Treatment of primary Sjögren's syndrome with hydroxychloroquine
Identifieur interne : 000034 ( Istex/Corpus ); précédent : 000033; suivant : 000035Treatment of primary Sjögren's syndrome with hydroxychloroquine
Auteurs : Robert I. Fox ; Edward Chan ; Laurie Benton ; Sherman Fong ; Mitchell Friedlaender ; Francis V. HowellSource :
- The American Journal of Medicine [ 0002-9343 ] ; 1988.
English descriptors
- Teeft :
- Alkaline phosphatase, American journal, Arthritis, Arthritis rheum, Artificial tears, Autoantibody, Autoantibody titers, Autoimmune disease, Beneficial effects, Biopsy, Cell surface, Clinical research, Different syndrome patients, Erythrocyte sedimentation rate, Erythrocyte sedimentation rate levels, Extraglandular sites, Factor paraprotein, Foreign antigens, Hydroxychloroquine, Hydroxychloroquine treatment, Hyperglobulinemia, Idiotype, Immune, Immune dysregulation, Immune response, Immunoglobulin, Immunoglobulin levels, Infiltrates, Kappa light chains, Laboratory features, Laboratory values, Little change, Lmmunol, Lymphocytic infiltration, Medicine volume, Moab, Monoclonal antibody, Multiple sclerosis, Ophthalmologic evaluation, Optical density, Oral mucositis, Patient group, Peripheral blood lymphocyte, Pokeweed mitogen, Primary syndrome, Primary syndrome patients, Regular basis, Representative patterns, Rheumatoid, Rheumatoid arthritis, Rheumatoid factor, Rheumatoid factor paraprotein, Rheumatoid factor samples, Salivary, Salivary gland, Salivary gland biopsies, Salivary gland biopsy, Significant change, Significant decrease, Syndrome, Syndrome patient, Syndrome patients, Systemic lupus erythematosus patients, Total immunoglobulin.
Abstract
Abstract: Sjögren's syndrome is an autoimmune disease characterized by lymphocytic infiltration of the salivary/lacrimal glands, autoantibody production, and polyclonal hyperglobulinemia. In view of the efficacy and relative safety of hydroxychloroquine in other autoimmune disorders, the potential benefit of hydroxychloroquine (200 mg per day for 12 months) in 10 patients with Sjögren's syndrome was evaluated. Changes in levels of total immunoglobulin, antibody against Sjögren's syndrome-associated antigen B, rheumatoid factor, and in vitro production of immunoglobulin in the serum were evaluated. For comparison, 10 patients matched according to age and sex, who did not receive hydroxychloroquine were studied. In the hydroxychloroquine-treated group, the following observations were made: (1) significantly decreased total immunoglobulin G (IgG) and IgA levels with little change in IgM levels; (2) significant decrease in IgA-rheumatoid factor with a smaller decrease in IgM-rheumatoid factor; (3) decreased IgG anti-Sjögren's syndrome-associated antigen B autoantibody; and (4) decreased erythrocyte sedimentation rate and increased hemoglobin level. Further, a specific idiotype present on their rheumatoid factor (defined by monoclonal antibody 17-109) was significantly decreased, with disappearance of detectable circulating paraprotein in two hydroxychloroquine-treated patients. Finally, rheumatoid factor production in vitro by lymphocytes from hydroxychloroquine-treated patients using a T cell-dependent mitogen was significantly decreased. These results suggest that hydroxychloroquine modulates lymphoproliferation in patients with Sjögren's syndrome and may prevent progression to extraglandular sites of neoplastic transformation.
