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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25059987 | Inhibition of adjuvant-induced arthritis by nasal administration of novel synthetic peptid | 2014 Jul 25 | BACKGROUND: Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease mediated by T cells. The aim of the present study was to investigate the therapeutic efficacy of synthetic peptides (HP-R1, HP-R2 and HP-R3), derived from the sequence of 65-kD mycobacterial heat shock protein (HSP), in the treatment of RA using adjuvant-induced arthritis (AA) animal model. METHODS: AA was induced by a single intradermal injection Freund's complete adjuvant in male Lewis rats. At the first clinical sign of disease, rats were administered nasally by micropipette of peptides or phosphate buffer saline (PBS). Disease progression was monitored by measurement of body weight, arthritis score and paw swelling. The changes of histopathology were assessed by hematoxylin eosin staining. The serum levels of tumor necrosis factor (TNF) - alpha and interleukin (IL)-4 were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: The peptides efficiently inhibited the footpad swelling and arthritic symptoms in AA rats. The synthetic peptides displayed significantly less inflammatory cellular infiltration and synovium hyperplasia than model controls. This effect was associated with a suppression of pro-inflammatory cytokine TNF-alpha production and an increase of anti-inflammatory cytokine IL-4 production after peptides treatment. CONCLUSIONS: These results suggest that the synthetic peptides derived from HSP65 induce highly effective protection against AA, which is mediated in part by down-regulation of inflammatory cytokines, and support the view that the synthetic peptides is a potential therapy for RA that may help to diminish both joint inflammation and destruction. | |
24468888 | Activated macrophage-like synoviocytes are resistant to endoplasmic reticulum stress-induc | 2014 May | OBJECTIVE: To explore the characteristic expression of endoplasmic reticulum (ER) stress protein in antigen-induced arthritis models and the role of ER stress in arthritis. METHODS: Effective animal models of rheumatoid arthritis in rabbits and rats were induced by methylated bovine serum albumin and Freund's complete adjuvant. Pathological changes were assessed by magnetic resonance imaging and histological analysis. The expression and localization of ER stress proteins in synovium and peritoneal macrophages (PMΦ) were analyzed by double immunofluorescence staining. RT-PCR was performed to detect mRNA expression of ER stress-related genes. Tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) levels in synoviocytes were measured by RT-PCR and radioimmunoassay. RESULTS: We found that the ER stress marker BiP was highly up-regulated in arthritis synovium and extensively expressed in fibroblast-like synoviocytes (FLS) and macrophage-like synoviocytes (MLS). The expression of the pro-apoptotic factor CHOP/GADD153 was slightly elevated in inflammatory synovium and mainly localized in FLS, but insignificant in MLS. Unexpectedly, increased expression of CHOP was observed in PMΦ in arthritis rats. Likewise, cleaved caspase-3 was rarely expressed in MLS. In addition, induction of ER stress by tunicamycin resulted in significantly increased expression of pro-inflammatory molecules such as IL-1β and TNF-α in cultured inflammatory FLS. CONCLUSION: Differential activation of the ER stress proteins in synovium MLS may contribute to the resistance of synoviocytes to ER stress-induced apoptosis. Furthermore, ER stress is a potential mediator of arthritis inflammation. | |
