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ID PMID Title PublicationDate abstract
15180353 Is Anti Cyclic citrullinated peptide a useful laboratory test for the diagnosis of rheumat 2004 Apr AIM OF THE STUDY: To evaluate Anti Cyclic citrullinated peptide (anti-CCP) and Rheumatoid Factor (RF) sensitivity and specificity in patients with Rheumatoid Arthritis (RA). MATERIALS AND METHODS: Anti-CCP and RAtest for the assessment of RF have been tried out in 35 patients with RA and in a group of 42 patients whose hands were affected by arthralgic/arthritis-like symptoms. RESULTS: Sensitivity of anti-CCP was 71,4% with 95,2% of specificity. RAtest sensitivity was 91,4% with specificity of 31%. Anti-CCP and RAtest both positive showed an overall 71.4% sensitivity and 95.2% specificity; sensitivity was 91.4% and specificity was 31.0%, if at least RAtest or anti-CCP resulted positive, The positive predictive value of the two test performed together was 97.0%, higher than that of anti-CCP (71.4%) and RAtest (88.5%9) alone. The negative predictive value of the two test performed together was 30.9% similar to that of the RAtest performed alone (30.9%). All patients affected by HCV related chronic liver disease were negative for anti-CCP test; 12/14 of them had RAtest positive. CONCLUSIONS: Anti-CCP antibody has a diagnostic specificity higher than RF. Anti-CCP and RA tests together prove to have the some specificity as anti-CCP alone and a lower sensitivity. Sensitivity is better when at least either RAtest or anti-CCP results positive. The best positive predictive value is obtained performing both anti-CCP and RAtest. Anti-CCP is a useful laboratory marker to confirm the diagnosis of rheumatoid arthritis; it seems to be very important to differentiate patients with RA from those with HCV related arthritis.
12044041 Technology evaluation: adalimumab, Abbott laboratories. 2002 Apr Adalimumab (D2E7), a human monoclonal antibody that binds to and neutralizes TNFa, is being developed by Abbott (formerly Knoll), under license from Cambridge Antibody Technology (CAT), for the potential treatment of inflammatory disorders such as rheumatoid arthritis (RA) and Crohn's disease. It is also being investigated for the potential treatment of coronary heart disease. Phase II studies for Crohn's disease and phase III for RA were ongoing throughout 2001. Limited data are only available for RA. In January 2002, it was reported that phase III trials of adalimumab for RA had been completed, but details have not been published in the primary literature so far. At this time CAT and Abbott expected to file for US approval in the second quarter of 2002 with a launch date anticipated for 2003. Phase III data are expected to be presented at the European League Against Rheumatism meeting in June 2002. In November 2000, Lehman Brothers predicted a US launch in June 2002 with peak US sales of $600 million in 2007 and a launch in non-US markets in 2003 with peak sales in these markets of $300 million in 2008. In December 2000, Merrill Lynch predicted regulatory clearance in the second half of 2003. The probability of adalimumab reaching the market is estimated to be 70%. In December 2000, Merrill Lynch predicted a 2003 launch, with estimated sales of pounds sterling 3.65 million in that year rising to pounds sterling 30.14 million in 2010. In March 2001, ABN AMRO predicted sales of $73 million in 2003 rising to $392 million in 2007.
12721703 Termination of disease-modifying antirheumatic drugs in rheumatoid arthritis and in psoria 2003 Apr 102 rheumatoid arthritis (RA) and 104 psoriatic arthritis (PsA) patients' records were analysed according to a standardised protocol. Using Cox regression, life-table analysis and log rank test, the effectiveness and toxicity of, and duration of disease modifying antirheumatic drug (DMARD) treatment were compared in RA and PsA. RA patients were treated with gold sodium thiomalate (GST), methotrexate (MTX) and sulphasalazine (SSZ) for a median duration of 35, 72 and 12 months respectively, whereas PsA patients were treated for 12, 12 and 17 months. The differences for GST and MTX were statistically significant (p=0.0043 and 0.0447). Drug toxicity was more frequently seen among patients with PsA (p=0.0023). No difference in efficacy could be proved. Results suggest that there is a significant difference between RA and PsA patients in terms of toxicity of these agents. Therefore, separate treatment strategies are needed, and earlier results with RA may not be directly applicable to PsA.
