Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
ID | PMID | Title | PublicationDate | abstract |
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16829993 | [Usefulness of ultrasonography and color Doppler sonography in the diagnosis of major sali | 2006 Apr | The algorithm for imaging of the salivary glands depends on the clinical scenario with which the patient presents to the clinician. Ultrasound has been increasingly used in recent years and thanks to high performance, easy to use apparatus, it can now be used for exploration of the salivary glands. This non invasive, painless and relatively inexpensive examination provides rapid visualisation of the salivary glands and is a useful adjunct to computed tomography and magnetic risonance imaging examination, particularly in tumour pathology. In recent years, publications have highlighted the potential uselfulness of salivary gland ultrasonography as a simple and non-invasive adjunctive test for the detection of gland involvement in Sjögren's syndrome (SS). SS is a chronic inflammatory disease of the salivary glands characterised by focal lymphocytic infiltrates that cause progressive destruction of the acinar structures. The findings of a previous study lead us to believe, in agreement with other examiners, that semiquantitative assessment of ultrasonographic images of the salivary glands is a sensitive and very useful means of evaluating salivary involvement in SS. Color Doppler sonography is a recently introduced method which makes it possible to evaluate intra- and perilesional vascularization and to perform a hemodynamic study of the area being explored. The color Doppler sonography can provide a useful adjunct to conventional ultrasound, increasing diagnostic accuracy in submandibular- parotid masses and to analyze physiologic changes that occur during salivary stimulation in normal subjects and the flow alterations that occur in diseased glands of SS patients. This article reviews the normal ultrasound anatomy of the salivary glands along with lithiasic, inflammatory, tumoral, and autoimmune disease such as SS. | |
16295789 | Adult onset Still's disease as a cause of acute severe mitral and aortic regurgitation. | 2005 Sep | Adult onset Still's disease (AOSD) is an uncommon acute systemic inflammatory disease of unknown origin. The clinical features include high spiking fever, arthralgia or arthritis, transient maculopapular rash, lymphadenopathy, hepatosplenomegaly, and serositis. Pericarditis is the most common cardiac manifestation of AOSD and occurs in approximately 30% of cases. A simultaneous occurrence of rapidly progressive bi-valvular regurgitation associated with AOSD has not been previously described. We report a case of a 55-year old woman who underwent mitral valve replacement and Bentall's operation due to acute severe mitral and aortic regurgitation associated with AOSD. | |
15880807 | Gene expression profiling of minor salivary glands clearly distinguishes primary Sjögren' | 2005 May | OBJECTIVE: To identify gene expression signatures in minor salivary glands (MSGs) from patients with primary Sjogren's syndrome (SS). METHODS: A 16K complementary DNA microarray was used to generate gene expression profiles in MSGs obtained from 10 patients with primary SS and 10 control subjects. The data were analyzed by 2 different strategies, one strict primary analysis and one subanalysis that allowed for inclusion of genes with no signal in more than 3 samples from each group. The results were validated by quantitative reverse transcriptase-polymerase chain reaction techniques. RESULTS: We found a distinct difference in gene expression levels in MSGs, enabling a simple class prediction method to correctly classify 19 of the 20 samples as either patient or control, based on the top 5 differentially expressed genes. The 50 most differentially expressed genes in the primary SS group compared with the control group were all up-regulated, and a clear pattern of genes involved in chronic inflammation was found. CXCL13 and CD3D were expressed in >/=90% of primary SS patients and in =10% of the controls. Lymphotoxin beta, as well as a number of major histocompatibility complex genes, cytokines, and lymphocyte activation factors, manifested its