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

ID PMID Title PublicationDate abstract
18296481 Decrease of RA-related orthopaedic surgery of the upper limbs between 1998 and 2004: data 2008 Apr OBJECTIVES: To describe the overall use and temporal trends in orthopaedic upper limb surgery associated with RA on a nation wide basis in Sweden between 1998 and 2004. METHODS: Data for all inpatient visits during 1998-2004 for patients older than 18 yrs with RA-related diagnoses were extracted from the Swedish National Hospital Discharge Registry (SNHDR). The SNHDR prospectively collects data on all hospital admissions in Sweden according to the International Classification of Diseases (ICD). Data were analysed with respect to orthopaedic surgery of the hand, elbow and shoulder. RESULTS: During the study period, 54,579 individual RA patients were admitted to a Swedish hospital and 9% of these underwent RA-related surgery of the upper limbs. The RA patient cohort underwent a total of 8251 RA-related upper limb surgical procedures. The hand (77%) was most frequently operated on, followed by the shoulder (13%) and the elbow (10%). There was a statistically significant decrease of 31% for all admissions associated with RA-related upper limb surgery during 1998-2004 (P = 0.001). Some 10% of all RA-related upper limb surgery was due to total joint arthroplasties (TJAs), mostly for the elbow (59%). During 1998-2004, all TJAs, elbow-TJAs and shoulder-TJAs had a stable occurrence. In contrast, the overall numbers of hand-TJAs significantly increased (P = 0.009). CONCLUSIONS: Rates of RA-related upper limb surgery decreased and TJAs had a stable occurrence in Sweden during 1998-2004. The findings of this study may reflect trends in disease management and health outcomes of RA patients in Sweden.
19022810 Why do people with rheumatoid arthritis still die prematurely? 2008 Dec Premature death has been long recognised as a manifestation of rheumatoid arthritis (RA). Three lines of evidence can explain why patients with RA die prematurely and why the mortality gap between patients with RA and the general population appears to widening. First, patients with RA have a higher risk of several serious comorbid conditions and they tend to experience worse outcomes after the occurrence of these illnesses. Second, patients with RA do not appear to receive optimal primary or secondary preventive care. And third, the systemic inflammation and immune dysfunction associated with RA appears to promote and accelerate comorbidity and mortality. This paper provides a brief summary and interpretation of the data underlying these findings. Together, these results provide a compelling argument in favour of a focused research programme aimed specifically at eliminating premature death in patients with RA.
17578850 Delay in presentation to primary care physicians is the main reason why patients with rheu 2007 Sep OBJECTIVES: To study the delay from the time of symptom onset to assessment by a Rheumatologist in patients with rheumatoid arthritis (RA) and to determine the contributions of patient and physician dependent factors to this delay. METHODS: Data were collected from 169 consecutive patients with RA at the time of assessment by Rheumatologists working in hospitals serving an inner city population in Birmingham, UK. Dates were recorded for: (i) onset of inflammatory joint symptoms; (ii) initial assessment in primary care; and (iii) referral from primary to secondary care. (iv) initial assessment by a rheumatologist in secondary care. RESULTS: The median delay from the onset of symptoms to a patient being assessed in secondary care was 23 weeks (IQR 12-54 weeks). The median delay before the patient was assessed in primary care was 12 weeks (IQR 4-28 weeks). For 96 patients (57%) more than half of the overall delay in assessment in secondary care was accounted for by a delay in assessment in primary care. CONCLUSIONS: Patient dependent factors, leading to a delay in consulting primary care physicians, are the principal reasons for the delay in patients with RA being seen by Rheumatologists in our population. A considerable body of evidence demonstrates that the earlier that therapy is introduced the better the clinical outcome. Consequently it is important to understand why some patients with RA delay in seeking medical advice, in order to allow effective interventions to reduce this delay.
