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ID PMID Title PublicationDate abstract
25414217 Unusual presentation of Sjögren's syndrome. 2014 Nov 20 We present a case of a 67-year-old woman admitted from the neurology clinic for further investigations of progressive ataxia and sensory symptoms. Neurological examination showed reduced pinprick and absent vibration sensations in the lower limbs. Motor system examination was normal. Her antinuclear antibodies titre was 1:100 with positive Ro antibodies. Her initial nerve conduction studies were normal. However, the lower limb somatosensory-evoked potentials (SSEP) demonstrated impairment of central sensory conduction pathway. Rheumatology review revealed a history of fatigue and Sicca symptoms and her Schirmer's test was strongly positive. This lead to the diagnosis of ganglionopathy associated to Sjögren's syndrome. She had an excellent response to intravenous methylprednisolone followed by oral prednisolone and intravenous cyclophosphamide infusions. This case highlights that dorsal column involvement can precede the diagnosis of primary Sjögren's syndrome.
24668540 Pulmonary involvement in Sjögren syndrome. 2014 Apr Sjögren syndrome (SS) is a chronic autoimmune disease characterized by lymphocytic inflammation of exocrine glands and a variety of extraglandular sites. Lung involvement as defined by symptoms and either pulmonary function testing or radiographic abnormalities occurs in approximately 10 to 20% of patients. Subclinical lung disease is even more frequent and often includes evidence of small airways disease and airway inflammation. In general, patients will have evidence of both airway and interstitial lung disease by radiographs and pathology. Bronchiolitis and bronchiectasis are the most common airway manifestations while the interstitial pathologies associated with SS include nonspecific interstitial pneumonitis, usual interstitial pneumonitis, and lymphocytic interstitial pneumonitis. Patients with SS are also at an increased risk of lymphoma. A protean of other lung abnormalities including amyloidosis, granulomatous lung disease, pseudolymphoma, pulmonary hypertension, and pleural disease have been described.
23845207 B-cell activating factor genetic variants in lymphomagenesis associated with primary Sjogr 2014 Jun Primary Sjogren's syndrome (pSS) is complicated by B-cell lymphoma in 5-10% of patients. Several clinical and serological features are proposed as adverse predictors for such complication and define a high risk pSS phenotype. We aimed to explore whether previously described polymorphisms of the B-cell activating factor (BAFF) could be related to pSS-related lymphomagenesis. Five single nucleotide polymorphisms (SNPs) of the BAFF gene (rs1224141, rs12583006, rs9514828, rs1041569 and the rs9514827) were evaluated in 111 low risk pSS patients (type II), 82 high risk/lymphoma patients (type I) and 137 healthy controls (HC) by PCR-based assays. The classification of pSS patients into types I and II was based on the presence or absence of risk factors or lymphoma development, respectively. Genotype and haplotype analysis was performed for all variants in the pSS groups. Since the rs1041569 SNP was not in Hardy-Weinberg equilibrium in the HC group (p < 0.001), haplotype analysis was performed in the remaining four out of the five SNPs tested when comparisons with HC individuals were performed. The high risk pSS group was characterized by higher frequency of the minor T allele of the rs9514828 BAFF polymorphism compared to HC. Compared to the low risk pSS patients but not the HC, the high risk pSS group exhibited lower frequencies of the AA genotype of the rs12583006 polymorphism as well as the TACAC and TACC haplotypes and higher frequency of the TTTC haplotype. The low risk pSS group exhibited higher frequency of the minor A allele and AA genotype of the rs12583006 variant compared to HC. Both pSS groups were characterized by increased frequency of the haplotype TATT and GTTC and decreased frequency of the TTCT when compared to HC. Taken together, these findings suggest the implication of the host's genetic background in pSS-related lymphomagenesis. The interaction of pSS-related BAFF gene haplotypes together with distinct BAFF genetic variants appears to contribute to this complication.