Url:
DOI: 10.1016/0002-9343(88)90365-8
Links to Exploration step
ISTEX:45836CB1252BFD52E6081B9F2A688D73E068F225Le document en format XML
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Fox</name><affiliation><mods:affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</mods:affiliation></affiliation></author><author><name sortKey="Chan, Edward" sort="Chan, Edward" uniqKey="Chan E" first="Edward" last="Chan">Edward Chan</name><affiliation><mods:affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</mods:affiliation></affiliation></author><author><name sortKey="Benton, Laurie" sort="Benton, Laurie" uniqKey="Benton L" first="Laurie" last="Benton">Laurie Benton</name><affiliation><mods:affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</mods:affiliation></affiliation></author><author><name sortKey="Fong, Sherman" sort="Fong, Sherman" uniqKey="Fong S" first="Sherman" last="Fong">Sherman Fong</name><affiliation><mods:affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</mods:affiliation></affiliation></author><author><name sortKey="Friedlaender, Mitchell" sort="Friedlaender, Mitchell" uniqKey="Friedlaender M" first="Mitchell" last="Friedlaender">Mitchell Friedlaender</name><affiliation><mods:affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</mods:affiliation></affiliation></author><author><name sortKey="Howell, Francis V" sort="Howell, Francis V" uniqKey="Howell F" first="Francis V." last="Howell">Francis V. 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In view of the efficacy and relative safety of hydroxychloroquine in other autoimmune disorders, the potential benefit of hydroxychloroquine (200 mg per day for 12 months) in 10 patients with Sjögren's syndrome was evaluated. Changes in levels of total immunoglobulin, antibody against Sjögren's syndrome-associated antigen B, rheumatoid factor, and in vitro production of immunoglobulin in the serum were evaluated. For comparison, 10 patients matched according to age and sex, who did not receive hydroxychloroquine were studied. In the hydroxychloroquine-treated group, the following observations were made: (1) significantly decreased total immunoglobulin G (IgG) and IgA levels with little change in IgM levels; (2) significant decrease in IgA-rheumatoid factor with a smaller decrease in IgM-rheumatoid factor; (3) decreased IgG anti-Sjögren's syndrome-associated antigen B autoantibody; and (4) decreased erythrocyte sedimentation rate and increased hemoglobin level. Further, a specific idiotype present on their rheumatoid factor (defined by monoclonal antibody 17-109) was significantly decreased, with disappearance of detectable circulating paraprotein in two hydroxychloroquine-treated patients. Finally, rheumatoid factor production in vitro by lymphocytes from hydroxychloroquine-treated patients using a T cell-dependent mitogen was significantly decreased. These results suggest that hydroxychloroquine modulates lymphoproliferation in patients with Sjögren's syndrome and may prevent progression to extraglandular sites of neoplastic transformation.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>hydroxychloroquine</json:string><json:string>rheumatoid</json:string><json:string>rheumatoid factor</json:string><json:string>moab</json:string><json:string>immunoglobulin</json:string><json:string>hydroxychloroquine treatment</json:string><json:string>syndrome</json:string><json:string>primary syndrome patients</json:string><json:string>autoantibody</json:string><json:string>primary syndrome</json:string><json:string>lmmunol</json:string><json:string>hyperglobulinemia</json:string><json:string>immune</json:string><json:string>idiotype</json:string><json:string>rheumatoid arthritis</json:string><json:string>infiltrates</json:string><json:string>salivary</json:string><json:string>american journal</json:string><json:string>autoantibody titers</json:string><json:string>immunoglobulin levels</json:string><json:string>erythrocyte sedimentation rate</json:string><json:string>syndrome patients</json:string><json:string>extraglandular sites</json:string><json:string>laboratory features</json:string><json:string>medicine volume</json:string><json:string>multiple sclerosis</json:string><json:string>patient group</json:string><json:string>foreign antigens</json:string><json:string>peripheral blood lymphocyte</json:string><json:string>beneficial effects</json:string><json:string>artificial tears</json:string><json:string>salivary gland biopsies</json:string><json:string>rheumatoid factor samples</json:string><json:string>biopsy</json:string><json:string>different syndrome patients</json:string><json:string>syndrome patient</json:string><json:string>optical density</json:string><json:string>cell surface</json:string><json:string>ophthalmologic evaluation</json:string><json:string>kappa light chains</json:string><json:string>factor paraprotein</json:string><json:string>pokeweed mitogen</json:string><json:string>oral mucositis</json:string><json:string>systemic lupus erythematosus patients</json:string><json:string>representative