Discoid lupus erythematosus‐like skin lesions in a patient with autosomal recessive chronic granulomatous disease
Identifieur interne : 002370 ( Istex/Corpus ); précédent : 002369; suivant : 002371Discoid lupus erythematosus‐like skin lesions in a patient with autosomal recessive chronic granulomatous disease
Auteurs : M. Strate ; F. Brandrup ; P. WangSource :
- Clinical Genetics [ 0009-9163 ] ; 1986-09.
English descriptors
- Teeft :
- Antimycotic treatment, Autosomal, Autosomal recessive, Autosomal recessive type, Case report, Cell damage, Chronic granulomatous disease, Clinical course, Clinical manifestations, Cytochrome, Discoid, Discoid lupus erythematosus, Discoid lupus skin lesions, Family history, Family members, Female carriers, Granulomatous, Hitzig seger, Lesion, Lupus, Mills quie, Nadph, Nadph oxidase, Neutrophil, Neutrophil function, Odense university hospital, Opportunistic infections, Recessive, Respiratory burst, Respiratory burst activity, Segal, Skin manifestations, Speckled staining, Strate, Superoxide, Superoxide dismutase, Superoxide production, Whole blood.
Abstract
A case of chronic granulomatous disease (CGD) in a 32‐year‐old female with two episodes of opportunistic infections is described. At the age of 29 the patient was suspected to be a carrier of X‐linked CGD on the basis of discoid lupus erythematosus‐like skin lesions. No respiratory burst activity, as measured by phorbol myristate acetate stimulated superoxide production, was observed in isolated neutrophils of the patient. Membrane‐rich fractions elicited no superoxide production in the presence of NADPH. The neutrophil content of cytochrome b_245 was within normal range. Family investigations revealed neither cellular abnormalities nor any history of skin diseases or opportunistic infections in first degree relatives. The parents of the patient were first cousins. On the basis of family history and the in‐vitro assessment of neutrophil function, the patient is believed to have autosomal recessive CGD. The presented case illustrates that lupus erythematosus‐like skin lesions are not restricted to female carriers of X‐linked CGD, but may also be found in the autosomal recessive type of the disease.
Url:
DOI: 10.1111/j.1399-0004.1986.tb00593.x
Links to Exploration step
ISTEX:B3CEE661EE44C291DC464CA3F16EA336CDFC3668Le document en format XML
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At the age of 29 the patient was suspected to be a carrier of X‐linked CGD on the basis of discoid lupus erythematosus‐like skin lesions. No respiratory burst activity, as measured by phorbol myristate acetate stimulated superoxide production, was observed in isolated neutrophils of the patient. Membrane‐rich fractions elicited no superoxide production in the presence of NADPH. The neutrophil content of cytochrome b_245 was within normal range. Family investigations revealed neither cellular abnormalities nor any history of skin diseases or opportunistic infections in first degree relatives. The parents of the patient were first cousins. On the basis of family history and the in‐vitro assessment of neutrophil function, the patient is believed to have autosomal recessive CGD. The presented case illustrates that lupus erythematosus‐like skin lesions are not restricted to female carriers of X‐linked CGD, but may also be found in the autosomal recessive type of the disease.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>neutrophil</json:string><json:string>granulomatous</json:string><json:string>chronic granulomatous disease</json:string><json:string>cytochrome</json:string><json:string>autosomal</json:string><json:string>nadph</json:string><json:string>recessive</json:string><json:string>female carriers</json:string><json:string>lupus</json:string><json:string>superoxide</json:string><json:string>strate</json:string><json:string>autosomal recessive</json:string><json:string>segal</json:string><json:string>lesion</json:string><json:string>family members</json:string><json:string>neutrophil function</json:string><json:string>skin manifestations</json:string><json:string>discoid</json:string><json:string>family history</json:string><json:string>respiratory burst</json:string><json:string>opportunistic infections</json:string><json:string>mills quie</json:string><json:string>discoid lupus erythematosus</json:string><json:string>discoid lupus skin lesions</json:string><json:string>nadph oxidase</json:string><json:string>odense university hospital</json:string><json:string>autosomal recessive type</json:string><json:string>clinical course</json:string><json:string>superoxide production</json:string><json:string>hitzig seger</json:string><json:string>antimycotic treatment</json:string><json:string>superoxide dismutase</json:string><json:string>whole blood</json:string><json:string>clinical manifestations</json:string><json:string>speckled staining</json:string><json:string>cell damage</json:string><json:string>respiratory burst activity</json:string><json:string>case report</json:string></teeft></keywords><author><json:item><name>M. 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At the age of 29 the patient was suspected to be a carrier of X‐linked CGD on the basis of discoid lupus erythematosus‐like skin lesions. No respiratory burst activity, as measured by phorbol myristate acetate stimulated superoxide production, was observed in isolated neutrophils of the patient. Membrane‐rich fractions elicited no superoxide production in the presence of NADPH. The neutrophil content of cytochrome b_245 was within normal range. Family investigations revealed neither cellular abnormalities nor any history of skin diseases or opportunistic infections in first degree relatives. The parents of the patient were first cousins. On the basis of family history and the in‐vitro assessment of neutrophil function, the patient is believed to have autosomal recessive CGD. 