23791632 Systemic sclerosis at the crossroad of polyautoimmunity. 2013 Sep OBJECTIVES: Several epidemiological studies have revealed the co-occurrence of other autoimmune diseases (AIDs) within patients with systemic sclerosis (SSc). However, some of these studies were based on small cohorts and wide ranges of prevalence have been reported. Therefore to overcome these limitations of individual studies, we sought to perform a meta-analysis to determine the accurate prevalence of polyautoimmunity in SSc. METHODS: We performed a systematic review and a meta-analysis of literature in MEDLINE and Embase databases from January 1960 to March 2013. All cohort studies reporting on prevalence of other AIDs known to be associated with SSc were analyzed. Prevalence of polyautoimmunity and of each AID were then calculated. RESULTS: Ten studies reporting polyautoimmunity were identified corresponding to a total of 6102 SSc patients. Overall 1432 patients with at least one AID were identified corresponding to a weighted prevalence of polyautoimmunity equal to 25.7% CI 95% [20.1%-31.6%]. Overall 208/5139 SSc-patients had at least two additional AIDs resulting in a weighted prevalence of 3.9% [3.3%-4.4%]. The most prevalent associated AIDs were autoimmune thyroid disease (10.4%) followed by Sjögren's syndrome (7.7%) and dermatopolymyositis/polymyositis (5.6%). CONCLUSION: Our results confirm that SSc polyautoimmunity is a frequent condition in SSc affecting a quarter of SSc-patients. The impact on the phenotype and also on the management and therapy will need to be addressed now in further works.
23664530 Clinical features distinguishing lymphoma development in primary Sjögren's Syndrome--a re 2013 Oct OBJECTIVE: The objective is to determine the relationship between clinical features and non-Hodgkin lymphoma (NHL) development in primary Sjögren's Syndrome (pSS), taking recently designed disease activity/severity scores into account. METHODS: Medical charts of pSS patients were retrospectively analyzed, scoring first and last visits with the (cumulative) EULAR Sjögren's Syndrome Disease Activity Index and counting extraglandular manifestations, comparing patients with and without NHL. RESULTS: One hundred ninety-five patients were analyzed with a median follow-up of 92 months (range 12-256). Twenty-one patients (11%) had NHL. Associations of parotid gland enlargement (OR 2.84) and low C4 (OR 7.71) with NHL were confirmed. In NHL patients, development of purpura, peripheral neuropathy (PNP), and glomerulonephritis (GN) concurred with lymphoma in 3/3, 5/7, and 2/2 of cases, respectively. Otherwise, purpura and PNP were not associated with NHL later on. This suggests that these symptoms might represent paraneoplastic events (in 16%, 24%, and 100% of our cases, respectively). Presence of IgM-kappa clonal components was associated with lymphoma in 64% of cases. Disease activity/severity scores at first visit could not predict lymphoma development, nor was the pSS disease course significantly worse in patients with NHL. CONCLUSIONS: In our cohort, no clinical manifestation or disease score could clearly select patients with subsequent lymphoma development. Presence of IgM-kappa clonal components and development of purpura, PNP, and GN should alert the clinician for the presence of lymphoma.
23555066 Multicentric reticulohistiocytosis presenting with papulonodular skin lesions and arthriti 2013 Multicentric reticulohistiocytosis is a rare multisystem disorder of unknown etiology that is characterized by erosive polyarthritis and papulonodular lesions on the skin, mucous membranes, and internal organs. We report the case of a 54-year-old female who was misdiagnosed as having rheumatoid arthritis and underwent numerous joint replacement surgeries for progressively destructive arthritis in her hands, shoulders, hips, and knees. The patient finally received a diagnosis of multicentric reticulohistiocytosis after histopathological examination of the patient's left knee arthroplasty which revealed a diffuse histiocytic infiltrate, multinucleated giant cells, and finely granulated eosinophilic cytoplasm with a ground-glass appearance.
26981679 Correction. 2013 Apr 3 Heather Hasthorpe, rheumatology specialist nurse at Norfolk and Norwich University Hospitals NHS Foundation Trust, and winner of the Innovations in Your Specialty award at the Nurse Awards 2013, was misquoted in our nurse awards supplement (March 13). Talking about her work with patients with rheumatoid arthritis, she was quoted as saying: 'My responsibility is to patients, to prevent the disability, pain and deformity associated with this degenerative disease.' Rather than describing the disease as 'degenerative', Ms Hasthorpe used the word 'destructive'. Nursing Standard apologises for the error.