16734620 Hydroxychloroquine potentiates Fas-mediated apoptosis of rheumatoid synoviocytes. 2006 Jun Inadequate apoptosis may contribute to the synovial hyperplasia associated with rheumatoid arthritis (RA). The Fas-associated death domain protein (FADD)-like interleukin (IL)-1beta-converting enzyme (FLICE)-inhibitory protein (FLIP), which is an apoptotic inhibitor, has been implicated in the resistance to Fas-mediated apoptosis of synoviocytes. This study investigated whether hydroxychloroquine (HCQ), an anti-rheumatic drug, induces the apoptosis of rheumatoid synoviocytes, and modulates the expression of FLIP. Fibroblast-like synoviocytes (FLS) were prepared from the synovial tissues of RA patients, and were cultured with various concentrations of HCQ in the presence or absence of the IgM anti-Fas monoclonal antibodies (mAb) (CH11). Treatment with HCQ, ranging from 1 to 100 microM, induced the apoptosis of FLS in a dose- and time-dependent manner. The increase in synoviocytes apoptosis by HCQ was associated with caspase-3 activation. A combined treatment of HCQ and anti-Fas mAb increased FLS apoptosis and caspase-3 activity synergistically, compared with either anti-Fas mAb or HCQ alone. The Fas expression level in the FLS was not increased by the HCQ treatment, while the FLIP mRNA and protein levels were decreased rapidly by the HCQ treatment. Moreover, time kinetics analysis revealed that the decreased expression of FLIP by HCQ preceded the apoptotic event that was triggered by HCQ plus anti-Fas mAb. Taken together, HCQ increases the apoptosis of rheumatoid synoviocytes by activating caspase-3, and also sensitizes rheumatoid synoviocytes to Fas-mediated apoptosis. Our data suggest that HCQ may exert its anti-rheumatic effect in rheumatoid joints through these mechanisms.
16829303 Human Fc receptors: critical targets in the treatment of autoimmune diseases and transplan 2006 Jul The receptors for the Fc region of immunoglobulins (FcR) are members of the immunoglobulin superfamily. They are expressed on various hematopoietic cells and constitute a link between humoral and cell-mediated immunity. The activation and downmodulation of immune responses are controlled by signals from activating and inhibitory FcR, expressed on the surface of immune cells. The signaling regions, defined as immunoreceptor-tyrosine-based activation motif and immunoreceptor-tyrosine-based inhibitory motif, are contained within the cytoplasmic domain of FcR or of the adaptor proteins associated with FcR. Activating and inhibitory FcR are usually coexpressed on the surface of the same cell and coengaged by the same ligand, functioning in concert to keep a balanced immune response. Impairment of the functional balance between activating and inhibitory FcR leads either to hyperactivity to foreign and self antigens or to unresponsiveness as seen in many autoimmune diseases and infections. Pathologic conditions in which immunoglobulin-FcR interactions play a major role, as well as the outcome of treatment with intravenous immunoglobulin and monoclonal antibodies, may be influenced by targeting FcR.
16945141 Fine mapping of genes within the IDDM8 region in rheumatoid arthritis. 2006 The IDDM8 region on chromosome 6q27, first identified as a susceptibility locus for type 1 diabetes, has previously been linked and associated with rheumatoid arthritis (RA). The region contains a number of potential candidate genes, including programmed cell death 2 (PDCD2), the proteosome subunit beta type 1 (PSMB1), delta-like ligand 1 (DLL-1) and TATA box-binding protein (TBP) amongst others. The aim of this study was to fine map the IDDM8 region on chromosome 6q27, focusing on the genes in the region, to identify polymorphisms that may contribute to susceptibility to RA and potentially to other autoimmune diseases. Validated single nucleotide polymorphisms (SNPs; n = 65) were selected from public databases from the 330 kb region of IDDM8. These were genotyped using Sequenom MassArray genotyping technology in two datasets; the test dataset comprised 180 RA cases and 180 controls. We tested 50 SNPs for association with RA and any significant associations were genotyped in a second dataset of 174 RA cases and 192 controls, and the datasets were combined before analysis. Association analysis was performed by chi-square test implemented in Stata software and linkage disequilibrium and haplotype analysis was performed using Helix tree version 4.1. There was initial weak evidence of association, with RA, of a number of SNPs around the loc154449 putative gene and within the KIAA1838 gene; however, these associations were not significant in the combined dataset. Our study has failed to detect evidence of association with any of the known genes mapping to the IDDM8 locus with RA.