patterns</json:string><json:string>erythrocyte sedimentation rate levels</json:string><json:string>significant change</json:string><json:string>laboratory values</json:string><json:string>rheumatoid factor paraprotein</json:string><json:string>alkaline phosphatase</json:string><json:string>immune dysregulation</json:string><json:string>clinical research</json:string><json:string>monoclonal antibody</json:string><json:string>immune response</json:string><json:string>significant decrease</json:string><json:string>little change</json:string><json:string>arthritis rheum</json:string><json:string>total immunoglobulin</json:string><json:string>salivary gland</json:string><json:string>lymphocytic infiltration</json:string><json:string>autoimmune disease</json:string><json:string>salivary gland biopsy</json:string><json:string>regular basis</json:string><json:string>arthritis</json:string></teeft></keywords><author><json:item><name>Robert I. Fox M.D., Ph.D.</name><affiliations><json:string>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</json:string></affiliations></json:item><json:item><name>Edward Chan Ph.D.</name><affiliations><json:string>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</json:string></affiliations></json:item><json:item><name>Laurie Benton</name><affiliations><json:string>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</json:string></affiliations></json:item><json:item><name>Sherman Fong Ph.D.</name><affiliations><json:string>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</json:string></affiliations></json:item><json:item><name>Mitchell Friedlaender M.D.</name><affiliations><json:string>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</json:string></affiliations></json:item><json:item><name>Francis V. Howell D.D.S.</name><affiliations><json:string>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</json:string></affiliations></json:item></author><articleId><json:string>88903658</json:string></articleId><arkIstex>ark:/67375/6H6-SW4CKVT1-M</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Sjögren's syndrome is an autoimmune disease characterized by lymphocytic infiltration of the salivary/lacrimal glands, autoantibody production, and polyclonal hyperglobulinemia. In view of the efficacy and relative safety of hydroxychloroquine in other autoimmune disorders, the potential benefit of hydroxychloroquine (200 mg per day for 12 months) in 10 patients with Sjögren's syndrome was evaluated. Changes in levels of total immunoglobulin, antibody against Sjögren's syndrome-associated antigen B, rheumatoid factor, and in vitro production of immunoglobulin in the serum were evaluated. For comparison, 10 patients matched according to age and sex, who did not receive hydroxychloroquine were studied. In the hydroxychloroquine-treated group, the following observations were made: (1) significantly decreased total immunoglobulin G (IgG) and IgA levels with little change in IgM levels; (2) significant decrease in IgA-rheumatoid factor with a smaller decrease in IgM-rheumatoid factor; (3) decreased IgG anti-Sjögren's syndrome-associated antigen B autoantibody; and (4) decreased erythrocyte sedimentation rate and increased hemoglobin level. Further, a specific idiotype present on their rheumatoid factor (defined by monoclonal antibody 17-109) was significantly decreased, with disappearance of detectable circulating paraprotein in two hydroxychloroquine-treated patients. Finally, rheumatoid factor production in vitro by lymphocytes from hydroxychloroquine-treated patients using a T cell-dependent mitogen was significantly decreased. These results suggest that hydroxychloroquine modulates lymphoproliferation in patients with Sjögren's syndrome and may prevent progression to extraglandular sites of neoplastic transformation.</abstract><qualityIndicators><score>8.963</score><pdfWordCount>4323</pdfWordCount><pdfCharCount>29307</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>6</pdfPageCount><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>220</abstractWordCount><abstractCharCount>1755</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>Treatment of primary Sjögren's syndrome with hydroxychloroquine</title><pmid><json:string>3177432</json:string></pmid><pii><json:string>0002-9343(88)90365-8</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>A clinical, pathological and serological study of 62 cases</title><language><json:string>unknown</json:string></language><pages><first>187</first><last>231</last></pages></serie><host><title>The American Journal of Medicine</title><language><json:string>unknown</json:string></language><publicationDate>1988</publicationDate><issn><json:string>0002-9343</json:string></issn><pii><json:string>S0002-9343(00)X0914-X</json:string></pii><volume>85</volume><issue>4</issue><pages><first>62</first><last>67</last></pages><genre><json:string>journal</json:string></genre><conference><json:item><name>Update in Rheumatology: Focus on Hydroxychloroquine, Hyatt Regency Cerromar Beach, Dorado, Puerto Rico 19871210 19871211</name></json:item></conference><editor><json:item><name>Nathan J. Zvaifler</name></json:item><json:item><name>M.D.