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DMARDs may cause adverse reactions and become less effective over time in some patients. Using changes in disease activity and X-ray findings as indicators, we retrospectively evaluated the long-term results of the step-wise administration of DMARDs in 200 patients with RA. The patients had been treated with gold compounds, SH compounds, and methotrexate, in this order, over a total of 10 years since initially being diagnosed with the disease in its relatively early stages. The step-wise administration of DMARDs had decreased and controlled RA activity and inflammatory response over the 10 years. Although X-ray findings for the wrists worsened over time in most of the patients, no knee or hip joint destruction was observed in patients in whom disease activity had been controlled well for a long period of time. The progression of destruction of major joints can be prevented in cases in which the Lansbury activity index and C-reactive protein are maintained at levels not more than 30% and 1.5 mg\u002Fdl, respectively. Since no drugs are now available which specifically prevent the progression of joint destruction, it is important to control RA activity for as long as possible.",{"EN":110},"Outcome of patients with rheumatoid arthritis treated by step-wise administration of disease-modifying antirheumatic drugs over a 10-year period",{"VOID":112},"[]",{"VOID":114},"10.1007\u002Fs101650300004","PUBLICATION","VERIFIED","2024-09-05T05:51:47.693+00:00","Auto Verify","https:\u002F\u002Facademic.oup.com\u002Fmr\u002Farticle-abstract\u002F13\u002F1\u002F27\u002F6315088?redirectedFrom=fulltext",[121,137,150,164],{"id":122,"sortIndex":19,"researcher":18,"roles":123,"affiliations":125,"properties":134,"displayName":136,"givenName":18,"familyName":18},"4a688950-e64b-4fdb-b3ec-edf32ed247e0",[124],"AUTHOR",[126],{"id":127,"sortIndex":19,"affiliation":128,"properties":18},"d84635be-7c55-423c-b3d8-3538e738409a",{"id":127,"createTime":18,"updateTime":18,"relativeEntities":129,"slug":18,"properties":130,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":133,"statistic":18},[],{"title":131},{"VI":132},"Department of Orthopaedic Surgery and Rheumatology, Tokushima Kensei (CO-OP) Hospital, 4-9-1 Shimosuketou,Tokushima 770-0805, Japan Tel. +81-88-622-7771; Fax +81-88-653-8480 e-mail: t-miniren@mb4.seikyou.ne.jp, , JP",[],{"title":135},{"VI":136},"Y. 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Infusions of rituximab ameliorated her neurological symptoms and serological inflammatory findings. Rituximab, a specific B cell-targeting therapy, might offer an alternative for refractory EGPA with possible advantages of cost and ease of use compared to IVIG, which also targets (at least in part) B lymphocytes and immunoglobulin production.",{"EN":246},"Successful treatment of eosinophilic granulomatosis with polyangiitis (EGPA; formerly Churg–Strauss syndrome) with rituximab in a case refractory to glucocorticoids, cyclophosphamide, and IVIG",{"VOID":112},{"VOID":249},"Cohen P, Pagnoux C, Mahr A, Arene JP, Mouthon L, Le Guern V, et al. Churg–Strauss syndrome with poor-prognosis factors: a prospective multicenter trial comparing glucocorticoids and six or twelve cyclophosphamide pulses in forty-eight patients. Arthritis Rheum. 2007;57:686–93.\nMukhtyar C, Guillevin L, Cid MC, Dasgupta B, de Groot K, Gross W, et al. EULAR recommendations for the management of primary small and medium vessel vasculitis. Ann Rheum Dis. 2009;68:310–17.\nTaniguchi M, Tsurikisawa N, Higashi N, Saito H, Mita H, Mori A, et al. Treatment for Churg–Strauss syndrome: induction of remission and efficacy of intravenous immunoglobulin therapy. Allergol Int. 2007;56:97–103.\nJones RB, Tervaert JW, Hauser T, Luqmani R, Morgan MD, Peh CA, et al. Rituximab versus cyclophosphamide in ANCA-associated renal vasculitis. J N Eng Med. 2010;363:211–20.\nStone JH, Merkel PA, Spiera R, Seo P, Langford CA, Hoffman GS, et al. Rituximab versus cyclophosphamide for ANCA-associated vasculitis. N Eng J Med. 2010;363:221–32.\nKaushik VV, Reddy HV, Bucknall RC. Successful use of rituximab in a patient with recalcitrant Churg–Strauss syndrome. Ann Rheum Dis. 2006;65:1116–7.\nKoukoulaki M, Smith KG, Jayne DR. Rituximab in Churg–Strauss syndrome. Ann Rheum Dis. 2006;65:557–9.\nPepper RJ, Fabre MA, Pavesio C, Gaskin G, Jones RB, Jayne D, et al. Rituximab is effective in the treatment of refractory Churg–Strauss syndrome and is associated with diminished T-cell interleukin-5 production. Rheumatology (Oxford). 2008;47:1104–5.\nSaech J, Owczarczyk K, Rosgen S, Petereit H, Hallek M, Rubbert-Roth A. Successful use of rituximab in a patient with Churg–Strauss syndrome and refractory central nervous system involvement. Ann Rheum Dis. 2010;69:1254–5.\nDonvik KK, Omdal R. Churg–Strauss syndrome successfully treated with rituximab. Rheumatol Int. 2011;31:89–91.\nCartin-Ceba R, Keogh KA, Specks U, Sethi S, Fervenza FC. Rituximab for the treatment of Churg–Strauss syndrome with renal involvement. Nephrol Dial Transplant. 2011;26:2865–71.\nSewell WA, Jolles S. Immunomodulatory action of intravenous immunoglobulin. Immunology. 2002;107:387–93.\nTsurikisawa N, Saito H, Oshikata C, Tsuburai T, Akiyama K. High-dose intravenous immunoglobulin treatment increases regulatory T cells in patients with eosinophilic granulomatosis with polyangiitis. J Rheumatol. 2012;39:1019–25.\nDanieli MG, Cappelli M, Malcangi G, Logullo F, Salvi A, Danieli G. Long term effectiveness of intravenous immunoglobulin in Churg–Strauss syndrome. Ann Rheum Dis. 2004;63:1649–54.