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We aimed to describe the clinical profiles and high-risk indicators of primary Sj\u00f6gren\u2019s syndrome (pSS) patients with central nervous system (CNS) involvement (pSS-CNS).<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>A total of 412 participants with pSS from a hospital in China from January 2012 to December 2019 were enrolled in the retrospective study. 42 pSS-CNS patients were compared with 370 pSS patients without CNS involvement. The clinical features, laboratory examinations, imaging characteristics, and treatment of the pSS-CNS cases were systematically analyzed. Potential risk factors related to pSS-CNS patients were identified by multivariate logistic regression analysis.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>The prevalence of central nervous system involvement in the studied pSS patients was 10.2% (42\/412), with 31.3% (14\/42) of pSS patients having neurological manifestations as the initial symptom. The manifestations of hemiparesis (35.7%, 15\/42), paraparesis (28.6%, 12\/42), dysphonia (31.0%, 13\/42), blurred vision (21.4%, 9\/42), and dysfunctional proprioception (23.8%, 10\/42) were more common in the pSS-CNS patients. Cerebral infarction (57.1%, 24\/42), demyelination (31.0%, 13\/42), myelitis (23.8%, 11\/42), and angiostenosis (21.4%, 9\/42) were most often found on MRI or CT scan imaging in the pSS-CNS patients. Intrathecal IgG level and total protein of cerebrospinal fluid were increased in 50% (8\/16) of the pSS-CNS group. In comparison with patients without CNS involvement, the pSS-CNS patients were found to also have kidney and lung involvement, hematologic abnormalities, positive ANA and anti-SSA antibody tests, and reduced complement 3 (C3) and complement 4 (C4) levels (all <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05). The prevalence of lung involvement, immune thrombocytopenia, and high-titer ANA (1:1000) were significantly higher in pSS-CNS disease activity compared to those in the moderately active group. Multivariate analysis identified lung involvement, anti-SSA positivity, and low C3 levels as prognostic factors for pSS-CNS. After high-dose glucocorticoids and immunosuppressive therapy, 60.5% (26\/38) of pSS-CNS patients improved, 36.8% (14\/38) were unresponsive to treatment, and 2.6% (1\/38) died.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>Clinical features are diverse in pSS-CNS patients, and the morbidity rate is low. CNS involvement was the initial presentation in state percentage here pSS patients. Pulmonary involvement, a positive anti-SSA antibody test, and reduced C3 levels are potential risk factors for CNS involvement in pSS. Treatment with high-dose glucocorticoids and immunosuppressive therapy appeared effective in 60% of pSS-CNS patients.<jats:table-wrap><jats:table><jats:tbody>\n                      <jats:tr>\n                        <jats:td colspan=\"2\"><jats:bold>Key Points<\/jats:bold><jats:italic>\u2022 The CNS manifestations of pSS are diverse, and CNS imaging and CSF analysis are important for the diagnosis.<\/jats:italic><jats:italic>\u2022 Pulmonary involvement, positive anti-SSA, and reduced C3 levels are potential risk factors of pSS-CNS.<\/jats:italic><jats:italic>\u2022 About 60% of pSS-CNS patients were responsive to high-dose glucocorticoid administration and immunosuppressive therapy.<\/jats:italic><\/jats:td>\n                      <\/jats:tr>\n                    <\/jats:tbody><\/jats:table><\/jats:table-wrap><\/jats:p>\n              <\/jats:sec>","DOI":"10.1007\/s10067-022-06448-w","type":"journal-article","created":{"date-parts":[[2022,11,19]],"date-time":"2022-11-19T02:02:32Z","timestamp":1668823352000},"page":"443-451","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Clinical features and high-risk indicators of central nervous system involvement in primary Sj\u00f6gren\u2019s syndrome"],"prefix":"10.1007","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0467-4355","authenticated-orcid":false,"given":"Wei","family":"Fan","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennefer","family":"Par-Young","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaiyan","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pingping","family":"Xiao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Hua","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lin","family":"Leng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuyan","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard","family":"Bucala","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2022,11,19]]},"reference":[{"issue":"10","key":"6448_CR1","doi-asserted-by":"publisher","first-page":"931","DOI":"10.1056\/NEJMcp1702514","volume":"378","author":"X Mariette","year":"2018","unstructured":"Mariette X, Criswell LA (2018) Primary Sj\u00f6gren\u2019s syndrome[J]. 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