23316808 | Citrulline: pharmacological perspectives and its role as an emerging biomarker in future. | 2013 Feb | L-Citrulline is a naturally occurring non-essential amino acid, an intermediate in urea cycle and conditionally essential in intestinal pathology. It is a potent hydroxyl radical scavenger and much more effective precursor of arginine and nitric oxide (NO) than arginine itself so exploited in therapeutics. Plasma citrulline concentration is used by clinicians to assess functional enterocyte mass in various chronic and acute small bowel pathologies like short bowel syndrome that has become an indication in clinical practice. Its supplementation is likely to be used in conditions like erectile dysfunction, sickle cell anemia, short bowel syndrome (to restore nitrogen balance), hyperlipidemia, cancer chemotherapy, hypercholestremia, in hyperoxic lung damage, urea cycle disorders, Alzheimers disease, multi-infarct dementia and as an immunomodulator. Its emerging role as a biomarker in intestinal pathology and early diagnosis of Rheumatoid arthritis has spread considerable interest. Antibody detection to Anti-cyclic citrullinated peptide (ACCP) antibodies can be recommended for early detection of RA decreasing joint damage and deformity, because these are detected well before the onset of disease manifestations of RA. The test is highly specific than RF (Rheumatoid factor), with moderate sensitivity, but much useful in differentiating RA from other disorders. Further studies and exploration is required in these areas. | |
25123039 | Biomarkers of cartilage and surrounding joint tissue. | 2014 | The identification and clinical demonstration of efficacy and safety of osteo- and chondro-protective drugs are met with certain difficulties. During the last few decades, the pharmaceutical industry has, in the field of rheumatology, experienced disappointments associated with the development of disease modification. Today, the vast amount of patients suffering from serious, chronic joint diseases can only be offered treatments aimed at improving symptoms, such as pain and acute inflammation, and are not aimed at protecting the joint tissue. This huge, unmet medical need has been the driver behind the development of improved analytical techniques allowing better and more efficient clinical trial design, implementation and analysis. With this review, we aim to provide a brief and general overview of biochemical markers of joint tissue, with special focus on neoepitopes. Furthermore, we highlight recent studies applying biochemical markers in joint degenerative diseases. These disorders, including osteoarthritis, rheumatoid arthritis and spondyloarthropathies, are the most predominant disorders in Europe and the USA, and have enormous socioeconomical impact. | |
23360886 | Carvedilol alleviates adjuvant-induced arthritis and subcutaneous air pouch edema: modulat | 2013 Apr 15 | Rheumatoid arthritis (RA) is a systemic inflammatory disease with cardiovascular complications as the leading cause of morbidity. Carvedilol is an adrenergic antagonist which has been safely used in treatment of several cardiovascular disorders. Given that carvedilol has powerful antioxidant/anti-inflammatory properties, we aimed to investigate its protective potential against arthritis that may add further benefits for its clinical usefulness especially in RA patients with concomitant cardiovascular disorders. Two models were studied in the same rat; adjuvant arthritis and subcutaneous air pouch edema. Carvedilol (10mg/kg/day p.o. for 21days) effectively suppressed inflammation in both models with comparable efficacy to the standard anti-inflammatory diclofenac (5mg/kg/day p.o.). Notably, carvedilol inhibited paw edema and abrogated the leukocyte invasion to air pouch exudates. The latter observation was confirmed by the histopathological assessment of the pouch lining that revealed mitigation of immuno-inflammatory cell influx. Carvedilol reduced/normalized oxidative stress markers (lipid peroxides, nitric oxide and protein thiols) and lowered the release of inflammatory cytokines (TNF-α & IL-6), and eicosanoids (PGE2 & LTB4) in sera and exudates of arthritic rats. Interestingly, carvedilol, per se, didn't present any effect on assessed biochemical parameters in normal rats. Together, the current study highlights evidences for the promising anti-arthritic effects of carvedilol that could be mediated through attenuation of leukocyte migration, alleviation of oxidative stress and suppression of proinflammatory cytokines and eicosanoids. | |