</name></json:item></editor></host><namedEntities><unitex><date><json:string>1894</json:string><json:string>19871210</json:string><json:string>1988</json:string></date><geogName></geogName><orgName><json:string>American Journal of Medicine</json:string><json:string>American Journal of Medicine The</json:string><json:string>Laboratory Values</json:string><json:string>American Journal of Medicine Volume</json:string><json:string>American Journal of Medicine Sjijgren</json:string><json:string>Department of Rheumatology</json:string><json:string>Department of Basic and Clinical Research</json:string><json:string>Calbiochem</json:string><json:string>Scripps Clinical and Research Foundation, La Jolla, California</json:string><json:string>Other Laboratory Values</json:string><json:string>NIH</json:string></orgName><orgName_funder><json:string>NIH</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Payne</json:string><json:string>Selection</json:string><json:string>K. Hench</json:string><json:string>D.D.S.La Jo</json:string><json:string>C. Robinson</json:string><json:string>M.D.</json:string><json:string>J. Curd</json:string><json:string>Robert I. Fox</json:string><json:string>E. Tan</json:string><json:string>MoAb</json:string><json:string>La Jolla</json:string><json:string>G. Williams</json:string><json:string>F. Kozin</json:string><json:string>ROBERT Fox</json:string><json:string>D. Carson</json:string></persName><placeName></placeName><ref_url></ref_url><ref_bibl><json:string>[4]</json:string><json:string>[27,32]</json:string><json:string>[34]</json:string><json:string>[22]</json:string><json:string>[8]</json:string><json:string>[28]</json:string><json:string>Lakhanpal et al</json:string><json:string>[21]</json:string><json:string>[11,14,18]</json:string><json:string>[20]</json:string><json:string>[9]</json:string><json:string>[29,30]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-SW4CKVT1-M</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - medicine, general & internal</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - general & internal medicine</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - General Medicine</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>1988</publicationDate><copyrightDate>1988</copyrightDate><doi><json:string>10.1016/0002-9343(88)90365-8</json:string></doi><id>45836CB1252BFD52E6081B9F2A688D73E068F225</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-SW4CKVT1-M/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-SW4CKVT1-M/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-SW4CKVT1-M/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Treatment of primary Sjögren's syndrome with hydroxychloroquine</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>elsevier</p></licence></availability><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M"></p><date>1988</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note>This work is supported in part by NIH grants AR 33983 and RR 00833. This is publication number 5162BCR from the Research Institute of Scripps Clinic, La Jolla, California.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Treatment of primary Sjögren's syndrome with hydroxychloroquine</title><author xml:id="author-0000"><persName><forename type="first">Robert I.</forename><surname>Fox</surname></persName><roleName type="degree">M.D., Ph.D.</roleName><note type="biography">Requests for reprints should be addressed to Dr. Robert I. Fox, Department of Basic and Clinical Research (BCR4), 10666 North Torrey Pines Road, La Jolla, California 92037.</note><affiliation>Requests for reprints should be addressed to Dr. Robert I. Fox, Department of Basic and Clinical Research (BCR4), 10666 North Torrey Pines Road, La Jolla, California 92037.</affiliation><affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Edward</forename><surname>Chan</surname></persName><roleName type="degree">Ph.D.</roleName><affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Laurie</forename><surname>Benton</surname></persName><affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Sherman</forename><surname>Fong</surname></persName><roleName type="degree">Ph.D.</roleName><affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Mitchell</forename><surname>Friedlaender</surname></persName><roleName type="degree">M.D.</roleName><affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Francis V.</forename><surname>Howell</surname></persName><roleName type="degree">D.D.S.</roleName><affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</affiliation></author><idno type="istex">45836CB1252BFD52E6081B9F2A688D73E068F225</idno><idno type="ark">ark:/67375/6H6-SW4CKVT1-M</idno><idno type="DOI">10.1016/0002-9343(88)90365-8</idno><idno type="PII">0002-9343(88)90365-8</idno><idno type="article-id">88903658</idno></analytic><monogr><title level="j">The American Journal of Medicine</title><title level="j" type="abbrev">AJM</title><idno type="pISSN">0002-9343</idno><idno type="PII">S0002-9343(00)X0914-X</idno><meeting><addName>Update in Rheumatology: Focus on Hydroxychloroquine, Hyatt Regency Cerromar Beach, Dorado, Puerto Rico</addName><date>19871210</date><date>19871211</date></meeting><editor xml:id="book-author-0000"><persName>Nathan J. Zvaifler</persName></editor><editor xml:id="book-author-0001"><persName>M.D.