Primary Sjögren syndrome‐related peripheral neuropathy: A systematic review and meta‐analysis

Liampas, Andreas; Parperis, Konstantinos; Erotocritou, Maria Faidra; Nteveros, Antonios; Papadopoulou, Marianna; Moschovos, Christos; Akil, Mohammed; Coaccioli, Stefano; Hadjigergiou, Georgios M.; Hadjivassiliou, Marios; Zis, Panagiotis

doi:10.1111/ene.15555

Cited by 26 publications

(16 citation statements)

References 72 publications

(301 reference statements)

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“…Gemignani et al suggested increasing age as a risk factor for the development of polyneuropathy in pSS patients [ 14 ]. Liampas et al also observed increasing age as one of risk factors for developing PN [ 15 ]. A possible explanation is microangiopathic changes in the endoneurial vessels [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

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Analysis of clinical features and risk factors of peripheral neuropathy in patients with primary Sjögren's syndrome

Wang

Chen

et al. 2023

Eur J Med Res

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Objective To observe the clinical features and efficacy of immunosuppressive therapy in patients with primary Sjögren's syndrome (PSS) combined with peripheral neuropathy (PN) syndrome and to explore the risk factors for PN in patients with PSS. Methods Sixty consecutive patients with PSS admitted to the Department of Rheumatology and Immunology, Wuhan No. 1 Hospital, from January 2014 to June 2020 were analysed retrospectively. Patients were divided into a PN group (N = 15) and a non-PN group (N = 45). The clinical characteristics of the two groups were compared, and the independent risk factors for PN combined with PSS were analysed by multivariate logistic regression. The patients with PSS combined with PN were followed up to observe the effect of immunosuppressive therapy. Results The patients with PN had a longer course of disease than those without PN (z = − 3.225, P = 0.001), and the incidence of Raynaud's phenomenon, anti-SSB antibody, rheumatoid factor and hyperglobulinaemia was higher (all P < 0.05) in patients with PN than in those without PN. Multivariate logistic regression analysis showed that hyperglobulinaemia, RF and anti-SSB antibodies were independent risk factors for PN with PSS (P < 0.05). Fourteen patients with PSS-PN were treated with immunosuppressants. The clinical symptoms of 10 patients were relieved, and mRS scores of 10 patients were decreased. Conclusion PN is a common complication in PSS patients. Patients with PSS combined with PN have a longer course of disease and a significantly higher percentage of Raynaud's phenomenon, positive anti-SSB antibody, positive RF and hyperglobulinaemia. Immunosuppressive therapy was effective for partial remission of PN with PSS.

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Section: Discussionmentioning

confidence: 99%

“…The recently published EULAR recommendations suggest first-line immunosuppressive therapy in patients with axonal sensory polyneuropathy [ 24 ]. Glucocorticoids are the most commonly used treatment option of managing pSS-related PN, when associated with vasculitis, followed by the use of IVIG [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

Analysis of clinical features and risk factors of peripheral neuropathy in patients with primary Sjögren's syndrome

Wang

Chen

et al. 2023

Eur J Med Res

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“…Sjogren's syndrome (SS) is a high-rate, common, and harmful global disease with higher potential morbidity and is an essential menopausal and aging disease [34][35][36]. The disease is characterized by xerostomia with dysfunction of salivary gland secretion as the initiating factor, which affects the whole body's health [37][38][39].…”

Section: Discussionmentioning

confidence: 99%

The Critical Biomarkers Identification of Insulin Signaling Involved in Initiating cAMP Signaling Mediated Salivary Secretion in Sjogren Syndrome: Transcriptome Sequencing in NOD Mice Model

et al. 2022

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Background Sjogren’s syndrome (SS) is an autoimmune disorder characterized by the destruction of exocrine glands, resulting in dry mouth and eyes. Currently, there is no effective treatment for SS, and the mechanisms associated with inadequate salivary secretion are poorly understood. Methods In this study, we used NOD mice model to monitor changes in mice’s salivary secretion and water consumption. Tissue morphology of the submandibular glands was examined by H&E staining, and Immunohistochemical detected the expression of AQP5 (an essential protein in salivary secretion). Global gene expression profiling was performed on submandibular gland tissue of extracted NOD mice model using RNA-seq. Subsequently, a series of bioinformatics analyses of transcriptome sequencing was performed, including differentially expressed genes (DEGs) identification, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, PPI network construction, hub gene identification, and the validity of diagnostic indicators using the dataset GSE40611. Finally, IFN-γ was used to treat the cells, the submandibular gland tissue of NOD mice model was extracted, and RT-qPCR was applied to verify the expression of hub genes. Results We found that NOD mice model had reduced salivary secretion and increased water consumption. H&E staining suggests acinar destruction and basement membrane changes in glandular tissue. Immunohistochemistry detects a decrease in AQP5 immunostaining within acinar. In transcriptome sequencing, 42 overlapping DEGs were identified, and hub genes (REN, A2M, SNCA, KLK3, TTR, and AZGP1) were identified as initiating targets for insulin signaling. In addition, insulin signaling and cAMP signaling are potential pathways for regulating salivary secretion and constructing a regulatory relationship between target-cAMP signaling-salivary secretion. Conclusion The new potential targets and signal axes for regulating salivary secretion provide a strategy for SS therapy in a clinical setting.