17133581 The -169C/T polymorphism in FCRL3 is not associated with susceptibility to rheumatoid arth 2006 Dec OBJECTIVE: In Japanese individuals, the -169C/T single-nucleotide polymorphism (SNP) in FCRL3 has been reported to be associated with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and autoimmune thyroid diseases. The objective of this study was to test the association of this SNP with RA and SLE, in a case-control study of Korean individuals. METHODS: The -169C/T SNP in FCRL3 was genotyped in 1,060 patients with RA, 457 patients with SLE, and 697 unaffected control subjects, using the MassARRAY SNP genotyping system. Associations were tested by multivariate logistic regression, with adjustments for age and sex. RESULTS: No association was detected between the -169C/T SNP and RA (odds ratio [OR] 1.11, 95% confidence interval [95% CI] 0.83-1.48, P = 0.50) or SLE (OR 1.00, 95% CI 0.73-1.37, P = 0.99). This SNP was not associated with rheumatoid factor status, shared epitope status, radiographic severity in patients with RA, or disease manifestations in patients with SLE. CONCLUSION: The association of the -169C/T SNP in FCRL3 with RA and SLE that was observed in Japanese patients was not replicated in a Korean population.
16518573 Local cell proliferation in rheumatoid synovial tissue: analysis by cyclin expression. 2006 Nov The immunohistochemical staining of cyclins was done to evaluate the proliferating cells in synovial tissue of rheumatoid arthritis (RA). Synovial specimens obtained from 18 patients with RA, 12 with osteoarthritis (OA), and 8 with traumatic arthritis (TA) were used for immunostaining of cyclins A and B1 and proliferating cell nuclear antigen (PCNA). The positive cells in lining layer (synoviocytes) and sublining layer (lymphoid and nonlymphoid cells) were counted. Moreover, the relationship between the frequency of their positive cells and clinical data of RA patients was analyzed statistically. In general, cyclin-A-, cyclin-B1-, and PCNA-positive cells in RA were more frequently observed as compared with those in OA and TA. Significant differences were found between RA and OA or TA in cyclin-A-, cyclin-B1-, and PCNA-positive sublining lymphoid cells, between RA and OA or TA in cyclin-B1- and PCNA-positive sublining nonlymphoid cells, and between RA and OA in cyclin-B1-positive synoviocytes. The ratio of cyclin-A- or cyclin-B1-positive cells per PCNA-positive cells was significantly higher in sublining lymphoid cells in RA than TA and in sublining lymphoid and nonlymphoid cells of RA than OA or TA. Moreover, a better relationship was observed between the frequency of cyclin-A-positive synoviocytes and age and between cyclin-A-positive sublining nonlymphoid cells and duration of the disease in RA patients. Our data demonstrated clearly that synoviocytes, as well as sublining lymphoid and nonlymphoid cells, could divide in situ, and more frequent cell division and a higher ratio of cyclin-A- or cyclin-B1-positive/PCNA-positive sublining cells could occur in RA than OA and TA.
