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Search for: rheumatoid arthritis    methotrexate    autoimmune disease    biomarker    gene expression    GWAS    HLA genes    non-HLA genes   

ID PMID Title PublicationDate abstract
18199025 Design and validation of methods searching for risk factors in genotype case-control studi 2008 Jan Accessibility of high-throughput genotyping technology allows genome-wide association studies for common complex diseases. This paper addresses two challenges commonly facing such studies: (i) searching an enormous amount of possible gene interactions and (ii) finding reproducible associations. These challenges have been traditionally addressed in statistics while here we apply computational approaches--optimization and cross-validation. A complex risk factor is modeled as a subset of single nucleotide polymorphisms (SNPs) with specified alleles and the optimization formulation asks for the one with the maximum odds ratio. To measure and compare ability of search methods to find reproducible risk factors, we propose to apply a cross-validation scheme usually used for prediction validation. We have applied and cross-validated known search methods with proposed enhancements on real case-control studies for several diseases (Crohn's disease, autoimmune disorder, tick-borne encephalitis, lung cancer, and rheumatoid arthritis). Proposed methods are compared favorably to the exhaustive search: they are faster, find more frequently statistically significant risk factors, and have significantly higher leave-half-out cross-validation rate.
17115099 Meta-analysis is no substitute for a comprehensive national registry. 2007 Jul Anti-tumor necrosis factor alpha (TNF-alpha) agents have become an established treatment option for rheumatoid arthritis (RA), but are not without risks. As TNF-alpha has a role in tumour surveillance, anti-TNF-alpha blockade could potentially increase the risk of malignancy. Recent meta-analysis by Bongartz et al. (JAMA 295:2275-2285, 2006) reported an increase in the incidence of malignancy attributed to anti-TNF-alpha antibodies, and the information has quickly and uncritically reached several secondary sources with huge effects on public perception of risks related to anti-TNF-alpha therapy. In contrast, the results from the British Society for Rheumatology Biologics Register show that in clinical practice, anti-TNF-alpha therapy in RA does not appear to increase the risk of malignancy in those patients with low risk of malignancy. We discuss the issues emerging from these published data and suggest caution against giving weight to meta-analysis of short-term drug studies.
19265617 Clinical tetrad of arthritis, urethritis, conjunctivitis, and mucocutaneous lesions (HLA-B 2008 Dec 15 A 21-year-old male patient with the clinical tetrad of arthritis, urethritis, conjunctivitis, and mucocutaneous lesions, commonly known as Reiter syndrome was presented. He was hospitalized in poor condition, with fever, bilateral conjunctivitis, swollen and painful knee and tarsal joints, low back pain, Achilles tendonitis, dactilitis, keratoderma blenorrhagica, purulent urethritis, circinate balanitis, and oral erosive lesions. Radiography and Computerized Axial Tomography (CAT) showed sacroileitis, spondilosis thoracalis, and arthritis of the feet. The laboratory studies revealed anemia, neutrophilic leukocytosis, elevated erythrocyte sedimentation rate (ESR), hypoalbuminemia, negative rheumatoid factor, pyuria, proteinuria, and the presence of HLA-B27. The microbiological examinations of samples from pustular lesions, throat, eyes, urethra, stool, and blood were sterile. Urethral smear was positive for Chlamydia trachomatis (PCR). The histopathological picture of skin lesions was consistent with pustular psoriasis. Systemic treatment with antibiotics, corticosteroids, and non-steroidal anti-inflammatory drugs produced clinical improvement. This clinical syndrome requires comprehensive evaluation and multidisciplinary management.
17706035 [Juvenile psoriatic arthritis]. 2007 Aug A case of juvenile psoriatic arthritis in a 12 year-old boy was reported. The patient had a history of one and half a year of bilateral heel pain, followed by pain in the right knee and ankle and right hip joint. He developed psoriatic lesions affecting his nails and skin. He had increased erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) contents. Human leukocyte antigen (HLA) B27 was detected but serum rheumatoid factor was not in the patient. A skin biopsy revealed psoriasis and ultrasonography demonstrated synovitis in right knee and ankle. Juvenile psoriatic arthritis was diagnosed based on his physical, laboratory and skin biopsy findings. A treatment with nonsteroidal anti-inflammatory drugs and sulfasalazine produced no effect. Leflunomide in conjunction with anti-TNF biologic agents (Etanercept) was administered, followed by symptomatic improvement 2 weeks later.