role in the pathogenesis of SS. Numerous type I interferon genes related to virus infection were found among the top 200 genes, with increased expression in primary SS. Interestingly, the expression of carbonic anhydrase II, which is essential in saliva production and secretion, and the apoptosis regulator Bcl-2-like 2 were down-regulated in primary SS patients. CONCLUSION: We have identified distinct gene expression profiles in MSGs from patients with primary SS that provide new knowledge about groups of genes that are up-regulated or down-regulated during disease, constituting an excellent platform for forthcoming functional studies. | |
17054763 | Sjögren's syndrome: why autoimmune epithelitis? | 2006 Nov | The expression 'autoimmune epithelitis' has been proposed as an alternative for Sjögren's syndrome (SS) based on data pointing out the central role of the epithelial cell in the pathogenesis of the syndrome. Clinically, apart from exocrine glands that are the main target, the epithelial component of the other organs such as kidneys, liver, lungs or thyroid is commonly affected resulting in various extraglandular manifestations. On the other hand, at the molecular and cellular level, the epithelial cell plays a major role in the initiation and perpetuation of the autoimmune lesion. Mechanisms such as antigen presentation, apoptosis, chemokine production or germinal center formation lie in the center of SS pathogenesis and the epithelial cell has a very important role. Herein, we present both aspects, review the data that support the proposed terminology and finally, suggest a unifying theory for the pathogenesis of SS. | |
16495845 | [Dyspareunia and Sjögren's syndrome]. | 2006 Jan | BACKGROUND: Dyspareunia is frequently associated with a psychiatric origin, particularly in patients with no obvious vulvovaginal or pelvic disease. The aim of this study was to assess the frequency of dry syndrome in patients with dyspareunia and to evaluate the main clinical and biological features and follow-up data for women with dyspareunia and dry syndrome. PATIENTS AND METHODS: Twenty-two patients presenting chronic idiopathic dyspareunia (without clear vulvovaginal dermatosis or infection) were included in this retrospective study. All patients underwent history-taking, gynecological examination, a Schirmer tear test, a sugar test, labial salivary gland biopsy assessment and immunological examination. A diagnosis of Sjögren's syndrome was considered where histological examination of the salivary glands showed a lymphocyte infiltration corresponding to stage 3 or 4 in the Chisholm classification. Diagnosis of dry syndrome without Sjögren's syndrome was made in patients with xerostomia and/or xerophthalmia without a specific histological picture of Sjögren's syndrome or immunological abnormalities at salivary gland biopsy. RESULTS: Based on our criteria, 10 patients (45%) had dry syndrome, including 4 with Sjögren's syndrome and 6 with dry syndrome without Sjögren's syndrome. 9 of these 10 patients presented either xerostomia (7 cases) and/or xerophthalmia (7 cases). Vaginal dryness was reported by 3 of the 10 women with dry syndrome but also by 4 of 12 women without dry syndrome. Examination of the vulva showed no particular clinical features and treatment with an emollient was not effective in all cases. DISCUSSION: This study showed a high frequency of dry syndrome in patients with chronic "idiopathic" dyspareunia. The incidence of the condition was even greater in women with functional conditions evocative of dry syndrome. Women presenting dyspareunia with no clearly related clinical causes should thus be carefully assessed for dry syndrome. | |
