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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17143981 | A study to standardize quantitative evaluation of parotid gland scintigraphy in patients w | 2006 Dec | OBJECTIVE: To standardize quantitative parotid gland scintigraphy for diagnosing Sjögren's syndrome (SS). METHODS: Forty-five patients with SS and 23 controls were studied. Dynamic images were obtained up to 50 min after the injection of 185 MBq 99mTc-pertechnetate and salivary excretion was stimulated with lemon juice orally at 40 min after the injection. Peak count and uptake speed in the uptake phase, and excretion speed and excretion fraction in the excretion phase were calculated. RESULTS: The levels of peak count, uptake speed, and excretion speed in the patients with SS were significantly lower than the levels in the controls, whereas there was no significant difference of excretion fraction level between the patients with SS and the controls. The calculations of peak count and excretion speed levels, which were closely related with the focus scores of minor salivary glands and the amount of stimulated whole saliva, showed higher reproducibility, sensitivity, and specificity than those of uptake speed and excretion fraction levels. CONCLUSION: The calculations of peak count and excretion speed were eligible to standardize quantitative parotid gland scintigraphy for diagnosing SS. | |
16792139 | Fanconi's syndrome and distal (type 1) renal tubular acidosis in a patient with primary Sj | 2006 Jun | Tubulointerstitial nephritis is a well-recognized complication in primary Sjögrens syndrome. Fanconi's syndrome is a far less frequent complication compared with distal tubular dysfunction. We here describe a 49-year-old woman with primary Sjögren's syndrome. In 1997, she was diagnosed with primary Sjögren's syndrome with tubulointerstitial nephritis, and was then treated with oral prednisolone for the tubulointerstitial nephritis. In 2002, she was referred to our hospital because of progressive fatigue. At that time, biclonal spike on serum protein (IgG-kappa and IgA-kappa) and Bence-Jones protein in urine were found. Bone marrow aspiration showed 1.0% plasma cell infiltration. Thus, a diagnosis of monoclonal gammopathy of undetermined significance (MGUS) was made. In 2004, she was again admitted to our hospital because of mild renal dysfunction and hypokalemia. Laboratory evaluation showed inappropriate, alkaline urine in hyperchloremic metabolic acidosis and a positive urine anion gap, indicating the presence of distal (Type 1) renal tubular acidosis (RTA). The urine concentration defect was also found. Further studies revealed proximal tubular dysfunction, including renal glycosuria, generalized aminoaciduria, phosphaturia, uricosuria and proximal RTA. The kidney biopsy represented diffuse and severe tubulointerstitial nephritis with dense infiltrates of lymphocytes and IgA and K light chain-positive plasma cells. No findings of multiple myeloma or malignant lymphoma were observed. In conclusion, our patient had Sjögren's syndrome with MGUS and exhibited dysfunction of both proximal tubule (Fanconi's syndrome) and distal tubule, which may be attributed to diffuse tubulointerstitial nephritis. | |
17911635 | Adiponectin enhances IL-6 production in human synovial fibroblast via an AdipoR1 receptor, | 2007 Oct 15 | Articular adipose tissue is a ubiquitous component of human joints, and adiponectin is a protein hormone secreted predominantly by differentiated adipocytes and involved in energy homeostasis. We investigated the signaling pathway involved in IL-6 production caused by adiponectin in both rheumatoid arthritis synovial fibroblasts and osteoarthritis synovial fibroblasts. Rheumatoid arthritis synovial fibroblasts and osteoarthritis synovial fibroblasts expressed the AdipoR1 and AdipoR2 isoforms of the adiponectin receptor. Adiponectin caused concentration- and time-dependent increases in IL-6 production. Adiponectin-mediated IL-6 production was attenuated by AdipoR1 and 5'-AMP-activated protein kinase (AMPK)alpha1 small interference RNA. Pretreatment with AMPK inhibitor (araA and compound C), p38 inhibitor (SB203580), NF-kappaB inhibitor, IkappaB protease inhibitor, and NF-kappaB inhibitor peptide also inhibited the potentiating action of adiponectin. Adiponectin increased the kinase activity and phosphorylation of AMPK and p38. Stimulation of synovial fibroblasts with adiponectin activated IkappaB kinase alpha/beta (IKK alpha/beta), IkappaBalpha phosphorylation, IkappaBalpha degradation, p65 phosphorylation at Ser (276), p65 and p50 translocation from the cytosol to the nucleus, and kappaB-luciferase activity. Adiponectin-mediated an increase of IKK alpha/beta activity, kappaB-luciferase activity, and p65 and p50 binding to the NF-kappaB element and was inhibited by compound C, SB203580 and AdipoR1 small interference RNA. Our results suggest that adiponectin increased IL-6 production in synovial fibroblasts via the AdipoR1 receptor/AMPK/p38/IKKalphabeta and NF-kappaB signaling pathway. | |
