionszzCT evaluation of the skull base is essential to establish this diagnosis and dis- Cliniques Universitaires Saint-Luc, tinguish aplasia from agenesis/hypoplasia (by the absence or hypoplasia of the carotid canal) or UCL, Avenue Hippocrate 10, from acquired ICA obstruction as demonstrated by angiographic CT. 1200 Woluwe-Saint-Lambert, J Clin Neurol 2014 Belgium Tel +32.472.93.34.80 Key Wordszzcongenital horner syndrome, internal carotid artery agenesis, Fax +32.81.42.35.05 heterochromia iridis, computed tomography. E-mail [email protected] Introduction spindly left ICA, which was misinterpreted as ICA thrombosis (Fig. 1). The left anterior cerebral artery and MCA were sup- Horner syndrome (HS), also known as Claude-Bernard-Horn- plied by a large posterior communicating artery from the bas- er syndrome or oculosympathetic palsy, comprises ipsilateral ilar artery. -
Reversal of Laser-Induced Hypopigmentation with a Narrow-Band UV-B Light Source in a Patient with Skin Type VI
Reversal of Laser-Induced Hypopigmentation with a Narrow-Band UV-B Light Source in a Patient with Skin Type VI Ã y yz ANETTA RESZKO, MD, PHD, SEAN A. SUKAL, MD, PHD, AND ROY G. GERONEMUS,MD Dr. Geronemus is on the Lumenis Medical Advisory Board. evus of Ota (nevus fuscoceruleus ophthalmo- tion after clearance of a nevus of Ota with a QSRL Nmaxillaris) is a benign dermal melanocytic in an African American Skin Type VI male with a hematoma clinically appearing as a bluish-brown narrow-band ultraviolet B (NB UV-B) source. discoloration in the ophthalmic and/or maxillary branches of the trigeminal nerve. The condition first Case described by Ota and Tanino occurs predominantly in Asians with estimated frequency of 0.014% to A 36-year-old African American male, Fitzpatrick 0.034%, but can be found in other ethnicities.1 Skin Type VI, with no significant medical history, Historical therapies for nevus of Ota include surgery, presented for treatment of a 10 Â 16-cm Tanino dermabrasion, electrodesiccation, skin grafting, and Stage III (V1 and V2 distribution) nevus of Ota cryotherapy and are all associated with a significant (Figure 1). The patient was treated with a QSRL, at a risk of dyschromia and scarring.2–5 fluence of 3 to 5 J, spot size 6.5 mm with no greater than 10% overlap between pulses. After 20 treat- The introduction of the theory of selective ment sessions, of which several were partial treat- photothermolysis and subsequent development of ments of the same area of the nevus of Ota over a Q-switched lasers revolutionized the treatment period of 6 years, the lesion was completely cleared. -
Table I. Genodermatoses with Known Gene Defects 92 Pulkkinen
92 Pulkkinen, Ringpfeil, and Uitto JAM ACAD DERMATOL JULY 2002 Table I. Genodermatoses with known gene defects Reference Disease Mutated gene* Affected protein/function No.† Epidermal fragility disorders DEB COL7A1 Type VII collagen 6 Junctional EB LAMA3, LAMB3, ␣3, 3, and ␥2 chains of laminin 5, 6 LAMC2, COL17A1 type XVII collagen EB with pyloric atresia ITGA6, ITGB4 ␣64 Integrin 6 EB with muscular dystrophy PLEC1 Plectin 6 EB simplex KRT5, KRT14 Keratins 5 and 14 46 Ectodermal dysplasia with skin fragility PKP1 Plakophilin 1 47 Hailey-Hailey disease ATP2C1 ATP-dependent calcium transporter 13 Keratinization disorders Epidermolytic hyperkeratosis KRT1, KRT10 Keratins 1 and 10 46 Ichthyosis hystrix KRT1 Keratin 1 48 Epidermolytic PPK KRT9 Keratin 9 46 Nonepidermolytic PPK KRT1, KRT16 Keratins 1 and 16 46 Ichthyosis bullosa of Siemens KRT2e Keratin 2e 46 Pachyonychia congenita, types 1 and 2 KRT6a, KRT6b, KRT16, Keratins 6a, 6b, 16, and 17 46 KRT17 White sponge naevus KRT4, KRT13 Keratins 4 and 13 46 X-linked recessive ichthyosis STS Steroid sulfatase 49 Lamellar ichthyosis TGM1 Transglutaminase 1 50 Mutilating keratoderma with ichthyosis LOR Loricrin 10 Vohwinkel’s syndrome GJB2 Connexin 26 12 PPK with deafness GJB2 Connexin 26 12 Erythrokeratodermia variabilis GJB3, GJB4 Connexins 31 and 30.3 12 Darier disease ATP2A2 ATP-dependent calcium 14 transporter Striate PPK DSP, DSG1 Desmoplakin, desmoglein 1 51, 52 Conradi-Hu¨nermann-Happle syndrome EBP Delta 8-delta 7 sterol isomerase 53 (emopamil binding protein) Mal de Meleda ARS SLURP-1 -
Other Relevant Data
4. Other Relevant Data 4.1 Transmission and absorption in biological tissues UVR may be transmitted, reflected, scattered or absorbed by chromophores in any layer of tissue, su ch as the skin and eye. Absorption is strongly related to wavelength, as it depends on the properties of the responsible chromophore(s). Accordingly, transmission is also wavelength-dependent. Transmission and other optical properties are affected by changes in the structure of the tissue and, especially in the case of the lens of the eye, by ageing. Absorption of radiation bya tissue chromophore is a prerequisite for any photochernical or photobiological effect; however, absorption does not necessarily have a biological con- sequence. 4.1.1 Epidermis Since UVR-induced skin cancer is an epidermal phenomenon, this section focuses on epidermis and excludes the dermis. The epidermis, a tissue with a high replication rate, can be divided functionally into two: an inner, living part (60-160-J-m thick in humans) of cells at various stages of differentiation and the outermost, non-living, terminally differentiated stratum corneum (8-15-J-m thick in humans). The dividing cell population is located in the innermost basal layer of the living epidermis. Optical properties have usually been studied using isolated strateum corneum or whole epidermis. Absorption and scattering of UVR by the stratum corneurn afford sorne protection to the living part of the epidermis from UVR exposure. Human and mouse epidermis have important structural differences. The living part and the stratum corneum of hum an epidermis have about 10 cell layers each. ln rnice, the living part has two to three celllayers and the stratum corne a one to two cell layers.