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ID PMID Title PublicationDate abstract
28899799 Neutrophil extracellular traps (NETs) in autoimmune diseases: A comprehensive review. 2017 Nov Neutrophil extracellular traps (NETs) are fibrous networks which protrude from the membranes of activated neutrophils. NETs are found in a variety of conditions such as infection, malignancy, atherosclerosis, and autoimmune diseases including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV), psoriasis, and gout. Studies suggest that an imbalance between "NETosis," which is a process by which NETs are formed, and NET degradation may be associated with autoimmune diseases. Neutrophils, interleukin-8, ANCA and other inflammatory molecules are considered to play a key role in NET formation. Prolonged exposure to NETs-related cascades is associated with autoimmunity and increases the chance of systemic organ damage. In this review, we discuss the roles of various inflammatory molecules in relation to NETs. We also describe the role of NETs in the pathogenesis of autoimmune diseases and discuss the possibility of using targeted therapies directed to NETs and associated molecules to treat autoimmune diseases.
27903507 Hydroxychloroquine inhibits proinflammatory signalling pathways by targeting endosomal NAD 2017 May OBJECTIVES: Hydroxychloroquine (HCQ) has been used for decades to treat patients with rheumatic diseases, for example, systemic lupus erythematosus (SLE), rheumatoid arthritis or the antiphospholipid syndrome (APS). We hypothesise that HCQ might target endosomal NADPH oxidase (NOX), which is involved in the signal transduction of cytokines as well as antiphospholipid antibodies (aPL). METHODS: For in vitro experiments, monocytic cells were stimulated with tumour necrosis factor α (TNFα), interleukin-1β (IL-1β) or a human monoclonal aPL and the activity of NOX was determined by flow cytometry. The expression of genes known to be induced by these stimuli was quantified by quantitative reverse transcription PCR. Live cell imaging was performed by confocal laser scanning microscopy. Finally, the effects of HCQ on NOX-induced signal transduction were analysed in an in vivo model of venous thrombosis. RESULTS: HCQ strongly reduces or completely prevents the induction of endosomal NOX by TNFα, IL-1β and aPL in human monocytes and MonoMac1 cells. As a consequence, induction of downstream genes by these stimuli is reduced or abrogated. This effect of HCQ is not mediated by direct interference with the agonists but by inhibiting the translocation of the catalytic subunit of NOX2 (gp91phox) into the endosome. In vivo, HCQ protects mice from aPL-induced and NOX2-mediated thrombus formation. CONCLUSIONS: We describe here a novel mechanism of action of HCQ, that is, interference with the assembly of endosomal NOX2. Since endosomal NOX2 is involved in many inflammatory and prothrombotic signalling pathways, this activity of HCQ might explain many of its beneficial effects in rheumatic diseases including the APS.
29696196 Remission induction by Raising the dose of Remicade in RA (RRRR) study: Rationale and stud 2017 Dec Infliximab, an inhibitor of TNF-α, is one of the most widely used biological disease-modifying antirheumatic drugs. Recent studies indicated that baseline serum TNF-α could be considered as a key indicator for optimal dosing of infliximab for RA treatment to achieve the clinical response and its sustained remission. The Remission induction by Raising the dose of Remicade in RA (RRRR) study is an open-label, parallel group, multicenter randomized controlled trial to compare the proportions of clinical remission based on the simplified disease activity index (SDAI) after 1 year of treatment and its sustained remission rate after another 1 year between the investigational treatment strategy (for which the dose of infliximab was chosen based on the baseline serum TNF) and the standard strategy of 3 mg/kg per 8 weeks of infliximab administration in infliximab-naïve patients with RA showing an inadequate response to MTX. The primary endpoint is the proportion of patients who kept discontinuation of infliximab 1 year after discontinued infliximab at the time of 54 weeks after the first administration of infliximab. The secondary endpoints are the proportion of clinical remission based on SDAI and changes in SDAI from baseline at each time point, other clinical parameters, quality of life measures and adverse events. Target sample size of randomized patients is 400 patients in total. The main results of the RRRR study are expected to be published at the end of 2017.