21794315 | Costs of the standard rheumatology care in active rheumatoid arthritis patients seen in a | 2006 May | OBJECTIVE: To assess the costs of standard care in patients with active rheumatoid arthritis (RA) seen in a tertiary care center in México City in the context of a clinical trial. To analyze the relationship between costs and utility units obtained by the patients in this scenario. PATIENTS AND METHODS: This economic evaluation was performed during a clinical trial with a 48-week followup in a tertiary care center in México City. The trial compared the efficacy of omega-3 fatty acids versus placebo in patients with active RA who also received standard rheumatology care. The costs of medical consultations, complementary tests and drugs were assessed. Other direct costs were also measured. Hypothetical scenarios with fewer medical consultations and complementary tests than those in the clinical trial were also analyzed. Utilities were assessed by the Health Utility Index. A cost-utility ratio was calculated using the baseline utilities score as comparator. A descriptive statistical analysis was performed. RESULTS: Ninety RA patients (83 women [92%], age [X ± SD] 43.2 ± 14.2 years with disease duration of 3.3 ± 4.6 years) were included. Data from 88 patients were analyzed. The total direct costs were 152,704.11 US$ 2005 divided into medical attention (78,386.43 US$ 2005, 51.33%), drugs (39,339.5 US$ 2005, 25.76%) and other direct costs (34,978.18 US$ 2005. 22.91%). In scenarios with fewer medical consultations and complementary tests than those in the clinical trial, the total direct costs ranged from 39,507.4 to 103,880.6 US$ 2005. Patients improved by a mean of 0.18 utility units on a 0-1 scale equivalent to 0.18 quality adjusted lifeyears (QALYs). The cost-utility ratios ranged from 2,494.1 to 9,640.38 US$ 2005 per QALY in the scenarios analyzed. CONCLUSIONS: The direct costs of the standard care of RA in the scenarios analyzed are substantial in the social and economic context of Mexico. The cost per gained QALY is high. | |
18292571 | Inhibition of monocyte chemoattractant protein-1 ameliorates rat adjuvant-induced arthriti | 2008 Mar 1 | Chemokines, including RANTES/CCL5 and MCP-1/CCL2, are highly expressed in the joints of patients with rheumatoid arthritis, and they promote leukocyte migration into the synovial tissue. This study was conducted to determine whether the inhibition of RANTES and MCP-1 therapeutically was capable of ameliorating rat of adjuvant-induced arthritis (AIA). Postonset treatment of AIA using a novel inhibitor for endogenous MCP-1 (P8A-MCP-1) improved clinical signs of arthritis and histological scores measuring joint destruction, synovial lining, macrophage infiltration, and bone erosion. Using immunohistochemistry, ELISA, real-time RT-PCR, and Western blot analysis, we defined joint inflammation, bony erosion, monocyte migration, proinflammatory cytokines, and bone markers, and p-p38 levels were reduced in rat AIA treated with P8A-MCP-1. In contrast, neither the dominant-negative inhibitor for endogenous RANTES (44AANA47-RANTES) nor the CCR1/CCR5 receptor antagonist, methionylated-RANTES, had an effect on clinical signs of arthritis when administered after disease onset. Additionally, therapy with the combination of 44AANA47-RANTES plus P8A-MCP-1 did not ameliorate AIA beyond the effect observed using P8A-MCP-1 alone. Treatment with P8A-MCP-1 reduced joint TNF-alpha, IL-1beta, and vascular endothelial growth factor levels. P8A-MCP-1 also decreased p38 MAPK activation in the joint. Our results indicate that inhibition of MCP-1 with P8A-MCP-1 after the onset of clinically detectable disease ameliorates AIA and decreases macrophage accumulation, cytokine expression, and p38 MAPK activation within the joint. | |