</persName></editor><imprint><publisher>ELSEVIER</publisher><date type="published" when="1988"></date><biblScope unit="volume">85</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="supplement">S1</biblScope><biblScope unit="page" from="62">62</biblScope><biblScope unit="page" to="67">67</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1988</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Sjögren's syndrome is an autoimmune disease characterized by lymphocytic infiltration of the salivary/lacrimal glands, autoantibody production, and polyclonal hyperglobulinemia. In view of the efficacy and relative safety of hydroxychloroquine in other autoimmune disorders, the potential benefit of hydroxychloroquine (200 mg per day for 12 months) in 10 patients with Sjögren's syndrome was evaluated. Changes in levels of total immunoglobulin, antibody against Sjögren's syndrome-associated antigen B, rheumatoid factor, and in vitro production of immunoglobulin in the serum were evaluated. For comparison, 10 patients matched according to age and sex, who did not receive hydroxychloroquine were studied. In the hydroxychloroquine-treated group, the following observations were made: (1) significantly decreased total immunoglobulin G (IgG) and IgA levels with little change in IgM levels; (2) significant decrease in IgA-rheumatoid factor with a smaller decrease in IgM-rheumatoid factor; (3) decreased IgG anti-Sjögren's syndrome-associated antigen B autoantibody; and (4) decreased erythrocyte sedimentation rate and increased hemoglobin level. Further, a specific idiotype present on their rheumatoid factor (defined by monoclonal antibody 17-109) was significantly decreased, with disappearance of detectable circulating paraprotein in two hydroxychloroquine-treated patients. Finally, rheumatoid factor production in vitro by lymphocytes from hydroxychloroquine-treated patients using a T cell-dependent mitogen was significantly decreased. These results suggest that hydroxychloroquine modulates lymphoproliferation in patients with Sjögren's syndrome and may prevent progression to extraglandular sites of neoplastic transformation.</p></abstract></profileDesc><revisionDesc><change when="1988">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-SW4CKVT1-M/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>AJM</jid><aid>88903658</aid><ce:pii>0002-9343(88)90365-8</ce:pii><ce:doi>10.1016/0002-9343(88)90365-8</ce:doi><ce:copyright type="unknown" year="1988"></ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>This work is supported in part by NIH grants AR 33983 and RR 00833. This is publication number 5162BCR from the Research Institute of Scripps Clinic, La Jolla, California.</ce:note-para></ce:article-footnote><ce:title>Treatment of primary Sjögren's syndrome with hydroxychloroquine</ce:title><ce:author-group><ce:author><ce:given-name>Robert I.</ce:given-name><ce:surname>Fox</ce:surname><ce:degrees>M.D., Ph.D.</ce:degrees><ce:cross-ref refid="COR1"><ce:sup loc="post">∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Edward</ce:given-name><ce:surname>Chan</ce:surname><ce:degrees>Ph.D.</ce:degrees></ce:author><ce:author><ce:given-name>Laurie</ce:given-name><ce:surname>Benton</ce:surname></ce:author><ce:author><ce:given-name>Sherman</ce:given-name><ce:surname>Fong</ce:surname><ce:degrees>Ph.D.</ce:degrees></ce:author><ce:author><ce:given-name>Mitchell</ce:given-name><ce:surname>Friedlaender</ce:surname><ce:degrees>M.D.</ce:degrees></ce:author><ce:author><ce:given-name>Francis V.</ce:given-name><ce:surname>Howell</ce:surname><ce:degrees>D.D.S.</ce:degrees></ce:author><ce:affiliation><ce:textfn>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Requests for reprints should be addressed to Dr. Robert I. Fox, Department of Basic and Clinical Research (BCR4), 10666 North Torrey Pines Road, La Jolla, California 92037.</ce:text></ce:correspondence></ce:author-group><ce:abstract class="author"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">Sjögren's syndrome is an autoimmune disease characterized by lymphocytic infiltration of the salivary/lacrimal glands, autoantibody production, and polyclonal hyperglobulinemia. In view of the efficacy and relative safety of hydroxychloroquine in other autoimmune disorders, the potential benefit of hydroxychloroquine (200 mg per day for 12 months) in 10 patients with Sjögren's syndrome was evaluated. Changes in levels of total immunoglobulin, antibody against Sjögren's syndrome-associated antigen B, rheumatoid factor, and <ce:italic>in vitro</ce:italic> production of immunoglobulin in the serum were evaluated. For comparison, 10 patients matched according to age and sex, who did not receive hydroxychloroquine were studied. In the