24701255 Anti-cyclic citrullinated peptide antibodies in psoriatic arthritis--cross-sectional study 2013 RATIONALE: Anti-CCP antibodies are detectable not only in rheumatoid arthritis (RA), but also in psoriatic arthritis (PsA). It is possible those anti-CCP antibodies are associated with features of PsA and that these auto-antibodies are useful in distinguishing PsA from RA. OBJECTIVE: to evaluate the prevalence and the associations of anti-CCP antibodies in PsA patients; to evaluate the usefulness of anti-CCP antibodies in distinguishing PsA from RA. METHODS AND RESULTS: The inquiry was designed as a cross-sectional study of 41 PsA patients, 139 RA patients and 147 normal subjects, which recorded demographic data, disease activity and serology: rheumatoid factor (RF), anti-CCP antibodies. Five PsA patients (12.2%) were anti-CCP positive. Compared to anti-CCP negative PsA patients, anti-CCP positive PsA patients had a more frequently a polyarticular disease pattern (p = 0.005), they were more frequently treated with biologics (p = 0.015) and less frequently with classic disease-modifying drugs (p < 0.001). An optimal positive cutoff value for anti-CCP titer was determined (11.6 U/mL), over which it is highly probable that a known PsA patient actually has RA and psoriasis. DISCUSSION: The more aggressive the disease of anti-CCP positive PsA patients indicates the need of a more intensive management regarding anti-rheumatic treatment and follow-up. Anti-CCP antibodies can be a useful tool in differentiating PsA from RA, especially in RA-like forms of PsA, which present no elements pertaining to spondyloarthropathies.
25396061 Pathogenic autoantibodies from patients with lupus nephritis cause reduced tyrosine phosph 2014 INTRODUCTION: The tertiary structure of normal podocytes prevents protein from leaking into urine. Patients with lupus nephritis (LN) develop proteinuria, and kidney biopsies from these patients display a number of podocyte abnormalities including retraction of podocyte processes. Autoantibodies have been shown to deposit in the kidneys of patients and mice with LN and are believed to play a key role in causing renal inflammation and dysfunction. The objective of this research was to study the effects of IgG antibodies from patients with LN on cultured human podocytes. METHODS: We exposed a human podocyte cell line to heat-inactivated (HI) plasma and purified polyclonal IgG from the following groups of subjects; patients with LN, patients with lupus without nephritis, patients with rheumatoid arthritis and healthy controls. We measured expression and intracellular distribution of podocyte-specific proteins and global phosphorylation of tyrosine. We then used mass spectrometry to identify the major protein targets of this phosphorylation. RESULTS: HI LN plasma did not alter expression or cellular distribution of podocyte-specific proteins but caused a significant reduction in podocyte protein tyrosine phosphorylation compared with plasma from healthy controls (p=0.0008). This result was replicated using purified IgG but was not seen with plasma from rheumatoid arthritis or non-renal lupus patients. The dominant tyrosine phosphorylated protein in podocytes was 55 kDa in size and was identified as tubulin. CONCLUSIONS: Since tubulin is an important component of podocyte major processes, these results suggest that autoantibodies from LN patients may exert an important pathogenic effect by dephosphorylation of this protein in podocytes.