16454534 | Fulfilling an unmet need in psoriasis : do biologicals hold the key to improved tolerabili | 2006 | Psoriasis is a chronic inflammatory disease of the skin affecting approximately 2% of the world's population. Traditional systemic treatments, including methotrexate, ciclosporin, psoralen plus UVA (PUVA), oral retinoids and fumaric acid esters, are widely used for severe disease and are effective in the short term. Severe psoriasis is a chronic disease and patients and physicians have expressed concerns about possible harm from organ toxicity, such as skin cancer (PUVA), hyperlipidaemia (retinoids), renal (ciclosporin) or hepatotoxicity (methotrexate). Long-term monitoring is required and may not detect early organ damage. The pathophysiology of psoriasis remains to be clarified, but advances toward the understanding of the immunological basis of psoriasis have uncovered the involvement of immunological pathways; for example, the role of tumour necrosis factor (TNF)-alpha, T cell proliferation and T cell activation, and migration to the epidermis. This advancement in knowledge combined with developments in recombinant technologies has led to the development of target-specific therapies. Biological agents are defined as proteins that can be extracted from animal tissue or produced via recombinant DNA technologies and possess pharmacological activity. Adalimumab, alefacept, infliximab, efalizumab and etanercept are examples of biological agents currently used for the treatment of psoriasis. Some of these are also therapy for other autoimmune conditions, such as rheumatoid arthritis and Crohn's disease. These biological agents are effective in psoriasis but raise new safety concerns. Information on the safety of biological agents in conditions such as rheumatoid arthritis and Crohn's disease can not be directly extrapolated to psoriasis. An increased incidence of lymphomas has been postulated to be associated with etanercept, infliximab and adalimumab; serious infections, such as tuberculosis, have also been reported with these three biologicals, all of which target TNF-alpha. Demyelinating disorders, such as multiple sclerosis, have been reported with some biologicals as has congestive heart failure. Alefacept, because of its mechanism of action of lowering the number of active T cells, is associated with low T cell counts. Efalizumab has been associated with thrombocytopenia and haemolytic anaemia. Data on the safety of >2.5 years' continuous treatment with efalizumab are reassuring and a valuable beginning to understanding the role and risk of harm of long-term therapy for a chronic disease. Longer follow-up studies and safety databases, for each of the biologicals used in psoriasis, are needed to ensure both prolonged efficacy and minimal risk of harm. | |
18046756 | Introduction to Genetic Analysis Workshop 15 summaries. | 2007 | The 15th biennial Genetic Analysis Workshop (GAW15) took place November 11-15, 2006 in St. Pete Beach, Florida. The workshop's primary focus was on the appropriate linkage, association, and other analyses of the increasingly large datasets generated by genetics research. A record number of participants (N=350) contributed 252 papers to GAW15. These contributions were organized into 17 presentation groups, with a range of 11 to 18 papers in each group (median of 15 papers per group). The data sets--or "problems"--for GAW15 included information from two real data sets and a simulated data set. The first problem utilizing real data included gene expression as the phenotype and genome-wide markers for linkage and association studies. The second problem allowed for detecting and characterizing genetic effects for rheumatoid arthritis. And the simulated problem was generated to reflect the data structure underlying the rheumatoid arthritis study. Further details on GAW15 are provided here, and the primary findings from the workshop are highlighted in the following group summary papers. | |
18805608 | Acquired Gitelman syndrome in a patient with primary Sjögren syndrome. | 2008 Dec | Acquired Gitelman syndrome (GS) associated with Sjögren syndrome (SS) is rare, and the test to determine the pathophysiological state of acquired GS in patients with primary SS has not been reported previously. A 47-year-old woman with sicca complex presented to our clinic with intermittent muscle cramping and weakness involving both lower extremities over several months. Laboratory findings showed hypokalemic metabolic alkalosis, hypomagnesemia, and hypocalciuria, which met the criteria for GS. Diagnostic evaluation identified primary SS as the cause of the acquired GS. Light microscopic examination of renal tissue from the patient showed mild tubulointerstitial nephritis. Immunohistochemical staining of renal tissue showed the absence of the sodium-chloride cotransporter (NCCT) in the distal convoluted tubules. Incubation of the patient's serum with normal mouse kidney tissue showed a pattern of NCCT in the distal convoluted tubules similar to that of incubation of normal mouse kidney with the rabbit polyclonal anti-NCCT antibody. This is a rare case of acquired GS associated with primary SS, and our findings suggest the presence of circulating autoantibodies to NCCT. | |
