Disorders of Pigmentation
Identifieur interne : 001932 ( Istex/Corpus ); précédent : 001931; suivant : 001933Disorders of Pigmentation
Auteurs : Susanna K. Fistarol ; Peter H. ItinSource :
- JDDG: Journal der Deutschen Dermatologischen Gesellschaft [ 1610-0379 ] ; 2010-03.
English descriptors
- Teeft :
- Abnormal, Abnormal melanogenesis, Abnormal transfer, Acad dermatol, Academy figure, Accurate diagnosis, Acth, Addison, Addison disease, Albinism, Albright syndrome, Algorithm, Anogenital regions, Antwort, Atopic dermatitis, Atrial myxomas, Authors journal compilation blackwell verlag gmbh, Autoimmune disorder, Autosomal, Average risk, Axillary freckling, Basal, Basal cell layer, Basal layer, Bedingt, Beim panhypopituitarismus entsteht, Berlin jddg, Berlin jddg academy, Berlin jddg jddg, Biochemical testing, Blue nevi, Brown color, Brown discoloration, Bullous porphyrias, Caucasian population, Clinical approach, Clinical examination, Congenital, Congenital hypopigmentation, Congenital lesion, Copper metabolism, Cowden syndrome, Crowe sign, Cutaneous, Depigmentation, Depigmented nevi, Depigmentosus, Dermatol, Dermatol clin, Differential diagnosis, Diffuse, Diffuse hyperpigmentation, Diffuse hypopigmentation, Diffuse variant, Dirty skin color, Disorder, Durch, Early childhood, Ectodermal dysplasias, Enzyme tyrosinase, Epidermal, Evidence level, Felty syndrome, First months, First years, Genetic disorder, Genetic mosaicism, Gmbh, Hautfarbe wird vorwiegend durch, Healthy newborns, Histology, Hyperpigmentation, Hypomelanosis, Hypophyseal tumors, Hypopigmentation, Hypopigmentation results, Important factor, Inflammatory skin disease, Iris hamartomas, Jddg, Keratinocytes, Lentigo, Leopard syndrome, Lesion, Leukoderma, Lichen sclerosus, Light hair, Linea alba, Lisch nodules, Localized, Localized depigmentation, Localized hyperpigmentation, Localized hypopigmentation, Lysosomal organelles, Malassezia furfur, Mature melanosomes, Medical history, Melanin, Melanin production, Melanin synthesis, Melanocyte, Melanocytic nevi, Melanoma, Melanosomes, Mucous membranes, Neural crest, Nevus, Nevus anaemicus, Nevus depigmentosus, Nevus depigmentosus simplex, Oral mucosa, Other factors, Other organs, Piebaldism, Pigmentary changes, Pigmentation, Pigmentation disorders, Pityriasis, Pityriasis alba, Pityriasis versicolor, Porphyria, Presumptive diagnosis, Primary biliary cirrhosis, Progressive hypomelanose, Progressive macular hypomelanosis, Proximal extremities, Psychomotor retardation, Renal insufficiency, Rete ridges, Richtig, Sclerosis, Secondary body hair, Segmental vitiligo, Simplex, Skin cancer, Skin color, Stratum corneum, Syndrome, Systemic diseases, Systemic sclerosis, Tuberous, Tuberous sclerosis, Tyrosinase activity, Various ethnicities, Various organs, Various therapies, Verdachtsdiagnose eines morbus addison wird gesichert durch, Verlag, Vitiligo, Vorwiegend, Waardenburg syndrome, Welche, Welche antwort, Wird, Wood light.
Abstract
Skin color is highly individual and the variations are controlled by numerous genes. The different skin colors result from the size and number of melanosomes and do not mirror the amount of melanocytes. Disorders of pigmentation can result from migration abnormalities of melanocytes from the neural crest to the skin during embryogenesis. In addition, impairment of melanosome transfer to the surrounding keratinocytes, an alteration in melanin synthesis and a defective degradation or removal of melanin may lead to abnormal skin pigmentation. Immunologic or toxic mediated destructions of melanocytes can end in pigmentation disorders. Disorders of pigmentation are classified in hypo‐ or hyperpigmentation which can occur as a genetic or acquired disease. They can manifest locally or diffuse. Congenital hypopigmentation can be restricted to the skin as in piebaldism or they represent a systemic disease as in Menkes disease or phenylketonuria. Localized hypo‐ or hyperpigmentation in children may serve as markers for systemic diseases. Ash‐leaf hypopigmentation are characteristic for tuberous sclerosis and more than 5 café‐au‐lait spots suggest neurofibromatosis 1 (von Recklinghausen disease). The most common autoimmune‐induced depigmentation is vitiligo. Generalized hyperpigmentation only rarely reflects a primary genetic disorder but is most often from acquired diseases as in Addison disease, secondary hemochromatosis or primary biliary cirrhosis. Treatment of pigmentation disorders are based on a diagnosis which sometimes allow a specific intervention. Cosmetically acceptable results are difficult to obtain.