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granulomatous disease</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>M.</givenNames><familyName>Strate</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>F.</givenNames><familyName>Brandrup</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>P.</givenNames><familyName>Wang</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="DK"><unparsedAffiliation>Department of Clinical Chemistry, Odense University Hospital, Odense, Denmark</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="DK"><unparsedAffiliation>Department of Dermatology, Odense University Hospital, Odense, Denmark</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Chronic granulomatous disease</keyword><keyword xml:id="k2">cytochrome b</keyword><keyword xml:id="k3">discoid lupus erythematosus‐like skin lesions</keyword><keyword xml:id="k4">neutrophil respiratory burst</keyword><keyword xml:id="k5">nitroblue tetrazolium slide test</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>A case of chronic granulomatous disease (CGD) in a 32‐year‐old female with two episodes of opportunistic infections is described. At the age of 29 the patient was suspected to be a carrier of X‐linked CGD on the basis of discoid lupus erythematosus‐like skin lesions. No respiratory burst activity, as measured by phorbol myristate acetate stimulated superoxide production, was observed in isolated neutrophils of the patient. Membrane‐rich fractions elicited no superoxide production in the presence of NADPH. The neutrophil content of cytochrome b_<sub>2</sub>45 was within normal range. Family investigations revealed neither cellular abnormalities nor any history of skin diseases or opportunistic infections in first degree relatives. The parents of the patient were first cousins. On the basis of family history and the in‐vitro assessment of neutrophil function, the patient is believed to have autosomal recessive CGD. The presented case illustrates that lupus erythematosus‐like skin lesions are not restricted to female carriers of X‐linked CGD, but may also be found in the autosomal recessive type of the disease.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Discoid lupus erythematosus‐like skin lesions in a patient with autosomal recessive chronic granulomatous disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Discoid lupus erythematosus‐like skin lesions in a patient with autosomal recessive chronic granulomatous disease</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Strate</namePart><affiliation>Department of Clinical Chemistry, Odense University Hospital, Odense, Denmark</affiliation><affiliation>Correspondence address: Department of Clinical Chemistry Odense University Hospital DK‐5000 Odense C Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F.</namePart><namePart type="family">Brandrup</namePart><affiliation>Department of Dermatology, Odense University Hospital, Odense, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Wang</namePart><affiliation>Department of Clinical Chemistry, Odense University Hospital, Odense, Denmark</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">1986-09</dateIssued><edition>Received 5 July 1985, revised, accepted for publication 3 May 1986</edition><copyrightDate encoding="w3cdtf">1986</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="references">20</extent><extent unit="linksCrossRef">4</extent></physicalDescription><abstract lang="en">A case of chronic granulomatous disease (CGD) in a 32‐year‐old female with two episodes of opportunistic infections is described. At the age of 29 the patient was suspected to be a carrier of X‐linked CGD on the basis of discoid lupus erythematosus‐like skin lesions. No respiratory burst activity, as measured by phorbol myristate acetate stimulated superoxide production, was observed in isolated neutrophils of the patient. Membrane‐rich fractions elicited no superoxide production in the presence of NADPH. The neutrophil content of cytochrome b_245 was within normal range. Family investigations revealed neither cellular abnormalities nor any history of skin diseases or opportunistic infections in first degree relatives. The parents of the patient were first cousins. On the basis of family history and the in‐vitro assessment of neutrophil function, the patient is believed to have autosomal recessive CGD. The presented case illustrates that lupus erythematosus‐like skin lesions are not restricted to female carriers of X‐linked CGD, but may also be found in the autosomal recessive type of the disease.</abstract><subject lang="en"><genre>keywords</genre><topic>Chronic granulomatous disease</topic><topic>cytochrome b</topic><topic>discoid lupus erythematosus‐like skin lesions</topic><topic>neutrophil respiratory burst</topic><topic>nitroblue tetrazolium slide test</topic></subject><relatedItem type="host"><titleInfo><title>Clinical Genetics</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">0009-9163</identifier><identifier type="eISSN">1399-0004</identifier><identifier type="DOI">10.1111/(ISSN)1399-0004</identifier><identifier type="PublisherID">CGE</identifier><part><date>1986</date><detail type="volume"><caption>vol.</caption><number>30</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>184</start><end>190</end><total>7</total></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>A variant form of X‐linked chronic granulomatous disease with normal nitroblue tetrazolium slide test and cytochrome b</title></titleInfo><name type="personal"><namePart type="given">N.</namePart><namePart type="family">Borregaard</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. 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