Sinus histiocytosis with massive lymphadenopathy: Presentation as giant granuloma annulare and detection of human herpesvirus 6
Identifieur interne : 000549 ( Istex/Corpus ); précédent : 000548; suivant : 000550Sinus histiocytosis with massive lymphadenopathy: Presentation as giant granuloma annulare and detection of human herpesvirus 6
Auteurs : Monica M. Scheel ; Peter L. Rady ; Stephen K. Tyring ; Amit G. PandyaSource :
- Journal of the American Academy of Dermatology [ 0190-9622 ] ; 1997.
English descriptors
- Teeft :
- Acad dermatol copyright, American academy, Brief communications, Case report, Control gene, Cutaneous, Dermatol, Dermatology, Dorfman, Electron beam radiation, Environmental dermatology, Erythrocyte sedimentation rate, Fourth digit, Herpesvirus, Histiocyte, Histiocytic, Histiocytosis, Human herpesvirus, Interferon, Interferon gamma, Intralesional steroids, Lymphadenopathy, Massive lymphadenopathy, Massive lymphadenopathy disease, Oligonucleotide probes, Original magnification, Plantar warts, Rosai, Schindl, Shml, Sinus, Sinus histiocytosis, Subcutaneous, Subcutaneous masses.
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DOI: 10.1016/S0190-9622(97)70186-5
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ISTEX:51D05340C48FED275A873FF1F46D3A434DDA08C8Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Sinus histiocytosis with massive lymphadenopathy: Presentation as giant granuloma annulare and detection of human herpesvirus 6</title><author><name sortKey="Scheel, Monica M" sort="Scheel, Monica M" uniqKey="Scheel M" first="Monica M." last="Scheel">Monica M. Scheel</name><affiliation><mods:affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. Dallas,a Departments of Microbiology and Immunologyb and the Department of Dermatology,c University of Texas Medical Branch at Galveston</mods:affiliation></affiliation></author><author><name sortKey="Rady, Peter L" sort="Rady, Peter L" uniqKey="Rady P" first="Peter L." last="Rady">Peter L. Rady</name><affiliation><mods:affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. Dallas,a Departments of Microbiology and Immunologyb and the Department of Dermatology,c University of Texas Medical Branch at Galveston</mods:affiliation></affiliation></author><author><name sortKey="Tyring, Stephen K" sort="Tyring, Stephen K" uniqKey="Tyring S" first="Stephen K." last="Tyring">Stephen K. Tyring</name><affiliation><mods:affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. Dallas,a Departments of Microbiology and Immunologyb and the Department of Dermatology,c University of Texas Medical Branch at Galveston</mods:affiliation></affiliation></author><author><name sortKey="Pandya, Amit G" sort="Pandya, Amit G" uniqKey="Pandya A" first="Amit G." last="Pandya">Amit G. Pandya</name><affiliation><mods:affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. 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Scheel</name><affiliation><mods:affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. Dallas,a Departments of Microbiology and Immunologyb and the Department of Dermatology,c University of Texas Medical Branch at Galveston</mods:affiliation></affiliation></author><author><name sortKey="Rady, Peter L" sort="Rady, Peter L" uniqKey="Rady P" first="Peter L." last="Rady">Peter L. Rady</name><affiliation><mods:affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. Dallas,a Departments of Microbiology and Immunologyb and the Department of Dermatology,c University of Texas Medical Branch at Galveston</mods:affiliation></affiliation></author><author><name sortKey="Tyring, Stephen K" sort="Tyring, Stephen K" uniqKey="Tyring S" first="Stephen K." last="Tyring">Stephen K. Tyring</name><affiliation><mods:affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. Dallas,a Departments of Microbiology and Immunologyb and the Department of Dermatology,c University of Texas Medical Branch at Galveston</mods:affiliation></affiliation></author><author><name sortKey="Pandya, Amit G" sort="Pandya, Amit G" uniqKey="Pandya A" first="Amit G." last="Pandya">Amit G. Pandya</name><affiliation><mods:affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. 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Pandya, MD, Department of Dermatology, U.T. Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75235-9069.</note><note>J Am Acad Dermatol 1997;37:643-6.</note><note>0190-9622/97/$5.00 + 0 16/54/82978</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Sinus histiocytosis with massive lymphadenopathy: Presentation as giant granuloma annulare and detection of human herpesvirus 6</title><author xml:id="author-0000"><persName><forename type="first">Monica M.</forename><surname>Scheel</surname></persName><roleName type="degree">MD, RPha</roleName><affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. Dallas,a Departments of Microbiology and Immunologyb and the Department of Dermatology,c University of Texas Medical Branch at Galveston</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Peter L.</forename><surname>Rady</surname></persName><roleName type="degree">MD, PhDb</roleName><affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. Dallas,a Departments of Microbiology and Immunologyb and the Department of Dermatology,c University of Texas Medical Branch at Galveston</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Stephen K.</forename><surname>Tyring</surname></persName><roleName type="degree">MD, PhDb,c</roleName><affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. Dallas,a Departments of Microbiology and Immunologyb and the Department of Dermatology,c University of Texas Medical Branch at Galveston</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Amit G.</forename><surname>Pandya</surname></persName><roleName type="degree">MDa</roleName><affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. 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Pandya, MD, Department of Dermatology, U.T. Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75235-9069.</ce:note-para></ce:article-footnote><ce:article-footnote><ce:label>☆☆</ce:label><ce:note-para>J Am Acad Dermatol 1997;37:643-6.</ce:note-para></ce:article-footnote><ce:article-footnote><ce:label>★</ce:label><ce:note-para>0190-9622/97/$5.00 + 0 <ce:bold>16/54/82978</ce:bold></ce:note-para></ce:article-footnote><ce:title>Sinus histiocytosis with massive lymphadenopathy: Presentation as giant granuloma annulare and detection of human herpesvirus 6</ce:title><ce:author-group><ce:author><ce:given-name>Monica M.</ce:given-name><ce:surname>Scheel</ce:surname><ce:degrees>MD, RPh<ce:sup>a</ce:sup></ce:degrees></ce:author><ce:author><ce:given-name>Peter L.</ce:given-name><ce:surname>Rady</ce:surname><ce:degrees>MD, PhD<ce:sup>b</ce:sup></ce:degrees></ce:author><ce:author><ce:given-name>Stephen K.</ce:given-name><ce:surname>Tyring</ce:surname><ce:degrees>MD, PhD<ce:sup>b,c</ce:sup></ce:degrees></ce:author><ce:author><ce:given-name>Amit G.</ce:given-name><ce:surname>Pandya</ce:surname><ce:degrees>MD<ce:sup>a</ce:sup></ce:degrees></ce:author><ce:affiliation><ce:textfn>Dallas and Galveston, Texas</ce:textfn></ce:affiliation><ce:affiliation><ce:textfn>From the Department of Dermatology, University of Texas Southwestern Medical Center. Dallas,<ce:sup>a</ce:sup> Departments of Microbiology and Immunology<ce:sup>b</ce:sup> and the Department of Dermatology,<ce:sup>c</ce:sup> University of Texas Medical Branch at Galveston</ce:textfn></ce:affiliation></ce:author-group></head><body><ce:sections><ce:para>Sinus histiocytosis with massive lymphadenopathy (SHML) is an uncommon disease of unknown cause. A small number of patients with skin or soft tissue manifestations but no lymphadenopathy has been described. <ce:cross-ref refid="bib1"><ce:sup>1</ce:sup></ce:cross-ref> We describe a patient with SHML presenting as giant lesions of granuloma annulare (GA) that were not associated with adenopathy. In addition, the patient had multiple soft tissue tumors that were found to be extranodal manifestations of SHML. Analysis of DNA from lesional skin revealed human herpesvirus 6 (HHV-6), variant B.</ce:para><ce:section><ce:section-title>CASE REPORT</ce:section-title><ce:para>A 44-year-old white man had a 10-year history of multiple, discrete 0.5 to 30 cm plaques with an erythematous pigmented border and central clearing on the face, neck, trunk, arms, and legs (<ce:cross-ref refid="fig1">Fig. 1 , <ce:italic>A</ce:italic></ce:cross-ref> ).