18513703 CT20126, a novel immunosuppressant, prevents collagen-induced arthritis through the down-r 2008 Jul 1 The colchicine-derived CT20126 compound has recently been shown to exert an immune regulatory effect and prolong the survival of allograft skins. In this study, we explored the anti-inflammatory and anti-arthritic effects of CT20126 in vivo and in vitro as well as investigated its underlying action mechanism. CT20126 suppressed the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2, tumor necrosis factor-alpha, and interleukin-1beta as well as the production of nitric oxide and prostaglandin E(2) in lipopolysaccharide (LPS)-treated macrophages as well as LPS-administered mice. This drug also inhibited the production of nitric oxide, prostaglandin E(2), and the chemokines, RANTES, GROalpha, and ENA-78, in cytokine-stimulated human synoviocytes. CT20126 suppressed NF-kappaB activation and iNOS promoter activity, which correlated with its inhibitory effect on phosphorylation-dependent IkappaB kinase activation, IkappaB phosphorylation and degradation, and NF-kappaB nuclear translocation, in LPS-stimulated macrophages. This compound also inhibited LPS-induced NF-kappaB-inducing kinase (NIK) and Akt phosphorylation, which are upstream of NF-kappaB activation. Furthermore, CT20126 significantly decreased the incidence and severity of arthritis as well as inhibited the expression of inflammatory cytokines, chemokines, iNOS, and cyclooxygenase-2 in the paws of collagen-induced arthritic mice. These findings indicate that CT20126 exerts an anti-inflammatory effect through NF-kappaB-responsive inflammatory gene expression by inhibiting the NIK- and Akt-dependent canonical NF-kappaB pathway and can be used as a therapeutic agent for rheumatoid arthritis related to chronic inflammation.
17956013 Cutaneous adverse reaction to infliximab: report of psoriasis developing in 3 patients. 2007 Sep Infliximab is a chimeric immunoglobulin G1kappa monoclonal antibody against tumor necrosis factor alpha (TNF-alpha), a proinflammatory cytokine that participates in both normal immune function and the pathogenesis of many autoimmune disorders. Treatment with infliximab reduces the biologic activities of TNF-alpha and thus is indicated in the treatment of rheumatoid arthritis, Crohn disease, ankylosing spondylitis, psoriatic arthritis, plaque psoriasis, and ulcerative colitis. To our knowledge, there have been 13 case reports of new-onset psoriasis, psoriasiform dermatitis, and palmoplantar pustular psoriasis that developed during treatment with infliximab. We report 3 additional cases of biopsy-proven new-onset psoriasis that developed while the patients underwent treatment with infliximab for inflammatory bowel disease. Although the mechanism for the development of psoriasis in these patients is unclear, several possible explanations are proposed. With increasing use of infliximab and other TNF-alpha inhibitors in clinical practice, more cases of similar reactions to these drugs probably will be reported and are necessary to determine the importance of this eruption.
18613763 New therapeutic applications for the anticoagulant, activated protein C. 2008 Aug BACKGROUND: Activated protein C (APC) is derived from its precursor, protein C (PC). Originally thought to be synthesised exclusively by the liver, recent reports have shown that PC is also produced by endothelial cells, smooth muscle cells, keratinocytes and some leukocytes. OBJECTIVE: To provide an update on the emerging therapeutic effects of APC. RESULTS/CONCLUSION: APC functions as an anticoagulant with cytoprotective, anti-inflammatory and antiapoptotic properties. In vitro and preclinical data have revealed that APC exerts its protective effects via an intriguing mechanism requiring endothelial protein C receptor and protease activated receptor-1. Approved as a therapeutic agent for severe sepsis, APC is emerging as a potential treatment for a number of autoimmune and inflammatory diseases including spinal cord injury, asthma, chronic wounds and possibly rheumatoid arthritis. The future therapeutic uses of APC look very promising.
18239925 Manifestation of palmoplantar pustulosis during or after infliximab therapy for plaque-typ 2008 Mar Infliximab is a monoclonal antibody directed against TNF-alpha. It has been approved for use in rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, psoriatic arthritis and plaque-type psoriasis. In case reports, positive effects on pustular variants of psoriasis have also been reported. However, paradoxically, manifestation of pustular psoriasis and plaque-type psoriasis has been reported in patients treated with TNF antagonists including infliximab for other indications. Here, we report on 5 patients with chronic plaque-type psoriasis who developed palmoplantar pustulosis during or after discontinuation of infliximab therapy. In two of the five cases, manifestation of palmoplantar pustulosis was not accompanied by worsening of plaque-type psoriasis. Possibly, site-specific factors or a differential contribution of immunological processes modulated by TNF inhibitors to palmoplantar pustulosis and plaque-type psoriasis may have played a role.