17075400 Hearing loss in rheumatoid arthritis. 2006 Nov OBJECTIVE: The objective of this study was to evaluate whether patients with rheumatoid arthritis (RA) are more likely to have subclinical hearing loss compared with persons without RA. METHODS: This is a case-control cross-sectional study of 29 patients with RA with disease duration greater than 5 years. Five males and five females were recruited into each decade category (age 40-49, 50-59, and 60-69). These cases were matched in a 1:1 ratio by sex and age to 30 control subjects. A comprehensive set of audiometric and disease severity assessments were performed. RESULTS: Seventeen (59%) of 29 patients with RA had abnormal hearing for at least one frequency (four in one ear, 13 in two ears) by audiometry as did 14 (47%) of 30 control subjects (five in one ear, nine in two ears). The percentage of patients with hearing loss (% RA vs. % control subjects) was: 45% versus 40% sensorineural, 10% versus 7% conductive, and 3% versus 0% mixed hearing loss. In RA versus control subjects, acoustic reflex threshold was abnormal in 17% versus 7%; speech reception threshold was abnormal in 10% versus 3%. Tympanometry and otoacoustic emission findings were similar in both groups. Word recognition did not differ between patients with RA and control subjects. In patients with RA/control subjects, hearing handicap, dizziness, and health assessment questionnaires were abnormal in 28%/7%, 14%/3%, and 72%/7%, respectively. CONCLUSION: There was no difference found in objective audiometric measurements in patients with RA compared with non-RA control subjects. Subjectively patients with RA were more likely to perceive themselves as having hearing disturbances, which may be related to overall disease related functional impairment.
18464310 Socioeconomic and occupational risk factors for rheumatoid arthritis: a nationwide study b 2008 Jun OBJECTIVE: To investigate possible associations between socioeconomic status, occupation, and hospitalization for rheumatoid arthritis (RA). METHODS: A nationwide database was constructed by linking the Swedish Census to the Hospital Discharge Register in order to obtain data on all first hospitalizations for RA in Sweden during the study period 1964 to 2004. Standardized incidence ratios (SIR) and 95% confidence intervals were calculated by socioeconomic status (education level) and occupation for men and women aged 30 years and older. Three cohorts were defined based on occupational titles recorded in Swedish census data in 1960, 1970, and 1980. RESULTS: A total of 13,820 male and 14,509 female hospitalizations for RA were identified during the study period. Men and women with an education level > 12 years had significantly decreased SIR. Among men, significantly increased SIR were present in all 3 cohorts among farmers, miners and quarry workers, electrical workers, other construction workers, and engine and motor operators. Among women, assistant nurses and religious, juridical, and other social-science-related workers had significantly increased SIR in all 3 cohorts. CONCLUSION: Socioeconomic status and occupation sometimes carry a significantly increased risk of hospitalization for RA. Future studies could investigate specific agents in the occupations for which increased risks are identified.
17627887 Cytokine inhibitors in rheumatoid arthritis and other autoimmune diseases. 2007 Aug The clinical success of TNFalpha blocking biologics in a growing number of immune-mediated pathologies, including rheumatoid arthritis, Crohn's disease, ankylosing spondylitis and psoriasis, confirms the importance of TNFalpha in driving chronic inflammation and represents an important step forward in the treatment of these conditions. TNFalpha blockade, however, is a treatment, rather than a cure, and is not effective in all patients or in all autoimmune diseases and further research is needed to get closer to a cure. Recently, the identification of a novel, IL-17 producing, T helper cell subset, that plays a dominant pathogenic role in animal models of autoimmunity, is a major advance on existing knowledge, although the role of these cells in human disease remains to be established. Cytokines driving angiogenesis are also important in disease chronicity and thus might be valid therapeutic targets.