\nHerrmann K, Gross WL, Moosig F. Extended follow-up after stopping mepolizumab in relapsing\u002Frefractory Churg–Strauss syndrome. Clin Exp Rheumatol. 2012;30:S62–5.\nGuilpain P, Auclair JF, Tamby MC, Servettaz A, Mahr A, Weill B, et al. Serum eosinophil cationic protein: a marker of disease activity in Churg–Strauss syndrome. Ann N Y Acad Sci. 2007;1107:392–9.\nHurst S, Chizzolini C, Dayer JM, Olivieri J, Roux-Lombard P. Usefulness of serum eosinophil cationic protein (ECP) in predicting relapse of Churg and Strauss vasculitis. 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Seventeen patients with lupus nephritis who had been resistant to corticosteroid and immunosuppressant therapy received weekly mizoribine pulse therapy. Mizoribine (350 mg) was administered three times at 12 h intervals over 2 consecutive days (700 mg for day 1 and 350 mg for day 2), followed by a washout period from day 3 to day 7. This therapeutic strategy enabled the peak blood levels of mizoribine to be increased to more than 3 μg\u002FmL in most of the patients. Although SLEDAI, anti-ds-DNA antibody titer, CH-50, and serum albumin level did not significantly improve, urinary protein levels decreased, and it was possible to taper the dose of concomitant steroids. Using our definition of clinical response, 10 of the 17 patients were responders and 4 of them were nonresponders. The average peak serum mizoribine concentration of the responders was as high as 3.5 μg\u002FmL. Elevation of serum liver enzymes was seen in 1 patient, and hyperuricemia occurred in 4 cases, but none of these adverse events were serious. 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Rinsyo-Iyaku. 1989;5(4):795–824 (in Japanese).",{},{"id":739,"text":740,"url":741,"identifiers":742},"1436dc66-a18b-4606-b5bc-d7de5c6dff66","Kuroda T, Hirose S, Tanabe N, Sato H, Nakatsue T, Ajiro J, et al. Mizoribine therapy for patients with lupus nephritis: the association between peak mizoribine concentration and clinical efficacy. Mod Rheumatol. 2007;17:206–12.","https:\u002F\u002Facademic.oup.com\u002Fmr\u002Farticle-abstract\u002F17\u002F3\u002F206\u002F6313751?redirectedFrom=fulltext",{"doi":743},"10.1007\u002Fs10165-007-0567-x",{"id":700,"text":745,"url":702,"identifiers":746},"Sonda K, Takahashi K, Tanabe K, Funchinoue S, Hayasaka Y, Kawaguchi H, et al. Clinical pharmacokinetic study of mizoribine in renal transplantation patients. Transpl Proc. 1996;28:3643–8.",{"doi":704},{"id":700,"text":748,"url":702,"identifiers":749},"Turka LA, Dayton J, Sinclair G, Thompson CB, Mitchell BS. Guanine ribonucleotide depletion inhibits T cell activation. Mechanism of action of the immunosuppressive drug mizoribine. J Clin Invest. 1991;87:940–8.",{"doi":704},{"id":700,"text":751,"url":702,"identifiers":752},"Hirohata S, Nakanishi K, Yanagida T. Inhibition of cyclin A gene expression in human B cells by an immunosuppressant mizoribine. Clin Exp Immunol. 2000;120:448–53.",{"doi":704},{"id":700,"text":754,"url":702,"identifiers":755},"Takahashi S, Wakui H, Gustafsson JA, Zilliacus J, Itoh H. Functional interaction of the immunosuppressant mizoribine with the 14-3-3 protein. Biochem Biophys Res Commun. 2000;274:87–92.",{"doi":704},{"id":700,"text":757,"url":702,"identifiers":758},"Ishida K, Kaneda H, Uemura O, Ushijima K, Ohta K, Goto Y, et al. Evaluation of limited sampling designs to estimate maximal concentration and area under the curve of mizoribine in pediatric patients with renal disease. Drug Metab Pharmacokinet. 2011;26:71–8.",{"doi":704},{"id":700,"text":760,"url":702,"identifiers":761},"Stypinski D, Obaidi M, Combs M, Weber M, Stewart AJ, Ishikawa H. Safety, tolerability and pharmacokinetics of high-dose mizoribine in healthy male volunteers. Br J Clin Pharmacol. 2006;63:459–68.",{"doi":704},{"id":18,"text":763,"url":18,"identifiers":764},"Yumura W, Uchida K, Kawashima A, Kobayashi H, Miwa N, Honda K et al. Evaluation of plasma concentration of mizoribine as an immunosuppressive agent in lupus nephritis patients. Kidney Dial. 1999;47:705–8. (in Japanese).",{},{"id":700,"text":766,"url":702,"identifiers":767},"Doi T, Masaki T, Shiraki N, Kawai T, Yorioka N. Oral mizoribine pulse therapy for steroid-dependent focal segmental glomerulosclerosis. Clin Nephrol. 2008;69:433–5.",{"doi":704},{"id":700,"text":769,"url":702,"identifiers":770},"Tanaka H, Tsugawa K, Nakahata T, Kudo M, Suzuki K, Ito E. Implication of the peak serum level of mizoribine for control of the serum anti-dsDNA antibody titer in patients with lupus nephritis. Clin Nephrol. 2005;63:417–22.",{"doi":704},{"id":772,"text":773,"url":774,"identifiers":775},"8f287da0-aa68-4a65-b812-d4dd53a1d056","Tanaka H, Tsugawa K, Oki E, Suzuki K, Ito E. Long-term mizoribine intermittent pulse therapy for young patients with flare of lupus nephritis. Clin Rheumatol. 2008;27:85–9.","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs00467-006-0120-8",{"doi":776},"10.1007\u002Fs00467-006-0120-8",{"id":700,"text":778,"url":702,"identifiers":779},"Suzuki K, Kameda H, Amano K, Nagasawa H, Takei H, Nishi E, et al. Single center prospective study of tacrolimus efficacy and safety in the treatment of various manifestations of systemic lupus erythematosus. Rheumatol Int. 2011;31:757–63.",{"doi":704},{"id":700,"text":781,"url":702,"identifiers":782},"Bao H, Liu Z-H, Xie H-L, Hu W-X, Zhang H-T, Li L-S. Successful treatment of class V + IV lupus nephritis with multitarget therapy. J Am Soc Nephrol. 2008;19:2001–10.",{"doi":704},{"id":784,"text":785,"url":786,"identifiers":787},"87a070e7-e1ea-4ed5-833c-989ae783c770","Aizawa-Yashiro T, Tsuruga K, Watanabe S, Oki E, Ito E, Tanaka H. Novel multidrug therapy for children with cyclosporine-resistant or -intolerant nephrotic syndrome. Pediatr Nephrol. 