23772084 | Hand bone loss in patients with psoriatic arthritis: posthoc analysis of IMPACT II data co | 2013 Aug | OBJECTIVE: In rheumatoid arthritis (RA), anti-tumor necrosis factor (anti-TNF) treatment is shown to reduce but not to arrest the rate of hand bone loss. This has not been assessed in psoriatic arthritis (PsA). Our objective was to examine changes in cortical hand bone density in patients with PsA treated with placebo or infliximab (IFX). METHODS: Patients in IMPACT II (Induction and Maintenance Psoriatic Arthritis Clinical Trial 2) were randomized to placebo or IFX. After Week 24, all received IFX. In a subset of 120 patients, cortical hand bone density was assessed at Weeks 0, 24, and 54 by digital X-ray radiogrammetry (dxr-BMD) on the same radiographs scored for joint damage. RESULTS: Changes from baseline to 24 weeks in dxr-BMD were -0.30% (SD 1.1%) in the placebo group and -0.08% (SD 1.4%) in the IFX group (p = 0.63). Between baseline and 54 weeks the changes were -0.71% (SD 2.1%) in the placebo group and 0.15% (SD 1.7%) in the IFX group (p = 0.07), and between 24 and 54 weeks -0.41% (SD 1.4%) and 0.23% (SD 0.8%), respectively (p = 0.05). No significant correlation was found between change in dxr-BMD and radiographic damage. CONCLUSION: This pilot study indicates that hand bone loss in PsA patients treated with anti-TNF can be arrested. Assessment of hand bone density may thus be a potential outcome measure for bone involvement and a response variable to treatment in PsA. | |
23784913 | Wnt inhibitory factor 1 deficiency uncouples cartilage and bone destruction in tumor necro | 2013 Sep | OBJECTIVE: Wnt signaling plays a pivotal role in skeletal development and in the control of cartilage and bone turnover. We have recently shown that the secreted Wnt antagonist Wnt inhibitory factor 1 (WIF-1) is mainly expressed in the upper layers of epiphyseal and articular cartilage and, to a lesser extent, in bone. Nevertheless, WIF-1(-/-) mice develop normally. In light of these findings, we undertook this study to analyze the role of WIF-1 in arthritis. METHODS: Expression analyses for WIF-1 were performed by real-time reverse transcription-polymerase chain reaction (RT-PCR). WIF-1(-/-) and tumor necrosis factor (TNF)-transgenic mice were crossbred, and the progression of arthritis in TNF-transgenic WIF-1(-/-) mice and littermate controls was evaluated. Structural joint damage was analyzed by histologic staining, histomorphometry, and micro-computed tomography. Wnt/β-catenin signaling was investigated by real-time RT-PCR and immunofluorescence on primary chondrocytes. RESULTS: WIF-1 expression was repressed by TNFα in chondrocytes and osteoblasts and down-regulated in experimental arthritis and in articular cartilage from patients with rheumatoid arthritis. WIF-1 deficiency partially protected TNF-transgenic mice against bone erosion and loss of trabecular bone, probably as a result of less osteoclast activity. In contrast, arthritis-related cartilage damage was aggravated by WIF-1 deficiency, while overexpression of WIF-1 attenuated cartilage degradation in TNF-transgenic mice. In chondrocytes, TNFα stimulated canonical Wnt signaling, which could be blocked by WIF-1, indicating a direct effect of TNFα and WIF-1 on Wnt signaling in this system. CONCLUSION: These data suggest that WIF-1 may take part in the fine-tuning of cartilage and bone turnover, promoting the balance of cartilage versus bone anabolism. | |
25386583 | Anterior ankle arthrodesis with molded plate: technique and outcomes. | 2014 Sep | BACKGROUND: There is still controversy regarding the best technique for ankle arthrodesis to acheive stable rigid fixation along with reconstructing a functional plantigrade foot. Moreover, existing techniques have complictions related to stability, soft tissue covering, fusion rate, and exposure. METHODS: With the anterior approach exactly on the tibialis anterior sheath, the joint was exposed and previous hardware, if any, was removed and with the safe direct approach, the ankle, hindfoot, and indirectly the subtalar joints were accessed. Then fresh cancellous bone was obtained and complete denudation was preformed. Lastly, a narrow 4.5 millimeter plate was carefully placed on what was determined to be the best final position.In this prospective study, 12 patients with severe ankle pain and arthritis enrolled from February 2010 to January 2012. Eight of them had posttraumatic arthritis and deformity with hardware, two had rheumatoid arthritis, one had poliomyelitis with severe deformity of the foot and knee, and another had chronic ulcerative synovitis of the ankle joint. The patients were assessed