14667551 Evaluating inflammatory joint disease: how and when can autoantibodies help? 2003 Dec The diagnosis of inflammatory joint disease rests on a constellation of symptoms, signs, laboratory test results and, occasionally, histological findings. Classification criteria have been developed by national learned societies, international panels of experts or, more rarely, an expert working alone. These criteria are intended to provide a common language for therapeutic trials and international publications. Yet, they are often inappropriately used as diagnostic tools for the individual patient. Identification of an early seroimmunologic marker with high sensitivity and specificity for classifying patients with recent-onset joint disease is a daunting challenge. Test performance characteristics such as sensitivity, specificity, positive and negative predictive values, and the positive or negative likelihood ratio help to assess the diagnostic usefulness of a laboratory test in a specific situation. The difference between the pretest and posttest likelihoods of obtaining a positive or negative result measures the usefulness, or performance, of a laboratory test in a specific situation according to the prevalence of the disease. A higher positive likelihood ratio indicates a more useful test. In a patient with inflammatory joint disease, the diagnosis can be sought by assaying a limited number of autoantibodies according to a decision tree. Thus, IgM rheumatoid factors (latex test or ELISA) and antibodies to filaggrin or other citrullinated proteins (antikeratin antibodies by indirect immunofluorescent assay or anticyclic citrullinated peptides by ELISA) identify more than 70% of cases of early rheumatoid arthritis with greater than 98% specificity. If these markers are negative, testing for antinuclear antibodies by indirect immunofluorescent assay on HEp-2 cells identifies 99% of cases of lupus and progressive systemic sclerosis. Confirmation of the diagnosis can be obtained by characterizing the autoantibodies: thus, presence of antidouble-stranded DNA (dsDNA, by the Farr radioimmunoassay, indirect immunofluorescent assay on Crithidia luciliae, or ELISA (IgG)) or of antinucleosome antibodies (ELISA) indicates lupus, whereas anticentromere, antitopoisomerase I (Scl 70), and antinucleolar antibodies point to progressive systemic sclerosis. A positive test for antibodies to soluble nuclear antigens of the U1 RNP type suggests mixed connective tissue disease or lupus but may indicate scleroderma. Anti-Sm antibodies are found in fewer than 10% of lupus patients but are highly specific. Anti-SSA (Ro) and anti-SSB (La) suggest lupus or primary Sjögren's syndrome. When tests are negative for ANA, several antibodies to cytoplasmic organelles are valuable diagnostic tools, such as anti-J01 for polymyositis syndromes and antiribosome antibodies for lupus, although their sensitivity is modest (20-25%). Finally antineutrophil cytoplasmic antibodies (ANCAs) ensure the diagnosis of small-vessel vasculitides, which often involve the lungs and kidneys. Thus, in diffuse Wegener's granulomatosis, ANCAs exhibiting the classic cytoplasmic pattern and corresponding by ELISA to anti-PR3 are found. In microscopic polyangiitis the ANCAs are peripheral and correspond by ELISA to antimyeloperoxidase antibodies. Tests for other antibodies are less often needed to evaluate inflammatory joint disease.