2011;26:1255–61.","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs00467-011-1876-z",{"doi":788},"10.1007\u002Fs00467-011-1876-z",{"id":790,"createTime":791,"updateTime":792,"relativeEntities":793,"slug":794,"properties":795,"entityType":115,"verifyStatus":116,"verifyTime":805,"verifyNote":118,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":806,"fullTextUrl":18,"authors":807,"publicationType":178,"publisherRelationship":901,"citationCount":18,"citationInfo":18,"publishDate":952,"publishYear":953,"citationAnalyzeStatus":232,"lastCitationAnalyze":954,"indexDatabases":955,"openAccess":18,"references":18,"isForceReanalyzing":235},"c891ddb9-457b-4f15-8134-36a1f4298a6c","2023-12-31T13:28:18.442+00:00","2026-07-10T13:50:36.292+00:00",[],"Rituximab-was-effective-on-refractory-thrombotic-thrombocytopenic-purpura-but-induced-a-flare-of-hemophagocytic-syndrome-in-a-patient-with-systemic-lupus-erythematosus",{"abstract":796,"title":798,"gsPaper":800,"references":801,"doi":803},{"EN":797},"We report the case of a patient with systemic lupus erythematosus (SLE) who first revealed hemophagocytic syndrome (HPS), which was treated successfully with glucocorticoid and intravenous cyclophosphamide. The patient then demonstrated refractory thrombotic thrombocytopenic purpura (TTP) with normal a disintegrin and metalloprotease with thrombospondin motifs (ADAMTS)-13 activity that responded well to rituximab. After rituximab treatment, the patient showed a flare of HPS that was controlled by additional intravenous cyclophosphamide treatment. This case showed that TTP with normal ADAMTS-13 activity is B-cell dependent and indicated that B-cell depletion might exacerbate some autoimmune conditions in SLE.",{"EN":799},"Rituximab was effective on refractory thrombotic thrombocytopenic purpura but induced a flare of hemophagocytic syndrome in a patient with systemic lupus erythematosus",{"VOID":112},{"VOID":802},"Lipsky PE. Systemic lupus erythematosus: an autoimmune disease of B cell hyperactivity. Nat Immunol. 2001;2:764–6.\nMartin F, Chan AC. B cell immunobiology in disease: evolving concepts from the clinic. Annu Rev Immunol. 2006;24:467–96.\nMizoguchi A, Bhan AK. A case for regulatory B cells. J Immunol. 2006;176(2):705–10.\nAnderton SM, Fillatreau S. Activated B cells in autoimmune diseases: the case for a regulatory role. Nat Clin Pract Rheumatol. 2008;4:657–66.\nSilverman GJ, Weisman S. Rituximab therapy and autoimmune disorders: prospects for anti-B cell therapy. Arthritis Rheum. 2003;48:1484–92.\nEisenberg R, Albert D. B-cell targeted therapies in rheumatoid arthritis and systemic lupus erythematosus. Nat Clin Pract Rheumatol. 2006;2:20–7.\nGunnarsson I, Sundelin B, Jónsdóttir T, Jacobson SH, Henriksson EW, van Vollenhoven RF. Histopathologic and clinical outcome of rituximab treatment in patients with cyclophosphamide-resistant proliferative lupus nephritis. Arthritis Rheum. 2007;56:1263–72.\nTokunaga M, Saito K, Kawabata D, Imura Y, Fujii T, Nakayamada S, et al. Efficacy of rituximab (anti-CD20) for refractory systemic lupus erythematosus involving the central nervous system. Ann Rheum Dis. 2007;66:470–5.\nLindholm C, Börjesson-Asp K, Zendjanchi K, Sundqvist AC, Tarkowski A, Bokarewa M. Long term clinical and immunological effects of anti-CD20 treatment in patients with refractory systemic lupus erythematosus. J Rheumatol. 2008;35(5):826–33.\nGeorge JN. Clinical practice. Thrombotic thrombocytopenic purpura. N Engl J Med. 2006;354:1927–35.\nGeorge JN, Woodson RD, Kiss JE, Kojouri K, Vesely SK. Rituximab therapy for thrombotic thrombocytopenic purpura: a proposed study of the Transfusion Medicine\u002FHemostasis Clinical Trials Network with a systematic review of rituximab Treatment of thrombotic thrombocytopenic purpura-hemolytic uremic syndrome in therapy for immune-mediated disorders. J Clin Apher. 2006;21:49–56.\nShah AA, Higgins JP, Chakravarty EF. Thrombotic microangiopathic hemolytic anemia in a patient with SLE: diagnostic difficulties. Nat Clin Pract Rheumatol. 2007;3:6–357.\nNiewold TB, Alpert D, Scanzello CR, Paget SA. Rituximab treatment of thrombotic thrombocytopenic purpura in the setting of connective tissue disease. J Rheumatol. 2006;33:1194–6.\nLimal N, Cacoub P, Sène D, Guichard I, Piette JC. Rituximab for the treatment of thrombotic thrombocytopenic purpura in systemic lupus erythematosus. Lupus. 2008;17:69–71.\nLetchumanan P, Ng HJ, Lee LH, Thumboo J. A comparison of thrombotic thrombocytopenic purpura in an inception cohort of patients with and without systemic lupus erythematosus. Rheumatology. 2009;48:399–403.\nMoake JL. Thrombotic microangiopathies. N Engl J Med. 2002;347:589–600.\nMiyamura T, Watanabe H, Takahama S, Sonomoto K, Nakamura M, Ando H, et al. Thrombotic thrombocytopenic purpura in patients with systemic lupus erythematosus. Nihon Rinsho Meneki Gakkai Kaishi. 2008;31:159–65. Japanese.\nLambotte O, Khellaf M, Harmouche H, Bader-Meunier B, Manceron V, Goujard C, et al. Characteristics and long-term outcome of 15 episodes of systemic lupus erythematosus-associated hemophagocytic syndrome. Medicine. 2006;85:169–82.\nKumakura S, Ishikura H, Kondo M, Murakawa Y, Masuda J, Kobayashi S. Autoimmune-associated hemophagocytic syndrome. Mod Rheumatol. 2004;14:205–15.\nZandman-Goddard G, Shoenfeld Y. Ferritin in autoimmune diseases. Autoimmun Rev. 2007;6:457–63.\nBruns A, Bläss S, Hausdorf G, Burmester GR, Hiepe F. Nucleosomes are major T and B cell autoantigens in systemic lupus erythematosus. Arthritis Rheum. 2000;43:2307–15.