Url:
DOI: 10.1111/j.1610-0387.2009.07137.x
Links to Exploration step
ISTEX:B4B8FC9CBBFD4695FDBE7579E26B7A8D3EADC199Le document en format XML
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xml:lang="en"><term>Abnormal</term><term>Abnormal melanogenesis</term><term>Abnormal transfer</term><term>Acad dermatol</term><term>Academy figure</term><term>Accurate diagnosis</term><term>Acth</term><term>Addison</term><term>Addison disease</term><term>Albinism</term><term>Albright syndrome</term><term>Algorithm</term><term>Anogenital regions</term><term>Antwort</term><term>Atopic dermatitis</term><term>Atrial myxomas</term><term>Authors journal compilation blackwell verlag gmbh</term><term>Autoimmune disorder</term><term>Autosomal</term><term>Average risk</term><term>Axillary freckling</term><term>Basal</term><term>Basal cell layer</term><term>Basal layer</term><term>Bedingt</term><term>Beim panhypopituitarismus entsteht</term><term>Berlin jddg</term><term>Berlin jddg academy</term><term>Berlin jddg jddg</term><term>Biochemical testing</term><term>Blue nevi</term><term>Brown color</term><term>Brown discoloration</term><term>Bullous porphyrias</term><term>Caucasian population</term><term>Clinical approach</term><term>Clinical examination</term><term>Congenital</term><term>Congenital hypopigmentation</term><term>Congenital lesion</term><term>Copper metabolism</term><term>Cowden syndrome</term><term>Crowe sign</term><term>Cutaneous</term><term>Depigmentation</term><term>Depigmented nevi</term><term>Depigmentosus</term><term>Dermatol</term><term>Dermatol clin</term><term>Differential diagnosis</term><term>Diffuse</term><term>Diffuse hyperpigmentation</term><term>Diffuse hypopigmentation</term><term>Diffuse variant</term><term>Dirty skin color</term><term>Disorder</term><term>Durch</term><term>Early childhood</term><term>Ectodermal dysplasias</term><term>Enzyme tyrosinase</term><term>Epidermal</term><term>Evidence level</term><term>Felty syndrome</term><term>First months</term><term>First years</term><term>Genetic disorder</term><term>Genetic mosaicism</term><term>Gmbh</term><term>Hautfarbe wird vorwiegend durch</term><term>Healthy newborns</term><term>Histology</term><term>Hyperpigmentation</term><term>Hypomelanosis</term><term>Hypophyseal tumors</term><term>Hypopigmentation</term><term>Hypopigmentation results</term><term>Important factor</term><term>Inflammatory skin disease</term><term>Iris hamartomas</term><term>Jddg</term><term>Keratinocytes</term><term>Lentigo</term><term>Leopard syndrome</term><term>Lesion</term><term>Leukoderma</term><term>Lichen sclerosus</term><term>Light hair</term><term>Linea alba</term><term>Lisch nodules</term><term>Localized</term><term>Localized depigmentation</term><term>Localized hyperpigmentation</term><term>Localized hypopigmentation</term><term>Lysosomal organelles</term><term>Malassezia furfur</term><term>Mature melanosomes</term><term>Medical history</term><term>Melanin</term><term>Melanin production</term><term>Melanin synthesis</term><term>Melanocyte</term><term>Melanocytic nevi</term><term>Melanoma</term><term>Melanosomes</term><term>Mucous membranes</term><term>Neural crest</term><term>Nevus</term><term>Nevus anaemicus</term><term>Nevus depigmentosus</term><term>Nevus depigmentosus simplex</term><term>Oral mucosa</term><term>Other factors</term><term>Other organs</term><term>Piebaldism</term><term>Pigmentary changes</term><term>Pigmentation</term><term>Pigmentation disorders</term><term>Pityriasis</term><term>Pityriasis alba</term><term>Pityriasis versicolor</term><term>Porphyria</term><term>Presumptive diagnosis</term><term>Primary biliary cirrhosis</term><term>Progressive hypomelanose</term><term>Progressive macular hypomelanosis</term><term>Proximal extremities</term><term>Psychomotor retardation</term><term>Renal insufficiency</term><term>Rete ridges</term><term>Richtig</term><term>Sclerosis</term><term>Secondary body hair</term><term>Segmental vitiligo</term><term>Simplex</term><term>Skin cancer</term><term>Skin color</term><term>Stratum corneum</term><term>Syndrome</term><term>Systemic diseases</term><term>Systemic sclerosis</term><term>Tuberous</term><term>Tuberous sclerosis</term><term>Tyrosinase activity</term><term>Various ethnicities</term><term>Various organs</term><term>Various therapies</term><term>Verdachtsdiagnose eines morbus addison wird gesichert durch</term><term>Verlag</term><term>Vitiligo</term><term>Vorwiegend</term><term>Waardenburg syndrome</term><term>Welche</term><term>Welche antwort</term><term>Wird</term><term>Wood light</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Skin color is highly individual and the variations are controlled by numerous genes. The different skin colors result from the size and number of melanosomes and do not mirror the amount of melanocytes. Disorders of pigmentation can result from migration abnormalities of melanocytes from the neural crest to the skin during embryogenesis. In addition, impairment of melanosome transfer to the surrounding keratinocytes, an alteration in melanin synthesis and a defective degradation or removal of melanin may lead to abnormal skin pigmentation. Immunologic or toxic mediated destructions of melanocytes can end in pigmentation disorders. Disorders of pigmentation are classified in hypo‐ or hyperpigmentation which can occur as a genetic or acquired disease. They can manifest locally or diffuse. Congenital hypopigmentation can be restricted to the skin as in piebaldism or they represent a systemic disease as in Menkes disease or phenylketonuria. Localized hypo‐ or hyperpigmentation in children may serve as markers for systemic diseases. Ash‐leaf hypopigmentation are characteristic for tuberous sclerosis and more than 5 café‐au‐lait spots suggest neurofibromatosis 1 (von Recklinghausen disease). The most common autoimmune‐induced depigmentation is vitiligo. Generalized hyperpigmentation only rarely reflects a primary genetic disorder but is most often from acquired diseases as in Addison disease, secondary hemochromatosis or primary biliary cirrhosis. Treatment of pigmentation disorders are based on a diagnosis which sometimes allow a specific intervention. Cosmetically acceptable results are difficult to obtain.