15189937 Increased arteriovenous carboxyhemoglobin differences in patients with inflammatory pulmon 2004 Jun PURPOSE: Exhaled carbon monoxide and arterial blood carboxyhemoglobin concentrations increase in inflammatory pulmonary diseases. The present study was undertaken to elucidate whether arteriovenous carboxyhemoglobin (a-vHb-CO) concentration differences are also useful to define the site of inflammation, either in the lung or organs other than the lung. MATERIALS AND METHODS: We examined concentrations of carboxyhemoglobin in both arterial and peripheral venous blood and exhaled carbon monoxide in patients with acute pulmonary inflammation including bronchial asthma (n = 18) and pneumonia (n = 33), and those in patients with extrapulmonary inflammatory diseases, including acute pyelonephritis (n = 28) and active rheumatoid arthritis (n = 16). RESULTS: The values of carboxyhemoglobin in both arterial and peripheral venous blood were significantly higher in patients with pulmonary and extrapulmonary inflammation compared with those in control subjects (n = 22). Furthermore, a-vHb-CO differences in patients with inflammatory pulmonary diseases were higher than those in patients with acute pyelonephritis and patients with rheumatoid arthritis, and than those in control subjects. The a-vHb-CO differences correlated with the WBC count of peripheral venous blood in patients with pneumonia. In patients with bronchial asthma, the a-vHb-CO differences inversely correlated with FEV(1), although they did not correlate with WBC count of peripheral venous blood. The a-vHb-CO differences in patients with acute pyelonephritis were higher than those in patients with active rheumatoid arthritis. CONCLUSION: The present study suggests that a-vHb-CO differences may be a useful means to define the site of inflammation, either in the lung or organs other than the lung, in patients with a fever of unknown origin. The large a-vHb-CO differences may be caused by carbon monoxide production in pulmonary inflammation.
15347489 Streptococcal toxic shock syndrome and sepsis manifesting in a patient with chronic rheuma 2004 Jul 15 Streptococcal-toxic-shock syndrome is caused by virulent strains of exotoxin-producing streptococcus, almost always group-A organisms such as Streptococcus pyogenes. It has often been described in the setting of surgical wounds, burns, childbirth, diabetics, elderly, neonates, and immunocompromised hosts, where the portal of entry is the skin. Our patient was on steroids and nonsteroidal anti-inflammatory drugs for chronic rheumatoid arthritis and developed this deadly infection after a fall.
12847681 Functional characterization of adherent synovial fluid cells in rheumatoid arthritis: dest 2003 Jul OBJECTIVE: To characterize the morphologic and immunologic features of adherent synovial fluid cells derived from patients with rheumatoid arthritis (RA), and to explore their potential function in vitro and in vivo by focusing on cartilage destruction. METHODS: Synovial fluid adherent cells obtained from patients with RA and from control subjects were characterized by immunohistochemistry, flow cytometry, and electron microscopy. In vitro, these cells were cultured in the presence of cartilage particles. Cartilage destruction was monitored by the release of sulfated glycosaminoglycans (sGAG) into the medium, and the level of matrix metalloproteinase 1 (MMP-1) in the cell culture supernatant was measured by enzyme-linked immunosorbent assay. To inhibit cartilage destruction in vitro, the MMP inhibitor marimastat was tested in this system. In vivo, in the SCID mouse coimplantation model, RA synovial fluid adherent cells and RA synovial fibroblasts (as positive controls) were coimplanted with human cartilage under the kidney capsule and maintained there for 60 days. RESULTS: In vitro, the synovial fluid adherent cells consisted of 2 subpopulations, large round-shaped macrophage-like cells (CD68+) and spindle-shaped fibroblast-like cells (Thy-1+). When passaged, the latter cells proliferated and organized themselves into 3-dimensional formations. This allowed them to reach collagen particles fixed with agarose. Fibroblasts derived from synovial tissues could not be used in this assay because they grew only in monolayers and not on agarose. The majority (>90%) of passaged RA synovial fluid adherent cells expressed the Thy-1+,CD45-,CD68-,CD86- phenotype. Electron microscopy did not reveal important morphologic differences between the 2 types of fibroblasts, those from synovial tissue or those from synovial fluid. However, synovial fluid adherent cells expressed lower levels of adhesion molecules, including CD54 and galectin 3, as well as the complement-regulatory molecule CD55. The in vitro release of sGAG associated with cell activity was 2.5-fold higher from RA synovial fluid adherent cells in comparison with that from negative control cells. The release of sGAG correlated with the concentration of MMP-1 and was inhibited by the broad-range MMP inhibitor marimastat in a dose-dependent manner. RA synovial fluid adherent cells coimplanted with cartilage in SCID mice showed the same invasive behavior as that displayed by tissue-derived RA synovial fibroblasts. CONCLUSION: Similar to tissue-derived RA synovial fibroblasts, RA synovial fluid adherent cells, which contain "floating" anchorage-independent fibroblast-like cells, mediate cartilage destruction independent of the hyperplastic synovial tissue.