\nUrbonaviciute V, Fürnrohr BG, Meister S, Munoz L, Heyder P, De Marchis F, et al. Induction of inflammatory and immune responses by HMGB1-nucleosome complexes: implications for the pathogenesis of SLE. J Exp Med. 2008;205:3007–18.\nMatsushita T, Yanab K, Bouaziz JD, Fujimoto M, Tedder TF. Regulatory B cells inhibit EAE initiation in mice while other B cells promote disease progression. J Clin Invest. 2008;118:3420–30.\nGoetz M, Atrey R, Ghalibafian M, Galle PR, Neurath MF. Exacerbation of ulcerative colitis after rituximab salvage therapy. Inflamm Bowel Dis. 2007;13:1365–8.\nDass S, Vital EM, Emery P. Development of psoriasis after B cell depletion with rituximab. Arthritis Rheum. 2007;56:2715–8.\nKfoury Baz EM, Mikati AR, Kanj NA. Reactive hemophagocytic syndrome associated with thrombotic thrombocytopenic purpura during therapeutic plasma exchange. Ther Apher. 2002;6:159–62.\nYamada T, Handa Y, Kamikawa T, Machino H, Suzuki K, Miyata K. A case of systemic lupus erythematosus associated with thrombotic thrombocytopenic purpura and hemophagocytic syndrome. Nihon Rinsho Meneki Gakkai Kaishi. 2006;29:384–8. Japanese.",{"VOID":804},"10.1007\u002Fs10165-009-0231-8","2024-06-24T00:41:30.671+00:00","https:\u002F\u002Facademic.oup.com\u002Fmr\u002Farticle-abstract\u002F20\u002F1\u002F81\u002F6315389?redirectedFrom=fulltext",[808,823,836,849,862,875,888],{"id":809,"sortIndex":19,"researcher":18,"roles":810,"affiliations":811,"properties":820,"displayName":822,"givenName":18,"familyName":18},"1450c03b-3545-4af5-8a2e-a27cb83b227c",[124],[812],{"id":813,"sortIndex":19,"affiliation":814,"properties":18},"67fea01d-9325-48ac-872a-db0b7615c5ca",{"id":813,"createTime":18,"updateTime":18,"relativeEntities":815,"slug":18,"properties":816,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":819,"statistic":18},[],{"title":817},{"VI":818},"Pulmonary Medicine and Clinical Immunology, Dokkyo University, School of Medicine, Mibu, Japan",[],{"title":821},{"VI":822},"Kuniyoshi 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36-year-old female patient who was diagnosed with chronic myocarditis as an initial manifestation of systemic lupus erythematosus (SLE) was admitted to our hospital. At her third occurrence of heart failure, we performed an endomyocardial biopsy and proved chronic myocarditis with SLE. Subsequently, she was treated with prednisolone and the immunosuppressive agent mizoribine (MZR), and her cardiac function improved. We describe for the first time treatment with MZR for chronic cardiac involvement of SLE.",{"EN":966},"Successful treatment of chronic lupus myocarditis with prednisolone and mizoribine",{"VOID":112},{"VOID":969},"Wijetunga M, Rockson S. Myocarditis in systemic lupus erythematosus. Am J Med. 2002;113:419–23.\nChan YK, Li EK, Tam LS, Chow LT, Ng HK. Intravenous cyclophosphamide improves cardiac dysfunction in lupus myocarditis. Scand J Rheumatol. 2003;32:306–8.\nGottenberg JE, Roux S, Assayag P, Clerc D, Mariette X. Specific cardiomyopathy in lupus patients: report of three cases. Joint Bone Spine. 2004;71:66–9.\nBrigden W, Bywaters EG, Lessof MH, Ross IP. The heart in systemic lupus erythematosus. Br Heart J. 1960;22:1–16.\nBidani AK, Roberts JL, Schwartz MM, Lewis EJ. Immunopathology of cardiac lesions in fatal systemic lupus erythematosus. Am J Med. 1980;69:849–58.\nBulkley BH, Roberts WC. The heart in systemic lupus erythematosus and the changes induced in it by corticosteroid therapy. A study of 36 necropsy patients. Am J Med. 1975;58:243–64.\nLogar D, Kveder T, Rozman B, Dobovisek J. Possible association between anti-Ro antibodies and myocarditis or cardiac conduction defects in adults with systemic lupus erythematosus. Ann Rheum Dis. 1990;49:627–9.\nVogel-Claussen J, Rochitte CE, Wu KC, Kamel IR, Foo TK, Lima JA, et al. Delayed enhancement MR imaging: utility in myocardial assessment. Radiographics. 2006;26:795–810.\nMahrholdt H, Goedecke C, Wagner A, Meinhardt G, Athanasiadis A, Vogelsberg H, et al. Cardiovascular magnetic resonance assessment of human myocarditis: a comparison to histology and molecular pathology. Circulation. 2004;109:1250–8.\nNaarendorp M, Kerr LD, Khan AS, Ornstein MH. Dramatic improvement of left ventricular function after cytotoxic therapy in lupus patients with acute cardiomyopathy: report of 6 cases. J Rheumatol. 1999;26:2257–60.\nTakahashi S, Wakui H, Gustafsson JA, Zilliacus J, Itoh H. Functional interaction of the immunosuppressant mizoribine with the 14-3-3 protein. Biochem Biophys Res Commun. 2000;274:87–92.\nChung JW, Joe DY, Park HJ, Kim HA, Park HS, Suh CH. Clinical characteristics of lupus myocarditis in Korea. Rheumatol Int. 2008;28:275–80.\nBusteed S, Sparrow P, Molloy C, Molloy MG. Myocarditis as a prognostic indicator in systemic lupus erythematosus. Postgrad Med J. 2004;80:366–7.\nSuri V, Varma S, Joshi K, Malhotra P, Kumari S, Jain S. Lupus myocarditis: marked improvement in cardiac function after intravenous immunoglobulin therapy. Rheumatol Int 2009. doi:10.1007\u002Fs00296-009-1098-x",{"VOID":971},"10.1007\u002Fs10165-010-0326-2","2024-06-24T02:09:53.813+00:00","https:\u002F\u002Facademic.oup.com\u002Fmr\u002Farticle-abstract\u002F20\u002F6\u002F606\u002F6304601?redirectedFrom=fulltext",[975,990,1003,1018,1031,1044,1057,1070,1083,1096,1109,1122,1135,1148],{"id":976,"sortIndex":19,"researcher":18,"roles":977,"affiliations":978,"properties":987,"displayName":989,"givenName":18,"familyName":18},"cbd3ce1a-65e4-440e-8821-e1a72f67cdeb",[124],[979],{"id":980,"sortIndex":19,"affiliation":981,"properties":18},"322272e3-6d08-438f-ab2a-77a921c97fba",{"id":980,"createTime":18,"updateTime":18,"relativeEntities":982,"slug":18,"properties":983,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":986,"statistic":18},[],{"title":984},{"VI":985},"Department of Rheumatology, Unit of Translational Medicine, Graduate School of Biomedical 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Takayasu arteritis—beyond pulselessness. Intern Med. 1999;38:226–32.",{"doi":704},{"id":1710,"text":1711,"url":1712,"identifiers":1713},"d6ec5bfd-e72e-458d-aa5c-1948829fc6eb","Hata A, Noda M, Moriwaki R, Numano F. Angiographic findings of Takayasu arteritis: new classification. Int J Cardiol. 