<ce:display><ce:figure id="fig1"><ce:label>Fig. 1</ce:label><ce:caption><ce:simple-para><ce:bold>A</ce:bold> , Multiple erythematous annular plaques with raised border and central clearing. <ce:bold>B,</ce:bold> Subcutaneous mass on left fourth digit.</ce:simple-para></ce:caption> <ce:link locator="gr1"></ce:link></ce:figure></ce:display>A firm subcutaneous mass was present on the left fourth digit (<ce:cross-ref refid="fig1">Fig. 1 , <ce:italic>B</ce:italic></ce:cross-ref> ). Similar subcutaneous masses were present on the right ankle, left second, third, and fourth toes, and distal left foot. Previous biopsy specimens of the skin had been interpreted as GA and cutaneous lymphoid hyperplasia. Examination of tissue removed from the subcutaneous masses had resulted in a diagnosis of giant cell tumors of tendon sheaths.</ce:para><ce:para>Laboratory examination revealed an erythrocyte sedimentation rate of 25, mild hypergammaglobulinemia, hemoglobin 12.2 gm/dl, hematocrit 36%, serum iron 64 μg/dl (normal, 75 to 175 μg/dl), and total iron binding capacity of 282 μg/dl, giving a saturation of 23% (low normal). Negative or normal laboratory results included leukocyte count, platelets, chemistry screen, antibodies for herpes simplex virus (HSV) 1, HSV2, and Epstein-Barr virus (EBV), urine culture, Lyme disease titer, HIV screen, stool ova and parasites, hepatitis A and B, RA latex, antinuclear antibody, VDRL, rapid plasma reagin, FTA, MHA-TP, T-cell receptor gene rearrangement studies on peripheral lymphocytes, free thyroxine, thyroid-stimulating hormone, delayed hypersensitivity patch tests, electrocardiogram, and chest x-ray.</ce:para><ce:para>The patient’s lesions had slowly enlarged over the past 10 years. A variety of medications had been tried, including dapsone, chloroquine, chlorambucil, cyclosporine, ketoconazole, cyclophosphamide, hydroxychloroquine, beta-carotene, topical tretinoin, quinacrine, metronidazole, fluconazole, isotretinoin, intralesional steroids, pentoxifylline, electron beam radiation (3000 rad), etretinate with PUVA, and nicotinamide. Both intralesional steroids and electron beam radiation caused moderate improvement, but the lesions quickly returned. Because the diagnosis of atypical GA was placed in doubt by the extensive and recalcitrant nature of his disease, it was decided to perform another biopsy. The specimen revealed a dermal infiltrate of histiocytes, lymphocytes, and plasma cells (<ce:cross-ref refid="fig2">Fig. 2</ce:cross-ref>) .
<ce:display><ce:figure id="fig2"><ce:label>Fig. 2</ce:label><ce:caption><ce:simple-para><ce:bold>A</ce:bold> , Dermal infiltrate with multiple pale-staining histiocytes and lymphocytes. (Hematoxylin-eosin stain; original magnification ×100). <ce:bold>B,</ce:bold> Pale-staining histiocyte displaying emperipolesis. (Hematoxylin-eosin stain; original magnification ×400.)</ce:simple-para></ce:caption> <ce:link locator="gr2"></ce:link></ce:figure></ce:display>There was a striking resemblance to the histiocytic form of GA. The principal infiltrating cells were histiocytes with a pale pink cytoplasm and an indistinct border. Stains for α-1-antichymotrypsin and lysozyme were positive. The large histiocytic cells were positive for S-100 antigen and displayed emperipolesis. On the basis of the pattern of the histiocytic infiltrate, the cytology of the individual cells, and the results of immunohistochemical staining, a diagnosis of SHML was made. The biopsy specimens of the patient’s subcutaneous masses were then reevaluated and found to have changes similar to those of the skin. A trial of intravenous vinblastine 10 mg weekly was unsuccessful. The patient was most recently treated with prednisone 20 mg daily along with a combination of oral methotrexate, 6-thioguanine, and leukovorin for 5 months. This caused a significant decrease in the size of the subcutaneous masses and thinning of the cutaneous plaques.