15130899 A good response to early DMARD treatment of patients with rheumatoid arthritis in the firs 2005 Jan OBJECTIVE: To describe the frequency and duration of remission in the Utrecht rheumatoid arthritis cohort of patients followed since diagnosis, and the clinical and treatment characteristics of patients with remission v those without. METHODS: In 1990 the Utrecht rheumatoid arthritis cohort study group started a clinical trial in which patients with recent onset of rheumatoid arthritis (<1 year) were randomised into four treatment groups: hydroxychloroquine (n = 169); intramuscular gold (n = 163); methotrexate (n = 166); and pyramid (n = 64). After two years, rheumatologists were allowed to prescribe any disease modifying antirheumatic drug. Remission was defined as: duration of morning stiffness < or =15 min, mean VAS pain < or =10 mm, Thompson joint score < or =10, and ESR < or =30 mm/h during at least six months. Cox regression analysis was used to determine baseline clinical, demographic, and treatment predictors of remission. RESULTS: Mean follow up duration was 62 months. Thirty six per cent achieved at least one period of remission. Median duration between diagnosis and the first remission period was 15 months for the intramuscular gold group, 18 months for the methotrexate and hydroxychloroquine groups, and 24 months for the pyramid group (NS). Predictors of remission were early response to initial treatment, less pain, rheumatoid factor negativity, and lower joint score at baseline. CONCLUSIONS: After a mean follow up duration of 62 months, only 36% of the patients had fulfilled the remission criteria at least once. A good response to treatment during the first year seems to be independently associated with remission rather than initial treatment alone.
12165097 Functional changes in rheumatoid fibroblast-like synovial cells through activation of pero 2002 Aug Peroxisome proliferator-activated receptor gamma (PPARgamma) is a ligand dependent transcriptional factor known to be a regulator of adipogenesis. Recent studies have also shown that stimulation of PPARgamma inhibits the transcriptional activities of other nuclear factors and down-regulates proinflammatory cytokine synthesis in T cells and monocytes. We examined, in the present study, the functional significance of PPARgamma expressed in fibroblast-like synovial cells (FLS) isolated from patients with rheumatoid arthritis (RA). Incubation of FLS with a synthetic PPARgamma ligand, troglitazone, inhibited endogenous production of TNF-alpha, IL-6 and IL-8, as well as matrix metalloprotease-3 (MMP-3), without inducing apoptosis of the cells. The gelatinase activity of FLS culture media was also inhibited by troglitazone. Electrophoretic mobility shift assay (EMSA) showed a significant reduction in the DNA binding activity of NF-kappaB in troglitazone-treated FLS in response to TNF-alpha or IL-1beta. Moreover, long-term cultivation of FLS with troglitazone resulted in morphological changes with marked lipid accumulation in these cells. Our results show a negative regulatory function for PPARgamma on cytokine and MMP production together with inhibition of cytokine-mediated inflammatory responses in rheumatoid synovial cells. Our results also suggest that FLS could differentiate into adipocyte-like cells in the presence of proper stimulatory signals including PPARgamma.
