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ID PMID Title PublicationDate abstract
15983755 [Pulmonary manifestations in rheumatic systemic diseases]. 2005 Jul Collagen based vascular diseases with pulmonary involvement comprise rheumatoid arthritis, systemic lupus erythematosus, progressive systemic sclerosis, dermatomyositis and polymyositis, ankylosing spondylitis, Sjögren's syndrome, and mixed connective tissue diseases. The different characteristics of pulmonary involvement are described. In such circumstances, early recognition of lung involvement is of considerable significance and the relationship to the corresponding disease has to be made. Frequently unrecognised pulmonary involvement ends up as fibrosis with irreversible deficits in respiratory function.
15756496 [Renal manifestations of rheumatic diseases]. 2005 Feb Inflammatory rheumatic diseases are frequently complicated by subclinical or overt renal manifestations. This is well known for the connective tissue diseases and vasculitides in which renal disease can be of significant prognostic value and therapeutic implication. However, rheumatoid arthritis and the spondyloarthritides can also be associated with direct renal manifestation or with secondary renal AA-amyloidosis. The clinician should be aware of the different glomerular (i. e. nephritic or nephritic syndrome, rapidly progressive renal disease) and tubulo-interstitial syndromes. In any case of renal dysfunction in a rheumatic patient, the differential diagnosis should include renal disease independent from the rheumatic condition, infection, and drug-induced renal toxicity.
15750665 Zinc in health and chronic disease. 2005 Zinc is a trace element essential for the optimal function of a variety of biochemical and physiological processes. Its role in healthy aging is particularly important as it prevents neo plastic cell growth, is involved in mitotic cell division, DNA and RNA repair. Although zinc is widely available in food, the daily intake in many persons may be suboptimal. Other causes of low zinc concentrations may be due to small bowel conditions that cause mucosal damage and thus decrease absorption. Chronic diseases associated with alterations in zinc status are bronchial asthma, rheumatoid arthritis and Alzheimer disease. At present it is uncertain if therapy with zinc would assist in the management of these chronic diseases. In view of the important cellular functions of zinc in the human body, a diet with an adequate zinc content is beneficial in promoting healthy aging and maintaining good health.
20704889 Can infections prevent or cure allergy and autoimmunity? 2005 Jun Extract: In western countries the prevalence and incidence of allergic and autoimmune diseases have been increasing dramatically over the last 50 years. In the last two decades, significant progress has been made towards understanding the genetic basis for susceptibility to autoimmunity or allergy. Genetic factors, however, cannot explain abrupt changes in disease incidence. It is therefore likely that environmental factors, specifically environmental factors that have changed over the last two generations, are critical for the increasing incidence of allergies and autoimmune diseases. Traditionally, autoimmune diseases such as multiple sclerosis (MS), type I diabetes, or rheumatoid arthritis (RA) are believed to have resulted from aberrant immune response to pathogens. In contrast, the "hygiene hypothesis," first postulated some 20 years ago, proposes that a lack of infections, especially during early childhood, predisposes one to the aberrant immune responses against harmless foreign antigens that cause allergic diseases such as rhinitis, atopic dermatitis, and allergic asthma. Several lines of epidemiological, clinical and experimental research point to more complex connections, either protective or pathogenic, between infection, allergy and autoimmunity.
16357728 Section 2: The importance of improving function in patients with pain. 2005 Apr When evaluating pain in the rheumatic diseases, assessment of adequate therapy has expanded from purely biochemical measures and joint counts to determining the degree of function. Because pain is an important predictor of function, instruments have been developed that attempt to measure how disease and pain affect parameters such as activities of daily living, quality of life, ability to work, and emotional well-being. Some measures, such as visual analogue scales, measure only the intensity of pain; multidimensional scales assess a variety of factors related to the patient's overall ability to function. The Short Form-36 measures the impact of disease on overall quality of life; adaptations have been made to some specific diseases. The Health Assessment Questionnaire was one of the first multidimensional questionnaires developed for rheumatic diseases, and this has been further refined for rheumatoid arthritis with the Multidimensional Health Assessment Questionnaire.