15971185 | Fast and high-resolution MR sialography using a small surface coil. | 2005 Jul | PURPOSE: To establish a fast and high-resolution MR sialographic technique that provides fast and high-resolution imaging. MATERIALS AND METHODS: MR sialography was performed on a 1.5-T MR imager using a small (47-mm) surface coil. We determined appropriate sequence parameters, and then applied the technique to the salivary glands of 143 patients with xerostomia (including those with Sjögren's syndrome or hyperlipidemia) or salivary gland inflammation. We compared the high-resolution MR sialography with conventional x-ray sialography in the patients with xerostomia to evaluate the effectiveness of the MR sialography technique. RESULTS: We found that a single-shot, single-slice MR sialography (TR/TR/number of signal acquisitions [NSA] = 8000 msec/1000 msec/6) using a small surface coil provides excellent duct images that are clinically feasible with fast (imaging time of 56 seconds) and high-resolution images. An alternative three-dimensional MR sialography technique provided better details of the branches at the expense of imaging time. The MR sialography technique using a small surface coil depicted effectively the ductal changes in the salivary glands in patients with or without Sjögren's syndrome, reflecting the severity of the diseases. CONCLUSION: We conclude that MR sialography can be performed using a fast and high-resolution sequence. | |
17085450 | The anti-rheumatic gold salt aurothiomalate suppresses interleukin-1beta-induced hyalurona | 2007 Jan 26 | Gold compounds are among the oldest disease-modifying drugs and are still widely used today for treating rheumatoid arthritis. Despite decades of use, little is known about the mode of action of this class of drugs. Here we have demonstrated that aurothiomalate (AuTM) suppresses hyaluronan accumulation by blocking interleukin (IL)-1beta-induced hyaluronan synthase-1 transcription. We have further demonstrated that, in fibroblast-like synoviocytes (FLSs), AuTM acts as a specific COX-2 transcriptional repressor in that IL-1beta-induced COX-2 transcription is blocked, whereas COX-1 transcription and translation is unaffected. As a consequence, PGE2 levels released by FLS are dose-dependently reduced in cells exposed to AuTM. Of similar importance is the demonstration that AuTM does block NFkappaB-DNA interaction. In addition, two other transcription factors implicated in inflammatory events, namely AP-1 and STAT3, are blocked as well. The effect on NFkappaB likely explains the inhibition of COX-2 as well as that of HAS1, as both are genes that depend on the activation of NFkappaB. Interestingly, AuTM does not interfere with IL-1beta-induced IkappaB alpha degradation, in most cases a prerequisite for subsequent NFkappaB activation. Furthermore, evidence is presented that, in FLS, AuTM blocks NFkappaB-DNA interaction neither by binding to NFkappaB binding sites nor by interacting with activated NFkappaB proteins. Taken together, AuTM treatment of FLS blocks two of the most important proinflammatory events that are associated with rheumatoid arthritis. AuTM blocks the release of PGE2 and prevents the activation of NFkappaB, therefore blocking IL-1beta-induced hyaluronan accumulation and likely a series of other pro-inflammatory NFkappaB-dependent genes. | |
15888112 | Congenital heart block associated with undiagnosed maternal Primary Sjögren's Syndrome -- | 2005 May | Congenital heart block (CHB) has been linked with Sjögren's Syndrome. This paper reports a case of previously undiagnosed maternal Primary Sjögren's Syndrome (1 degrees SS) that was only discovered following the birth of the patient's first child with CHB. The possible pathophysiological mechanisms underlying CHB associated with 1 degrees SS are discussed. | |
17127687 | Response to intramuscular methyl prednisolone in inflammatory hand pain: evidence for a ta | 2007 May | BACKGROUND: Hand pain with stiffness is a common clinical presentation to early arthritis clinics, with outcome varying from resolution to the development of rheumatoid arthritis. OBJECTIVE: To assess the response and predictors of response to intramuscular methylprednisolone (MP) and hydroxychloroquine (HCQ) using a standardised treatment protocol. METHODS: Patients with inflammatory hand pain (IHP), defined as predominantly hand pain and morning stiffness of at least 30 min duration, received a standardised assessment prior to receiving intramuscular MP. Response (primary outcome) at 4 weeks was a 50% improvement in symptoms as perceived by the patient; responders who relapsed received repeat intramuscular MP and HCQ. RESULTS: 102 patients were recruited, of which 21% were rheumatoid factor (RF) positive, 23% had clinical synovitis, 25% had raised C-reactive protein level and 55% had ultrasound-detected synovitis. 