28879043 Fully automated joint space width measurement and digital X-ray radiogrammetry in early RA 2017 OBJECTIVES: To study fully automated digital joint space width (JSW) and bone mineral density (BMD) in relation to a conventional radiographic scoring method in early rheumatoid arthritis (eRA). METHODS: Radiographs scored by the modified Sharp van der Heijde score (SHS) in patients with eRA were acquired from the SWEdish FarmacOTherapy study. Fully automated JSW measurements of bilateral metacarpals 2, 3 and 4 were compared with the joint space narrowing (JSN) score in SHS. Multilevel mixed model statistics were applied to calculate the significance of the association between ΔJSW and ΔBMD over 1 year, and the JSW differences between damaged and undamaged joints as evaluated by the JSN. RESULTS: Based on 576 joints of 96 patients with eRA, a significant reduction from baseline to 1 year was observed in the JSW from 1.69 (±0.19) mm to 1.66 (±0.19) mm (p<0.01), and BMD from 0.583 (±0.068) g/cm(2) to 0.566 (±0.074) g/cm(2) (p<0.01). A significant positive association was observed between ΔJSW and ΔBMD over 1 year (p<0.0001). On an individual joint level, JSWs of undamaged (JSN=0) joints were wider than damaged (JSN>0) joints: 1.68 mm (95% CI 1.70 to 1.67) vs 1.54 mm (95% CI 1.63 to 1.46). Similarly the unadjusted multilevel model showed significant differences in JSW between undamaged (1.68 mm (95% CI 1.72 to 1.64)) and damaged joints (1.63 mm (95% CI 1.68 to 1.58)) (p=0.0048). This difference remained significant in the adjusted model: 1.66 mm (95% CI 1.70 to 1.61) vs 1.62 mm (95% CI 1.68 to 1.56) (p=0.042). CONCLUSIONS: To measure the JSW with this fully automated digital tool may be useful as a quick and observer-independent application for evaluating cartilage damage in eRA. TRIAL REGISTRATION NUMBER: NCT00764725.
27538899 Ganglionic acetylcholine receptor autoantibodies in patients with autoimmune diseases incl 2017 Jul OBJECTIVES: Autonomic dysfunction is closely associated with autoimmune diseases (AID) including primary biliary cirrhosis (PBC). The objective of this study was to determine the prevalence of anti-ganglionic (nicotinic) acetylcholine receptor (gAChR) antibodies in patients with AID. METHODS: We determined the presence of gAChR antibodies in serum samples from 146 patients (systemic lupus erythematosus [SLE] = 32; rheumatoid arthritis [RA] = 43; systemic sclerosis [SSc] = 38; PBC= 33) without information regarding autonomic symptoms, as well as 34 patients with other neurological diseases [OND], and 73 healthy controls [HC]. We specifically analyzed sera for anti-gAChRα3 and -β4 antibodies using the luciferase immunoprecipitation system (LIPS) assay. RESULTS: LIPS assay detected anti-gAChRα3 and -β4 antibodies in the sera from patients with SLE (12.5%, 4/32), RA (18.6%, 8/43), SSc (13.2%, 5/38), PBC (9.1%, 3/33), OND (2.9%, 1/34), and HC (0.0%, 1/73). There were no significant correlations between the levels of anti-gAChRα3 and -β4 antibodies, and the total titers of autoantibodies in AID. CONCLUSIONS: The results demonstrated a significant prevalence of anti-gAChR antibodies in patients with AID, which is independent of the production of other autoantibodies in patients with autoimmune diseases. These anti-gAChR antibodies could mediate the autonomic dysfunction involved in the autoimmune mechanisms of AID.
28633956 A time-adjustable pulsatile release system for ketoprofen: In vitro and in vivo investigat 2017 Oct A time-adjustable pulsatile release system (TAPS) containing ketoprofen (KF) as an active pharmaceutical agent was developed having been designed for bedtime dosing and releasing drug in the early morning to control the symptoms of rheumatoid arthritis (RA). The formulation involved a tablet core (KF) and a control-release layer, and the coating membrane was composed of EC and Eudragit L100. A single-factor study, a central composite design and a response surface method were selected to optimize the formula and the optimum prescription was as follows: tablet core (KF 50mg, MCC 70mg, lactose 40mg, L-HPC 38mg), and film (EC 7.8g, Eudragit L100 4.2g, PEG 6000 1.8g in 95% alcohol each 200ml). The in vivo release behavior of the tablets was evaluated in Beagle dogs after a parallel oral administration of KF TAPS tablets and commercial KF capsules, when it was found that the KF TAPS tablets released the drug after a lag-time of 3.458h and the T(max) was 5.833h. The relative bioavailability was 85.01%, and the two formulations were bioequivalent in terms of C(max) and AUC(0-t) and the in vitro- in vivo correlations indicated that test formulation had a good in vivo-in vitro correlation (r=0.9703). These results show that the novel drug delivery system (TAPS) has the potential to be used as a KF preparation with chronophamacokinetics characteristics.