16137943 [Risk factors for osteoporosis in Japan]. 2005 Sep Risk factors for osteoporosis based on literally analysis were reviewed. For the prevention for the incidence of osteoporosis, the risk factors were low BMI, smoking and low impact exercise. Calcium and Vitamin D intake was the important preventive factor for the disease. Risk factors to assess the prevalent osteoporosis early were also reviewed. Finally, risk assessment for osteoporosis integrated by members of WHO collaborating centre for metabolic bone diseases were stated. They have undertaken a series of meta-analyses to identify clinical risk factors for fracture to determine their dependence upon age and sex. These were based on the individual data from prospective population-based studies. They concluded the risk factors for osteoporosis were age female-sex, low BMI, family history of fracture, current smoking, ever use of systemic corticosteroids, alcohol intake more than two units per day, rheumatoid arthritis and low BMD at the femoral neck or total hip.
17029106 Identification of three novel peptides that inhibit CD40-CD154 interaction. 2005 The CD40-CD154 interaction is an attractive target for therapeutic intervention in various autoimmune disorders, including rheumatoid arthritis, systemic lupus erythematosus (SLE), multiple sclerosis, and myasthenia gravis. In this study, to develop a new disruption strategy of the CD40-CD154 interaction, we screened for peptides with inhibitory effects on such ligation. 2 x 10(11) phage display libraries displaying liner peptides of 12-mer amino acids were screened by CD40-Ig binding assay and eight phages which expressed a different respective peptide (40BP-1 to -8) were able to specifically bind to CD40. Competitive inhibition analyses showed that 3 of the 8 peptides (40BP-N1-1 - APELPNMTPSWT; 40BP-N1-2 - APRPHTSYSPLP; and 40BP-N1-3 - GMTAPPPPRLTQ) blocked CD40-CD154 interaction when used at high concentrations. A consensus sequence (APxPPxxT) was conserved in these three peptides. These peptides may constitute a useful and novel strategy for the inhibition of the interaction between CD40 and CD154 molecules.
16609823 The burden of musculoskeletal disease--a global perspective. 2006 Nov Musculoskeletal diseases are one of the major causes of disability around the world and have been a significant reason for the development of the Bone and Joint Decade. Rheumatoid arthritis, osteoarthritis and back pain are important causes of disability-adjusted-life years in both the developed and developing world. COPCORD studies in over 17 countries around the world have identified back and knee pain as common in the community and are likely to increase with the ageing population. Musculoskeletal conditions are an enormous cost to the community in economic terms, and these figures emphasise how governments need to invest in the future and look at ways of reducing the burden of musculoskeletal diseases by encouraging exercise and obesity prevention campaigns.
15940563 Pleural amyloidosis as the first sign of IgD multiple myeloma. 2005 Jun We describe a case of IgD myeloma with amyloid and plasmocytic pleural localisations. At the onset of the disease it mimicked rheumatoid arthritis, which can be the first presentation of both AL amyloidosis and multiple myeloma. Pleural effusion can happen first in IgD myeloma, but our observation is of interest in that it confirms the very rare possibility of pleural amyloid and plasmocytic localisations devoid of pleural effusion.
17034761 Auranofin, as an anti-rheumatic gold compound, suppresses LPS-induced homodimerization of 2006 Dec 1 Toll-like receptors (TLRs), which are activated by invading microorganisms or endogenous molecules, evoke immune and inflammatory responses. TLR activation is closely linked to the development of many chronic inflammatory diseases including rheumatoid arthritis. Auranofin, an Au(I) compound, is a well-known and long-used anti-rheumatic drug. However, the mechanism as to how auranofin relieves the symptom of rheumatoid arthritis has not been fully clarified. Our results demonstrated that auranofin suppressed TLR4-mediated activation of transcription factors, NF-kappaB and IRF3, and expression of COX-2, a pro-inflammatory enzyme. This suppression was well correlated with the inhibitory effect of auranofin on the homodimerization of TLR4 induced by an agonist. Furthermore, auranofin inhibited NF-kappaB activation induced by MyD88-dependent downstream signaling components of TLR4, MyD88, IKKbeta, and p65. IRF3 activation induced by MyD88-independent signaling components, TRIF and TBK1, was also downregulated by auranofin. Our results first demonstrate that auranofin suppresses the multiple steps in TLR4 signaling, especially the homodimerization of TLR4. The results suggest that the suppression of TLR4 activity by auranofin may be the molecular mechanism through which auranofin exerts anti-rheumatic activity.