73% responded, with associated significant reductions in morning stiffness, Health Assessment Questionnaire, painful and tender joint counts, and visual analogue scores (p < or = 0.006 for all). Ultrasound-detected synovitis (p<0.001) and RF (p = 0.04), but not clinical synovitis (p = 0.74), were significantly associated with response to intramuscular MP. 86% who remained on HCQ long term reported a benefit. CONCLUSIONS: Patients with IHP have significant improvement in symptoms and function following intramuscular MP. Further placebo-controlled trials are required to assess the role of intramuscular MP and ultrasonography in managing this patient group. | |
16295756 | [Pyoderma gangrenosum in dakar: about 14 cases]. | 2005 | From January 1990 to December 2001, we undertook a retrospective study in the dermatology department of Aristide le Dantec hospital in order to assess the epidemiologic, clinical and evolutionary profiles of pyoderma gangrenosum (P.G). All files of patients diagnosed with PG were reviewed. The diagnosis was based on clinical and histological aspects. Fourteen files of patients with PG were reviewed. They were constituted of 8 males and 6 females, with a median age of 24.5 (extreme 4 and 54 years). Paediatric forms represented 30 % of the cases. The typical aspect with an ulceration with elevated edge comprising of purulent hutchs was observed in all the cases. The localization on the level of the lower limbs was noted among 12 patients (85.7 %). The PG was associated to chronic ulcerative colitis (1 case), rheumatoid spondylitis (1 case) and rheumatoid arthritis in all cases. After 11 weeks treatment by oral corticothérapy at the daily posology of 1 mg/kg/, cicatrization of cutaneous lesions were noted in all the cases. Five reccurences were observed. P.G remains a rare pathology with no difference on races and regions . this is particularly true on children. Our serie, is remarkable by the high frequency of its paediatric forms. As for clinical and evolutive aspects as well as associated pathologies, findings are comparable with those described other series | |
15944295 | The non-MHC quantitative trait locus Cia5 contains three major arthritis genes that differ | 2005 Jun 15 | Cia5 is a locus on rat chromosome 10 which regulates the severity of collagen- and pristane-induced arthritis (CIA and PIA). To refine the region toward positional identification, Cia5 subcongenic strains were generated and studied in PIA and CIA. The protective effect of the telomeric locus Cia5a was confirmed in both models. A second arthritis severity locus (Cia5d) was identified within the most centromeric portion of Cia5. DA.F344(Cia5d) rats had a significantly lower median arthritis severity index in PIA, but not in CIA, compared with DA. On histologic analyses DA.F344(Cia5a) and DA.F344(Cia5d) congenics with PIA preserved a nearly normal joint architecture compared with DA, including significant reduction in synovial hyperplasia, pannus, angiogenesis, inflammatory infiltration, bone and cartilage erosions. Cia5 and Cia5a synovial levels of IL-1beta mRNA were reduced. Although both DA.F344(Cia5) and DA.F344(Cia5a) rats were protected in CIA, the arthritis scores of DA.F344(Cia5) were significantly higher than those of DA.F344(Cia5a), suggesting the existence of a third locus where F344-derived alleles centromeric from Cia5a contribute to increased arthritis severity. The existence of the third locus was further supported by higher levels of autoantibodies against rat type II collagen in DA.F344(Cia5) congenics compared with DA.F344(Cia5a). Our results determined that Cia5 contains three major arthritis severity regulatory loci regulating central events in the pathogenesis of arthritis, and differentially influencing CIA and PIA. These loci are syntenic to regions on human chromosomes 17q and 5q implicated in the susceptibility to rheumatoid arthritis, suggesting that the identification of these genes will be relevant to human disease. | |
