Treatment of primary Sjögren's syndrome with hydroxychloroquine
Identifieur interne : 003229 ( Main/Exploration ); précédent : 003228; suivant : 003230Treatment of primary Sjögren's syndrome with hydroxychloroquine
Auteurs : Robert I. Fox [États-Unis] ; Edward Chan [États-Unis] ; Laurie Benton [États-Unis] ; Sherman Fong [États-Unis] ; Mitchell Friedlaender [États-Unis] ; Francis V. Howell [États-Unis]Source :
- 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
Affiliations:
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Howell</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Basic and Clinical Research, Divisions of Clinical Rheumatology and Ophthalmology, Scripps Clinical and Research Foundation, La Jolla, California</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">The American Journal of Medicine</title><title level="j" type="abbrev">AJM</title><idno type="ISSN">0002-9343</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1988">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><idno type="ISSN">0002-9343</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0002-9343</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Alkaline phosphatase</term><term>American journal</term><term>Arthritis</term><term>Arthritis rheum</term><term>Artificial tears</term><term>Autoantibody</term><term>Autoantibody titers</term><term>Autoimmune disease</term><term>Beneficial effects</term><term>Biopsy</term><term>Cell surface</term><term>Clinical research</term><term>Different syndrome patients</term><term>Erythrocyte sedimentation rate</term><term>Erythrocyte sedimentation rate levels</term><term>Extraglandular sites</term><term>Factor paraprotein</term><term>Foreign antigens</term><term>Hydroxychloroquine</term><term>Hydroxychloroquine treatment</term><term>Hyperglobulinemia</term><term>Idiotype</term><term>Immune</term><term>Immune dysregulation</term><term>Immune response</term><term>Immunoglobulin</term><term>Immunoglobulin levels</term><term>Infiltrates</term><term>Kappa light chains</term><term>Laboratory features</term><term>Laboratory values</term><term>Little change</term><term>Lmmunol</term><term>Lymphocytic infiltration</term><term>Medicine volume</term><term>Moab</term><term>Monoclonal antibody</term><term>Multiple sclerosis</term><term>Ophthalmologic evaluation</term><term>Optical density</term><term>Oral mucositis</term><term>Patient group</term><term>Peripheral blood lymphocyte</term><term>Pokeweed mitogen</term><term>Primary syndrome</term><term>Primary syndrome patients</term><term>Regular basis</term><term>Representative patterns</term><term>Rheumatoid</term><term>Rheumatoid arthritis</term><term>Rheumatoid factor</term><term>Rheumatoid factor paraprotein</term><term>Rheumatoid factor samples</term><term>Salivary</term><term>Salivary gland</term><term>Salivary gland biopsies</term><term>Salivary gland biopsy</term><term>Significant change</term><term>Significant decrease</term><term>Syndrome</term><term>Syndrome patient</term><term>Syndrome patients</term><term>Systemic lupus erythematosus patients</term><term>Total immunoglobulin</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml: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.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li></region></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Fox, Robert I" sort="Fox, Robert I" uniqKey="Fox R" first="Robert I." last="Fox">Robert I. Fox</name></region><name sortKey="Benton, Laurie" sort="Benton, Laurie" uniqKey="Benton L" first="Laurie" last="Benton">Laurie Benton</name><name sortKey="Chan, Edward" sort="Chan, Edward" uniqKey="Chan E" first="Edward" last="Chan">Edward Chan</name><name sortKey="Fong, Sherman" sort="Fong, Sherman" uniqKey="Fong S" first="Sherman" last="Fong">Sherman Fong</name><name sortKey="Friedlaender, Mitchell" sort="Friedlaender, Mitchell" uniqKey="Friedlaender M" first="Mitchell" last="Friedlaender">Mitchell Friedlaender</name><name sortKey="Howell, Francis V" sort="Howell, Francis V" uniqKey="Howell F" first="Francis V." last="Howell">Francis V. Howell</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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