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>hyperpigmentation</json:string><json:string>hypopigmentation</json:string><json:string>melanocyte</json:string><json:string>pigmentation</json:string><json:string>jddg</json:string><json:string>melanin</json:string><json:string>nevus</json:string><json:string>vitiligo</json:string><json:string>durch</json:string><json:string>melanosomes</json:string><json:string>wird</json:string><json:string>authors journal compilation blackwell verlag gmbh</json:string><json:string>gmbh</json:string><json:string>verlag</json:string><json:string>depigmentation</json:string><json:string>dermatol</json:string><json:string>albinism</json:string><json:string>localized</json:string><json:string>addison disease</json:string><json:string>epidermal</json:string><json:string>welche</json:string><json:string>basal</json:string><json:string>hypomelanosis</json:string><json:string>leukoderma</json:string><json:string>porphyria</json:string><json:string>depigmentosus</json:string><json:string>cutaneous</json:string><json:string>lentigo</json:string><json:string>keratinocytes</json:string><json:string>syndrome</json:string><json:string>addison</json:string><json:string>richtig</json:string><json:string>bedingt</json:string><json:string>piebaldism</json:string><json:string>diffuse hyperpigmentation</json:string><json:string>melanoma</json:string><json:string>welche antwort</json:string><json:string>antwort</json:string><json:string>autosomal</json:string><json:string>vorwiegend</json:string><json:string>early childhood</json:string><json:string>pityriasis</json:string><json:string>tuberous</json:string><json:string>congenital</json:string><json:string>tuberous sclerosis</json:string><json:string>differential diagnosis</json:string><json:string>nevus depigmentosus simplex</json:string><json:string>melanin production</json:string><json:string>diffuse hypopigmentation</json:string><json:string>mature melanosomes</json:string><json:string>segmental vitiligo</json:string><json:string>berlin jddg</json:string><json:string>clinical approach</json:string><json:string>sclerosis</json:string><json:string>tyrosinase activity</json:string><json:string>localized hyperpigmentation</json:string><json:string>localized hypopigmentation</json:string><json:string>beim panhypopituitarismus entsteht</json:string><json:string>stratum corneum</json:string><json:string>skin color</json:string><json:string>hautfarbe wird vorwiegend durch</json:string><json:string>diffuse</json:string><json:string>disorder</json:string><json:string>acth</json:string><json:string>algorithm</json:string><json:string>histology</json:string><json:string>simplex</json:string><json:string>progressive macular hypomelanosis</json:string><json:string>brown discoloration</json:string><json:string>waardenburg syndrome</json:string><json:string>abnormal transfer</json:string><json:string>verdachtsdiagnose eines morbus addison wird gesichert durch</json:string><json:string>academy figure</json:string><json:string>basal cell layer</json:string><json:string>berlin jddg academy</json:string><json:string>atopic dermatitis</json:string><json:string>pityriasis alba</json:string><json:string>pigmentation disorders</json:string><json:string>clinical examination</json:string><json:string>berlin jddg jddg</json:string><json:string>presumptive diagnosis</json:string><json:string>caucasian population</json:string><json:string>rete ridges</json:string><json:string>depigmented nevi</json:string><json:string>lesion</json:string><json:string>abnormal</json:string><json:string>biochemical testing</json:string><json:string>healthy newborns</json:string><json:string>genetic mosaicism</json:string><json:string>ectodermal dysplasias</json:string><json:string>nevus anaemicus</json:string><json:string>congenital lesion</json:string><json:string>medical history</json:string><json:string>pigmentary changes</json:string><json:string>wood light</json:string><json:string>first months</json:string><json:string>diffuse variant</json:string><json:string>proximal extremities</json:string><json:string>localized depigmentation</json:string><json:string>autoimmune disorder</json:string><json:string>dirty skin color</json:string><json:string>important factor</json:string><json:string>various organs</json:string><json:string>lichen sclerosus</json:string><json:string>first years</json:string><json:string>hypophyseal tumors</json:string><json:string>secondary body hair</json:string><json:string>renal insufficiency</json:string><json:string>various therapies</json:string><json:string>abnormal melanogenesis</json:string><json:string>lysosomal organelles</json:string><json:string>genetic disorder</json:string><json:string>average risk</json:string><json:string>brown color</json:string><json:string>oral mucosa</json:string><json:string>anogenital regions</json:string><json:string>evidence level</json:string><json:string>inflammatory skin disease</json:string><json:string>linea alba</json:string><json:string>other organs</json:string><json:string>accurate diagnosis</json:string><json:string>bullous porphyrias</json:string><json:string>systemic sclerosis</json:string><json:string>felty syndrome</json:string><json:string>mucous membranes</json:string><json:string>hypopigmentation results</json:string><json:string>axillary freckling</json:string><json:string>crowe sign</json:string><json:string>iris hamartomas</json:string><json:string>lisch nodules</json:string><json:string>albright syndrome</json:string><json:string>cowden syndrome</json:string><json:string>various ethnicities</json:string><json:string>psychomotor retardation</json:string><json:string>leopard syndrome</json:string><json:string>melanocytic nevi</json:string><json:string>atrial myxomas</json:string><json:string>blue nevi</json:string><json:string>pityriasis versicolor</json:string><json:string>malassezia furfur</json:string><json:string>copper metabolism</json:string><json:string>dermatol clin</json:string><json:string>acad dermatol</json:string><json:string>enzyme