16529878 | The effect on health of alternate day calorie restriction: eating less and more than neede | 2006 | Restricting caloric intake to 60-70% of normal adult weight maintenance requirement prolongs lifespan 30-50% and confers near perfect health across a broad range of species. Every other day feeding produces similar effects in rodents, and profound beneficial physiologic changes have been demonstrated in the absence of weight loss in ob/ob mice. Since May 2003 we have experimented with alternate day calorie restriction, one day consuming 20-50% of estimated daily caloric requirement and the next day ad lib eating, and have observed health benefits starting in as little as two weeks, in insulin resistance, asthma, seasonal allergies, infectious diseases of viral, bacterial and fungal origin (viral URI, recurrent bacterial tonsillitis, chronic sinusitis, periodontal disease), autoimmune disorder (rheumatoid arthritis), osteoarthritis, symptoms due to CNS inflammatory lesions (Tourette's, Meniere's) cardiac arrhythmias (PVCs, atrial fibrillation), menopause related hot flashes. We hypothesize that other many conditions would be delayed, prevented or improved, including Alzheimer's, Parkinson's, multiple sclerosis, brain injury due to thrombotic stroke atherosclerosis, NIDDM, congestive heart failure. Our hypothesis is supported by an article from 1957 in the Spanish medical literature which due to a translation error has been construed by several authors to be the only existing example of calorie restriction with good nutrition. We contend for reasons cited that there was no reduction in calories overall, but that the subjects were eating, on alternate days, either 900 calories or 2300 calories, averaging 1600, and that body weight was maintained. Thus they consumed either 56% or 144% of daily caloric requirement. The subjects were in a residence for old people, and all were in perfect health and over 65. Over three years, there were 6 deaths among 60 study subjects and 13 deaths among 60 ad lib-fed controls, non-significant difference. Study subjects were in hospital 123 days, controls 219, highly significant difference. We believe widespread use of this pattern of eating could impact influenza epidemics and other communicable diseases by improving resistance to infection. In addition to the health effects, this pattern of eating has proven to be a good method of weight control, and we are continuing to study the process in conjunction with the NIH. | |
16849501 | PKC-theta-deficient mice are protected from Th1-dependent antigen-induced arthritis. | 2006 Aug 1 | T cell effector functions contribute to the pathogenesis of rheumatoid arthritis. PKC-theta transduces the signal from the TCR through activation of transcription factors NF-kappaB, AP-1, and NFAT. We examined the effects of PKC-theta deficiency on two Th1-dependent models of Ag-induced arthritis and found that PKC-theta-deficient mice develop disease, but at a significantly diminished severity compared with wild-type mice. In the methylated BSA model, cellular infiltrates and articular cartilage damage were mild in the PKC-theta-deficient mice as compared with wild-type mice. Quantitation of histopathology reveals 63 and 77% reduction in overall joint destruction in two independent experiments. In the type II collagen-induced arthritis model, we observed a significant reduction in clinical scores (p < 0.01) in three independent experiments and diminished joint pathology (p < 0.005) in PKC-theta-deficient compared with wild-type littermates. Microcomputerized tomographic imaging revealed that PKC-theta deficiency also protects from bone destruction. PKC-theta-deficient CD4(+) T cells show an impaired proliferative response, decreased intracellular levels of the cytokines IFN-gamma, IL-2, and IL-4, and significantly diminished cell surface expression of the activation markers CD25, CD69, and CD134/OX40 on memory T cells. We demonstrate decreased T-bet expression and significantly reduced IgG1 and IgG2a anti-collagen II Ab levels in PKC-theta-deficient mice. Collectively, our results demonstrate that PKC-theta deficiency results in an attenuated response to Ag-induced arthritis, which is likely mediated by the reduced T cell proliferation, Th1/Th2 cell differentiation and T cell activation before and during disease peak. | |