15358625 Proinflammatory mediators elicit secretion of the intracellular B-lymphocyte stimulator po 2005 Jan 15 We have recently shown that granulocyte-colony-stimulating factor (G-CSF)- and interferon-gamma (IFN-gamma)-activated human neutrophils accumulate and release remarkable amounts of soluble B-lymphocyte stimulator (BLyS) in vitro. In this study, we provide evidence that neutrophils migrating into skin window exudates (SWEs) developed in healthy volunteers and in patients with rheumatoid arthritis (RA), synthesized, and released BLyS in response to locally produced G-CSF. Accordingly, the concentrations of soluble BLyS in SWEs were significantly more elevated than in serum. Because the levels of SWE BLyS, but not SWE G-CSF, were higher in patients with RA than in healthy subjects, we examined the effect of CXCL8/IL-8, C5a, and other proinflammatory mediators that dramatically accumulate in RA SWEs and in inflamed synovial fluids. We show that CXCL1/GROalpha, CXCL8/IL-8, C5a, immune complexes, tumor necrosis factor-alpha (TNF-alpha), leukotriene B4, N-formyl-methionyl-leucyl-phenylalanine (fMLP), and lipopolysaccharide (LPS), which by themselves do not induce BLyS de novo synthesis, act as potent secretagogues for BLyS, which is mainly stored in Golgi-related compartments within G-CSF-treated neutrophils, as determined by immunogold electron microscopy. This action is pivotal in greatly amplifying neutrophil-dependent BLyS release in SWEs of patients with RA compared with healthy subjects. Collectively, our data uncover a novel mechanism that might dramatically exacerbate the release of BLyS by neutrophils during pathologic inflammatory responses.
14586405 Induction of Notch signaling by tumor necrosis factor in rheumatoid synovial fibroblasts. 2003 Oct 30 Rheumatoid arthritis (RA) is characterized by progressive inflammation associated with abberrant proliferation of synoviocytes. In order to explore the characteristics of rheumatoid synovial fibroblasts (RSF), we performed the comparative gene expression profile analysis between RSF and normal synovial fibroblasts (NSF) upon tumor necrosis factor (TNF) stimulation. As an initial screening for the genes preferentially induced by TNF in RSF compared with NSF, we have adopted a cDNA array containing well-defined sets of genes responsible for cell growth, cell fate determination, and cellular invasiveness. Differentially expressed genes of interest were confirmed using real-time RT-PCR. We found that TNF induced the expression of Notch-1, Notch-4, and Jagged-2 in RSF. The expression of these proteins was detected in the RA synovial tissues. The nucleus of RA synoviocytes showed strong staining with anti-Notch-1 and Notch-4 antibody. TNF induced the nuclear translocation of Notch intracellular domain in RSF, indicating the elicitation of the Notch signaling. Notch-1, Notch-4, and Jagged-2 proteins were also detected in the developing synovium of mouse embryo. Thus, RSF may have re-acquired the primordial phenotype, accounting for the hyperproliferation and aggressive invasiveness, exhibiting tumor-like phenotype.
14712356 Clinical course of bucillamine-induced nephropathy in patients with rheumatoid arthritis. 2003 Dec BACKGROUND: Bucillamine, a disease-modifying antirheumatic drug widely prescribed in Japan, is reported to be a cause of proteinuria. However, to date, the clinical course of the nephropathy associated with the use of bucillamine has not been described in detail. METHODS: We analyzed renal biopsy findings from 10 patients with rheumatoid arthritis and concomitant bucillamine-induced nephropathy. Each patient was followed up until proteinuria had resolved. RESULTS: Proteinuria appeared 2-11 months after the initiation of the treatment with bucillamine. Nine patients, who stopped bucillamine treatment immediately (within 3 months) after the onset of proteinuria, were diagnosed as having stage I membranous nephropathy. Only one patient, who used bucillamine for 9.5 months after the onset of proteinuria, was diagnosed as having stage II membranous nephropathy. In all patients with stage I membranous nephropathy, the proteinuria disappeared within 7 months after they stopped bucillamine treatment. On the other hand, in the patient with stage II membranous nephropathy, the proteinuria persisted for 14 months after the use of bucillamine was stopped. In all the patients, the proteinuria resolved completely without deterioration of renal function. None of the patients has experienced recurrence of proteinuria. CONCLUSIONS: In patients with proteinuria induced by treatment with bucillamine, membranous nephropathy is the most common disorder. Immediate withdrawal of bucillamine results in prompt and complete resolution of proteinuria without deterioration of renal function.Bucillamine, a disease-modifying antirheumatic drug widely prescribed in Japan, is reported to be a cause of proteinuria. However, to date, the clinical course of the nephropathy associated with the use of bucillamine has not been described in detail.