29066483 Aquaporin-4 Blockage by siRNA Protects Rat Articular Chondrocytes from IL-1β-induced Apop 2017 Sep Accumulating evidence reveals that articular chondrocytes undergo increased apoptosis in rheumatoid arthritis (RA) and inhibiting chondrocyte apoptosis might be a promising therapeutic strategy. We recently found that aquaporin-4 (AQP4) protein level in the cartilage of rats with adjuvant-induced arthritis was higher than normal rats. Herein, cultured rat articular chondrocyte impaired by interleukin-1 beta (IL-1β) was used as an in vitro model of chondrocyte apoptosis. We observed the protective effect of AQP4 blockage by siRNA on IL-1β-induced chondrocyte apoptosis and explored the underlying mechanisms. Our findings revealed that AQP4 siRNA protected articular chondrocytes from IL-1β-induced apoptosis, evidenced by increased cell proliferation (MTT assay), few observations of apoptotic morphologic changes (Hoechst 33258 staining assay) and decreased cell apoptosis rates (Annexin V-FITC/PI staining assay). Additionally, AQP4 siRNA remarkably decreased Bax and caspase 3 mRNA levels and increased Bcl-2 mRNA level, accompanied by reducing phosphorylated-p38 (P-p38) protein level, without affecting p38 protein. The above effects of AQP4 siRNA were similar to SB203580, a specific p38 inhibitor. Together, AQP4 siRNA attenuated IL-1β-induced chondrocyte apoptosis by regulating apoptosis-related gene expressions and inhibiting p38 MAPK. Our results provide experimental evidence that AQP4 inhibition contributes to preventing chondrocyte apoptosis in joint diseases such as RA and provide a novel therapeutic target for RA.
28589321 Latent tuberculosis infection and tuberculosis in patients with rheumatic diseases treated 2017 Aug The introduction of biological agents, especially the tumor necrosis factor inhibitors (anti-TNF), for the treatment of rheumatic diseases increased the risk of developing tuberculosis (TB). Screening for latent TB infection (LTBI) is strongly recommended before starting therapy with anti-TNF agents. The objective of this study was to identify the prevalence of LTBI and TB among patients with rheumatic diseases on anti-TNF agents. This is a cross-sectional study. The electronic medical records of all adult patients (≥18 years old) undergoing anti-TNF treatment were reviewed. Every patient underwent tuberculin skin test (TST) before starting anti-TNF treatment. In total, 176 patients were included; the mean age was 51.9 ± 12.4 years, 34.7% were males, and 90.9% were white. The underlying diseases were rheumatoid arthritis (RA) in 50.6% (N = 89), ankylosing spondylitis (AS) in 27.8% (N = 49), and psoriatic arthritis (PsA) in 17.6% (N = 31). The prevalence of positive TST was 29.5%. Household contact with TB was significantly associated with a positive TST (p = 0.020). RA patients had lower TST reactions than AS patients (p = 0.022). There were six cases of TB (3.4%) diagnosed during anti-TNF therapy. We demonstrated a high prevalence of positive TST (29.5%) among patients with rheumatic diseases in a region with high TB prevalence. Our data corroborates the ACR's recommendation that patients who live in high TB incidence settings should be tested annually for LTBI.
31644093 Gold Preparations. 2012 Gold salts, including auranofin and gold sodium thiomalate, have been used for the therapy of rheumatoid arthritis for many decades, but have recently been replaced by more modern disease-modifying antirheumatic drugs. Parenteral gold therapy (chrysotherapy) can cause acute, clinically apparent hepatitis that is usually cholestatic and self-limited in nature, but can be severe and even fatal. In contrast, oral gold preparations (such as auranofin) are associated with a low rate of serum enzyme elevations during treatment, but have not been convincingly linked to clinically apparent liver injury.
28542532 Correction: Comorbidities of rheumatoid arthritis: Results from the Korean National Health 2017 [This corrects the article DOI: 10.1371/journal.pone.0176260.].