tyrosinase</json:string><json:string>basal layer</json:string><json:string>other factors</json:string><json:string>primary biliary cirrhosis</json:string><json:string>systemic diseases</json:string><json:string>congenital hypopigmentation</json:string><json:string>light hair</json:string><json:string>nevus depigmentosus</json:string><json:string>melanin synthesis</json:string><json:string>neural crest</json:string><json:string>progressive hypomelanose</json:string><json:string>skin cancer</json:string></teeft></keywords><author><json:item><name>Susanna K. Fistarol</name><affiliations><json:string>Department of Dermatology, Basel University Hospital, Switzerland</json:string></affiliations></json:item><json:item><name>Peter H. Itin</name><affiliations><json:string>Department of Dermatology, Basel University Hospital, Switzerland</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>disorder of pigmentation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>hypopigmentation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>hyperpigmentation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>genodermatosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>melanocytes</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>melanosomes</value></json:item></subject><articleId><json:string>DDG7137</json:string></articleId><arkIstex>ark:/67375/WNG-GTVR0X92-F</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Skin color is highly individual and the variations are controlled by numerous genes. The different skin colors result from the size and number of melanosomes and do not mirror the amount of melanocytes. Disorders of pigmentation can result from migration abnormalities of melanocytes from the neural crest to the skin during embryogenesis. In addition, impairment of melanosome transfer to the surrounding keratinocytes, an alteration in melanin synthesis and a defective degradation or removal of melanin may lead to abnormal skin pigmentation. Immunologic or toxic mediated destructions of melanocytes can end in pigmentation disorders. Disorders of pigmentation are classified in hypo‐ or hyperpigmentation which can occur as a genetic or acquired disease. They can manifest locally or diffuse. Congenital hypopigmentation can be restricted to the skin as in piebaldism or they represent a systemic disease as in Menkes disease or phenylketonuria. Localized hypo‐ or hyperpigmentation in children may serve as markers for systemic diseases. Ash‐leaf hypopigmentation are characteristic for tuberous sclerosis and more than 5 café‐au‐lait spots suggest neurofibromatosis 1 (von Recklinghausen disease). The most common autoimmune‐induced depigmentation is vitiligo. Generalized hyperpigmentation only rarely reflects a primary genetic disorder but is most often from acquired diseases as in Addison disease, secondary hemochromatosis or primary biliary cirrhosis. Treatment of pigmentation disorders are based on a diagnosis which sometimes allow a specific intervention. Cosmetically acceptable results are difficult to obtain.</abstract><qualityIndicators><refBibsNative>true</refBibsNative><abstractWordCount>227</abstractWordCount><abstractCharCount>1630</abstractCharCount><keywordCount>6</keywordCount><score>9.724</score><pdfWordCount>6944</pdfWordCount><pdfCharCount>47252</pdfCharCount><pdfVersion>1.4</pdfVersion><pdfPageCount>16</pdfPageCount><pdfPageSize>595.276 x 841.89 pts (A4)</pdfPageSize><pdfWordsPerPage>434</pdfWordsPerPage><pdfText>true</pdfText></qualityIndicators><title>Disorders of Pigmentation</title><pmid><json:string>19788584</json:string></pmid><genre><json:string>article</json:string></genre><host><title>JDDG: Journal der Deutschen Dermatologischen Gesellschaft</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1610-0387</json:string></doi><issn><json:string>1610-0379</json:string></issn><eissn><json:string>1610-0387</json:string></eissn><publisherId><json:string>DDG</json:string></publisherId><volume>8</volume><issue>3</issue><pages><first>187</first><last>202</last><total>16</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>2010</json:string></date><geogName></geogName><orgName><json:string>National Institutes of Health</json:string><json:string>NIH</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>J.Dermatol</json:string><json:string>Histology</json:string><json:string>Peter Itin</json:string><json:string>The</json:string><json:string>Jan C. 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Prof. Dr. med. Peter Itin
Dermatologie
Universitätsspital
Petersgraben 4
CH‐4031 Basel, Schweiz
Tel.: +41‐61‐265‐4084
Fax: +41‐61‐265‐4885
E‐mail: <email>pitin@uhbs.ch</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:DDG.DDG7137.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Submitted: 9. 2. 2009 | Accepted: 21. 4. 2009</unparsedEditorialHistory><countGroup><count type="figureTotal" number="13"></count><count type="tableTotal" number="3"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="22"></count><count type="linksCrossRef" number="47"></count></countGroup><titleGroup><title type="main">Disorders of Pigmentation</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Susanna K.</givenNames><familyName>Fistarol</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Peter H.