16777581 Ankylosing spondylitis and symptom-modifying vs disease-modifying therapy. 2006 Jun The main objectives of medical therapy in ankylosing spondylitis (AS) are to relieve pain, stiffness and fatigue and to prevent structural damage. The Assessment in Ankylosing Spondylitis Working Group has proposed different domains with specific instruments to assess the efficacy of therapeutic agents classified as symptom-modifying and disease-controlling antirheumatic drugs. Non-steroidal antiinflammatory drugs (NSAIDs) are still the first-line treatment in the management of AS, and they are effective in controlling symptoms such as pain and stiffness and maintaining mobility in many patients. A recent randomized trial suggested that the progression of radiological damage occurs less on continuous use of celecoxib compared with on-demand use. If such findings were confirmed by other studies, the therapeutic value of NSAIDs in AS may extend beyond symptom control. However, for each individual patient, the expected advantages of treatment with NSAIDs should be weighted against any possible gastrointestinal and cardiovascular disadvantages. Disease-modifying antirheumatic drugs (DMARDs) are widely used for second-line therapy in AS, but the evidence for their efficacy is poor. The term 'DMARD' has been borrowed from rheumatoid arthritis, and none of the DMARDs have been shown to prevent or significantly decrease the rate of progression of structural damage which is required to be qualified as a disease-controlling antirheumatic drug for AS. Sulphasalazine is the most extensively studied DMARD and studies suggest some degree of clinical benefit confined to peripheral joint involvement, but no evidence of benefit in axial disease. Methotrexate, which is the gold standard DMARD in rheumatoid arthritis, does not seem to have a substantial therapeutic effect in AS on axial or peripheral joint involvement. Leflunomide appears to exert little beneficial effect, if any, even on peripheral joint involvement. There is also good evidence that local therapy with corticosteroids is effective and may be used in selected patients. Oral corticosteroids may be somewhat effective in relieving the symptoms of AS, but this has not been formally studied. Small studies have reported favourable results with intravenous methylprednisolone pulse therapy, but the effect is temporary. Pamidronate and thalidomide have been used in some preliminary trials but need further studies to assess their potential role in treating AS patients resistant or intolerant to other forms of treatment. Treatment with tumour necrosis factor blockers is not discussed in this review.
16128605 Biologics in the treatment of transplant rejection and ischemia/reperfusion injury: new ap 2005 Tumor necrosis factor (TNF)-alpha inhibitors have proven efficacy in various autoimmune diseases such as Crohn disease, rheumatoid arthritis, psoriasis, and ankylosing spondylitis. Indeed, some TNFalpha inhibitors have already been approved for the management of the inflammatory manifestations associated with Crohn disease and rheumatoid arthritis. These agents are increasingly used for treatment of corticosteroid-resistant graft-versus-host disease after bone marrow transplantation, and case reports have documented their efficacy in treating corticosteroid- and muromonab-resistant rejection after intestinal transplantation. Thus, the potential role of TNFalpha inhibitors in transplantation of other vascularized solid organs is worthy of investigation. Experimental evidence indicates that TNFalpha plays a key role in mediating ischemia/reperfusion (IR) injury after liver, kidney, intestine, heart, lung, and pancreas transplantation. TNFalpha was also identified as a marker cytokine during organ rejection. Single-center studies evaluating the role of TNFalpha inhibitors in kidney transplantation have been initiated but the results are not yet available. TNFalpha is known to be a contributing factor in kidney allograft rejection, and may have value in predicting the onset of steroid-resistant acute rejection after liver transplantation. Experimental and preliminary clinical data have shown that circulating levels of TNFalpha are increased during cardiac graft rejection, and indicate that TNFalpha plays a role in the pathogenesis of acute cardiac allograft rejection. Anti-TNFalpha therapy was shown to prolong cardiac allograft survival when used alone or in combination with other drugs. TNFalpha genotype has been strongly associated with mortality in humans due to acute cell-mediated heart transplant rejection. In addition, there is evidence for a genetic predisposition toward acute rejection after kidney and simultaneous kidney-pancreas transplantation. TNFalpha inhibition has been used successfully as part of an induction therapy for pancreatic islet cell transplantation. Apart from IR injury and acute rejection after lung transplantation, TNFalpha was also found to be involved in the pathoimmunology of obliterative bronchiolitis. In conclusion, a substantial body of experimental evidence and preliminary clinical data suggest that TNFalpha inhibitors may play an important role in solid-organ transplantation, both in the amelioration of IR injury and in the treatment and prevention of acute rejection. Pharmacodynamic monitoring and pharmacogenetic screening may help to identify patients most likely to benefit from TNFalpha blockade. Randomized controlled trials in patients undergoing solid-organ transplantation are needed to further elucidate the clinical value of TNFalpha inhibition.