12149230 Blockade of Fas-dependent apoptosis by soluble Fas in LGL leukemia. 2002 Aug 15 Altered expression of the Fas-Fas ligand apoptotic pathway leads to lymphoproliferative and autoimmune diseases. In lpr/lpr mice and children with autoimmune lymphoproliferative syndrome, defective apoptosis is due to Fas mutations. Large granular lymphocyte (LGL) leukemia is a clonal lymphoproliferative disorder associated with rheumatoid arthritis. Leukemic LGLs are resistant to Fas-dependent apoptosis despite expressing high levels of Fas. Such resistance can be overcome by activating leukemic LGLs in vitro, suggesting inhibition of Fas signaling in leukemic cells. We report that sera from patients with LGL leukemia contain high levels of soluble Fas. Ten of these 33 patients with LGL leukemia also had rheumatoid arthritis. Cloning and sequencing revealed expression of multiple Fas messenger RNA variants in leukemic LGL. These Fas variants, including 3 newly described here, encode soluble Fas molecules. Supernatants from cells transfected with these Fas variants blocked Fas-dependent apoptosis of leukemic LGLs. These results suggest that blockade of Fas-signaling by soluble Fas may be a mechanism leading to apoptosis resistance in leukemic LGLs.
12747285 Molecular differences in anticytokine therapies. 2003 Mar Biologic agents that inhibit proinflammatory cytokines have made a profound impact on the treatment of rheumatoid arthritis (RA). Of the agents that are currently approved by the US Food and Drug Administration (FDA) for this indication, etanercept and infliximab neutralize tumor necrosis factor (TNF), and anakinra inhibits interleukin-1 (IL-1). Adalimumab, which was just recently approved by the FDA, is also a TNF inhibitor. Despite their common ability to inhibit cytokine bioactivity, the molecular structures and mechanisms of action of these biologic agents are significantly different. The TNF-binding moiety of etanercept is derived from soluble TNF receptor subunits. Infliximab is a chimeric (mouse-human) monoclonal antibody to TNF, while adalimumab is a fully human anti-TNF monoclonal antibody. Anakinra has yet another mechanism of action: it is an IL-1 receptor antagonist. The molecular characteristics of these agents may be relevant to clinical efficacy and safety. These agents are still relatively new: to date, the longest reporting time is 5 years, for etanercept. Additional long-term data will be required to determine the relative benefits and drawbacks of different molecular characteristics in these anticytokine agents.
12114272 A role for sex steroids in autoimmune diseases: a working hypothesis and supporting data. 2002 Jun In recent years there has been a continuingly increasing interest in novel research subjects, as yet poorly explored, either because they relate to aspects previously thought to be marginal with respect to classical fields of investigation, or because they require both specialized competence and intense cross-talk by researchers from disparate areas. The potential interaction between immunity and cancer has generated a remarkable number of studies, including those related to the newly explored immune-neuro-endocrine system. In this paper, we review a few autoimmune diseases as examples of a mutual relationship between immune diseases and malignancies. We also review our previous studies on patients with rheumatoid arthritis (RA). In particular, aiming to define the hormone-responsive or -sensitive status of synovial tissues and cells, we have inspected different endocrine end-points, including (1) high- and low-affinity sites of androgen and estrogen binding; (2) the activity of key enzymes of steroid metabolism; and (3) the hormonal profile of synovial fluids as an indication of local endocrine milieu. Overall, our data provide convincing evidence for synovial macrophage-like cells and a subset of T lymphocytes to be considered as target cells for gonadal steroids. This provides a basis for developing new strategies for alternative treatments of RA and possibly unveils novel perspectives in both research and the clinic for other autoimmune diseases as well. In addition, the association of autoimmunity and cancer may disclose promising new avenues of research linking steroid hormones, the immune system, and malignant transformation.