18383379 Genetic association of vasoactive intestinal peptide receptor with rheumatoid arthritis: a 2008 Apr OBJECTIVE: Vasoactive intestinal peptide (VIP) has been shown to be one of the endogenous factors involved in the maintenance of immune tolerance. Administration of VIP ameliorates clinical signs in various experimental autoimmune disorders. This study was undertaken to investigate whether the exacerbated inflammatory autoimmune response in rheumatoid arthritis (RA) might result directly from altered expression and/or signaling of VIP receptors in immune cells. METHODS: The effect of specific agonists of different VIP receptors on collagen-induced arthritis in mice was investigated by clinical and histologic assessment and measurement of cytokine and chemokine production. Expression of VIP receptor type 1 (VPAC1) in synovial cells and monocytes from RA patients was determined by flow cytometry. Potential associations of VPAC1 genetic polymorphisms with RA susceptibility were investigated. RESULTS: A VPAC1 agonist was very efficient in the treatment of experimental arthritis, and deficient expression of VPAC1 in immune cells of RA patients was associated with the predominant proinflammatory Th1 milieu found in this disease. Immune cells derived from RA patients were less responsive to VIP signaling than were cells from healthy individuals and showed reduced VIP-mediated immunosuppressive activity, rendering leukocytes and synovial cells more proinflammatory in RA. A significant association between multiple-marker haplotypes of VPAC1 and susceptibility to RA was found, suggesting that the reduced VPAC1 expression in RA-derived immune cells is associated with the described VPAC1 genetic polymorphism. CONCLUSION: These findings are highly relevant to the understanding of RA pathogenesis. They suggest that VIP signaling through VPAC1 is critical to maintaining immune tolerance in RA. In addition, the results indicate that VPAC1 may be a novel therapeutic target in RA.
19035419 Risk of cardiovascular mortality in patients with rheumatoid arthritis: a meta-analysis of 2008 Dec 15 OBJECTIVE: To determine the magnitude of risk of cardiovascular mortality in patients with rheumatoid arthritis (RA) compared with the general population through a meta-analysis of observational studies. METHODS: We searched Medline, EMBase, and Lilacs databases from their inception to July 2005. Observational studies that met the following criteria were assessed by 2 researchers: 1) prespecified RA definition, 2) clearly defined cardiovascular disease (CVD) outcome, including ischemic heart disease (IHD) and cerebrovascular accidents (CVAs), and 3) reported standardized mortality ratios (SMRs) and 95% confidence intervals (95% CIs). We calculated weighted-pooled summary estimates of SMRs (meta-SMRs) for CVD, IHD, and CVAs using the random-effects model, and tested for heterogeneity using the I(2) statistic. RESULTS: Twenty-four studies met the inclusion criteria, comprising 111,758 patients with 22,927 cardiovascular events. Overall, there was a 50% increased risk of CVD death in patients with RA (meta-SMR 1.50, 95% CI 1.39-1.61). Mortality risks for IHD and CVA were increased by 59% and 52%, respectively (meta-SMR 1.59, 95% CI 1.46-1.73 and meta-SMR 1.52, 95% CI 1.40-1.67, respectively). We identified asymmetry in the funnel plot (Egger's test P = 0.002), as well as significant heterogeneity in all main analyses (P < 0.0001). Subgroup analyses showed that inception cohort studies (n = 4, comprising 2,175 RA cases) were the only group that did not show a significantly increased risk for CVD (meta-SMR 1.19, 95% CI 0.86-1.68). CONCLUSION: Published data indicate that CVD mortality is increased by approximately 50% in RA patients compared with the general population. However, we found that study characteristics may influence the estimate.
18085742 Influence of patient education on exercise compliance in rheumatoid arthritis: a prospecti 2008 Feb OBJECTIVE: To determine the effect of education on the exercise habits of patients with rheumatoid arthritis (RA) after 6 and 12 months. METHODS: We studied 208 outpatients recruited between June 2001 and December 2002. This was a prospective controlled randomized trial. The active group received a multidisciplinary education program, including training in home-based exercises and guidelines for leisure physical activity (PA). The control group received a booklet added to usual medical care. Compliance with home-based exercises was defined as a practice rate >or= 30% of the prescribed training. Compliance with leisure PA was defined as >or= 20% increase in Baecke questionnaire score. Additional assessments involved possible predictors of compliance and changes with regard to the compliance. RESULTS: At 6-month followup, home-based exercise and leisure PA compliance were significantly higher [13.5% vs 1%, respectively (p = 0.001); and 28.2% vs 13.8% (p = 0.02)], but were not at 12 months. Predictors of leisure PA compliance at 6 months included participating in the active group (odds ratio 2.74, 95% CI 1.17 to 6.38) and previous low leisure PA (OR 6.01, 95% CI 2.47 to 14.61), with decreased fatigue (FACIT-F mean -2.94 +/- 8.04 vs -0.1 +/- 7.25 for noncompliant subjects; p = 0.04) and improved psychological status (Arthritis Impact Measurement Scale mean -1.25 +/- 3.12 vs 0.11 +/- 3.39; p = 0.03). CONCLUSION: Education of patients with RA may increase compliance especially with leisure PA, particularly when it is poor at baseline, but these effects are limited and short-term.