17329922 | Successful treatment of primary Sjögren's syndrome with chronic natural killer lymphocyto | 2007 | We report a patient with Sjögren's syndrome and chronic natural killer lymphocytosis, who developed severe neutropenia, autoimmune hemolytic anemia, and immune thrombocytopenia. High-dose prednisolone therapy improved the hemolytic anemia and thrombocytopenia, but not the CD16(+) CD56(-) NK lymphocytosis completely. Interestingly, indomethacin farnesil (a prodrug of indomethacin) was effective for myalgia and also decreased the number of CD16(+) CD56(-) NK cells. NK lymphocytosis is rarely associated with autoimmune disease, but the combination of indomethacin and steroid therapy may have a favorable effect for such patients. | |
16699050 | Lymphoma and other malignancies in primary Sjögren's syndrome. | 2006 Jun | Low peripheral CD4+ counts or low CD4+/CD8+ ratios may be important risk factors for lymphoma in SS | |
18754812 | Dendritic cells modulated by innate immunity improve collagen-induced arthritis and induce | 2009 Jan | Dendritic cells (DCs) mediate interactions between innate and specific immunity and may induce regulatory mechanisms. We investigated the effects of modulated DCs in mice with collagen-induced arthritis (CIA) and tested the responses of cells to induced naturally occurring regulatory T cells. DCs were stimulated or not with DNA or lipopolysaccharide (LPS) for 24 hr. DC maturation was assayed, and then modulated DCs were intraperitoneally injected on day 14 into DBA/1 mice to treat CIA. In addition to arthritis scores and type 2 collagen (CII) response, the induction of CD4(+) CD25(+) T cells was analysed by flow cytometry in peripheral blood and the expression of Foxp3, transforming growth factor (TGF)-beta, interleukin (IL)-10 and cytotoxic T-lymphocyte antigen (CTLA)-4 was quantified. Finally, the expression of indoleamine-2,3-dioxygenase (IDO) was assayed in DCs. In comparison with LPS-stimulated DCs, plasmid-stimulated DCs expressed lower levels of major histocompatibility complex (MHC) class II, CD40, CD80 and CD86 molecules and secreted less IL-12p70, interferon (IFN)-gamma, IL-10 and TNF-alpha, displaying a semi-mature phenotype. Compared with non-stimulated DCs, stimulated DCs improved arthritis scores when injected after immunization, without modifying the T helper type 1 (Th1)/Th2 balance of the immune response against collagen. Stimulated DCs induced markers for regulatory T cells (Foxp3, TGF-beta1 and CTLA-4) in vivo. Only LPS-stimulated DCs expressed IDO, which may explain their better therapeutic efficacy. Regulatory mechanisms were induced using DCs modulated by innate immunity stimulators. Innate immunity mechanisms do not require the presence of the disease-causing antigen, even in T- and B-cell specific diseases. Our results have implications for the treatment of rheumatoid arthritis, an autoimmune disease whose triggering antigen has not been identified, and substantially clarify the role of regulatory T cells in CIA. | |
18583934 | New roles for the major human 3'-5' exonuclease TREX1 in human disease. | 2008 Jun 15 | Aicardi-Goutières syndrome (AGS), Systemic Lupus Erythematosus (SLE), Familial Chilblain Lupus (FCL) and Retinal Vasculopathy and Cerebral Leukodystrophy (RVCL) {a new term encompassing three independently described conditions with a common etiology--Cerebroretinal Vasculopathy (CRV), Hereditary Vascular Retinopathy (HVR) and Hereditary Endotheliopathy, Retinopathy and Nephropathy (HERNS)}--have previously been regarded as distinct entities. However, recent genetic analysis has demonstrated that each of these diseases maps to chromosome 3p21 and can be caused by mutations in TREX1, the major human 3'-5' exonuclease. In this review, we discuss the putative functions of TREX1 in relationship to the clinical, genetic and functional characteristics of each of these conditions. | |
18494743 | Self-application of single-use eyedrop containers in an elderly population: comparisons wi | 2008 Dec | PURPOSE: To test whether patients aged >or=80 years can safely and successfully apply eyedrops from a single-use eyedrop container without support, and to compare the results with those of younger patients using single-use containers and older patients using standard eyedrop bottles. METHODS: Patients aged >or=80 years who had no physical or mental conditions hindering self-application of eyedrops and actually did so because of glaucoma or dry eyes were included consecutively in the study group (n = 44) in order to perform self-application of eyedrops from single-use eyedrop containers. Patients were observed meticulously by two investigators, who documented practical problems during the procedure in a checklist. In control group A (n = 22), glaucoma or sicca patients aged between 50 and 65 years applied drops from single-use eyedrop containers; in control group B (n = 28), glaucoma or sicca patients aged >or=80 years used a traditional eyedrop bottle. RESULTS: Successful application of the drops into the conjunctival sac was achieved by 57% in the study group (95% and 89% in control groups A and B, respectively). Scratching of the eyedrop container along the conjunctiva or cornea was observed in 68% of the study group (41% and 61% in control groups A and B, respectively). Frequency of problems during opening and self-application of single-use eyedrop containers in the study group showed an inverse correlation to visual acuity in the better eye and previous experience with this kind of eyedrop container. CONCLUSION: Older patients have massive problems in self-administering eyedrops from single-use containers. Factors influencing the success of self-application may include the patient's previous experience with this kind of eyedrop container and the patient's visual acuity. | |
18355474 | [Primary Gougerot-Sjogren's syndrome presenting as a cerebellar syndrome]. | 2007 Dec | Primary Sjogren's syndrome is an autoimmune exocrinopathy with various extraglandular complications. Central neurological manifestations were described in 20 percent of cases. Cerebellar syndrome is uncommon in Sjogren's syndrome, but can occur after diagnosis, or rarely as an inaugural sign of the disease. We report the case of a 54-year-old man who presented a cerebellar syndrome with xerostomy and xerophthalmos. The diagnosis of primary Sjorgren's syndrome was confirmed on the accessory salivary gland biopsy. The patient received oral and intravenous corticosteroid therapy associated with cyclophosphamide monthly. Outcome was good. | |
17762603 | An important role for B-cell activation factor and B cells in the pathogenesis of Sjögren | 2007 Sep | PURPOSE OF REVIEW: This review provides an update on the specific, strong association between dysregulated production of the cytokine B-cell activation factor and Sjögren's syndrome, and offers new perspectives on potential pathogenic mechanisms. RECENT FINDINGS: Excess B-cell activation factor in mice triggers Sjögren's syndrome-like symptoms, and elevated serum B-cell activation factor in humans correlates with Sjögren's syndrome. B-cell activation factor is produced locally by activated monocytes, T cells and dendritic cells, and by epithelial cells and infiltrating B cells. Moreover, recent data in humans suggest that the innate immune system plays a role as an initiator of immune disorders in inflamed tissues. SUMMARY: Recent data have demonstrated the critical role of B-cell activation factor and B cells in the pathogenesis of Sjögren's syndrome, and its association with B lymphomas. Moreover, B-cell depleting treatments have confirmed the critical role of B cells in Sjögren's syndrome. Excess B-cell activation factor possibly corrupts B-cell tolerance and allows the emergence of self-reactive B cells that efficiently present antigen to T cells. In addition, B-cell activation factor may stimulate T-cell independent activation of B cells via Toll-like receptors; this recently identified mechanism could also play a separate, detrimental role in autoimmunity. | |
17341155 | Recurrence after topical nonpreserved methylprednisolone therapy for keratoconjunctivitis | 2007 Feb | BACKGROUND: The aim of this study was to evaluate the prevalence of long-term recurrence after topical nonpreserved methylprednisolone pulse therapy for the treatment of keratoconjunctivitis sicca (KCS) with Sjögren's syndrome. METHODS: A total of 106 eyes of 53 Sjögren's syndrome patients were included in the study. All patients were treated with topical nonpreserved 1% methylprednisolone solution. Initial therapy consisted of eyedrops 4 times a day for 2 weeks, and then patients were reevaluated and tapered off the medication every 2 weeks until discontinuation. Tear film breakup time (TBUT), Schirmer test, corneal fluorescein staining, and subjective symptom scores were measured. Additionally, impression cytology of the bulbar conjunctiva was performed. The over-all success rates and success period were determined using the Kaplan-Meier survival curve. RESULTS: A reduction in subjective symptoms and fluorescein staining, and an improvement in TBUT and Schirmer test results, was observed after treatment (P<0.001). Impression cytology specimens revealed a significantly increased number of periodic acid-Schiff-positive cells after treatment. After the first pulse therapy, mean survival was 56.6 weeks and 11 (20.8%) patients recurred. After the second pulse therapy, mean survival was 72.4 weeks and only 1 patient recurred. No serious complications, including intraocular pressure elevation and cataract formation, were encountered during the entire follow-up period. CONCLUSIONS: Topical nonpreserved methylprednisolone pulse therapy proved to be a safe, effective long-term treatment of improving subjective and objective dry eye factors in KCS patients with Sjögren's syndrome. | |