15764045 Adalimumab (Humira): a brief review for dermatologists. 2004 Dec Adalimumab is a new purely human TNF-alpha monoclonal antibody that has been approved for the treatment of rheumatoid arthritis as monotherapy or in combination with methotrexate. It is administered by subcutaneous injection in a 40-mg dose every other week. The one published Phase II trial of adalimumab for psoriasis has provided very encouraging results for its efficacy. Its most important side effects relate to the development of infection while it is being used. It is a promising medication and research regarding its use continues.
12760319 A therapy-resistant chronic leg ulcer treated successfully with topical basic fibroblast g 2003 Mar We report a patient with rheumatoid arthritis who had a chronic leg ulcer with long-standing resistance to therapy. Topical basic fibroblast growth factor (bFGF) at a dose of 30 micrograms/day for 3 months was clinically effective in reducing the ulcer area by promoting angiogenesis, re-epithelization, granulation and scar formation. bFGF may be an effective treatment for therapy-resistant leg ulcers.
12056295 [Chrysiasis]. 2002 Apr We describe the case of a 78-year old woman, with rheumatoid arthritis, 3 years of regular parenteral gold administration and Chrysiasis. Chrysiasis is a rare permanent pigmentation of the skin resulting from the parenteral administration of gold. The cause of the pigmentation is multifactorial and not fully established at the moment.
12378169 A medium-term follow-up study of 44 Souter-Strathclyde elbow arthroplasties carried out fo 2002 Sep The results of 44 primary Souter-Strathclyde total elbow arthroplasties performed on 36 patients with rheumatoid arthritis are reported, with a mean follow-up of 6 years (range, 17 months-12 years; median, 6 years). Of these patients, 63% reported complete freedom from pain in the elbow, 25% mild intermittent pain, and 12% moderate pain. The mean range of motion at follow-up was 97 degrees (range, 40 degrees -135 degrees ). This represented a mean gain of 16.5 degrees of flexion, but only a 1.5 degrees gain in extension. Twenty-sevenelbows had a range of motion of 100 degrees or greater compared with 13 before surgery. There was 1 permanent ulnar nerve palsy and 1 deep infection requiring debridement. Six cases (4%) required revision, 2 for olecranon fractures and 4 for loosening. In patients with rheumatoid arthritis with low functional demand, the Souter-Strathclyde total elbow arthroplasty performs well in abolishing pain and increasing independence in carrying out the activities of daily living.
15494359 A linguistic framework for assessing the quality of written patient information: its use i 2005 Jun Patient information leaflets are an important adjunct to verbal exchange between doctor and patient. Their value is dependent upon whether they contain useful information from the viewpoint of the patient and are easily understood. We developed a framework based upon linguistic theory for assessing the quality of written patient information and applied it to a set of leaflets about methotrexate treatment. Items included the overall structure of the text, the technicality of the vocabulary used, the number of content words per clause ('lexical density'), and the clarity of the role relationship between author and reader. The leaflets consisted of up to nine identifiable sections (range 3-8): background information about the drug, summary of its use, dosage instructions, outline of benefits and side-effects, monitoring information, constraints on patient behavior, storage instructions, and clinical contact availability. Most leaflets contained a high number of content words per clause and the identity of the author was clear in only three (17%). Linguistic analysis provides highly relevant information about written patient information. Together with critical assessment of factual and visual aspects, consideration of key linguistic features should improve the quality of informational texts for our patients.