</givenNames><familyName>Itin</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="CH"><unparsedAffiliation>Department of Dermatology, Basel University Hospital, Switzerland</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">disorder of pigmentation</keyword><keyword xml:id="k2">hypopigmentation</keyword><keyword xml:id="k3">hyperpigmentation</keyword><keyword xml:id="k4">genodermatosis</keyword><keyword xml:id="k5">melanocytes</keyword><keyword xml:id="k6">melanosomes</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Summary</title><p>Skin color is highly individual and the variations are controlled by numerous genes. The different skin colors result from the size and number of melanosomes and do not mirror the amount of melanocytes. Disorders of pigmentation can result from migration abnormalities of melanocytes from the neural crest to the skin during embryogenesis. In addition, impairment of melanosome transfer to the surrounding keratinocytes, an alteration in melanin synthesis and a defective degradation or removal of melanin may lead to abnormal skin pigmentation. Immunologic or toxic mediated destructions of melanocytes can end in pigmentation disorders. Disorders of pigmentation are classified in hypo‐ or hyperpigmentation which can occur as a genetic or acquired disease. They can manifest locally or diffuse. Congenital hypopigmentation can be restricted to the skin as in piebaldism or they represent a systemic disease as in Menkes disease or phenylketonuria. Localized hypo‐ or hyperpigmentation in children may serve as markers for systemic diseases. Ash‐leaf hypopigmentation are characteristic for tuberous sclerosis and more than 5 café‐au‐lait spots suggest neurofibromatosis 1 (von Recklinghausen disease). The most common autoimmune‐induced depigmentation is vitiligo. Generalized hyperpigmentation only rarely reflects a primary genetic disorder but is most often from acquired diseases as in Addison disease, secondary hemochromatosis or primary biliary cirrhosis. Treatment of pigmentation disorders are based on a diagnosis which sometimes allow a specific intervention. Cosmetically acceptable results are difficult to obtain.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="n-fnt-1" numbered="no"><p>Section Editor
Prof. Dr. Jan C. Simon,
Leipzig</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Disorders of Pigmentation</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Disorders of Pigmentation</title></titleInfo><name type="personal"><namePart type="given">Susanna K.</namePart><namePart type="family">Fistarol</namePart><affiliation>Department of Dermatology, Basel University Hospital, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter H.</namePart><namePart type="family">Itin</namePart><affiliation>Department of Dermatology, Basel University Hospital, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2010-03</dateIssued><edition>Submitted: 9. 2. 2009 | Accepted: 21. 4. 2009</edition><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">13</extent><extent unit="tables">3</extent><extent unit="formulas">0</extent><extent unit="references">22</extent><extent unit="linksCrossRef">47</extent></physicalDescription><abstract lang="en">Skin color is highly individual and the variations are controlled by numerous genes. The different skin colors result from the size and number of melanosomes and do not mirror the amount of melanocytes. Disorders of pigmentation can result from migration abnormalities of melanocytes from the neural crest to the skin during embryogenesis. In addition, impairment of melanosome transfer to the surrounding keratinocytes, an alteration in melanin synthesis and a defective degradation or removal of melanin may lead to abnormal skin pigmentation. Immunologic or toxic mediated destructions of melanocytes can end in pigmentation disorders. Disorders of pigmentation are classified in hypo‐ or hyperpigmentation which can occur as a genetic or acquired disease. They can manifest locally or diffuse. Congenital hypopigmentation can be restricted to the skin as in piebaldism or they represent a systemic disease as in Menkes disease or phenylketonuria. Localized hypo‐ or hyperpigmentation in children may serve as markers for systemic diseases. Ash‐leaf hypopigmentation are characteristic for tuberous sclerosis and more than 5 café‐au‐lait spots suggest neurofibromatosis 1 (von Recklinghausen disease). The most common autoimmune‐induced depigmentation is vitiligo. Generalized hyperpigmentation only rarely reflects a primary genetic disorder but is most often from acquired diseases as in Addison disease, secondary hemochromatosis or primary biliary cirrhosis. Treatment of pigmentation disorders are based on a diagnosis which sometimes allow a specific intervention. Cosmetically acceptable results are difficult to obtain.</abstract><subject lang="en"><genre>keywords</genre><topic>disorder of pigmentation</topic><topic>hypopigmentation</topic><topic>hyperpigmentation</topic><topic>genodermatosis</topic><topic>melanocytes</topic><topic>melanosomes</topic></subject><relatedItem type="host"><titleInfo><title>JDDG: Journal der Deutschen Dermatologischen Gesellschaft</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">1610-0379</identifier><identifier type="eISSN">1610-0387</identifier><identifier type="DOI">10.1111/(ISSN)1610-0387</identifier><identifier type="PublisherID">DDG</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>187</start><end>202</end><total>16</total></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>What controls variation in human skin color?</title></titleInfo><name type="personal"><namePart type="given">GS</namePart><namePart type="family">Barsh</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Barsh GS. What controls variation in human skin color? PLoS Biol 2003; 1: 19–22.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>1</number></detail><extent unit="pages"><start>19</start><end>22</end></extent></part><relatedItem type="host"><titleInfo><title>PLoS Biol</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>1</number></detail><extent unit="pages"><start>19</start><end>22</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit2"><titleInfo><title>Nordlund JJ, Boissy RE, Hearing VJ, King R, Oetting W, Ortonne JP. The Pigmentary System, 2nd Edition, Wiley‐Blackwell, 2006.</title></titleInfo><note type="citation/reference">Nordlund JJ, Boissy RE, Hearing VJ, King R, Oetting W, Ortonne JP. The Pigmentary System, 2nd Edition, Wiley‐Blackwell, 2006.</note><name type="personal"><namePart type="given">JJ</namePart><namePart type="family">Nordlund</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RE</namePart><namePart type="family">Boissy</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">VJ</namePart><namePart type="family">Hearing</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">King</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Oetting</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JP</namePart><namePart type="family">Ortonne</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>book</genre><originInfo><publisher>Wiley‐Blackwell</publisher></originInfo><part><date>2006</date></part></relatedItem><relatedItem type="references" displayLabel="cit3"><titleInfo><title>Early central nervous system evolution: an era of skin brains?