28779588 Erratum regarding inaccurate authorship attributions noted. 2017 May For the paper entitled Pain improvement in rheumatoid arthritis with hyperbaric oxygen: report of three cases,' which appeared in the July-August 2016 issue of UHM (43-4), author attributions read as: John B. Slade MD, Mary V. Potts RN, Alan M. Flower DO, Michelle T. Sit MD, Thomas W. Schmidt MD. Undersea Hyperb Med. 2016 Jul-Aug; 43(4): 467-472. The corrected authorship reads as: John B. Slade MD, Mary V. Potts RN, Alan M. Flower DO, Karen M. Sky, MD, FACP, FACR, Michelle T. Sit MD, Thomas W. Schmidt MD. Undersea Hyperb Med. 2016 Jul-Aug; 43(4): 467-472. Dr. Karen M. Sky was inadvertently deleted from the list of authors. UHM apologizes for the omission.
27635862 Early Subchondral Bone Loss at Arthritis Onset Predicted Late Arthritis Severity in a Rat 2017 Jun Synovitis is usually observed before loss of articular function in rheumatoid arthritis (RA). In addition to the synovium and according to the "Inside-Outside" theory, bone compartment is also involved in RA pathogenesis. Then, we investigated time dependent articular bone loss and prediction of early bone loss to late arthritis severity on the rat adjuvant-induced arthritis (AIA) model. Lewis female rats were longitudinally monitored from arthritis induction (day 0), with early (day 10) and late (day 17) steps. Trabecular and cortical microarchitecture parameters of four ankle bones were assessed by microcomputed tomography. Gene expression was determined at sacrifice. Arthritis occurred at day 10 in AIA rats. At this time, bone erosions were detected on four ankle bones, with cortical porosity increase (+67%) and trabecular alterations including bone volume fraction (BV/TV: -13%), and trabecular thickness decrease. Navicular bone assessment was the most reproducible and sensitive. Furthermore, strong correlations were observed between bone alterations at day 10 and arthritis severity or bone loss at day 17, including predictability of day 10 BV/TV to day 17 articular index (R(2)  = 0.76). Finally, gene expression at day 17 confirmed massive osteoclast activation and interestingly provided insights on strong activation of bone formation inhibitor markers at the joint level. In rat AIA, bone loss was already observed at synovitis onset and was predicted late arthritis severity. Our results reinforced the key role of subchondral bone in arthritis pathogenesis, in favour to the "Inside-Outside" theory. Mechanisms of bone loss in rat AIA involved resorption activation and formation inhibition changes. J. Cell. Physiol. 232: 1318-1325, 2017. © 2016 Wiley Periodicals, Inc.
28530020 Golimumab: A Review in Inflammatory Arthritis. 2017 Jun Golimumab (Simponi(®)), a fully human monoclonal antibody against tumour necrosis factor-alpha (TNFα), is given once monthly by subcutaneous injection. In the EU, golimumab is approved as monotherapy and/or in combination with methotrexate for the treatment of inflammatory arthritis, including rheumatoid arthritis (RA), psoriatic arthritis (PsA) and axial spondyloarthritis [comprising ankylosing spondylitis (AS) and non-radiographic axial spondyloarthritis (nr-axSpA)] in adults, and polyarticular juvenile idiopathic arthritis (pJIA) in children. These approvals were based on the observations that golimumab was generally well tolerated and conferred some or all of the following benefits in pivotal studies in these settings: reduced signs and symptoms of arthritis; improved physical functioning and health-related quality of life; and slowed radiographic progression. Of note, data from long-term extensions (LTEs) of pivotal studies in RA, PsA and AS have confirmed that the safety and efficacy of golimumab are sustained through 5 years of treatment; the long-term tolerability profile of the drug is similar to that of other TNFα inhibitors (TNFis). Like other subcutaneous TNFis, golimumab offers patients the convenience and flexibility of home-based self-injection, although it has the added potential advantage of requiring less frequent administration, in particular compared with older, first generation agents, such as etanercept and adalimumab. Thus, golimumab is an effective, generally well tolerated and potentially convenient option for the treatment of RA, PsA, AS and nr-axSpA in adults, and pJIA in children.