16490750 RANKL protein is expressed at the pannus-bone interface at sites of articular bone erosion 2006 Sep OBJECTIVES: Receptor activator of NF-kappaB ligand (RANKL) and osteoprotegerin (OPG) have been demonstrated to be critical regulators of osteoclast generation and activity. In addition, RANKL has been implicated as an important mediator of bone erosion in rheumatoid arthritis (RA). However, the expression of RANKL and OPG at sites of pannus invasion into bone has not been examined. The present study was undertaken to further elucidate the contribution of this cytokine system to osteoclastogenesis and subsequent bone erosion in RA by examining the pattern of protein expression for RANKL, OPG and the receptor activator of NF-kappaB (RANK) in RA at sites of articular bone erosion. METHODS: Tissues from 20 surgical procedures from 17 patients with RA were collected as discarded materials. Six samples contained only synovium or tenosynovium remote from bone, four samples contained pannus-bone interface with adjacent synovium and 10 samples contained both synovium remote from bone and pannus-bone interface with adjacent synovium. Immunohistochemistry was used to characterize the cellular pattern of RANKL, RANK and OPG protein expression immediately adjacent to and remote from sites of bone erosion. RESULTS: Cellular expression of RANKL protein was relatively restricted in the bone microenvironment; staining was focal and confined largely to sites of osteoclast-mediated erosion at the pannus-bone interface and at sites of subchondral bone erosion. RANK-expressing osteoclast precursor cells were also present in these sites. OPG protein expression was observed in numerous cells in synovium remote from bone but was more limited at sites of bone erosion, especially in regions associated with RANKL expression. CONCLUSIONS: The pattern of RANKL and OPG expression and the presence of RANK-expressing osteoclast precursor cells at sites of bone erosion in RA contributes to the generation of a local microenvironment that favours osteoclast differentiation and activity. These data provide further evidence implicating RANKL in the pathogenesis of arthritis-induced joint destruction.
17966397 Control of osteoclast activity and bone loss by IKK subunits: new targets for therapy. 2007 Transcription factor NF-kappaB has been well recognized as a pivotal player in osteclastogenesis and inflammation-induced bone loss. Here, we discuss our recent results obtained using a genetic approach in mice that indicate the importance of IKKbeta, and not IKKalpha, as a transducer of signals from receptor activator of NF-kappaB (RANK) to NF-kappaB. Ablation of IKKbeta results in lack of osteoclastogenesis and unresponsiveness of IKKbeta-deficient mice to inflammation-induced bone loss. In the need of a more effective therapy for the treatment of inflammatory diseases causing bone resorption, specific inhibition of IKKbeta represents a logical alternative strategy to the current therapies.
17182267 Long-term results of infliximab therapy in rheumatoid arthritis: experience acquired by th 2007 Jan OBJECTIVE: Infliximab is effective in patients with rheumatoid arthritis (RA). Add-on infliximab therapy in patients on methotrexate results in a rapid gain in effectiveness, which lasts at least 1 year. The objective of this study was to evaluate the effectiveness and continuation rate of infliximab in patients with RA after the first year of treatment. METHODS: The first 50 patients with RA who were given infliximab in the North-Pas-de-Calais region of France were included in a multicenter open-label study. The patients had severe RA or failed to respond to conventional medications. Infliximab was given in a dosage of 3 mg/kg every 8 weeks in combination with methotrexate. Effectiveness was evaluated using the DAS28-3 score and EULAR response criteria. The dates and reasons of infliximab discontinuations were recorded. RESULTS: The 2-year infliximab continuation rate was 70%. Serious adverse events requiring infliximab discontinuation occurred in 7 patients. Mean DAS28-3 scores in the 35 patients who took infliximab for at least 2 years were 6.42 at baseline, 4.33 after 30 weeks, 4.31 after 54 weeks, and 3.86 after 102 weeks. According to EULAR criteria after 102 weeks, there were 12 good responders, 18 moderate responders, and 5 nonresponders. CONCLUSION: Experience acquired in the North-Pas-de-Calais district of France suggests that infliximab is continued for more than 2 years in more than two-thirds of patients and remains effective over this period.