1996;54(Suppl):S155–63.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS0167527396028136",{"doi":1714},"10.1016\u002Fs0167-5273(96)02813-6",{"id":700,"text":1716,"url":702,"identifiers":1717},"Maksimowicz-McKinnon K, Clark TM, Hoffman GS. Limitations of therapy and a guarded prognosis in an American cohort of Takayasu arteritis patients. Arthritis Rheum. 2007;56:1000–9.",{"doi":704},{"id":18,"text":1719,"url":18,"identifiers":1720},"Kerr GS, Hallahan CW, Giordano J, Leavitt RY, Fauci AS, Rottem M, et al. Takayasu arteritis. Ann Intern Med. 1994;120:919–29.",{},{"id":700,"text":1722,"url":702,"identifiers":1723},"Vanoli M, Daina E, Salvarani C, Sabbadini MG, Rossi C, Bacchiani G, et al. Takayasu’s arteritis: a study of 104 Italian patients. Arthritis Rheum. 2005;53:100–7.",{"doi":704},{"id":18,"text":1725,"url":18,"identifiers":1726},"Zamani F, Shakeri R, Modiramani O, Malekzadeh R. Abdominal pain as presentation of Takayasu’s arteritis in an adolescent male patient. Med Gen Med. 2006;8:69.",{},{"id":700,"text":1728,"url":702,"identifiers":1729},"Mehta R, Deepak S, John A, Shine S, Raj V, Balakrishnan V. Takayasu arteritis presenting as chronic mesenteric ischemia. Indian J Gastroenterol. 2004;23:73–4.",{"doi":704},{"id":18,"text":1731,"url":18,"identifiers":1732},"Desai KA, Cotter NM, Doucet L, Veillon DM, Cotelingam JD, Herrera GA, et al. Pathology case of the month. 39-Year-old woman with abdominal pain and weight loss. Takayasu’s arteritis (TA). J La State Med Soc. 2004;156:230–4.",{},{"id":18,"text":1734,"url":18,"identifiers":1735},"Nakao K, Ikeda M, Kimata S, Niitani H, Niyahara M. Takayasu’s arteritis: clinical report of eighty-four cases and immunological studies of seven cases. Circulation. 1967;35:1141–55.",{},{"id":700,"text":1737,"url":702,"identifiers":1738},"Hata J, Haruma K, Suenaga K, Yoshihara M, Yamamoto G, Tanaka S, et al. Ultrasonographic assessment of inflammatory bowel disease. Am J Gastroenterol. 1992;87:443–7.",{"doi":704},{"id":700,"text":1740,"url":702,"identifiers":1741},"Morita Y, Yamamura M, Suwaki K, Mima A, Ishizu T, Hirohata M, et al. Takayasu’s arteritis associated with ulcerative colitis; genetic factors in this association. Intern Med. 1996;35:574–8.",{"doi":704},{"id":18,"text":1743,"url":18,"identifiers":1744},"Maksimowicz-McKinnon K, Hoffman GS. Crohn’s disease plus Takayasu’s arteritis: more than coincidence? Ann Med Interne (Paris). 2003;154:75–6.",{},{"id":700,"text":1746,"url":702,"identifiers":1747},"Taniguchi N, Itoh K, Honda M, Obayashi T, Nakamura M, Kawai F, et al. Comparative ultrasonographic and angiographic study of carotid arterial lesions in Takayasu’s arteritis. Angiology. 1997;48:9–20.",{"doi":704},{"id":700,"text":1749,"url":702,"identifiers":1750},"Tso E, Flamm SD, White RD, Schvartzman PR, Mascha E, Hoffman GS. Takayasu arteritis: utility and limitations of magnetic resonance imaging in diagnosis and treatment. Arthritis Rheum. 2002;46:1634–42.",{"doi":704},{"id":700,"text":1752,"url":702,"identifiers":1753},"Yamada I, Nakagawa T, Himeno Y, Numano F, Shibuya H. Takayasu arteritis: evaluation of the thoracic aorta with CT angiography. Radiology. 1998;209:103–9.",{"doi":704},{"id":1755,"text":1756,"url":1757,"identifiers":1758},"7d716d76-abc5-4d3c-9647-68a32fede2ad","Umekita K, Takajo I, Miyauchi S, Tsurumura K, Ueno S, Kusumoto N, et al. [18F] fluorodeoxyglucose positron emission tomography is a useful tool to diagnose the early stage of Takayasu’s arteritis and to evaluate the activity of the disease. Mod Rheumatol. 2006;16:243–7.","https:\u002F\u002Facademic.oup.com\u002Fmr\u002Farticle-abstract\u002F16\u002F4\u002F243\u002F6313622?redirectedFrom=fulltext",{"doi":1759},"10.1007\u002Fs10165-006-0485-3",{"id":1761,"createTime":1762,"updateTime":1763,"relativeEntities":1764,"slug":1765,"properties":1766,"entityType":115,"verifyStatus":116,"verifyTime":1776,"verifyNote":118,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1777,"fullTextUrl":18,"authors":1778,"publicationType":178,"publisherRelationship":1822,"citationCount":18,"citationInfo":18,"publishDate":1872,"publishYear":422,"citationAnalyzeStatus":232,"lastCitationAnalyze":1873,"indexDatabases":1874,"openAccess":18,"references":18,"isForceReanalyzing":235},"3cc9c33c-b9a6-4e39-811b-c5b26e248587","2024-01-09T00:26:38.125+00:00","2026-05-01T05:08:24.197+00:00",[],"Simultaneous-quantitative-analysis-of-the-expression-of-CD64-and-CD35-on-neutrophils-as-markers-to-differentiate-between-bacterial-and-viral-infections-in-patients-with-rheumatoid-arthritis",{"abstract":1767,"title":1769,"gsPaper":1771,"references":1772,"doi":1774},{"EN":1768},"The expression level of CD64 on neutrophils can be used to differentiate between an infection and a disease flare in rheumatoid arthritis (RA) patients. However, the CD64 expression is elevated by both bacteria and viruses, so it cannot be used to distinguish the type of infection. We herein investigated the results of a simultaneous quantitative analysis of the expression of CD64 and CD35 on neutrophils to