28988489 Fatty infiltration of the minor salivary glands is a selective feature of aging but not Sj 2017 Dec OBJECTIVE: Determine the presence and assess the extent of fatty infiltration of the minor salivary glands (SG) of primary SS patients (pSS) as compared to those with non-SS sicca (nSS). METHODS: Minor SG biopsy samples from 134 subjects with pSS (n = 72) or nSS (n = 62) were imaged. Total area and fatty replacement area for each glandular cross-section (n = 4-6 cross-sections per subject) were measured using Image J (National Institutes of Health, Bethesda, MD). The observer was blinded to subject classification status. The average area of fatty infiltration calculated per subject was evaluated by logistic regression and general linearized models (GLM) to assess relationships between fatty infiltration and clinical exam results, extent of fibrosis and age. RESULTS: The average area of fatty infiltration for subjects with pSS (median% (range) 4.97 (0.05-30.2)) was not significantly different from that of those with nSS (3.75 (0.087-41.9). Infiltration severity varied widely, and subjects with fatty replacement greater than 6% were equivalently distributed between pSS and nSS participants (χ(2) p = .50). Age accounted for all apparent relationships between fatty infiltration and fibrosis or reduced saliva flow. The all-inclusive GLM for prediction of pSS versus non-SS classification including fibrosis, age, fatty replacement, and focus score was not significantly different from any desaturated model. In no iteration of the model did fatty replacement exert a significant effect on the capacity to predict pSS classification. CONCLUSIONS: Fatty infiltration is an age-associated phenomenon and not a selective feature of Sjögren's syndrome. Sicca patients who do not fulfil pSS criteria have similar rates of fatty infiltration of the minor SG.
28528377 Correlation between corneal innervation and inflammation evaluated with confocal microscop 2017 Sep PURPOSE: To evaluate corneal innervation and inflammatory cell infiltration using in vivo confocal microscopy (IVCM) and to correlate these findings with subjective symptoms of dry eye, as measured by the Ocular Surface Disease Index (OSDI) in patients with non-Sjögren's (NSDE) and Sjögren's syndrome dry eyes (SSDE). METHODS: Central corneal images were prospectively captured from 10 age-matched healthy control eyes, 24 eyes with clinically diagnosed NSDE and 44 eyes with clinically diagnosed SSDE, using IVCM (HRT III RCM). Density, tortuosity and reflectivity of corneal nerves, presence of inflammatory dendritic cells (DCs) and OSDI scores were evaluated. RESULTS: Images obtained by IVCM from 78 eyes were analyzed. The density of nerve fibers was 1562 ± 996 μm/frame in the SSDE group, 2150 ± 1015 μm/frame in the NSDE group and 2725 ± 687 μm/frame in the control group (P < 0.05, ANOVA). In comparison to the control group, the density of nerve fibers was decreased in the SSDE (P < 0.001) and the NSDE groups (P = 0.06), with increased nerve tortuosity and decreased reflectivity in both groups (both P < 0.05). The density of DCs was 71.65 ± 72.54 cells/mm(2) in the SSDE group, 40.33 ± 31.63 cells/mm(2) in the NSDE group and 27.53 ± 5.58 cells/mm(2) in the control group (P < 0.05, ANOVA). In comparison to the control group, the density of DCs was increased in the SSDE (P < 0.001) and the NSDE groups (P = 0.07). Significant correlations were found between the nerve density and DC density (r = -0.57, P < 0.001), between the nerve density and OSDI scores (r = -0.91, P < 0.001) and between the nerve reflectivity and OSDI scores (r = -0.75, P < 0.001). CONCLUSIONS: The corneas of eyes affected with NSDE and SSDE are characterized by alterations in corneal innervation and infiltration of inflammatory DCs. Corneal nerve density and reflectivity are correlated with severity of subjective dry eye symptoms, as measured by OSDI score.
28476437 Sjogren's syndrome from the perspective of ophthalmology. 2017 Sep Sjogren's syndrome (SS) is an autoimmune disease affecting the lacrimal glands resulting in dry eye disease (DED). Ophthalmologists may be the first line of detection of Sjogren's syndrome given the frequency of DED in SS and that dry eye is often the presenting symptom. Numerous symptom questionnaires and tests have been developed to help diagnose DED, but as of yet, there is no "gold standard." Minimally invasive objective metrics are needed for a reliable diagnosis of DED. Currently there is no single test to diagnose SS-associated DED. Although there are several approaches to treatment, none are specific for DED in SS, and, generally, several methods need to be tried to find what works best for a specific patient. Treatment for DED continues to be an unmet medical need, especially given that DED in SS is typically on the severe end of the spectrum.
28532741 Coexistence of sarcoidosis and adult onset Still disease. 2019 Sep Sarcoidosis is a chronic, inflammatory disease with unknown cause characterized by non-caseating granuloma formations. It can be presented with bilateral hilar lymphadenopathy, skin lesions, eye involvement and locomotor system findings. Adult onset Still disease (AOSD) is a chronic inflammatory disease which presents with fever, arthritis and typical skin rashes. The disease is rare and can be misdiagnosed due to the absence of typical clinical and laboratory findings. The association of sarcoidosis and AOSD has not been previously reported in the literature. Herein we reported the development of AOSD in a patient followed by the diagnosis of sarcoidosis. The patient did not respond to high-dose corticosteroids and methotrexate therapy, and the disease was under control with anti-IL-6 (Tocilizumab) drug.