16005870 | Male NOD mouse external lacrimal glands exhibit profound changes in the exocytotic pathway | 2006 Jan | The lacrimal glands of male NOD mice exhibit many of the features of the human lacrimal gland in patients afflicted with the autoimmune disease, Sjögren's syndrome, including loss of secretory functions and lymphocytic infiltration into the lacrimal gland. To elucidate the early changes in the secretory pathway associated with development of Sjögren's syndrome, we investigated the organization of the exocytotic pathway in lacrimal glands of age-matched male BALB/c and NOD mice. Cryosections from lacrimal glands from 1 and 4 month male BALB/c and NOD mice were processed for confocal fluorescence and electron microscopic evaluation of different participants in exocytosis. No changes in apical actin filaments were noted in glands from NOD mice, but these glands exhibited thickening of basolateral actin relative to that seen in the BALB/c mice. Rab3D immunofluorescence associated with mature secretory vesicles was distributed abundantly in a continuous vesicular network concentrated beneath the apical plasma membrane in glands from 1 and 4 month BALB/c mice. In glands from 1 month NOD mice, rab3D immunofluorescence exhibited marked discontinuity and irregularity in the vesicular labeling pattern. While this change was also detected in glands from 4 month NOD mice, many of these glands exhibited an additional extension of rab3D labeling through the cell to the basolateral membrane. Electron microscopic analysis confirmed the formation of irregularly shaped, unusually large secretory vesicles in lacrimal glands from NOD mice. Quantitation of multiple secretory vesicles from electron micrographs revealed a significant (p< or =0.05) increase in the percentage of secretory vesicles incorporated into multivesicular aggregates in lacrimal glands from 1 and 4 month NOD mice compared to BALB/c mice. The M3 muscarinic receptor, a key signaling effector of exocytosis, was redistributed away from its normally basolateral locale in glands from BALB/c mice, with concomitant enrichment in intracellular aggregates in glands from NOD mice. These findings show that lacrimal glands in NOD mice as young as 1 month contain aberrant secretory vesicles with altered effector composition that undergo premature cytoplasmic fusion, and that changes in the distribution of the M3 muscarinic receptor occur within the same time frame. | |
17599026 | Pooled analysis of 857 published adult fever of unknown origin cases in Turkey between 199 | 2007 Jul | BACKGROUND: The aim of this study was a systematic review of the literature related to adult fever of unknown origin (FUO) in Turkey. MATERIAL/METHODS: To find the published series, three national and two international databases were searched. RESULTS: Data for 857 patients with the diagnosis of fever of unknown origin were obtained from 13 articles. FUO was defined as fever over 38.3 degrees C that continues at least for three weeks with no diagnosis reached after one week of inpatient investigation in all series (Petersdorf and Beason criteria). Infections, collagen vascular diseases, and neoplasms were found to be the reason of fever in 403 (47.0%), 137 (15.9%), and 126 (14.7%) of the in all 857 patients. The most common infectious disease was tuberculosis (147/403, 36.4%) followed by brucellosis (51/403, 12.6%) and infective endocarditis (39/403, 9.6%). The most common collagen vascular disease was adult-onset Still's Disease (49/137, 35.7%), followed by systemic lupus erythematosus (23/137, 16.7%). The most common neoplasms were Hodgkin's disease (32/126, 25.3%) and non-Hodgkin's lymphoma (32/126, 25.3%). The reason of fever could not be defined in 138/857 (16.1%) patients. CONCLUSIONS: Tuberculosis and brucellosis remain common causes of FUO in Turkey. In addition, lymphomas and adult-onset Still's disease should be considered in the differential diagnosis of a patient admitted with FUO. | |
16857298 | [Exophtalmia revealing a mantle cell lymphoma]. | 2006 Sep | INTRODUCTION: Mantle cell lymphoma reached rarely ophtalmic sphere and salivary glands. CAS REPORT: We reported a dry syndrome seen in a 67 year-old patient. The first patological analysis of accessory salivary glands evoked a primary Gougerot-Sjögren syndrome. Secondary, he presented a mantle cell lymphoma. DISCUSSION: The pathological lack of specifity and the discovery of atypical Gougerot-Sjögren syndrome must encourage complementary immunohistochemical study of salivary glands biopsy. | |
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. |