23480265 The significance of non-human primates as preclinical models of human arthritic disease. 2008 Mar BACKGROUND: The broad immunological gap between inbred SPF-raised strains of mice and rats and the diverse rheumatoid arthritis (RA) patient population limits the predictive value of the existing disease models for clinical success of new therapies, in particular for those using highly specific biologicals. OBJECTIVE: This review argues that because of their closer immunological and physiological proximity to patients, disease models in non-human primates (NHPs) may bridge this gap and help reduce the failure of many (± 80%) new therapies in clinical trials. In various research areas, NHPs are an accepted intermediate between disease models in rodents and the ultimate introduction for clinical use in patients. However, with the exception of transplantation, this is not the case for immune-mediated inflammatory disorders, such as RA, although useful preclinical models are being developed. METHOD: The validity and use of the rhesus monkey model of collagen-induced arthritis as a preclinical RA model is reviewed. The discussion comprises present genetic and immunological aspects, biomarkers, and an overview of published preclinical therapy evaluations. CONCLUSION: It is time to consider the use of NHPs with a greater evolutionary proximity to humans as models for preclinical evaluation of new human-specific drugs for arthritic disease.
16779871 PhiC31 integrase mediates integration in cultured synovial cells and enhances gene express 2006 Aug BACKGROUND: Gene transfer to synovium in joints has been shown to be an effective approach for treating pathologies associated with rheumatoid arthritis (RA) and related joint disorders. However, the efficiency and duration of gene delivery has been limiting for successful gene therapy for arthritis. The transient gene expression that often accompanies non-viral gene delivery can be prolonged by integration of vector DNA into the host genome. We report a novel approach for non-viral gene therapy to joints that utilizes phage phiC31 integrase to bring about unidirectional genomic integration. METHODS: Rabbit and human synovial cells were co-transfected with a plasmid expressing phiC31 integrase and a plasmid containing the transgene and an attB site. Cells were cultured with or without G418 selection and the number of neo-resistant colonies or eGFP cells determined, respectively. Plasmid rescue, PCR query, and DNA sequence analysis were performed to reveal integration sites in the rabbit and human genomes. For in vivo studies, attB-reporter gene plasmids and a plasmid expressing phiC31 integrase were intra-articularly injected into rabbit knees. Joint sections were used for histological analysis of beta-gal expression, and synovial cells were isolated to measure luciferase expression. RESULTS: We demonstrated that co-transfection of a plasmid expressing phiC31 integrase with a plasmid containing the transgene and attB increased the frequency of transgene expression in rabbit synovial fibroblasts and primary human RA synoviocytes. Plasmid rescue and DNA sequence analysis of plasmid-chromosome junctions revealed integration at endogenous pseudo attP sequences in the rabbit genome, and PCR query detected integration at previously characterized integration sites in the human genome. Significantly higher levels of transgene expression were detected in vivo in rabbit knees after intra-articular injection of attB-reporter gene plasmids and a plasmid expressing phiC31 integrase. CONCLUSION: The ability of phiC31 integrase to facilitate genomic integration in synovial cells and increase transgene expression in the rabbit synovium suggests that, in combination with more efficient DNA delivery methods, this integrase system could be beneficial for treatment of rheumatoid arthritis and other joint disorders.