determine whether these molecules can be used to distinguish between bacterial and viral infections in RA patients. We collected blood from 22 RA patients with pathogen-proven infections (15 bacterial and 7 viral infections). Blood samples were stained with QuantiBRITE CD64PE\u002FCD45PerCP and CD35PE, and the mean fluorescence intensities were assessed by a flow cytometer. The mean numbers of molecules were calculated using QuantiBrite PE beads. We calculated the ratio of CD64 to the CD35 level (CD35\u002FCD64), and used a cut-off value of 2.8 for the CD35\u002FCD64 ratio. At this value, the sensitivity for diagnosing a bacterial infection was 87%, and the specificity was 86%. Simultaneous quantitative analysis of CD64 and CD35 expression on neutrophils might be useful to distinguish between bacterial and viral infections in RA patients.",{"EN":1770},"Simultaneous quantitative analysis of the expression of CD64 and CD35 on neutrophils as markers to differentiate between bacterial and viral infections in patients with rheumatoid arthritis",{"VOID":112},{"VOID":1773},"Wolfe F, Mitchell DM, Sibley JT, Fries JF, Bloch DA, Williams CA, et al. The mortality of rheumatoid arthritis. Arthritis Rheum. 1994;37:481–94.\nBuckle AM, Hogg N. The effect of IFN-gamma and colony-stimulating factors on the expression of neutrophil cell membrane receptors. J Immunol. 1989;143:2295–301.\nKerst JM, de Haas M, van der Schoot CE, Slaper-Cortenbach IC, Kleijer M, von dem Borne AE, et al. Recombinant granulocyte colony-stimulating factor administration to healthy volunteers: induction of immunophenotypically and functionally altered neutrophils via an effect on myeloid progenitor cells. Blood. 1993;82:3265–72.\nNeuman E, Huleatt JW, Jack RM. Granulocyte-macrophage colony-stimulating factor increases synthesis and expression of CR1 and CR3 by human peripheral blood neutrophils. J Immunol. 1990;145:3325–32.\nCapsoni F, Minonzio F, Colombo G, Ongari AM, Bonara P, Rizzardi GP, et al. Membrane expression and function of complement receptors CR1 and CR3 on neutrophils from HIV-infected subjects: modulation by rTNF-alpha and rGM-CSF. Scand J Immunol. 1992;36:541–6.\nDavis BH, Olsen SH, Ahmad E, Bigelow NC. Neutrophil CD64 is an improved indicator of infection or sepsis in emergency department patients. Arch Pathol Lab Med. 2006;130:654–61.\nNuutila J, Hohenthal U, Laitinen I, Kotilainen P, Rajamaki A, Nikoskelainen J, et al. Simultaneous quantitative analysis of FcgammaRI (CD64) expression on neutrophils and monocytes: a new, improved way to detect infections. J Immunol Methods. 2007;328:189–200.\nFjaertoft G, Hakansson L, Ewald U, Foucard T, Venge P. Neutrophils from term and preterm newborn infants express the high affinity Fcgamma-receptor I (CD64) during bacterial infections. Pediatr Res. 1999;45:871–6.\nNg PC, Li K, Wong RP, Chui KM, Wong E, Fok TF. Neutrophil CD64 expression: a sensitive diagnostic marker for late-onset nosocomial infection in very low birthweight infants. Pediatr Res. 2002;51:296–303.\nAllen E, Bakke AC, Purtzer MZ, Deodhar A. Neutrophil CD64 expression: distinguishing acute inflammatory autoimmune disease from systemic infections. Ann Rheum Dis. 2002;61:522–5.\nMatsui T, Ohsumi K, Ozawa N, Shimada K, Sumitomo S, Shimane K, et al. CD64 on neutrophils is a sensitive and specific marker for detection of infection in patients with rheumatoid arthritis. J Rheumatol. 2006;33:2416–24.\nNishino J, Tanaka S, Kadono Y, Matsui T, Komiya A, Nishimura K, et al. The usefulness of neutrophil CD64 expression in the diagnosis of local infection in patients with rheumatoid arthritis in daily practice. J Orthop Sci. 2010;15:547–52.\nLeino L, Sorvajärvi K, Katajisto J, Laine M, Lilius EM, Pelliniemi TT, et al. Febrile infection changes the expression of IgG Fc receptors and complement receptors in human neutrophils in vivo. Clin Exp Immunol. 1997;107:37–43.\nAlemán M, Beigier-Bompadre M, Borghetti C, de la Barrera S, Abbate E, Isturiz M, et al. Activation of peripheral blood neutrophils from patients with active advanced tuberculosis. Clin Immunol. 2001;100:87–95.\nNuutila J, Hohenthal U, Laitinen I, Kotilainen P, Rajamaki A, Nikoskelainen J, et al. Quantitative analysis of complement receptors, CR1 (CD35) and CR3 (CD11b), on neutrophils improves distinction between bacterial and viral infections in febrile patients: comparison with standard clinical laboratory data. J Immunol Methods. 2006;315:191–201.\nJalava-Karvinen P, Hohenthal U, Laitinen I, Kotilainen P, Rajamäki A, Nikoskelainen J, et al. Simultaneous quantitative analysis of Fc gamma RI (CD64) and CR1 (CD35) on neutrophils in distinguishing between bacterial infections, viral infections, and inflammatory diseases. Clin Immunol. 2009;133:314–23.\nArnett FC, Edworthy SM, Bloch DA, McShane DJ, Fries JF, Cooper NS, et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum. 1988;31:315–24.\nAletaha D, Nell VP, Stamm T, Uffmann M, Pflugbeil S, Machold K, et al. Acute phase reactants add little to composite disease activity indices for rheumatoid arthritis: validation of a clinical activity score. Arthritis Res Ther. 2005;7:R796–806.\nTanaka S, Nishino J, Matsui T, Komiya A, Nishimura K, Tohma S. Neutrophil CD64 expression in the diagnosis of local musculoskeletal infection and the impact of antibiotics. J Bone Jt Surg Br. 2009;91:1237–42.\nQuayle JA, Watson F, Bucknall RC, Edwards SW. Neutrophils from the synovial fluid of patients with rheumatoid arthritis express the high affinity immunoglobulin G receptor, Fc gamma RI (CD64): role of immune complexes and cytokines in induction of receptor expression. Immunology. 