16859536 Epratuzumab (humanised anti-CD22 antibody) in primary Sjögren's syndrome: an open-label p 2006 This open-label, phase I/II study investigated the safety and efficacy of epratuzumab, a humanised anti-CD22 monoclonal antibody, in the treatment of patients with active primary Sjögren's syndrome (pSS). Sixteen Caucasian patients (14 females/2 males, 33-72 years) were to receive 4 infusions of 360 mg/m2 epratuzumab once every 2 weeks, with 6 months of follow-up. A composite endpoint involving the Schirmer-I test, unstimulated whole salivary flow, fatigue, erythrocyte sedimentation rate (ESR), and immunoglobulin G (IgG) was devised to provide a clinically meaningful assessment of response, defined as a > or = 20% improvement in at least two of the aforementioned parameters, with > or = 20% reduction in ESR and/or IgG considered as a single combined criterion. Fourteen patients received all infusions without significant reactions, 1 patient received 3, and another was discontinued due to a mild acute reaction after receiving a partial infusion. Three patients showed moderately elevated levels of Human anti-human (epratuzumab) antibody not associated with clinical manifestations. B-cell levels had mean reductions of 54% and 39% at 6 and 18 weeks, respectively, but T-cell levels, immunoglobulins, and routine safety laboratory tests did not change significantly. Fifty-three percent achieved a clinical response (at > or = 20% improvement level) at 6 weeks, with 53%, 47%, and 67% responding at 10, 18, and 32 weeks, respectively. Approximately 40%-50% responded at the > or = 30% level, while 10%-45% responded at the > or = 50% level for 10-32 weeks. Additionally, statistically significant improvements were observed in fatigue, and patient and physician global assessments. Further, we determined that pSS patients have a CD22 over-expression in their peripheral B cells, which was downregulated by epratuzumab for at least 12 weeks after the therapy. Thus, epratuzumab appears to be a promising therapy in active pSS, suggesting that further studies be conducted.
16922642 Clinical pharmacology of etoricoxib. 2005 Aug Etoricoxib is a highly selective COX-2 inhibitor (coxib) approved in Europe for the treatment of osteoarthritis (OA), rheumatoid arthritis and acute gouty arthritis. Etoricoxib is an effective analgesic drug that has shown some improved efficacy versus traditional NSAIDs and it is the only coxib approved for the treatment of acute gouty arthritis. Moreover, recent studies evidence its efficacy in patients with ankylosing spondylitis. In the Etoricoxib Diclofenac Gastrointestinal Evaluation study performed in patients with OA, etoricoxib significantly reduced the rate of discontinuation by 50% due to gastrointestinal adverse events versus diclofenac. Comparable rates of thrombotic cardiovascular events were detected. Rates of discontinuation due to hypertension-related adverse effects were higher on etoricoxib than diclofenac. Similarly to other selective COX-2 inhibitors, etoricoxib is contraindicated in patients with ischaemic heart disease or stroke and it should be used with caution in patients with risk factors for heart disease. The European Medicines Agency has contraindicated the use of etoricoxib in patients with uncontrolled hypertension. Selective COX-2 inhibitors remain an appropriate choice in patients at low cardiovascular risk, but with increased risk of gastrointestinal complications.
16152852 Early results with the thrust plate prosthesis in young patients with osteoarthritis of th 2005 Apr The purpose of this study was to evaluate the results of the Thrust Plate Prosthesis as a treatment option for osteoarthritis of the hip in young patients. Of the fifty patients (63 hips) reviewed, 31 (62%) were males and 19 (38%) females. Pre-operative diagnosis included primary osteoarthritis (23), developmental dysplasia (8), avascular necrosis (7), Perthes (4), post-traumatic arthritis (3), rheumatoid arthritis (2), ankylosing spondylitis (1), psoriatic arthropathy (1) and slipped upper femoral epiphysis (1). All components were implanted uncemented with metal-on-metal articulation. The average follow-up was 4.04 years (range 12 months-8.5 years). The mean age of the patients was 42.3 years (range 21-57 years). The mean pre-operative Harris Hip Score was 41.9 (range 12-89) and at final follow-up 89.91 (range 41-100). In 25 hips with > or = 5 yr follow-up, the average HHS at final follow-up was 84.5 (range 50-100). Complications included dislocation (2), transient sciatic nerve palsy (1), discomfort from lateral strap (2), implantation of wrong femoral head (1), revision (3 = 4.76%) and implant loosening (4) (6.35%). The thrust plate prosthesis is a useful alternative in young patients with hip arthritis and the results are comparable with other uncemented hip replacements. The added advantage is preservation of the proximal femoral bone stock, which can prove useful in future revisions.