19035473 Splenic suppressor of cytokine signaling 3 transgene expression affects T cell responses a 2008 Dec OBJECTIVE: Members of the suppressor of cytokine signaling (SOCS) family are key negative intracellular regulators of cytokine and growth factor responses, including those that regulate immune responses in autoimmune disorders, such as rheumatoid arthritis (RA). The aim of this study was to investigate modulation of T cell immunity for the treatment of experimental arthritis, via enhanced expression of SOCS-3 in splenic antigen-presenting cells (APCs) obtained after intravenous injection of adenovirus encoding SOCS-3. METHODS: DBA/1 mice were immunized with type II collagen, and adenovirus vectors were administered by intravenous injection before the clinical onset of collagen-induced arthritis (CIA). Splenic cellular responses were analyzed by measuring cytokine production, using Luminex multi-analyte technology. Th cell populations were analyzed by flow cytometry. RESULTS: Systemic delivery of adenovirus encoding SOCS-3 resulted in enhanced transgene expression in splenic APCs, which led to decreased production of interleukin-23 (IL-23), IL-6, and tumor necrosis factor alpha, but significantly higher production of antiinflammatory IL-10, by these cells. Fluorescence-activated cell sorting analysis showed increased numbers of splenic CD4+ T cells after SOCS-3 treatment. In the presence of SOCS-3-transduced APCs, however, purified splenic CD3+ T cells showed reduced antigen-specific proliferation and a significant reduction in the production of interferon-gamma (-43%), IL-4 (-41%), and IL-17 (-70%). Interestingly, the altered splenic cellular responses were accompanied by a protective effect on CIA development, and histologic analysis of knee joints showed reduced joint inflammation and connective tissue destruction. CONCLUSION: This study demonstrates effective prevention of CIA after intravenously induced overexpression of SOCS-3; this is probably caused by the generation of tolerogenic APCs, which have an inhibitory effect on Th1, Th2, and especially, Th17 cell activity.
16696922 [Effects of kangfengshi granules on expressions of osteoprotegerin, RANKL and M-CSF in bon 2006 May OBJECTIVE: To observe the effects of Kangfengshi Granules (KFSG) on expressions of the mRNAs of osteoprotegerin (OPG), receptor activator of nuclear factor-kappaB ligand (RANKL) and macrophage colony stimulating factor (M-CSF) in bone tissues of rats with collagen-induced arthritis. METHODS: Forty SD rats were randomly divided into four groups: normal control group, untreated group, cyclosporine A (CsA)-treated group and KFSG-treated group. Except the rats in the normal control group, all the other rats received subcutaneous injection of collagen II to establish collagen-induced arthritis (CIA) models. Then the rats in each group were fed normal saline or corresponding drugs for four weeks. Total RNA was extracted from carpal and digital bones. The expressions of OPG, RANKL and M-CSF mRNAs were examined by real-time PCR. RESULTS: The total incidence of arthritis induced by collagen II in the rats was approximately 90%. The expression levels of RANKL and M-CSF mRNAs and the RANKL mRNA/OPG mRNA ratio in the untreated group, KFSG-treated group and CsA-treated group were all significantly higher than those in the normal control group, while the expression levels of OPG mRNA in those three groups were significantly lower than that in the normal control group. The expression level of OPG mRNA in the KFSG-treated group was obviously higher while the expression level of M-CSF mRNA and the RANKL mRNA/OPG mRNA ratio in the same group were both lower as compared with those in the untreated group. CONCLUSION: The molecular mechanism of effects of KFSG on bone erosion and destruction induced by rheumatoid arthritis is closely correlated with up-regulating the expression of OPG mRNA, down-regulating the expression of M-CSF mRNA and RANKL mRNA/OPG mRNA ratio.
18600328 Mucosal administration of an altered CII263-272 peptide inhibits collagen-induced arthriti 2008 Nov Rheumatoid arthritis (RA) is a systemic autoimmune disease mediated by T cells. Collagen type II (CII) is one of the autoantigens associated with RA. CII263-272 is a predominant CII antigenic peptide that can induce T-cell activation upon binding to MHC and interaction with the appropriate T-cell receptor (TCR). Altered CII263-272 peptides with substitution of specific amino acids could bind to RA-associated HLA-DR4/1 with no T cell stimulating effects and could inhibit T cell activation in RA. We performed this study to evaluate the effect of mucosal administration and to explore the mechanism of the inhibitory effect of altered CII263-272 peptide (267Q-->A, 270K-->A and 271G-->A) on collagen induced arthritis (CIA). CIA was induced in Lewis rats by immunization with bovine CII. Altered CII263-272 peptide was given intranasally beginning from arthritis onset. Wild CII263-272 peptide or PBS was administered as controls. Therapeutic effects were evaluated by arthritis scores, body weight change, and joint pathologic scores. The anti-CII antibody and its subtypes and the cytokines, IFN-gamma, IL-10, and IL-17 were measured with ELISA. Foxp3+CD4+CD25+ regulatory T cell induction was assessed by FACS analysis. Following treatment with the altered CII263-272 peptide, arthiritis scores were reduced and body weight was increased. The altered CII263-272 peptide could retard the histologic lesion of the joints. The titers of anti-CII antibodies IgG2a in altered CII263-272 peptide treated rats decreased markedly compared to PBS-treated rats. The serum levels of IFN-gamma in rats treated with altered peptide was lower than that of rats treated with wild CII263-272 peptide and PBS. No differences were observed in the levels of serum IL-10 among the three groups. The altered CII263-272 peptide could decrease serum level of IL-17 and increase peripheral Foxp3+CD4+CD25+ T cells at early stage of CIA. Mucosal administration of altered CII263-272 peptide could effectively inhibit the progression of CIA. Altered CII263-272 peptide could suppress Th17 cells and expand regulatory T cells in the early stage of the disease. The IgG2a subtype of anti-CII antibodies and IFN-gamma were reduced and in vivo Th1 responses were inhibited as a result of altered CII peptide treatment. Altered CII peptide is likely therapeutic in RA.