24239715 Anti-proliferative effect of recombinant human endostatin on synovial fibroblasts in rats 2014 Jan 15 Rheumatoid arthritis (RA) is characterized by pronounced synovial hyperplasia resulting in pannus formation, cartilage erosion and ultimately joint destruction. Activated RA synovial fibroblasts (SFs) mediate the invasion and destruction of cartilage and bone. We previously demonstrated that recombinant human endostatin (rhEndostatin) is sufficient to induce SF apoptosis in adjuvant arthritis (AA) rats. However, the effect of this protein on SF proliferation is unknown. This study was designed to assess the inhibitory effect and mechanisms of rhEndostatin on the proliferation of cultured AA SFs. MTT assay and flow cytometric detection were performed to investigate SF proliferation and cell cycle progression, respectively. Also, the expression levels of p53, p21, cyclin D1, CDK4 and PCNA in AA SFs were detected by real-time PCR and western blotting assays. Our data revealed that AA SF proliferation was significantly inhibited by rhEndostatin in a concentration-dependent manner. In addition, rhEndostatin (50μg/ml) caused the G0/G1 cell cycle arrest of AA SFs. There were significant decreases in the expression levels of p53, p21, cyclin D1 and PCNA in AA SFs treated with rhEndostatin, and a significant increase in CDK4 expression. Collectively, our data suggest that rhEndostatin inhibits AA SF proliferation, which is preceded by cell cycle arrest at the G0/G1 phase. This is partly due to the inhibitory effect of rhEndostatin on cyclin D1 and PCNA by a p53-p21-CDK4-independent mechanism. Taken together, these findings highlight the potential use of rhEndostatin for RA treatment.
25174532 Psychosocial factors associated with increased physical activity in insufficiently active 2015 Sep OBJECTIVES: Although physical activity can potentially reduce symptoms of arthritis, 50% of people with arthritis are insufficiently active. The aim was to identify psychosocial factors associated with increased physical activity in mid-age adults with arthritis who did not meet recommended physical activity levels. DESIGN: Longitudinal cohort study. METHODS: Data were from 692 insufficiently active men and women (mean age 55 ± 6.6 years) with arthritis, who answered mailed surveys in 2007 and 2009 in the HABITAT study. Increased physical activity was defined as a change of ≥ 200 MET min/week in walking, moderate and vigorous activities from 2007 to 2009. Scale scores were used to measure psychosocial factors including intention, experiences, attitudes, efficacy, barriers, motivation, social support, and health professional advice. Associations between (1) 2007 psychosocial factors and (2) 2007-2009 improvement (≥ +1 standard deviation) in psychosocial factors and increased physical activity were examined with logistic regression models. Results were adjusted for education, body mass index, and self-rated health. RESULTS: Between 2007 and 2009, 296 participants (42.8%) increased their physical activity. Engagement, mastery and physical activity intention in 2007 were associated with this increase in physical activity (engagement OR = 1.11, 99% confidence interval (CI) = 1.05-1.17; mastery OR = 1.12, 99%CI = 1.02-1.22; physical activity intention OR = 1.29, 99%CI = 1.06-1.56). Improved scores for encouragement (OR = 2.07, CI = 1.07-4.01) and self-efficacy (OR =2 .27, CI = 1.30-3.97) were also significantly associated with increased physical activity. CONCLUSIONS: Positive physical activity experiences and intentions were predictors of increased physical activity among people with arthritis. Improved physical activity confidence and social support were associated with increased physical activity. It is important to consider these psychosocial factors when planning physical activity interventions for people with arthritis.
24497204 Peptidylarginine deiminase 4 contributes to tumor necrosis factor α-induced inflammatory 2014 Jun OBJECTIVE: Peptidylarginine deiminase 4 (PAD4) is a citrullinating enzyme that has multiple associations with inflammation. In rheumatoid arthritis, PAD4 and protein citrullination are increased in inflamed joints, and anti-citrullinated protein antibodies (ACPAs) form against citrullinated antigens are formed. ACPA immune complexes can deposit in the joint and induce the production of tumor necrosis factor α (TNFα), a critical inflammatory cytokine in the pathogenesis of rheumatoid arthritis. Further, in other settings, TNFα has been shown to induce PAD4 activity and modulate antibody formation. We undertook this study to investigate whether TNFα and PAD4 may synergistically exacerbate autoantibody production and inflammatory arthritis. METHODS: To determine whether TNFα and PAD4 augment autoantibody production and inflammatory arthritis, we first used a multiplex assay to determine whether mice with chronic inflammatory arthritis due to overexpression of TNFα develop autoantibodies against native and citrullinated antigens. With TNF(+) PAD4(+/+) and TNF(+) PAD4(-/-) mice, we then compared serum autoantibody levels by multiplex array, lymphocyte activation by flow cytometry, total serum IgG levels by enzyme-linked immunosorbent assay, arthritis by clinical and histologic scoring, and systemic inflammation using microfluidic devices. RESULTS: TNFα-overexpressing mice had increased levels of autoantibodies reactive against native and citrullinated antigens. PAD4(-/-) mice with TNFα-induced arthritis had lower levels of autoantibodies reactive against native and citrullinated antigens, decreased T cell activation and total IgG levels, and reduced inflammation and arthritis compared to PAD4(+/+) TNFα-overexpressing mice. CONCLUSION: PAD4 mediates autoantibody production and inflammatory arthritis downstream of TNFα.