17123065 | FR180204, a novel and selective inhibitor of extracellular signal-regulated kinase, amelio | 2007 Jan | Extracellular signal-regulated kinase (ERK), a serine/threonine protein kinase of the mitogen-activated protein kinase superfamily, is activated by various stimuli in inflammatory cells. We recently described FR180204 (5-(2-phenylpyrazolo[1,5-a]pyridin-3-yl)-1H-pyrazolo[3,4-c]pyridazin-3-amine), a novel selective ERK inhibitor. In this paper, we investigated the effect of FR180204 on collagen-induced arthritis (CIA) in DBA/1 mice, an animal model of rheumatoid arthritis (RA) mediated by type II collagen (CII)-reactive T cells and anti-CII antibodies. Preventive administration of FR180204 (100 mg/kg, i.p., b.i.d.) significantly ameliorated the clinical arthritis and body weight loss occurring in the CIA mice. Further, FR180204-treated mice showed a significant decrease in plasma anti-CII antibody levels (62%). FR180204 also attenuated delayed-type hypersensitivity in CII-immunized DBA/1 mice, an inflammatory response elicited by CII-reactive T cells, in a dose-dependent manner (52 and 62% inhibition at 32 and 100 mg/kg, respectively). Moreover, FR180204 inhibited in vitro CII-induced proliferation of lymph node cells prepared from CII-immunized mice, in which CII-specific T cells are known to undergo specific proliferation. In conclusion, our results suggest that ERK regulates both the cell-mediated and humoral immune responses in the development of CIA. ERK inhibitors may be useful as therapeutic reagents for the treatment of RA. | |
16385511 | Interleukin-6 modulates production of T lymphocyte-derived cytokines in antigen-induced ar | 2006 Jan | OBJECTIVE: To determine the cellular mediators of antigen-induced arthritis (AIA) and the relative contribution of members of the interleukin-6 (IL-6) family and tumor necrosis factor (TNF) in AIA. METHODS: AIA was induced in mice deficient in T and B lymphocytes, IL-6 (IL-6(-/-)), TNF (TNF(-/-)), IL-11 receptor, and oncostatin M receptor, by immunization with methylated bovine serum albumin (mBSA) followed 7 days later by intraarticular injection of mBSA. Arthritis severity was assessed histologically, and T lymphocyte responses were assessed in vitro. Anti-TNF neutralizing antibody was administered to wild-type mice during AIA. Bone marrow osteoclasts were generated in vitro via culture with RANKL and macrophage colony-stimulating factor. RESULTS: AIA was dependent on CD4+ T lymphocytes, but not CD8+ T lymphocytes or B cells. IL-6(-/-) mice had reduced AIA severity and fewer osteoclasts at sites of bone erosion. This protective effect was not seen with a deficiency of other IL-6 family members and was similar to that in TNF(-/-) mice or wild-type mice receiving TNF blockade treatment. IL-6(-/-) CD4+ T lymphocytes from draining lymph nodes had reduced antigen-induced proliferation and produced less IL-17 and less RANKL, relative to osteoprotegerin, than cells from wild-type mice. Bone marrow from IL-6(-/-) mice generated fewer osteoclasts in vitro than bone marrow from either wild-type or TNF(-/-) mice. CONCLUSION: AIA is driven by CD4+ T lymphocytes. IL-6 is an important mediator of bone destruction in AIA because it regulates T lymphocyte production of key osteoclastogenic cytokines and inflammation-induced bone marrow osteoclast differentiation. These findings have implications for reducing bone and joint damage in rheumatoid arthritis. | |
16607767 | Temporomandibular joint ankylosis. A possible complication in juvenile psoriatic rheumatis | 2005 Jul | The authors present a rare case of bilateral temporomandibular joint ankylosis secondary to polyarticular juvenile psoriatic arthritis in a 24 year-old man. The patient first presented with arthritis of his right elbow joint at the age of 9, followed by involvement of the distal inter-phalangeal joints of his right foot and both sacroiliac joints. Serum rheumatoid factor was not detected. At the age of 16 he developed psoriatic lesions affecting his nails and skin. By the age of 20, clinical and radiological evidence of arthritis was detected in his temporomandibular joint (TMJ). Subsequently, the patient developed bilateral TMJ ankylosis over a period of 4 years. The patient was managed by bilateral resection of the ankylosis bone blocks, mobilization of the mandible and interposition of Dacron material between the two neo-articular surfaces. 10 months postoperatively the patient maintained an inter-incisal distance of 3 cm. Postoperative mechano-therapy was hindered by the limited use of the patients' hands. | |