16574782 (5R)-5-hydroxytriptolide attenuated collagen-induced arthritis in DBA/1 mice via suppressi 2006 Jul (5R)-5-Hydroxytriptolide (LLDT-8) displays strong immunosuppressive activities both in vitro and in vivo in our previous studies. This study aims to investigate whether LLDT-8 has antiarthritic potential in a murine model of type II bovine collagen (CII)-induced arthritis (CIA) and to show the mechanism(s) of LLDT-8 action. DBA/1 mice were immunized with CII to induce arthritis and administered with LLDT-8. The severity of arthritis was evaluated according to the clinical score and joint damage. The effects of LLDT-8 on immune responses were determined by measurement of serum antibody levels, lymphocyte proliferation assay, cytokine assay, nitric oxide (NO) production, arginase activity assays, fluorescence-activated cell sorting analysis of splenic Mac-1+ cells, as well as polymerase chain reaction analysis for interferon-gamma (IFN-gamma)-related gene expression. We showed that LLDT-8 treatment significantly reduced the incidence and severity of CIA. The preventive and therapeutic effects of LLDT-8 are associated with 1) reduction of serum anti-CII immunoglobulin (Ig) G, IgG2a, and IgG1 levels; 2) inhibition of CII-specific lymphocyte proliferation, IFN-gamma and interleukin-2 production; 3) blockade of gene expressions in IFN-gamma signaling, including IFN-gamma production pathways [signal transducer and activator of transcription (STAT) 1, T-box transcription factor, interleukin 12Rbeta2, and STAT4] and IFN-gamma-induced chemokine transcription [macrophage inflammatory protein (Mip)-1alpha, Mip-1beta, regulated on activation normally T cell expressed and secreted, and inducible protein 10]; and 4) retardation of the abnormal increase of NO via IFN-gamma/STAT1/interferon regulatory factor 1/inducible nitric-oxide synthase pathway and arginase activity. Moreover, the mRNA transcription of chemokine receptors was also suppressed [including C-C chemokine receptor (CCR) 1, CCR5, and C-X-C chemokine receptor 3]. In conclusion, our data suggest that the antiarthritic effect of LLDT-8 is closely related to the blockade of IFN-gamma signaling. LLDT-8 may have a therapeutic value in the treatment of rheumatoid arthritis.
17558048 A clinical study of psoriatic arthropathy. 2007 May BACKGROUND: The incidence of uncomplicated psoriasis is 1-3% in the general population. Arthritis is found in increased frequency in psoriatic patients and its incidence is estimated to be 5-7%. AIM: To assess the prevalence of arthritis in psoriatic patients. METHODS: Four hundred and seventy-two psoriatic patients were enrolled in the study out of which 40 patients had (psoriatic) arthropathy (PsA). Severity of psoriasis was assessed by the psoriasis area and severity index (PASI). Routine blood investigations were carried out along with radiological investigations. RESULTS: Forty percent of the 40 PsA patients were in the age group of 51-60 years. Seven patients out of the 40 (17.5%) psoriatic arthropathic (PsA) patients had a family history of psoriasis. Nail involvement was observed in 37 cases (92.5%). Rheumatoid factor was present in five out of the 40 (12.5%) PsA patients. Serum uric acid levels were above normal in eighteen out of the 40 (45%) PsA patients. Asymmetric oligoarthropathy was the most commonly observed feature in 42.5% of the 40 PsA patients. Narrowing of joint spaces and erosions were observed in 62.5% and 45% of the 40 PsA patients. CONCLUSION: There is an association between the duration of skin lesions and duration of arthropathy. Similarly the PASI score is also directly related with arthropathy.