clinically and radiographically for an average of two years (range: 13 months to 4 years) for functional recovery, range of motion, stability of the ankle, and imaging evidence of union. RESULTS: Ankle deformities and pain in all 12 cases were corrected. With a short healing time and rapid recovery period, after six weeks all of the patients could walk independently. Also, scores of the Manchester-Oxford Foot Questionnaire (MOXFQ) improved significantly from 69 preoperatively to 33 postoperatively). CONCLUSIONS: Anterior ankle arthrodesis with molded plating can be an easy and safe way to manage deformities and it has excellent fusion rate and sufficient rigid fixation. | |
24292720 | Osteoblast ontogeny and implications for bone pathology: an overview. | 2014 Jan | Osteoblasts are specialized mesenchyme-derived cells accountable for bone synthesis, remodelling and healing. Differentiation of osteoblasts from mesenchymal stem cells (MSC) towards osteocytes is a multi-step process strictly controlled by various genes, transcription factors and signalling proteins. The aim of this review is to provide an update on the nature of bone-forming osteoblastic cells, highlighting recent data on MSC-osteoblast-osteocyte transformation from a molecular perspective and to discuss osteoblast malfunctions in various bone diseases. We present here the consecutive stages occurring in the differentiation of osteoblasts from MSC, the transcription factors involved and the role of miRNAs in the process. Recent data concerning the pathogenic mechanisms underlying the loss of bone mass and architecture caused by malfunctions in the synthetic activity and metabolism of osteoblasts in osteoporosis, osteogenesis imperfecta, osteoarthritis and rheumatoid arthritis are discussed. The newly acquired knowledge of the ontogeny of osteoblasts will assist in unravelling the abnormalities taking place during their differentiation and will facilitate the prevention and/or treatment of bone diseases by therapy directed against altered molecules and mechanisms. | |
24981072 | Increased levels of serum galectin-3 in patients with primary Sjögren's syndrome: associa | 2014 Oct | OBJECTIVES: To explore the potential values of serum galectin-3 (Gal-3) levels in diagnosis of interstitial lung disease (ILD) for patients with primary Sjögren's syndrome (pSS). METHODS: The concentrations of serum Gal-3 and interleukin (IL)-17 were measured by enzymelinked immunosorbent assay (ELISA) in 87 patients with pSS and 30 healthy controls (HC). The levels of plasma C-reactive protein (CRP), rheumatoid factor (RF), immunoglobulin (Ig)G, complement (C3), albumin (ALB) and Fibrinogen (FIB) and erythrocyte sedimentation rate (ESR) were measured. ILD was identified on high-resolution computed tomography. RESULTS: The levels of serum Gal-3 and IL-17 were significantly higher in pSS patients than in HC. Stratification analyses indicated significantly higher levels of Gal-3 in pSS patients with ILD and in those with positive ANCA. In comparison with that of pSS patients without ILD, significantly higher levels of ESR, CRP, FIB, IgG, C3 and lower ALB were detected in pSS patients with ILD. The levels of galectin-3 were correlated positively with the values of CRP, FIB, IgG or IL-17 in patients with pSS. CONCLUSIONS: These findings suggest that higher levels of serum galectin-3 may be associated with the development of pSS, particularly with ILD. | |
24739520 | Alum, an aluminum-based adjuvant, induces Sjögren's syndrome-like disorder in mice. | 2014 Mar | OBJECTIVES: Adjuvant-induced innate immune responses have been suspected to play a role in the initiation of certain autoimmune disorders. This study investigates the role of alum, an aluminum-based adjuvant in the induction of Sjögren's syndrome-like disorder in mice. METHODS: Inbred, female New Zealand Mixed (NZM) 2758 strain of mice were injected with alum. Control mice were treated similarly with PBS. The mice were monitored for salivary gland dysfunction by measuring pilocarpine-induced salivation. Presence of lymphocytic infiltrates within the submandibular glands was studied by histopathology. Autoantibodies to Ro and La proteins were analysed by ELISA and the presence of anti-nuclear antibodies (ANA) was analysed by indirect immunofluorescence. RESULTS: By eight weeks after treatment, the saliva production in the alum-treated mice was significantly decreased in comparison to the PBS-treated mice. This functional loss persisted till the termination of experiments at 20 wks. The incidence and severity of sialoadenitis was significantly higher in the alum-treated mice. Although there were no differences in the levels of anti-Ro/La autoantibodies in sera of alum and PBS-treated groups, the alum group showed higher ANA reactivity. CONCLUSIONS: In the NZM2758 mice, alum induces a Sjögren's syndrome-like disorder that is characterised by chronic salivary gland dysfunction and the presence of lymphocytic infiltrates within the salivary glands. Thus, the potential of aluminum-based adjuvants for induction of autoimmunity should be closely monitored in individuals genetically susceptible to developing autoimmune disorders. | |
24060278 | Reciprocal relation between GADD153 and Del-1 in regulation of salivary gland inflammation | 2013 Dec | Endoplasmic reticulum (ER) stress response is a pivotal regulator of inflammation and cell death. An integral component of ER stress-induced apoptosis is expression of growth arrest- and DNA damage-inducible protein 153 (GADD153). Further, ER stress response is implicated in leukocyte adhesion and recent studies have discovered endogenous inhibitors of leukocyte adhesion including the developmental endothelial locus-1 (Del-1). Accordingly, we tested the hypothesis that Sjögren's syndrome (SS) is associated with increased salivary gland expression of GADD153 and increased leukocyte infiltration in association with decreased Del-1 thereby contributing to inflammation and cell death. We utilized the non-obese diabetic (NOD) mice, a model of SS-like disease, in association with immunostaining and flow cytometry-based studies. Salivary glands of 14-week-old NOD mice displayed a) increased GADD153 expression, b) marked reduction in Del-1, c) inflammatory cell infiltrates including CD3+ T and CD19+ B lymphocytes as well as M1 and M2 macrophages and d) increased pro-inflammatory interleukin (IL)-17 but reduced anti-inflammatory cytokine, IL-10. These changes were accompanied with disruption of mitochondrial membrane potential and significant increase in apoptosis and necrosis of salivary gland cells of NOD than control mice. Our collective observations suggested that GADD153 directly and/or indirectly through downregulation of Del-1 contributes importantly to salivary gland inflammation and cell death. To establish the relevance of GADD153 and Del-1 for the human condition, lower lip biopsy samples of non-SS subjects and those with a diagnosis of SS were subjected to immunohistochemistry. The results show intense GADD153 immunostaining but marked reduction in Del-1 expression in biopsy samples of SS compared to non-SS subjects. Collectively, the results indicate that GADD153 regulates inflammation and cell death in salivary gland in SS. Further, Del-1 expression likely provides a mechanistic link between increased GADD153 and leukocyte infiltration and accompanying inflammation of salivary gland tissue in this condition. | |
23117086 | Evaluation of the effect of losartan and methotrexate combined therapy in adjuvant-induced | 2013 Jan 5 | There is increasing body of evidence documenting the involvement of angiotensin II in inflammatory diseases. Moreover the up-regulation of angiotensin II AT(1) receptors in the synovium of rheumatoid arthritis patients has been previously described. This study aimed at investigating the anti-inflammatory effect of losartan, the selective angiotensin II AT(1) receptor blocker, and comparing the efficacy of methotrexate alone and in combination with losartan in adjuvant arthritis in rats. Twelve days post adjuvant injection, Sprague-Dawley rats were treated with methotrexate (1mg/kg/week), losartan (20mg/kg/day) and their combination for 15 days. Severity of arthritis was assessed by hind paw swelling, arthrogram scores. Serum was analyzed for measurement of albumin, C-reactive protein (CRP), nitrite/nitrate concentrations, interleukin 1β (IL-1β), tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), aspartate transaminase (AST) and alanine transaminase (ALT). Histopathological examination was done for hind paws and livers. Methotrexate