25291981 Sjögren's syndrome and neuromyelitis optica spectrum disorders (NMOSD)--a case report and 2014 Oct 9 BACKGROUND: Neuromyelitis optica (NMO) is a rare relapsing auto-immune disease of the central nervous system which is sometimes found in association with other autoimmune disorders including Sjogren's syndrome. We present the case of a middle aged female with Sjogren's syndrome (SS) and Neuromyelitis optica spectrum disorders (NMOSD) who had a rapidly declining neurological illness that responded to immunosuppressive therapy. CASE PRESENTATION: A 51-year-old female with Sjogren's syndrome and recent history of varicella zoster infection presented with right upper and lower extremity weakness of one week duration. She was noted to have contrast enhancement at C2-C4 cord levels on cervico-thoracic MRI. Comprehensive work up was negative except for presence of a mild lymphocytic pleocytosis and oligoclonal bands in the CSF. She was diagnosed with transverse myelitis secondary to varicella zoster infection and was treated with high dose steroids in addition to acyclovir with improvement in her symptoms. Two months later she developed left upper and lower extremity weakness, bilateral dysesthesias and urinary incontinence. Repeat MRI of the cervico-thoracic spine revealed worsening enhancement at lower cervical cord levels (C5-7) with extension to T1. CSF analysis was unchanged; however immunological work up was abnormal for elevated NMO-IgG/AQP4 antibody. She was diagnosed with NMOSD and was treated with immunosuppressive therapy. Initially with IV methylprednisone and Cyclophosphamide therapy followed by Mycophenolate mofetil (MMF) maintenance therapy with good response. Repeat MRI 6 months later showed near complete resolution of previous abnormal cord signal changes. CONCLUSION: One needs to recognize the relationship between autoimmune diseases especially SS and NMOSD. The presence of NMO antibody has been associated with a relapsing disease course and a careful follow-up, besides use of remission maintenance agents such as MMF and Azathioprine are important to consider.
24333103 A comprehensive review of autoantibodies in primary Sjögren's syndrome: clinical phenotyp 2014 Jun Sjögren's syndrome (SS) is a systemic autoimmune disease characterized by periepithelial lymphocytic infiltrates in affected tissues and the production of plethora of autoantibodies. Among them autoimmune responses against Ro/SSA and La/SSB are of major importance since their detection is routinely used for disease diagnosis and clinical characterization. Although the exact mechanisms underlying disease pathogenesis are not fully understood, the important role of salivary gland epithelial cells (SGEC) in the initiation and development of the local immune responses is well-established. SGECs are also capable to mediate the exposure of the Ro/SSA and La/SSB autoantigens to the immune system by elevated apoptosis and autoantigen release in apoptotic bodies and/or by the secretion of autoantigen-containing exosomes. The expression of these autoantigens in epithelial cells appears to be tightly regulated. Up-to-date, signaling of certain innate immunity receptors, such as TLR3, appear to be implicated in the regulation of Ro/SSA and La/SSB expression by SGECs, whereas the deregulated expression of certain miRNAs that are predicted to target them in SS patients suggests a regulatory feedback at the post-transcriptional level. In the periphery, the humoral autoimmune responses are further regulated by the development of an active network of idiotypic-antiidiotypic antibodies. The plethora of mechanisms suggests that autoimmune humoral responses in SS are tightly regulated. In this review, the major humoral autoimmune responses, recent advances on the role of epithelial cells in their development, as well as possible regulatory mechanisms will be discussed.