15987482 The differential contribution of tumour necrosis factor to thermal and mechanical hyperalg 2005 Therapies directed against tumour necrosis factor (TNF) are effective for the treatment of rheumatoid arthritis and reduce pain scores in this condition. In this study, we sought to explore mechanisms by which TNF contributes to inflammatory pain in an experimental model of arthritis. The effects of an anti-TNF agent, etanercept, on behavioural pain responses arising from rat monoarthritis induced by complete Freund's adjuvant were assessed and compared with expression of TNF receptors (TNFRs) by dorsal root ganglion (DRG) cells at corresponding time points. Etanercept had no effect on evoked pain responses in normal animals but exerted a differential effect on the thermal and mechanical hyperalgesia associated with rat arthritis induced by complete Freund's adjuvant (CFA). Joint inflammation was associated with increased TNFR1 and TNFR2 expression on DRG cells, which was maintained throughout the time course of the model. TNFR1 expression was increased in neuronal cells of the DRG bilaterally after arthritis induction. In contrast, TNFR2 expression occurred exclusively on non-neuronal cells of the macrophage-monocyte lineage, with cell numbers increasing in a TNF-dependent fashion during CFA-induced arthritis. A strong correlation was observed between numbers of macrophages and the development of mechanical hyperalgesia in CFA-induced arthritis. These results highlight the potential for TNF to play a vital role in inflammatory hyperalgesia, both by a direct action on neurons via TNFR1 and by facilitating the accumulation of macrophages in the DRG via a TNFR2-mediated pathway.
16406545 Retrospective case review of pediatric patients with uveitis treated with infliximab. 2006 Feb PURPOSE: To assess the response and adverse events associated with infliximab treatment for refractory, noninfectious pediatric uveitis. DESIGN: Retrospective noncomparative case series of pediatric patients with refractory uveitis treated with infliximab. PARTICIPANTS: Six patients were identified. Diagnoses of the participants included idiopathic uveitis (n = 1), juvenile rheumatoid arthritis with uveitis (n = 3), idiopathic retinal vasculitis with uveitis (n = 1), and bilateral pars planitis, with vitreitis and papillitis of the left eye (n = 1). Uveitis developed in the patients (5 female, 1 male) at a mean age of 9.0 years (+/-5.0 years; range, 0.9-14.8 years). All patients had bilateral eye involvement. These patients were refractory to or dependent on topical steroids (n = 4), oral prednisone (n = 3), or both, and were also refractory to the following therapies: methotrexate (n = 6), cyclosporine (n = 3), mycophenolate mofetil (n = 3), etanercept (n = 3), and daclizumab (n = 1). INTERVENTION: All patients initially received infliximab at doses between 5 and 10 mg/kg at 2- to 4-week intervals, and then were maintained at 4- to 8-week intervals at doses of 5 to 18 mg/kg. Mean follow-up time on treatment has been 48.1 weeks (+/-14.9 weeks; range, 32-74 weeks). MAIN OUTCOME MEASURES: Primary outcome measures included the quantitative measurement of the amount of ocular inflammation in different locations within the eye. Patients were monitored for infusion reactions as well as other potential side effects. The children's clinical status, complete blood counts, and liver function panels were monitored by pediatric rheumatologists every 6 weeks. RESULTS: All 6 patients showed reduction in their intraocular inflammation after infliximab therapy was initiated. Furthermore, control of ocular inflammation was achieved while receiving infliximab therapy. Topical and systemic corticosteroids were able to be discontinued in all patients except for 1 patient, who is currently weaning off prednisone. The only adverse reactions seen were the development of vitreous hemorrhage in 1 patient and a case of transient upper respiratory infusion reaction. No patient has had to discontinue treatment. CONCLUSIONS: Infliximab seems to be an effective agent for the treatment of refractory pediatric uveitis without apparent serious toxicity in this series of patients.