</ce:para><ce:section><ce:section-title>DNA analysis</ce:section-title><ce:para>DNA from a fresh skin lesion on the thigh was isolated by means of a nonorganic DNA extraction kit (ONCOR, Gaithersburg, Md.). Each series of polymerase chain reaction (PCR) consisted of a normal control DNA (Clontech Labs, Palo Alto, Calif.) and known HHV-6, HHV-7, HHV-8, and EBV positive control DNA. The primer and conditions of the PCR analysis for HHV-6, HHV-7, HHV-8, and EBV have been described. <ce:cross-refs refid="bib2 bib3 bib4"><ce:sup>2-4</ce:sup></ce:cross-refs> Amplification of the interferon gamma internal control gene was included to indicate the quality of DNA samples. Primers for the interferon gamma internal control gene were designed to give a 173 bp sized amplicon. <ce:cross-ref refid="bib5"><ce:sup>5</ce:sup></ce:cross-ref> Amplification was carried out in 40 consecutive cycles by means of AmpliTaq DNA polymerase (Perkin Elmer, Roche Molecular Systems, Inc., Branchburg, N.J.). Fragment fractionation of the PCR mixture was carried out on a 2% Seakem GTG agarose gel (FMC, Rockland, Me.) stained with ethidium bromide. Specificity of the amplification of viral and internal gene fragments was confirmed by a Southern blot hybridization procedure by means of oligonucleotide probes specific to the amplified DNA sequences of HHV-6 variant A and B, HHV-7, HHV-8, EBV, and interferon gamma internal control gene. Multiple precautions were observed in all procedures. The transfer of PCR products onto membranes, end-labeling of oligonucleotide probes, hybridization, and washing steps were performed as described. <ce:cross-ref refid="bib6"><ce:sup>6</ce:sup></ce:cross-ref></ce:para><ce:para>Agarose gel electrophoresis and subsequent Southern blot analysis revealed viral DNA of HHV-6 variant B but no PCR products specific for HHV-6 variant A, HHV-7, HHV-8, or EBV.</ce:para></ce:section></ce:section><ce:section><ce:section-title>DISCUSSION</ce:section-title><ce:para>SHML is a rare histiocytic proliferative disorder, <ce:cross-ref refid="bib1"><ce:sup>1</ce:sup></ce:cross-ref> first described by Rosai and Dorfman. <ce:cross-refs refid="bib7 bib8"><ce:sup>7,8</ce:sup></ce:cross-refs> Good descriptive studies of SHML have been limited because of its rarity and clinical heterogeneity. Laboratory abnormalities most frequently encountered are leukocytosis and neutrophilia, elevated erythrocyte sedimentation rate, and chronic anemia, most often normochromic and normocytic. <ce:cross-ref refid="bib7"><ce:sup>7</ce:sup></ce:cross-ref> Our patient had a mild iron deficiency anemia, although no source of blood loss was found. Hypergammaglobulinemia (usually polyclonal) as well as an elevated titer of antibodies to EBV are common, suggesting an impaired or disordered immune response to an infectious agent or antigen. <ce:cross-ref refid="bib9"><ce:sup>9</ce:sup></ce:cross-ref></ce:para><ce:para>The cause and pathogenesis of SHML are unknown. Proposed causes include a specific infectious process leading to a histiocytic response by the body, and an accumulation of histiocytic cells resulting from an immunologic defect. <ce:cross-refs refid="bib8 bib10"><ce:sup>8,10</ce:sup></ce:cross-refs> A previous study found that 7 of 9 patients with SHML had detectable HHV-6 by in situ hybridization. <ce:cross-ref refid="bib11"><ce:sup>11</ce:sup></ce:cross-ref> The presence of HHV-6 in tissue samples from our patient suggests a causative function of this virus in SHML. On the other hand, HHV-6 may be present because of defective immunity in patients with SHML. A patient with SHML confined to the skin was recently described in whom the disease coincided with both an HSV infection and a polybacterial urinary tract infection. <ce:cross-ref refid="bib12"><ce:sup>12</ce:sup></ce:cross-ref> Studies to detect HSV and HHV-6 DNA in skin were negative.</ce:para><ce:para>Because of the rarity of SHML and its tendency to clear spontaneously, a standard approach to treatment has been lacking. Antibiotics are of no benefit. <ce:cross-ref refid="bib8"><ce:sup>8</ce:sup></ce:cross-ref> Systemic steroids partially and temporarily decrease nodal size or symptoms, <ce:cross-ref refid="bib8"><ce:sup>8</ce:sup></ce:cross-ref> as demonstrated in our patient. There have been reports of a transient decrease in adenopathy or extranodal involvement after irradiation, but regrowth frequently occurs. <ce:cross-ref refid="bib10"><ce:sup>10</ce:sup></ce:cross-ref> There are many case reports of SHML treated with various chemotherapeutic regimens, but most have shown only partial improvement. <ce:cross-ref refid="bib10"><ce:sup>10</ce:sup></ce:cross-ref> A few cases of complete clearing have been reported, including a 45-year-old man with aggressive systemic disease who responded to vinblastine-loaded platelets, <ce:cross-ref refid="bib13"><ce:sup>13</ce:sup></ce:cross-ref> and a 48-year-old man with papules and nodules of the skin who responded to thalidomide. <ce:cross-refs refid="bib14 bib15"><ce:sup>14,15</ce:sup></ce:cross-refs> Our patient has responded to a combination of methotrexate, 6-thioguanine, leukovorin, and prednisone.