and losartan monotherapies significantly reduced all parameters of inflammation and arthritis with better results in the methotrexate group except for the transaminases where losartan caused more significant reduction in their serum levels. The combined therapy showed better results than methotrexate and losartan alone. Hind paws showed better improvement of inflammatory cell infiltration and bone resorption in the combined therapy group. Disturbances in liver architecture and fibrosis caused by adjuvant arthritis were reverted to normal status in the combined therapy group in contrast to losartan and methotrexate monotherapies. In conclusion, methotrexate and losartan combined therapy provided more effective anti-inflammatory and hepatoprotective effects than either drug alone. | |
24633988 | Transoral approach to extradural non-neoplastic lesions of the craniovertebral junction. | 2014 Jun | BACKGROUND: The transoral approach allows for an unobstructed anterior view of the craniovertebral junction from the lower clivus to C1 and C2. It can be applied to a heterogeneous spectrum of pathological lesions involving this area including craniovertebral junction malformations, atlanto-axial synovial cysts, pseudoarthrosis following odontoid fractures, selected cases of retro-odontoid pannus, and vertical translocation in rheumatoid patients. METHODS: Microsurgical strategy is dictated by the nature and site of the target lesion. Atlas preservation during transoral approach (atlas-sparing technique) minimizes postoperative instability and is suitable for the majority of extradural non-neoplastic lesions of the craniovertebral junction. The transoral trans-atlas approach allows for a wider exposure of the anterior craniovertebral junction, but at the price of a higher incidence of postoperative instability; it is usually required in patients with severe basilar invagination or irreducible vertical translocation in rheumatoid arthritis. CONCLUSIONS: The transoral corridor is an effective route to approach a variety of anterior extradural lesions of the craniovertebral junction. Tailoring the approach to each specific lesion provides the needed exposure whilst limiting postoperative instability. | |
24077977 | Clinical characteristics of children with positive anti-SSA/SSB antibodies. | 2014 Aug | This study aimed to characterize the manifestations of clinical symptoms and signs, primary rheumatic diseases, and other autoantibodies in pediatric patients with positive anti-SSA and/or anti-SSB antibodies. Subjects under age 18 with positive anti-SSA and/or anti-SSB antibodies were screened and enrolled in a tertiary hospital in Taiwan. Data were collected via medical records,including age, gender, onset of the primary rheumatic disease, clinical symptoms and signs, and the medication used. Schirmer test for Sjögren's syndrome (SS) screening was performed in all enrolled patients. Among twenty enrolled subjects, seventeen of them had systemic lupus erythematosus; four of them were diagnosed as SS with positive Schirmer test. In addition to antinuclear antibodies and anti-DNA antibodies, other common autoantibodies were anti-RNP antibodies (50 %) and anti-Sm antibodies(30 %). The most common symptoms were arthritis (60 %)followed by malar rash (40 %). In conclusion, we observed that a low proportion of childhood SS (4/20) exists in our patients with positive SSA and/or anti-SSB antibodies. It is suggested that clinicians should focus more on the clinical symptoms in these patients, rather than undertaking invasive diagnostic interventions to rule out Sjögren's syndrome. | |
22886469 | Primary Sjögren's syndrome and B-non-Hodgkin lymphoma: role of CD4+ T lymphocytopenia. | 2013 Apr | Primary Sjögren's syndrome (PSS) is associated with increased risk of lymphoproliferative malignancy, and B-cell non-Hodgkin lymphoma (B-NHL) is the most frequent type. To evaluate CD4+ T lymphocytes distributions in patients with (PSS) and the association of CD4+ T lymphocytopenia with the development of (B-NHL), this study included 8 (PSS) patients associated with B-NHL (group I), 50 (pSS) patients without B-NHL (group II), and 30 healthy volunteers who served as controls. The frequency of circulating CD4+ and CD8+ T lymphocytes distributions and CD4+/CD8+ T cell ratio was assessed