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“…This caused a great quantity of proin ammatory lymphocyte in ltration, when the SG tissue chemokines of NOD mice increased signi cantly, such as Th17 cells in ltrating into SG tissue, and the in ltrating pro-in ammatory lymphocytes will secrete pro-in ammatory cytokines to form a vicious circle, leading to the permanence of autoimmunity. Massive lymphocyte in ltration leads to decreased secretion of the affected gland [35,36]. We found that the increase of CD4 + GRK2, Th17 + CXCR3 in mice spleen promoted lymphocyte in ltration into SG tissue, and a large number of Th17 cells appear in SG tissues and peripheral tissues of mice, Treg cells are reduced, and the proportion of Th17/Treg cells is out of balance, it promotes the progression of pSS.…”

Section: Discusstionmentioning

confidence: 94%

CXCL9, 10, 11/CXCR3 Axis Contributes to the Progress of Primary Sjogren’s Syndrome by Activating GRK2 to Promote T Lymphocyte Migration

Zhang

Shi

et al. 2023

Inflammation

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Primary Sjogren's syndrome (pSS) is a systemic autoimmune disease that causes dysfunction of secretory glands and the speci c pathogenesis is still unknown. The CXCL9, 10, 11/CXCR3 axis and G protein-coupled receptor kinase 2 (GRK2) involved in many in ammation and immunity processes. We used NOD/Ltj mice, a spontaneous SS animal model, to elucidate the pathological mechanism of CXCL9, 10, 11/CXCR3 axis promoting T lymphocyte migration by activating GRK2 in pSS. We found that CD4+GRK2, Th17+CXCR3 was apparently increased and Treg+CXCR3 was signi cantly decreased in the spleen of 4W NOD mice without sicca symptom compared to ICR mice (control group). The protein levels of IFN-γ, CXCL9, 10, 11 increased in submandibular gland (SG) tissue accompanied by obvious lymphocytic in ltration and Th17 cells overwhelmingly in ltrated relative to Treg cells at the sicca symptom occurs, and we found that the proportion of Th17 cells was increased, whereas that of Treg cells was decreased in spleen. In vitro, we used IFN-γ to stimulate human salivary gland epithelial cells (HSGECs) co-culture with Jurkat cells, and the results showed that CXCL9, 10, 11 was increased by IFN-γ activates JAK2/STAT1 signal pathway and Jurkat cells migration increased with the raised of cell membrane GRK2 expression. HSGECs with tofacitinib or Jurkat cells with GRK2 siRNA can reduce the migration of Jurkat cells. The results indicate that CXCL9, 10, 11 signi cantly increased in SG tissue through IFN-γ stimulating HSGECs, and the CXCL9, 10, 11/CXCR3 axis contributes to the progress of pSS by activating GRK2 to promote T lymphocyte migration.

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Primary Sjögren syndrome‐related peripheral neuropathy: A systematic review and meta‐analysis

Abstract: This is a repository copy of Primary Sjögren syndrome-related peripheral neuropathy: a systematic review and meta-analysis.

Cited by 26 publications

References 72 publications

Analysis of clinical features and risk factors of peripheral neuropathy in patients with primary Sjögren's syndrome

Analysis of clinical features and risk factors of peripheral neuropathy in patients with primary Sjögren's syndrome

The Critical Biomarkers Identification of Insulin Signaling Involved in Initiating cAMP Signaling Mediated Salivary Secretion in Sjogren Syndrome: Transcriptome Sequencing in NOD Mice Model

CXCL9, 10, 11/CXCR3 Axis Contributes to the Progress of Primary Sjogren’s Syndrome by Activating GRK2 to Promote T Lymphocyte Migration

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