1997;91:266–73.\nJones J, Laffafian I, Cooper AM, Williams BD, Morgan BP. Expression of complement regulatory molecules and other surface markers on neutrophils from synovial fluid and blood of patients with rheumatoid arthritis. Br J Rheumatol. 1994;33:707–12.",{"VOID":1775},"10.1007\u002Fs10165-011-0587-4","2024-06-23T11:28:37.374+00:00","https:\u002F\u002Facademic.oup.com\u002Fmr\u002Farticle-abstract\u002F22\u002F5\u002F750\u002F6303838?redirectedFrom=fulltext",[1779,1794,1809],{"id":1780,"sortIndex":19,"researcher":18,"roles":1781,"affiliations":1782,"properties":1791,"displayName":1793,"givenName":18,"familyName":18},"fd858cfc-d9d0-4dfa-90a9-a1bb07810f32",[124],[1783],{"id":1784,"sortIndex":19,"affiliation":1785,"properties":18},"93092117-262d-4cdc-9eff-6b00fc24f228",{"id":1784,"createTime":18,"updateTime":18,"relativeEntities":1786,"slug":18,"properties":1787,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1790,"statistic":18},[],{"title":1788},{"VI":1789},"Department of Internal Medicine, Center for Rheumatic Diseases, Dohgo Spa Hospital, Matsuyama, Japan",[],{"title":1792},{"VI":1793},"Sho Mokuda",{"id":1795,"sortIndex":88,"researcher":18,"roles":1796,"affiliations":1797,"properties":1806,"displayName":1808,"givenName":18,"familyName":18},"78b0439a-4b9e-44b1-986d-9373d327dc4c",[124],[1798],{"id":1799,"sortIndex":19,"affiliation":1800,"properties":18},"b74340c7-c6f1-4155-8d77-5264eb814591",{"id":1799,"createTime":18,"updateTime":18,"relativeEntities":1801,"slug":18,"properties":1802,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1805,"statistic":18},[],{"title":1803},{"VI":1804},"Department of Clinical Laboratory, Center for Rheumatic Diseases, Dohgo Spa Hospital, Matsuyama, Japan",[],{"title":1807},{"VI":1808},"Osamu Doi",{"id":1810,"sortIndex":152,"researcher":18,"roles":1811,"affiliations":1812,"properties":1819,"displayName":1821,"givenName":18,"familyName":18},"3dd0f5f4-fc91-40b7-84e2-1dbb839fd584",[124],[1813],{"id":1784,"sortIndex":19,"affiliation":1814,"properties":18},{"id":1784,"createTime":18,"updateTime":18,"relativeEntities":1815,"slug":18,"properties":1816,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1818,"statistic":18},[],{"title":1817},{"VI":1789},[],{"title":1820},{"VI":1821},"Kiyoshi Takasugi",{"url":1777,"publisher":1823,"properties":1868},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1824,"slug":10,"properties":1825,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1828,"manageAffiliations":1837,"indexDatabases":1848,"url":18,"thumbnailPath":18,"statistic":1863,"gsStatistic":18,"type":18,"analyzePriority":18},[],{"issn":1826,"title":1827},{"VOID":13},{"EN":15},[1829,1833],{"id":22,"createTime":18,"updateTime":18,"relativeEntities":1830,"label":1831,"description":1832,"parentId":18,"standard":18,"scholarHubFieldId":18},[],{"EN":25},{},{"id":28,"createTime":18,"updateTime":18,"relativeEntities":1834,"label":1835,"description":1836,"parentId":18,"standard":18,"scholarHubFieldId":18},[],{"EN":31},{},[1838,1843],{"id":35,"createTime":18,"updateTime":18,"relativeEntities":1839,"slug":18,"properties":1840,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1842,"statistic":18},[],{"title":1841},{"EN":39},[],{"id":42,"createTime":18,"updateTime":18,"relativeEntities":1844,"slug":18,"properties":1845,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1847,"statistic":18},[],{"title":1846},{"EN":46},[],[1849,1856],{"id":50,"indexDatabase":1850,"url":63,"indexYears":18,"academicFieldIds":1855,"indexDatabaseRanking":18},{"id":52,"createTime":18,"updateTime":18,"relativeEntities":1851,"label":1852,"description":1853,"key":59,"publicationTags":1854,"standard":18},[],{"EN":55,"VI":55},{"EN":57,"VI":58},[61,62],[65],{"id":67,"indexDatabase":1857,"url":78,"indexYears":79,"academicFieldIds":1862,"indexDatabaseRanking":83},{"id":69,"createTime":18,"updateTime":18,"relativeEntities":1858,"label":1859,"description":1860,"key":75,"publicationTags":1861,"standard":18},[],{"EN":72,"VI":72},{"EN":72,"VI":74},[77],[81,82],{"impactFactor":19,"impactFactorByYear":1864,"i10Index":19,"i10IndexLast5Year":19,"totalPublication":86,"totalPublicationByYear":1865,"totalCitation":90,"totalCitationByYear":1866,"totalCitationPerPublication":93,"totalCitationPerPublicationByYear":1867,"hindexLast5Year":88,"hindex":88},{},{"2000":88,"2001":88,"2002":89},{"2000":88,"2002":92},{"2000":88,"2002":95},{"pages":1869,"volume":1871},{"VOID":1870},"750-757",{"VOID":1543},"2012-01-12","2026-05-01T05:08:24.196+00:00",[83,61],{"id":1876,"createTime":1877,"updateTime":1878,"relativeEntities":1879,"slug":1880,"properties":1881,"entityType":115,"verifyStatus":116,"verifyTime":1891,"verifyNote":118,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1892,"fullTextUrl":18,"authors":1893,"publicationType":178,"publisherRelationship":1991,"citationCount":18,"citationInfo":18,"publishDate":2041,"publishYear":1212,"citationAnalyzeStatus":232,"lastCitationAnalyze":1878,"indexDatabases":2042,"openAccess":18,"references":18,"isForceReanalyzing":235},"ec9b284a-f773-4fa3-80f0-2d4b62faa389","2023-12-08T14:58:06.799+00:00","2026-04-12T02:23:57.076+00:00",[],"Efficacy-and-safety-of-orally-administered-pilocarpine-hydrochloride-for-patients-with-juvenile-onset-Sj%C3%B6gren-s-syndrome",{"abstract":1882,"title":1884,"gsPaper":1886,"references":1887,"doi":1889},{"EN":1883},"The number of patients with juvenile-onset Sjögren’s syndrome (SS) has recently increased. However, there is no drug that is safe and effective for the xerostomia that occurs in patients of this age group. We evaluated the efficacy and safety of orally administered pilocarpine