</title></titleInfo><name type="personal"><namePart type="given">ND</namePart><namePart type="family">Holland</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Holland ND. Early central nervous system evolution: an era of skin brains? Nat Rev Neurosci 2003; 4: 617–27.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>617</start><end>27</end></extent></part><relatedItem type="host"><titleInfo><title>Nat Rev Neurosci</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>617</start><end>27</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit4"><titleInfo><title>The genetics of sun sensitivity in humans</title></titleInfo><name type="personal"><namePart type="given">JL</namePart><namePart type="family">Rees</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Rees JL. The genetics of sun sensitivity in humans. Am J Hum Genet 2004; 75: 739–51.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>75</number></detail><extent unit="pages"><start>739</start><end>51</end></extent></part><relatedItem type="host"><titleInfo><title>Am J Hum Genet</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>75</number></detail><extent unit="pages"><start>739</start><end>51</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit5"><titleInfo><title>Hereditary hypo/de‐pigmented dermatoses: an overview</title></titleInfo><name type="personal"><namePart type="given">VN</namePart><namePart type="family">Seghal</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Srivastva</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Seghal VN, Srivastva G. Hereditary hypo/de‐pigmented dermatoses: an overview. Int J Dermatol 2008; 47: 1041–50.</note><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>47</number></detail><extent unit="pages"><start>1041</start><end>50</end></extent></part><relatedItem type="host"><titleInfo><title>Int J Dermatol</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>47</number></detail><extent unit="pages"><start>1041</start><end>50</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit6"><titleInfo><title>Hypomelanotic conditions of the newborn and infant</title></titleInfo><name type="personal"><namePart type="given">R</namePart><namePart type="family">Ruiz‐Maldonado</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Ruiz‐Maldonado R. Hypomelanotic conditions of the newborn and infant. Dermatol Clin 2007; 25: 373–82.</note><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><extent unit="pages"><start>373</start><end>82</end></extent></part><relatedItem type="host"><titleInfo><title>Dermatol Clin</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><extent unit="pages"><start>373</start><end>82</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit7"><titleInfo><title>A clinical approach to leukoderma</title></titleInfo><name type="personal"><namePart type="given">J</namePart><namePart type="family">Bolognia</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Bolognia J. A clinical approach to leukoderma. Int J Dermatol 1999; 38: 568–72.</note><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>38</number></detail><extent unit="pages"><start>568</start><end>72</end></extent></part><relatedItem type="host"><titleInfo><title>Int J Dermatol</title></titleInfo><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>38</number></detail><extent unit="pages"><start>568</start><end>72</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit8"><titleInfo><title>Piebaldism and neurofibromatosis type 1: horses of very different colors</title></titleInfo><name type="personal"><namePart type="given">RA</namePart><namePart type="family">Spritz</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PH</namePart><namePart type="family">Itin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DH</namePart><namePart type="family">Gutmann</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Spritz RA, Itin PH, Gutmann DH. Piebaldism and neurofibromatosis type 1: horses of very different colors. J Invest Dermatol 2004; 122: 34–5.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>122</number></detail><extent unit="pages"><start>34</start><end>5</end></extent></part><relatedItem type="host"><titleInfo><title>J Invest Dermatol</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>122</number></detail><extent unit="pages"><start>34</start><end>5</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit9"><titleInfo><title>Monogenic pigmentary skin disorders: genetics and patho‐physiology</title></titleInfo><name type="personal"><namePart type="given">D</namePart><namePart type="family">Herskovitz</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Sprecher</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Herskovitz D, Sprecher E. Monogenic pigmentary skin disorders: genetics and patho‐physiology. Isr Med Assoc J 2008; 10: 713–7.</note><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>713</start><end>7</end></extent></part><relatedItem type="host"><titleInfo><title>Isr Med Assoc J</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>713</start><end>7</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit10"><titleInfo><title>Mosaic manifestations of monogenic skin diseases</title></titleInfo><name type="personal"><namePart type="given">P</namePart><namePart type="family">Itin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Burger</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Itin P, Burger B. Mosaic manifestations of monogenic skin diseases. J Dtsch Dermatol Ges 2009; 7: 744–9.