hydroxychloroquine-treated group, the following observations were made: (1) significantly decreased total immunoglobulin G (IgG) and IgA levels with little change in IgM levels; (2) significant decrease in IgA-rheumatoid factor with a smaller decrease in IgM-rheumatoid factor; (3) decreased IgG anti-Sjögren's syndrome-associated antigen B autoantibody; and (4) decreased erythrocyte sedimentation rate and increased hemoglobin level. Further, a specific idiotype present on their rheumatoid factor (defined by monoclonal antibody 17-109) was significantly decreased, with disappearance of detectable circulating paraprotein in two hydroxychloroquine-treated patients. Finally, rheumatoid factor production <ce:italic>in vitro</ce:italic> by lymphocytes from hydroxychloroquine-treated patients using a T cell-dependent mitogen was significantly decreased. These results suggest that hydroxychloroquine modulates lymphoproliferation in patients with Sjögren's syndrome and may prevent progression to extraglandular sites of neoplastic transformation.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Treatment of primary Sjögren's syndrome with hydroxychloroquine</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Treatment of primary Sjögren's syndrome with hydroxychloroquine</title></titleInfo><name type="personal"><namePart type="given">Robert I.</namePart><namePart type="family">Fox</namePart><namePart type="termsOfAddress">M.D., Ph.D.</namePart><affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</affiliation><description>Requests for reprints should be addressed to Dr. Robert I. Fox, Department of Basic and Clinical Research (BCR4), 10666 North Torrey Pines Road, La Jolla, California 92037.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Edward</namePart><namePart type="family">Chan</namePart><namePart type="termsOfAddress">Ph.D.</namePart><affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Laurie</namePart><namePart type="family">Benton</namePart><affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sherman</namePart><namePart type="family">Fong</namePart><namePart type="termsOfAddress">Ph.D.</namePart><affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mitchell</namePart><namePart type="family">Friedlaender</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Francis V.</namePart><namePart type="family">Howell</namePart><namePart type="termsOfAddress">D.D.S.</namePart><affiliation>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California, USA</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">1988</dateIssued><copyrightDate encoding="w3cdtf">1988</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Sjögren's syndrome is an autoimmune disease characterized by lymphocytic infiltration of the salivary/lacrimal glands, autoantibody production, and polyclonal hyperglobulinemia. In view of the efficacy and relative safety of hydroxychloroquine in other autoimmune disorders, the potential benefit of hydroxychloroquine (200 mg per day for 12 months) in 10 patients with Sjögren's syndrome was evaluated. Changes in levels of total immunoglobulin, antibody against Sjögren's syndrome-associated antigen B, rheumatoid factor, and in vitro production of immunoglobulin in the serum were evaluated. For comparison, 10 patients matched according to age and sex, who did not receive hydroxychloroquine were studied. In the hydroxychloroquine-treated group, the following observations were made: (1) significantly decreased total immunoglobulin G (IgG) and IgA levels with little change in IgM levels; (2) significant decrease in IgA-rheumatoid factor with a smaller decrease in IgM-rheumatoid factor; (3) decreased IgG anti-Sjögren's syndrome-associated antigen B autoantibody; and (4) decreased erythrocyte sedimentation rate and increased hemoglobin level. Further, a specific idiotype present on their rheumatoid factor (defined by monoclonal antibody 17-109) was significantly decreased, with disappearance of detectable circulating paraprotein in two hydroxychloroquine-treated patients. Finally, rheumatoid factor production in vitro by lymphocytes from hydroxychloroquine-treated patients using a T cell-dependent mitogen was significantly decreased. These results suggest that hydroxychloroquine modulates lymphoproliferation in patients with Sjögren's syndrome and may prevent progression to extraglandular sites of neoplastic transformation.</abstract><note>This work is supported in part by NIH grants AR 33983 and RR 00833. This is publication number 5162BCR from the Research Institute of Scripps Clinic, La Jolla, California.</note><relatedItem type="host"><titleInfo><title>The American Journal of Medicine</title></titleInfo><titleInfo type="abbreviated"><title>AJM</title></titleInfo><name type="conference"><namePart>Update in Rheumatology: Focus on Hydroxychloroquine, Hyatt Regency Cerromar Beach, Dorado, Puerto Rico</namePart><namePart type="date">19871210</namePart><namePart type="date">19871211</namePart></name><name type="personal"><namePart>Nathan J. 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