28460510 [Coexistence of sarcoidosis and primary Sjögren syndrome: a clinical analysis and literat 2017 May 1 Four patients with coexistence of sarcoidosis and primary Sjögren syndrome (pSS) were retrospectively analyzed.All patients were female, who were referred to our department mainly because of respiratory symptoms.Positive antinuclear antibody(ANA) was detected in 2 patients and anti-Sjögrens syndrome A (SSA) antibody positive in 1 patient.All patients presented specific histologic patterns of both sarcoidosis and pSS.Publications related to coexistence of these two diseases were reviewed.Forty-one patients were finally included in the analysis, among whom 37 confirmed patients were from literature search.There were 37 women and 4 men.The main clinical features presentation were xerophthalmia in 40, xerostomia in 38, hilaradenopathies in 28, interstitial lung disease in 15, respiratory symptoms in 13.The main immunologic data were positive ANA in 23, SSA antibody in 19, anti-Sjögrens syndrome B antibody in 10 and rheumatoid factor in 12.All patients presented specific histologic patterns of both diseases.Patients with both sarcoidosis and pSS of ten represent multisystemic involvement and positive immunologic parameters, as well as the dual expression of specific histologic characteristics.
28425227 Primary Sjögren's syndrome in patients with celiac disease. 2017 Apr 18 BACKGROUND/AIM: Many autoimmune diseases occur concomitantly with celiac disease (CD). We aimed to determine the frequency of Sjögren's syndrome (SS) in CD patients based on SS-specific serology verified by minor labial salivary biopsy. MATERIALS AND METHODS: Eight-two patients with CD were included in the study. After examination for objective evidence of sicca complex, all patients were tested for serological presence of rheumatoid factor (RF) and antinuclear antibodies (ANAs) and for ANA profile. Minor labial salivary biopsy was performed for patients with positive serology and/or clinical signs of SS. RESULTS: Of the patients included, 24 (29.3%) had dry eye symptoms while 20 (24.4%) had dry mouth symptoms. Dry eye was detected by Schirmer test in 10 patients (12.2%) and by ocular staining score in only 2 patients (2.4%). All samples were negative for RF while 12 (14.6%) samples were positive for ANAs. Of 82 patients with CD, the diagnosis of SS was established in only one patient (1.2%), while one patient (1.2%) was diagnosed with morphea and 4 patients (4.9%) were classified as having undifferentiated connective tissue disease. CONCLUSION: The prevalence of SS in CD is low, so there is no need for serologic screening of all patients with CD for SS.
27817092 Comparisons of presentations and outcomes of neuromyelitis optica patients with and withou 2017 Feb Patients with neuromyelitis optica (NMO) often have an accompanying autoimmune disease, most commonly, but not limited to Sjögren's syndrome (SS). The aim of this study was to compare clinical and laboratory features between NMO patients with and without SS and to investigate the prognosis of NMO in patients with and without SS. Twenty-three NMO patients with SS and 42 NMO patients without SS were included. Clinical and laboratory profiles were compared, including annual relapse rate and time from onset of NMO to Expanded Disability Status Scale (EDSS) scores of 4.0 and 6.0. More NMO patients with SS than those without SS had anti-nuclear antibody, anti-SS-A/Ro and anti-SS-B/La antibodies (91.3 vs. 35.7%, p < 0.001, 87.0 vs. 2.3%, p < 0.001, and 34.8 vs. 0.0%, p < 0.001, respectively). Serum immunoglobulins (IgA, IgM and IgG) were markedly increased in NMO patients with SS in comparison with those without SS. Annual relapse rate and the time from disease onset to an EDSS score of 4.0 and 6.0 were not significantly different between the two groups. No differences between the two groups were found for the other parameters, including AQP-4 antibody status, length of spinal cord lesion and brain lesions. These results imply that NMO in SS more likely represents coexistence with SS rather than representing the result of direct central nervous system involvement in SS. Autoimmune response appears to be more intense in the NMO group with SS, but did not cause a more severe prognosis in comparison with the group without SS, indicating that we should pay attention to the potential benefit of the antinuclear antibodies in NMO.