hydrochloride for juvenile-onset SS patients. Five female patients, aged from 9 to 16 years, received 5–10 mg\u002Fday for 4 weeks. On days 1 and 28, salivary production was measured by the Saxon test, and patients completed subjective self-evaluations of xerostomia symptoms and were asked about changes in water intake and overall improvement of dry mouth on day 28. After 4 weeks of pilocarpine administration, salivary production increased significantly in all patients, and overall status was assessed as “improved” in all patients. One patient had excessive sweating. No serious adverse events or laboratory examination abnormalities correlated with pilocarpine administration were found. In conclusion, the results of this study suggest that orally administered pilocarpine is safe and effective for treating xerostomia in juvenile-onset SS patients. This is the first report of the efficacy of pilocarpine for juvenile SS patients; further evaluations are needed to confirm our result.",{"EN":1885},"Efficacy and safety of orally administered pilocarpine hydrochloride for patients with juvenile-onset Sjögren’s syndrome",{"VOID":112},{"VOID":1888},"Tomiita M, Saito K, Kohno Y, Shimojo N, Fujikawa S, Niimi H. The clinical features of Sjögren’s syndrome in Japanese children. Acta Paediatr Jpn. 1997;39:268–72.\nCimaz R, Casadei A, Rose C, Bartunkova J, Sediva A, Falcini F, et al. Primary Sjögren syndrome in paediatric age: a multicentre survey. Eur J Pediatr. 2003;162:661–5.\nSinger NG, Tomaowa-Soltys I, Lowe R. Sjögren’s syndrome in childhood. Curr Rheumatol Rep. 2008;10:147–55.\nFujibayashi T, Sugai S, Miyasaka N, Hayashi Y, Tsubota K. Revised Japanese criteria for Sjögren’s syndrome (1999): availability and validity. Mod Rheumatol. 2004;14:425–34.\nTaylor P. Cholinergic agonists. In: Gilman AG, Rall TW, Nies AS, Taylor P, editors. Goodman and Gilman’s the pharmacological basis of therapeutics. 8th ed. New York: Pergamon Press; 2004. p. 122–30.\nNaito Y, Matsumoto I, Wakamatsu E, et al. Muscarinic acetylcholine receptor autoantibodies in patients with Sjögren’s syndrome. Ann Rheum Dis. 2005;64:510–1.\nNakamura Y, Wakamatsu E, Matsumoto I, et al. High prevalence of autoantibodies to muscarinic-3 acetylcholine receptor in patients with juvenile-onset Sjögren syndrome. Ann Rheum Dis. 2008;67:136–7.\nJorkjend L, Bergenholtz A, Johansson AK, et al. Effect of pilocarpine on impaired salivary secretion in patients with Sjögren’s syndrome. Swed Dent J. 2008;32:49–56.\nRosas J, Ramos-Casals M, Ena J, et al. Usefulness of basal and pilocarpine-stimulated salivary flow in primary Sjögren’s syndrome. Correlation with clinical, immunological and histological features. Rheumatology. 2002;41:670–5.\nPeluso G, De Santis M, Inzitari R, et al. Proteomic study of salivary peptides and proteins in patients with Sjögren’s syndrome before and after pilocarpine treatment. Arthritis Rheum. 2007;56:2216–22.\nPapas AS, Sherrer YS, Charney M, et al. Successful treatment of dry mouth and dry eye symptoms in Sjögren’s syndrome patients with oral pilocarpine: a randomized, placebo-controlled, dose-adjustment study. J Clin Rheumatol. 2004;10:169–77.\nKuar A, Singla V, Khokhar S, et al. Efficacy of oral pilocarpine in patients with Sjögren’s syndrome. Indian J Rheumatol. 2006;1:93–8.\nSugai S, Koike T, Miyasaka N, et al. Dose-finding study of oral pilocarpine for the treatment of xerostomia associated with Sjögren’s syndrome. Jpn Pharmacol Ther. 2007;35:s141–53.\nKonno A, Nishio M, Origasa H. Oral pilocarpine for radiation-induced xerostomia: a randomized, double-blind, placebo-controlled trial. Jpn Pharmacol Ther. 2007;35:s131–9.",{"VOID":1890},"10.1007\u002Fs10165-010-0313-7","2024-05-15T21:54:56.285+00:00","https:\u002F\u002Fdoi.org\u002F10.3109\u002Fs10165-010-0313-7",[1894,1909,1924,1937,1950,1965,1978],{"id":1895,"sortIndex":19,"researcher":18,"roles":1896,"affiliations":1897,"properties":1906,"displayName":1908,"givenName":18,"familyName":18},"9fc596f4-d9a2-4d4c-a6b0-9c77a3cb89a0",[124],[1898],{"id":1899,"sortIndex":19,"affiliation":1900,"properties":18},"4b4185a4-6a1c-4740-a59b-a6735d5177f0",{"id":1899,"createTime":18,"updateTime":18,"relativeEntities":1901,"slug":18,"properties":1902,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1905,"statistic":18},[],{"title":1903},{"VI":1904},"Department of Pediatrics, Graduate School of Medicine, Chiba University, Chiba, Japan",[],{"title":1907},{"VI":1908},"Minako Tomiita",{"id":1910,"sortIndex":88,"researcher":18,"roles":1911,"affiliations":1912,"properties":1921,"displayName":1923,"givenName":18,"familyName":18},"6234245c-f1f0-4cff-867d-3c997856ec95",[124],[1913],{"id":1914,"sortIndex":19,"affiliation":1915,"properties":18},"36bbdaf7-65e0-4a2f-9993-9bdf978b00fb",{"id":1914,"createTime":18,"updateTime":18,"relativeEntities":1916,"slug":18,"properties":1917,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1920,"statistic":18},[],{"title":1918},{"VI":1919},"Department of Pediatrics, Kagoshima University Medical and Dental Hospital, Kagoshima, Japan",[],{"title":1922},{"VI":1923},"Syuji Takei",{"id":1925,"sortIndex":152,"researcher":18,"roles":1926,"affiliations":1927,"properties":1934,"displayName":1936,"givenName":18,"familyName":18},"f977a94f-c916-442a-8818-cb86df3685e9",[124],[1928],{"id":1914,"sortIndex":19,"affiliation":1929,"properties":18},{"id":1914,"createTime":18,"updateTime":18,"relativeEntities":1930,"slug":18,"properties":1931,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1933,"statistic":18},[],{"title":1932},{"VI":1919},[],{"title":1935},{"VI":1936},"Naomi 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