23878841 Salivary and serum B-cell activating factor (BAFF) levels after hydroxychloroquine treatme 2013 PURPOSE: Some evidence implicates a role of hydroxychloroquine (HQ) in the management of Sjögren's syndrome. This study evaluated the effect of HQ on saliva B-cell activating factor (BAFF) levels as well as health related quality of life (QoL) in patients with primary Sjögren's syndrome (pSS). MATERIALS AND METHODS: Ten pSS patients who had been treated with HQ for at least 2 years and 15 healthy controls (HC) were included in the study. First, HQ was withdrawn for 12 weeks, then baseline evaluation was performed. Subsequently, HQ was restarted and further evaluations were carried out after 12 and 24 weeks of HQ treatment. Oral infection foci were eliminated by dental and periodontal treatments in both groups before enrollment. BAFF levels were evaluated with ELISA in serum and unstimulated mixed saliva. Salivary flow rates of patients and the control group were measured as well. Oral health quality of life (QoL) was evaluated by an oral health impact profile-14 (OHIP-14) questionnaire. RESULTS: Salivary BAFF levels (median: 12.39 ng/ml) were significantly decreased by using HQ both at 12 (2.78 ng/ml, P = 0.008) and 24 weeks (0.54 ng/ml, P = 0.011). Similarly, decreases in serum BAFF levels (5.23 ng/ml) were seen at 12 and 24 weeks after HQ treatment (2.18 ng/ml, P = 0.008 and 0.0 ng/ml, P = 0.012, respectively). Serum and salivary BAFF levels were significantly lower in healthy controls (0.37 ng/ml and 0.0 ng/ml, resp.) compared to those of pSS before HQ therapy (P = 0.006 and P = 0.001, resp.). Unstimulated salivary flows were similar in patients treated with HQ after 12 (0.38 ml/min) and 24 weeks (0.50 ml/min) (P = 0.51) but higher than the patients' rate at baseline (0.04 ml/min) (P = 0.008). CONCLUSION: Salivary and serum BAFF levels were lowered in patients with pSS when treated with HQ. In addition, decreased disease activity and increased salivary flows can be achieved with HQ in pSS patients.
24847722 Salivary gland ultrasound in children: a useful tool in the diagnosis of juvenile Sjögren 2014 Jul Primary Sjögren's syndrome (pSS) is a systemic autoimmune disease uncommon in children, clinically characterized by recurrent parotitis at the onset, which is a common disorder in childhood, most of them of infectious origin. Juvenile pSS diagnosis is based on clinical symptoms and presence of autoantibodies, after exclusion of infectious or lymphoproliferative diseases. However, salivary gland ultrasound (SGU) shows typical features of pSS that can add useful information for the diagnosis of this disorder. We describe three patients who presented with recurrent parotitis in which characteristic autoantibodies and typical SGU pattern allow us to make the diagnosis of juvenile pSS. We suggest that in children with recurrent parotitis SGU and autoantibodies should be routinely performed.
24822219 The association between serological biomarkers and primary Sjogren's syndrome associated w 2014 BACKGROUND AND AIM: The sensitivity and specificity of biomarkers used for predicting peripheral neuropathy of Sjogren's syndrome (SJS) patients remain unsatisfactory. This study aimed to determine the prognostic value of circulating autoantibodies levels in SJS patients with peripheral neuropathy. METHODS: Two hundred and fifty serological positive (either anti-Ro or anti-La positive) SJS patients' data were collected retrospectively. The titers of autoantibodies, electrophysiology reports, and clinical manifestation were reviewed. RESULTS: The prevalence rate of peripheral neuropathy is 7.2% in our study. Regarding classification of peripheral neuropathy, 12 had mixed sensorimotor polyneuropathy, six had cranial neuropathy. After stepwise logistic regression analysis, anti- β 2 glycoprotein I (a β 2GP I) and perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA) were significantly associated with peripheral neuropathy in serology positive SJS (P = 0.01, P = 0.046, resp.). CONCLUSION: The occurrence of peripheral neuropathy among SJS patients is not frequent and easily overlooked. Our study demonstrated that a β 2GP I and p-ANCA levels may imply the danger of the occurrence of neuropathy in SJS patients, and they can be considered a biomarker that should be added to the panel of conventional autoantibody in SJS patients.