18984408 Genes and Sjögren's syndrome. 2008 Nov The evidence for a strong genetic component conferring susceptibility to primary Sjögren's syndrome (SS) is mounting. Several associations with SS have been reported and provide evidence that the HLA region harbors important susceptibility loci and that multiple genes outside the HLA region play a role. Genetic discovery lags behind success observed in related autoimmune diseases. Identifying genetic factors that cause SS will allow more precise definition of pathogenic mechanisms leading to the overall SS phenotype and clinically heterogeneous subsets of patients. Critical opportunities are certain to follow for translation into improved diagnosis and therapies for SS and its spectrum diseases.
17491316 [A case of multiple nodular pulmonary amyloidosis complicated with primary Sjogren syndrom 2007 Apr A 79-year-old woman was admitted to the Department of Orthopedics Surgery for treatment of osteoarthritis in her knee. Multiple pulmonary nodular lesions were found on preoperative chest x-ray film screening. Metastatic lung tumor was suspected, but no tumorous lesions were detected in other organs. CT guided lung biopsy was performed. Histopathological examination revealed amyloid consisting of homogenous eosinophilic materials. No amyloid deposits were detected in other organs, so we diagnosed localized nodular pulmonary amyloidosis. She was subsequently given a diagnosis of primary Sjögren syndrome. We believe that such a case of multiple nodular pulmonary amyloidosis with Sjögren syndrome is rare, and the case showed interesting radiological findings, such as mimicking metastatic lung tumor.
18276740 Stress, coping strategies and social support in patients with primary Sjögren's syndrome 2009 Jan OBJECTIVES: Previous evidence suggests the role of psychological stress in triggering the onset of autoimmunity. We aimed to investigate whether stress following major and minor life events could precede the onset of primary Sjögren's syndrome (pSS). The role of coping strategies and social support, as compensating buffering mechanisms, was also explored. METHODS: 47 patients with pSS were compared with two control groups: 35 patients with lymphoma (disease controls, DC) and 120 healthy controls (HC) with disease onset within the previous year. All subjects completed questionnaires assessing the occurrence of major and minor stressful events, coping strategies and social support prior to disease onset. Data analysis was performed by univariate and multivariate logistic regression models. RESULTS: A higher number of patients with pSS reported the occurrence of negative stressful life events prior to disease onset compared with patients with lymphoma and HC, while the number and impact of daily hassles did not differ between the three groups. Coping strategies were defective and the overall social support was lower in patients with pSS compared with DC and HC groups. In the multivariate model, pSS status was associated with maladaptive coping and lower overall social support relative to DC and HC, as well as with an increased number of negative stressful life events compared with HC but not DC. CONCLUSIONS: Prior to disease onset, patients with pSS experience high psychological stress following major negative life events, without developing satisfactory adaptive coping strategies to confront their stressful life changes. Lack of social support may contribute to the relative risk of disease development.
18193229 Correspondence between clinical improvement and proteomic changes of the salivary peptide 2008 Jun The aberrant induction of salivary/lacrimal proteins is considered to be crucial in the pathogenesis of sicca-symptoms related to primary Sjögren syndrome (SS). We report the case of an 11-year-old boy who was admitted to hospital due to recurrent bilateral parotid gland enlargement and keratoconjunctivitis, which were diagnosed as primary SS upon a combination of laboratory and instrumental tests. The proteomic analysis of the salivary peptide complex in the patient's salivary fluid near diagnosis and after 6 months of pharmacological therapy revealed quantitative and mostly qualitative differences. This observation reveals that clinical and functional changes of the salivary glands driven by non-steroidal antinflammatory drugs might be reflected in different proteomic patterns of the salivary fluid.
17992587 Persistent viral infection in primary Sjogren's syndrome: review and perspectives. 2007 Jun Exocrine gland pathology in primary Sjogren's syndrome is characterized by destruction of acinar epithelial cells and chronic lymphocytic infiltrates surrounding ductal epithelial cells. These cells seem to be activated, as it is inferred by their immunophenotype. The cause of this activation and the chronic inflammatory response that targets epithelial cells remain unknown. Here, we will review the evidence pointing to a persistent viral infection as a probable cause of primary Sjogren's syndrome and discuss potential directions for future research.