</note><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>7</number></detail><extent unit="pages"><start>744</start><end>9</end></extent></part><relatedItem type="host"><titleInfo><title>J Dtsch Dermatol Ges</title></titleInfo><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>7</number></detail><extent unit="pages"><start>744</start><end>9</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit11"><titleInfo><title>Congenital and genetic disorders associated with hypopigmentation</title></titleInfo><name type="personal"><namePart type="given">SJ</namePart><namePart type="family">Orlow</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Orlow SJ. Congenital and genetic disorders associated with hypopigmentation. Curr Probl Derm 1994; 161–84.</note><part><date>1994</date><extent unit="pages"><start>161</start><end>84</end></extent></part><relatedItem type="host"><titleInfo><title>Curr Probl Derm</title></titleInfo><part><date>1994</date><extent unit="pages"><start>161</start><end>84</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit12"><titleInfo><title>Clinical practice</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Taieb</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Picardo</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Taieb A, Picardo M. Clinical practice. Vitiligo. N Engl J Med 2009; 360: 160–9.</note><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>360</number></detail><extent unit="pages"><start>160</start><end>9</end></extent></part><relatedItem type="host"><titleInfo><title>Vitiligo. N Engl J Med</title></titleInfo><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>360</number></detail><extent unit="pages"><start>160</start><end>9</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit13"><titleInfo><title>Origin, clinical presentation, and diagnosis of hypomelanotic skin disorders</title></titleInfo><name type="personal"><namePart type="given">I</namePart><namePart type="family">Mollet</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Ongenae</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JM</namePart><namePart type="family">Naeyaert</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Mollet I, Ongenae K, Naeyaert JM. Origin, clinical presentation, and diagnosis of hypomelanotic skin disorders. Dermatol Clin 2007; 25: 363–71.</note><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><extent unit="pages"><start>363</start><end>71</end></extent></part><relatedItem type="host"><titleInfo><title>Dermatol Clin</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><extent unit="pages"><start>363</start><end>71</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit14"><titleInfo><title>Postinflammatory hypopigmentation and hyperpigmentation</title></titleInfo><name type="personal"><namePart type="given">R</namePart><namePart type="family">Ruiz‐Maldonado</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">ML</namePart><namePart type="family">Orozco‐Covarrubias</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Ruiz‐Maldonado R, Orozco‐Covarrubias ML. Postinflammatory hypopigmentation and hyperpigmentation. Sem Cutan Med Surg 1997; 16: 36–43.</note><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><extent unit="pages"><start>36</start><end>43</end></extent></part><relatedItem type="host"><titleInfo><title>Sem Cutan Med Surg</title></titleInfo><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><extent unit="pages"><start>36</start><end>43</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit15"><titleInfo><title>Progressive macular hypomelanosis: an overview</title></titleInfo><name type="personal"><namePart type="given">GN</namePart><namePart type="family">Relyveld</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HE</namePart><namePart type="family">Menke</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Westerhof</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Relyveld GN, Menke HE, Westerhof W. Progressive macular hypomelanosis: an overview. Am J Clin Dermatol 2007; 8: 13–9.</note><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><extent unit="pages"><start>13</start><end>9</end></extent></part><relatedItem type="host"><titleInfo><title>Am J Clin Dermatol</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><extent unit="pages"><start>13</start><end>9</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit16"><titleInfo><title>Risk factors associated with pulmonal arterial hypertension in colombian patients with systemic sclerosis: review of the literature</title></titleInfo><name type="personal"><namePart type="given">P</namePart><namePart type="family">Coral‐Alvarado</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Rojas‐Villarraga</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MC</namePart><namePart type="family">Latorre</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RD</namePart><namePart type="family">Mantilla</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JF</namePart><namePart type="family">Restrepo</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AL</namePart><namePart type="family">Pardo</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Chalem</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Rondón</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Jáuregui</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JC</namePart><namePart type="family">Rueda</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Cañas</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">ME</namePart><namePart type="family">Hincapie</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Pineda‐Tamayo</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Alvarez</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Iglesia‐Gamarra</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">FJ</namePart><namePart type="family">Diaz</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JM</namePart><namePart type="family">Anaja</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Coral‐Alvarado P, Rojas‐Villarraga A, Latorre MC, Mantilla RD, Restrepo JF, Pardo AL, Chalem P, Rondón F, Jáuregui E, Rueda JC, Cañas C, Hincapie ME, Pineda‐Tamayo R, Alvarez F, Iglesia‐Gamarra A, Diaz FJ, Anaja JM. Risk factors associated with pulmonal arterial hypertension in colombian patients with systemic sclerosis: review of the literature. J Rheumatol 2008; 35: 244–50.