24200611 [Sjogren's syndrome-associated neuropathy]. 2013 Nov Sjogren's syndrome is a systemic autoimmune disease characterized by xerophthalmia and xerostomia; it is associated with widespread systemic visceral involvement. A wide variety of neurological complications are characteristic features of Sjogren's syndrome, of which peripheral neuropathy is a major neurological manifestation. Based on the predominant neuropathic symptoms, patients can be considered to have several forms of neuropathies, including sensory ataxic neuropathy, painful sensory neuropathy without sensory ataxia, multiple mononeuropathy, multiple cranial neuropathy, trigeminal neuropathy, autonomic neuropathy, and radiculoneuropathy. Acute or subacute onset is observed more frequently in multiple mononeuropathy and multiple cranial neuropathies, whereas disease progression is usually chronic in other forms of neuropathies. Sensory symptoms without substantial motor involvement are observed predominantly in sensory ataxic, painful sensory, trigeminal, and autonomic neuropathies. In contrast, motor impairment is apparent in multiple mononeuropathy, multiple cranial neuropathy, and radiculoneuropathy. Autonomic symptoms such as abnormal pupils and orthostatic hypotension are particularly noted in patients with sensory ataxic, painful, trigeminal, and autonomic neuropathies. Sural nerve biopsy specimens reveal predominantly large fiber loss in sensory ataxic neuropathy and predominantly small fiber loss in painful sensory neuropathy. Vasculitis is observed most frequently in multiple mononeuropathy. The autopsy findings of patients with sensory ataxic and painful neuropathies demonstrate neuronal loss in the dorsal root ganglia and sympathetic ganglia with CD8-positive cytotoxic T lymphocytes. Differential therapeutic responses to corticosteroids and intravenous immunoglobulin can be seen among the various neuropathic forms. In conclusion, the clinicopathological features of neuropathies associated with Sjogren's syndrome are highly variable. The neuropathy classification is important from a therapeutic point of view.
23852065 [The function of osteopontin and other cytokines in the diagnosis of Sjoigren's syndrome]. 2013 Jun PURPOSE: To explore the relationship of serum concentrations of osteopontin(OPN), TNF-α and TGF-β1 in Sjoigren's syndrome patients. METHODS: Forty Sjoigren's syndrome (SS) patients were determined by pathological examination, which included 15 primary SS and 25 secondary SS. Serum level of OPN, TNF-alpha and TGF-beta 1 were examined by enzyme linked immunosorbent assay (ELISA). Multiple correlation analysis was performed using SPSS13.0 software package. RESULTS: Serum OPN, TNF-alpha levels increased in SS compared with healthy subjects (P<0.05).Serum TGF-beta 1 level in secondary SS significantly increased than primary SS (P<0.05). On the contrary, serum TGF-beta1 level had no significant change compared with the controls. OPN was correlated with TGF-beta 1. CONCLUSIONS: OPN and TNF-alpha may be used as adjunctive diagnostic parameter. TGF-beta 1 can be used as an index in differential diagnosis of primary and secondary SS. OPN and TGF-beta 1 have different effects and interactions between them, demonstrating mutuality, diversity and integrity of the cytokine network.
25028690 Ankylosis of temporomandibular joint caused by psoriatic arthritis: a report of four cases 2014 Psoriatic arthritis (PsA) is an inflammatory joint disease associated with psoriasis. PsA is often confused with other diseases such as osteoarthritis and rheumatoid arthritis. PsA involving temporomandibular joints (TMJs) are uncommon: only 19 articles with 43 cases have been documented in the literature. TMJ ankylosis caused by PsA is rare, with only six cases having been reported. The authors present four cases of ankylosis of the TMJ secondary to PsA and review the literature. The findings of this study suggest that more attention should be paid to psoriasis patients with TMJ symptoms and proper treatment should be taken to prevent irreversible TMJ damage.