16802368 | Increased extracellular levels of the novel proinflammatory cytokine high mobility group b | 2006 Jul | OBJECTIVE: To investigate the expression of the novel proinflammatory cytokine high mobility group box chromosomal protein 1 (HMGB-1) in the salivary glands of patients with Sjögren's syndrome (SS) and patients with sicca symptoms. METHODS: Biopsy samples from the minor labial salivary glands of patients with SS, patients with sicca symptoms but no diagnosis of SS, and healthy controls were investigated. Expression of HMGB-1, tumor necrosis factor (TNF), and interleukin-1beta (IL-1beta) was analyzed using immunohistochemical staining on consecutive cryosections. RESULTS: Increased expression of HMGB-1 was observed among the large infiltrates of mononuclear cells found in biopsy samples from patients with SS, and the degree of extracellular HMGB-1 was significantly higher in patients with SS compared with patients with sicca symptoms and with healthy controls (P < 0.05 and P < 0.01, respectively). Cellular expression of TNF was increased in patients with SS and in patients with sicca symptoms. In addition, the level of secreted TNF was significantly higher in patients with SS than in healthy controls (P < 0.05). Intracellular expression of IL-1beta was detected in all groups, while extracellular IL-1beta was observed almost exclusively among the infiltrating mononuclear cells of patients with SS. CONCLUSION: The increased amount of extracellular HMGB-1 observed in salivary glands of patients with SS indicates that HMGB-1 is involved in the inflammatory process of the disease. This cytokine, along with TNF and IL-1beta, may form a proinflammatory loop that promotes the chronic features of the glandular inflammation in SS. | |
16316423 | Elevated serum levels of soluble E-cadherin in patients with primary Sjögren's syndrome. | 2005 Dec | The aim of this study was to investigate serum levels of soluble E-cadherin (sE-cadherin) in relation to lymphocytic organization and to characterize the expression of E-cadherin and integrin alphaEbeta7/CD103 in salivary gland epithelium of patients with Sjögren's syndrome (SS). Serum levels of sE-cadherin were significantly increased in SS compared to non-SS and nonsignificantly in germinal centre (GC)+ compared to GC- patients. Membrane-bound E-cadherin was detected on the majority of acinar and ductal epithelial cells in both SS and non-SS. alphaEbeta7/CD103-positive cells were found scattered in focal infiltrates and GC, and in small clusters close to ductal and acinar epithelium at an increased level in SS compared to non-SS. Interestingly, E-cadherin-positive cells were detected randomly dispersed in focal lymphocytic infiltrates in 10/21 patients. By double-labelling, the cells with the E-cadherin-positive component were identified as CD68(+) macrophages. Elevated serum levels of sE-cadherin indicate an increased epithelial cell turnover and shedding, and sE-cadherin deserves further analysis as a potential diagnostic tool for SS. | |
15761725 | Coexisting ankylosing spondylitis and Sjogren's syndrome: a case report. | 2005 Aug | Sjogren's syndrome and ankylosing spondylitis can occur either alone or in conjunction with other disorders. In this article we report a female patient afflicted with ankylosing spondylitis and Sjogren's syndrome. | |
17057945 | Anti-beta2-glycoprotein I in Sjogren's syndrome is associated with parkinsonism. | 2007 May | The nervous system may be involved in up to 30% of patients with Sjogren's syndrome (SS). We describe three patients with Sjogren's syndrome and a concomitant parkinsonian syndrome. Elevated titers of anti-beta2-glycoprotein I IgG were found in the serum of all three patients. This autoantibody is strongly associated with anticardiolipin (aCL) antibodies, antiphospholipid syndrome (APS), and thromboembolic phenomena, but its role in the pathogenesis of the parkinsonian disorder in SS is unclear. These patients may present a subtype of SS patients in which the presence of aCL antibodies is associated with central nervous system involvement predominantly in the basal ganglia. |