16948117 Identification of fibronectin neoepitopes present in human osteoarthritic cartilage. 2006 Sep OBJECTIVE: Fibronectin fragments are present at high concentrations in the cartilage of patients with rheumatoid arthritis and patients with osteoarthritis (OA) and have been shown to promote cartilage catabolism in human cartilage cultures, suggesting that fibronectin fragments participate in the initiation and progression of arthritic disease. This study was undertaken to 1) identify the major fibronectin fragments in human OA cartilage and confirm their ability to elicit cartilage catabolism, 2) identify the cleavage sites in fibronectin and generate the corresponding neoepitope antibodies, and 3) explore the utility of fibronectin neoepitopes as biomarkers. METHODS: Fibronectin fragments were purified from human OA cartilage using affinity chromatography; their N-termini were then identified by sequencing. Bovine nasal cartilage was treated with affinity-purified fibronectin fragments and assayed for aggrecan breakdown by monitoring the release of glycosaminoglycans and the aggrecan neoepitope 1771AGEG. Fibronectin neoepitopes were detected by Western blotting in cytokine-treated media of human cartilage explants, and by immunohistochemical analyses of human OA cartilage. RESULTS: Multiple fibronectin fragments were isolated from human OA cartilage, and all contained the N-terminus 272VYQP. These fragments induced aggrecanase-mediated cartilage catabolism in bovine cartilage explants. Fibronectin fragments with the N-terminus 272VYQP and fragments with the C-terminus VRAA271 were detected following cytokine treatment of human cartilage extracts. These neoepitopes localized with areas of aggrecan loss in OA cartilage. CONCLUSION: Human OA cartilage contains fibronectin fragments with catabolic activity and a major cleavage site within fibronectin. This study is the first to characterize fibronectin neoepitopes in OA cartilage, suggesting that they may represent a novel biomarker of arthritis.
16937151 Bilateral total knee replacement under a single anaesthetic, using a cementless implant is 2007 Mar Bilateral knee replacement under single anaesthetic is not a common procedure. There is a general agreement that this is associated with greater morbidity and mortality. However, there is a suggestion in literature that using a cementless implant could reduce this risk. We wanted to make a prospective comparison of safety and clinical results, between unilateral and bilateral cementless knee replacements performed under a single anaesthetic. A prospective non-randomised matched cohort study on 87 consecutive patients who had bilateral simultaneous/sequential knee replacement and 174 consecutive patients who had unilateral knee replacement between the period of 1997 and 2002 were included in this study. All patients had a cementless mobile-bearing implant. All patients had an independent objective assessment at follow-up. There was no significant difference between the two groups in terms of age, sex, primary diagnosis (osteoarthritis or rheumatoid arthritis), co-morbidity, ASA grade, average range of motion and average American knee society score and post-operative surgical complications. There was one early death in the bilateral group, and three in the unilateral group. The clinical results of bilateral group were as good as the unilateral group. Our study showed that in terms of postoperative medical and surgical complications, bilateral simultaneous/sequential knee replacement using a cementless mobile-bearing implant is as safe as a unilateral knee replacement. With careful patient selection, bilateral knee replacement under a single anaesthetic would be a suitable option for patients who present with bilateral symptomatic arthritis of the knee.
16542849 Anti-TNF therapies in the management of acute and chronic uveitis. 2006 Feb 21 Patients with anterior uveitis may be treated with topical therapy alone but patients with posterior uveitis and those with sight threatening complications of anterior uveitis usually require systemic treatment especially if the disease is bilateral. The mainstay of treatment is corticosteroids and additional immunosuppressive agents such as cyclosporin and mycophenolate are used when necessary. There remains a significant cohort of patients in whom this therapy is either not tolerated or is ineffective. The use of the anti-tumour necrosis factor (TNF) antibodies has been very successful in controlling other immune-mediated disorders such as rheumatoid arthritis and has subsequently been extended to use in other arthritidies and other disorders such as psoriasis and Crohn's disease. TNF is known to play a key role in ocular inflammation as shown by animal studies and its detection in the ocular fluids of inflamed eyes in man. In some disorders all types of anti-TNF antibodies have similar efficacy but that does not appear to be the case with uveitis where infliximab is at present looking to be more effective than etanercept. The data on the use of anti-TNF drugs in uveitis is presented together with new data on its role as a steroid sparing agent.