</note><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>35</number></detail><extent unit="pages"><start>244</start><end>50</end></extent></part><relatedItem type="host"><titleInfo><title>J Rheumatol</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>35</number></detail><extent unit="pages"><start>244</start><end>50</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit17"><titleInfo><title>Primary disorders of hyperpigmentation</title></titleInfo><name type="personal"><namePart type="given">ChS</namePart><namePart type="family">Fulk</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Fulk ChS. Primary disorders of hyperpigmentation. J Am Acad Dermatol 1984; 10: 1–16.</note><part><date>1984</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>1</start><end>16</end></extent></part><relatedItem type="host"><titleInfo><title>J Am Acad Dermatol</title></titleInfo><part><date>1984</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>1</start><end>16</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit18"><titleInfo><title>Diffuse hyperpigmentation of the skin: a clinicopathologic approach to diagnosis</title></titleInfo><name type="personal"><namePart type="given">CM</namePart><namePart type="family">Stefanato</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Bhawan</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Stefanato CM, Bhawan J. Diffuse hyperpigmentation of the skin: a clinicopathologic approach to diagnosis. Sem Cutan Med Surg 1997; 16: 61–3.</note><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><extent unit="pages"><start>61</start><end>3</end></extent></part><relatedItem type="host"><titleInfo><title>Sem Cutan Med Surg</title></titleInfo><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><extent unit="pages"><start>61</start><end>3</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit19"><titleInfo><title>Cutaneous hyperpigmentation caused by systemic drugs</title></titleInfo><name type="personal"><namePart type="given">JD</namePart><namePart type="family">Hendrix Jr</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KE</namePart><namePart type="family">Greer</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Hendrix JD Jr, Greer KE. Cutaneous hyperpigmentation caused by systemic drugs. Int J Dermatol 1992; 31: 458–66.</note><part><date>1992</date><detail type="volume"><caption>vol.</caption><number>31</number></detail><extent unit="pages"><start>458</start><end>66</end></extent></part><relatedItem type="host"><titleInfo><title>Int J Dermatol</title></titleInfo><part><date>1992</date><detail type="volume"><caption>vol.</caption><number>31</number></detail><extent unit="pages"><start>458</start><end>66</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit20"><titleInfo><title>Genodermatosis with reticulate, patchy and mottled pigmentation of the neck – a clue to rare dermatologic disorders</title></titleInfo><name type="personal"><namePart type="given">PH</namePart><namePart type="family">Itin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Lautenschlager</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Itin PH, Lautenschlager S. Genodermatosis with reticulate, patchy and mottled pigmentation of the neck – a clue to rare dermatologic disorders. Dermatology 1998; 197: 281–90.</note><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>197</number></detail><extent unit="pages"><start>281</start><end>90</end></extent></part><relatedItem type="host"><titleInfo><title>Dermatology</title></titleInfo><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>197</number></detail><extent unit="pages"><start>281</start><end>90</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit21"><titleInfo><title>The diagnostic value of café‐au‐lait macules</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Landau</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">BR</namePart><namePart type="family">Krafchik</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Landau M, Krafchik BR. The diagnostic value of café‐au‐lait macules. J Am Acad Dermatol 1999; 40: 877–90.</note><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>40</number></detail><extent unit="pages"><start>877</start><end>90</end></extent></part><relatedItem type="host"><titleInfo><title>J Am Acad Dermatol</title></titleInfo><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>40</number></detail><extent unit="pages"><start>877</start><end>90</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit22"><titleInfo><title>Postinflammatory hyperpigmentation: a common but troubling condition</title></titleInfo><name type="personal"><namePart type="given">NL</namePart><namePart type="family">Lacz</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Vafaie</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">NI</namePart><namePart type="family">Kihiczak</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RA</namePart><namePart type="family">Schwartz</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Lacz NL, Vafaie J, Kihiczak NI, Schwartz RA. Postinflammatory hyperpigmentation: a common but troubling condition. Int J Dermatol 2004; 43: 362–5.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>43</number></detail><extent unit="pages"><start>362</start><end>5</end></extent></part><relatedItem type="host"><titleInfo><title>Int J Dermatol</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>43</number></detail><extent unit="pages"><start>362</start><end>5</end></extent></part></relatedItem></relatedItem><identifier type="istex">B4B8FC9CBBFD4695FDBE7579E26B7A8D3EADC199</identifier><identifier type="ark">ark:/67375/WNG-GTVR0X92-F</identifier><identifier type="DOI">10.1111/j.1610-0387.2009.07137.x</identifier><identifier type="ArticleID">DDG7137</identifier><accessCondition type="use and reproduction" contentType="copyright">© The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Converted from (version ) to MODS version 3.6.</recordOrigin><recordCreationDate encoding="w3cdtf">2019-11-14</recordCreationDate></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-GTVR0X92-F/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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