using flow cytometry coulter EPICS-XL and compared between patients groups and controls. There was statistically significant CD4+ T lymphocytopenia in (PSS) patients with B-NHL than those without lymphoma and controls (P = 0.001). Moreover, a significant low CD4+/CD8+ T cell ratio 0.8 in group I than group II and controls (P = 0.001) was found. Significant positive correlations of CD4+ T lymphocytopenia with other risk factors (parotid swelling, vasculitis, rheumatoid factors, low complement, cryoglobulinemia) were detected. CD4+ T lymphocytopenia is associated with B-NHL developed in patients with PSS and can be considered as an important predictor of lymphoma. | |
22484709 | Renal involvement in primary Sjogren syndrome of childhood: case report and literature rev | 2013 Jan | Renal tubular acidosis (RTA) is common in adults with primary Sjogren syndrome (pSS) but to date this condition has only been identified in 12 pediatric cases of pSS. Here we present the case of a 13-year-old, otherwise asymptomatic girl in whom the search for the etiology of incidentally found nephrocalcinosis led to diagnosis of distal RTA and nephrogenic diabetes insipidus secondary to SS-associated tubulointerstitial nephritis. Immunosupressive treatment and alkali/electrolyte supplementation resulted in stable renal function over the 6-year follow-up. A review of the literature focuses on two aspects of pSS: (1) the difficulties in diagnosing pSS in childhood and (2) clinical-pathological features, treatment and outcome of renal tubulointerstitial disease in childhood pSS. SS should be considered in older children, particularly females with otherwise unexplained RTA. A careful search for other renal dysfunctions is necessary, and renal biopsy may be of value in assessing the extent of renal damage and the need for immunomodulatory therapy. | |
24477732 | Adult Still's disease associated with ovarian cancer: case report. | 2013 Nov | We report a case of adult-onset Still's disease in a female patient with fever, myalgia, vanishing rash and bilateral inguinal lymphadenopathy, diagnosed after extensive workup to exclude other rheumatic, infectious and neoplastic diseases. The patient initially responded to corticosteroid therapy, but progressed to increased lymph nodes size that when biopsied, revealed serous ovarian adenocarcinoma. To our knowledge, this is the first report of ovarian neoplasm associated with adult-onset Still's disease. | |
23588513 | Primary Sjögren's syndrome prevalence in a major metropolitan area in Brazil. | 2013 Feb | There has been no previous prevalence study about of Sjögren's syndrome (SS) in Brazil. The aim was to evaluate the SS prevalence in a general population in Vitória, ES, Brazil. This was an epidemiological, observational, and cross-sectional study conducted on 1,205 randomized people, aged 18-65 years, who lived in Vitória. The subjects were screened for xerostomia and xerofphthalmia through home interviews. Those with sicca symptoms were asked to report to a hospital for further medical evaluation, unstimulated salivary flow, Schirmer I test, blood analysis and minor labial salivary biopsy. Sicca symptoms were found in 18% (217 subjects) of the sample. Of the 217 subjects with sicca symptoms, 127 (58%) were available for examination. In this sample, 61.7% were female and 46.8% were under medication. Sicca syndrome was confirmed in 12% by at least one examination (salivary flow or Schirmer I). Two patients (0.17%) matched four criteria according to American-European Criteria (95% CI = 0.020-0.5983). | |
25398925 | Pulmonary co-infection with Nocardia and Aspergillus in a patient with adult-onset Still's | 2014 Nov 14 | Patients on immunosuppression are at risk of unusual infections. We present a man diagnosed to have adult-onset Still's disease who, on high-dose oral steroid and tacrolimus, developed a cavitating pneumonia due to co-infection with Aspergillus flavus and Nocardia. Timely diagnosis and institution of appropriate therapy resulted in a favourable clinical outcome. Such co-infection in a patient receiving tacrolimus is rare in the published literature. This case serves to emphasise the need to be vigilant for unusual infections in patients who are immunosuppressed, either due to drugs or underlying disease condition. |