18633631 Similar results with 21 Kudo and 21 Souter-Strathclyde total elbow arthroplasties in patie 2008 Oct INTRODUCTION: The results of different prostheses used for total elbow arthroplasty (TEA) in rheumatoid arthritis (RA) have been reported in only a few studies. Small differences in survival or function between implants have been reported. We retrospectively evaluated the results of 42 Souter-Strathclyde and Kudo TEAs. MATERIALS AND METHODS: Between 1988 and 1994, 21 consecutive patients with RA and severe elbow destruction underwent a Souter-Strathclyde TEA. Between 1994 and 1998, another group comprising 21 consecutive patients with RA with severe elbow destruction underwent a Kudo TEA. RESULTS: There were six revisions for the groups combined, including four aseptic loosenings, one fracture and one liner wear and metallosis. The 5-year survival for the Souter-Strathclyde and the Kudo were 85% (95% CI 69-100) and 95% (95% CI 85-100), respectively. The difference between the groups was not statistically significant as tested by the Cox regression analysis. The majority of the patients were free of pain at follow-up. More than half of the patients were able to perform only light housekeeping tasks and a considerable proportion even had difficulties in maintaining personal hygiene. The elbow range of motion improved only slightly after the operation. CONCLUSION: Both the Souter-Strathclyde and the Kudo TEAs provide good pain relief in the arthritic elbow leading to high patient satisfaction despite the residual disabilities. Only small differences in the results between the Souter-Strathclyde and the Kudo TEAs were found. More than half of the patients were able to perform only light housekeeping tasks and a considerable proportion even had difficulties in maintaining personal hygiene. The elbow range of motion improved only slightly after the operation.
18645970 Results of acetabular wiremesh and autograft in protrusio acetabuli. 2008 Jan Between 1990 and 2005, 25 acetabular reconstructions in 25 patients were performed using autogenous morcellized bone-graft and acetabular wiremesh due to acetabular bone stock loss. The most frequent preoperative diagnosis in our patients were severe hip arthrosis (50%), and rheumatoid arthritis (15%).The mean follow up was 8.6 years (range 2-15 years). The most frequent long-term complication was the appearence of radiolucent lines.A cemented acetabular cup was used in all cases. Preoperative mean Harris Hip Score was 42.3, rising to 90.6 at follow-up after surgery. None of the patients had any loosening of the acetabular component and only one had radiolucent lines >2mm which did not progress. Kohler's line remained intact in all cases.Results of this study suggests bone-grafting and acetabular wiremesh is an effective and simple method to arrest the progresion of acetabular protrusio.
17967717 Inflammatory molecules: a target for treatment of systemic autoimmune diseases. 2007 Nov Inflammation is a process to protect the host against infection and danger signals. However, many pathologic conditions, including autoimmune diseases, are sustained by perpetual activation of the inflammatory process. In the past few years our knowledge about the molecular basis of inflammation have been uncovered and now much is known about the primary role of pro-inflammatory cytokines such as IL-1 and TNF. In the early '90s, anti-cytokine therapies started and confirmed the primary role of TNF in autoimmune diseases, such as rheumatoid arthritis, Crohn's Disease and psoriasis. Increasing understanding of the role of inflammatory mediators in inflammation and diseases is opening new avenues for the treatment of inflammatory-based diseases through selective targeting of cytokines and lipid mediators.