</ce:para><ce:para>Our patient is the first reported case of SHML presenting as GA and the first to have typing of the HHV-6 variant B from a tissue sample. 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granuloma annulare and detection of human herpesvirus 6</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Sinus histiocytosis with massive lymphadenopathy: Presentation as giant granuloma annulare and detection of human herpesvirus 6</title></titleInfo><name type="personal"><namePart type="given">Monica M.</namePart><namePart type="family">Scheel</namePart><namePart type="termsOfAddress">MD, RPha</namePart><affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. Dallas,a Departments of Microbiology and Immunologyb and the Department of Dermatology,c University of Texas Medical Branch at Galveston</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter L.</namePart><namePart type="family">Rady</namePart><namePart type="termsOfAddress">MD, PhDb</namePart><affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. Dallas,a Departments of Microbiology and Immunologyb and the Department of Dermatology,c University of Texas Medical Branch at Galveston</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stephen K.</namePart><namePart type="family">Tyring</namePart><namePart type="termsOfAddress">MD, PhDb,c</namePart><affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. Dallas,a Departments of Microbiology and Immunologyb and the Department of Dermatology,c University of Texas Medical Branch at Galveston</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Amit G.</namePart><namePart type="family">Pandya</namePart><namePart type="termsOfAddress">MDa</namePart><affiliation>Dallas and Galveston, TexasFrom the Department of Dermatology, University of Texas Southwestern Medical Center. Dallas,a Departments of Microbiology and Immunologyb and the Department of Dermatology,c University of Texas Medical Branch at Galveston</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1997</dateIssued><copyrightDate encoding="w3cdtf">1997</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><note>Reprint requests: Amit G. Pandya, MD, Department of Dermatology, U.T. Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75235-9069.</note><note>J Am Acad Dermatol 1997;37:643-6.</note><note>0190-9622/97/$5.00 + 0 16/54/82978</note><relatedItem type="host"><titleInfo><title>Journal of the American Academy of Dermatology</title></titleInfo><titleInfo type="abbreviated"><title>YMJD</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><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1997</dateIssued></originInfo><identifier type="ISSN">0190-9622</identifier><identifier type="PII">S0190-9622(05)X7238-3</identifier><part><date>1997</date><detail type="volume"><number>37</number><caption>vol.</caption></detail><detail type="issue"><number>4</number><caption>no.</caption></detail><extent unit="issue-pages"><start>523</start><end>672</end></extent><extent unit="pages"><start>643</start><end>646</end></extent></part></relatedItem><identifier type="istex">51D05340C48FED275A873FF1F46D3A434DDA08C8</identifier><identifier type="ark">ark:/67375/6H6-R3FGNT47-C</identifier><identifier type="DOI">10.1016/S0190-9622(97)70186-5</identifier><identifier type="PII">S0190-9622(97)70186-5</identifier><accessCondition type="use and reproduction" contentType="copyright">©1997 American Academy of Dermatology, Inc</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>American Academy of Dermatology, Inc, ©1997</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-R3FGNT47-C/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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