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ID PMID Title PublicationDate abstract
15837451 Factors associated with patients' loss to follow-up after finishing randomized clinical tr 2005 Feb OBJECTIVES: To study patient's follow-up after finishing participation in randomized clinical trials (RCTs), and to identify factors associated with loss to follow-up (FU). PATIENTS AND METHODS: Medical charts of 212 rheumatoid arthritis (RA) and osteoarthritis (OA) patients from a rheumatological out-patient center were analyzed. Loss to FU was considered when patients did not return to their regular appointments within the first year after finishing their participation in an RCT assessing anti-cyclooxygenase-2 non-steroidal anti-inflammatory drugs (anti-COX-2 NSAIDs). Mann-Whitney U-test, chi2 test and Wilcoxon test were performed as appropriate. Logistic regression was performed to identify factors which might be related to loss to FU. A survey was conducted to obtain lost to FU patients' opinions. p values less than 0.05 were considered significant. RESULTS: The mean frequency of patients' visits in the year before enrollment in an RCT was 3.73 SD 2.06, and during the year after participation was 2.6 SD 1.96 (p<0.0001). Fifty patients (23.6%) did not return to their usual rheumatologic visit. On multivariate analysis, the number of daily tablets of study medication (odds ratio (OR)=2.64, 95% confidence interval (CI) 1.1 to 6.3) and the frequency of clinical visits (OR=0.56, 95% CI 0.37 to 0.85) were associated with loss to FU (p<0.008). Lost to FU patients' opinions did not support these findings. CONCLUSIONS: After participating in a RCT assessing anti-COX-2 NSAIDs, many patients return with less frequency, or do not return at all to their regular rheumatologic visit. Although a high number of tablets of the investigational drug and a low frequency of protocol visits may be contributors to patient loss to FU, investigators should consider that personal situations not related to the RCTs may also influence patients' return to consultation in the private setting.
16859519 Diagnostic value of antibodies against a modified citrullinated vimentin in rheumatoid art 2006 Antibodies directed against citrullinated vimentin are members of the family of autoantibodies reactive with citrullinated proteins and are among the most specific serological markers for the diagnosis of rheumatoid arthritis (RA). This study was performed to test the diagnostic value of a newly developed enzyme-linked immunosorbent assay (ELISA) for the detection of antibodies against a genetically modified citrullinated vimentin (anti-MCV) in comparison with a second-generation anti-cyclic citrullinated peptides (anti-CCP2) ELISA test system. Blinded sera from 631 patients (409 consecutive out-patients and 222 randomly selected stored sera) with RA (n = 164) and non-RA (osteoarthritis [n = 120], polymyalgia rheumatica/giant cell arteritis [n = 80], spondyloarthritis [n = 36], and other inflammatory rheumatic or non-inflammatory disease [n = 67]) were tested for the presence of anti-MCV and anti-CCP2 antibodies according to the manufacturers' instructions. The diagnostic performance of the anti-MCV was comparable with the anti-CCP2 assay for the diagnosis of RA according to the calculated area under the curve (0.824; 95% confidence interval (CI) 0.778-0.870 versus 0.818; 95% CI 0.767-0.869) as analysed by receiving operating characteristic curve. When categorised with a cutoff value of 20.0 U/ml (as recommended by the manufacturer), sensitivity and specificity of the anti-MCV ELISA were 69.5% (95% CI 61.9%-76.5%) and 90.8% (86.9%-93.8%), respectively, compared with 70.1% (62.5%-77.0%) and 98.7% (96.7%-99.6%) of the anti-CCP2 assay. Using the cutoff values of 19.0 U/ml and 81.5 U/ml for the anti-MCV test to obtain a sensitivity and specificity identical to the anti-CCP2 assay, showed a reduced specificity (89.8%; 85.8%-92.9%) and sensitivity (53.7%; 45.7%-61.5%), respectively, of the anti-MCV ELISA compared with the anti-CCP2 test. In conclusion, the serum ELISA testing for anti-MCV antibodies as well as the anti-CCP-2 assay perform comparably well in the diagnosis of RA. In the high-specificity range, however, the anti-CCP2 assay appears to be superior to the anti-MCV test.
17207425 Reliability and validity of the American Orthopaedic Foot and Ankle Society Clinical Ratin 2006 Dec BACKGROUND: The use of clinical outcomes instruments is essential for the effective interpretation of individual patient progress as well as the comparison of treatment groups. An outcomes instrument must be reliable and valid to obtain any meaningful data. The purpose of the present study was to examine the reliability and validity of the American Orthopaedic Foot and Ankle Society (AOFAS) clinical rating scale for the hallux metatarsophalangeal-interphalangeal and lesser toes metatarsophalangeal-interphalangeal joints. METHODS: Eleven patients (one man, 10 women) with an average age of 54 (range 40 to 72) years and with classic rheumatoid arthritis not currently treated for foot complaints were enrolled in the present study. The average duration of rheumatoid arthritis was 14 years. Each patient completed a set of two outcomes instruments and had a physical examination by a single clinician at the initial visit and returned at 1 week for completion of the same scales and examination. The outcomes scales used were the AOFAS clinical rating scale for the hallux, the AOFAS clinical rating scale for the lesser toes, and the previously validated Foot Function Index (FFI). Test-retest reliability was evaluated using intraclass correlation coefficients between week 1 and week 2 for the summary scores as well as for the subscales of pain and activity. Consistency between the two instruments was evaluated with Pearson correlation coefficients. RESULTS: The AOFAS clinical rating scale for the hallux and lesser toes is repeatable between 1-week trials (ICC 0.95; p < 0.05; ICC 0.80; p < 0.05, respectively). Moderately strong correlations were found between the mean values for the AOFAS hallux and FFI (r = -0.81; p < 0.05). Weaker correlations were seen between the mean values for the AOFAS lesser toes and FFI scales (r = -0.69; p < 0.05). CONCLUSIONS: The hallux subscale for pain correlates strongly with the FFI subscale for pain, suggesting high content validity (r = -0.94; p < 0.001). Ceiling effects were seen with the AOFAS lesser toe subscale for activity, limiting its usefulness in a general patient population. The AOFAS lesser toe subscale for pain and the AOFAS hallux subscale for activity correlated weakly with the FFI values (r = -0.31; r = -0.37; p > 0.05, respectively). CONCLUSIONS: Although the AOFAS hallux and lesser toe scales were found to be reliable in a rheumatoid patient population, their validity remains in question. These findings must be confirmed with larger subject numbers, with the inclusion of symptomatic patients before recommended routine use of the hallux clinical rating and lesser toe clinical rating scales.
16385351 [Biologic therapy with anti-TNFα in rheumathoid arthritis]. 2005 OBJECTIVE: To evaluate the efficacy, the tolerability, and treatment survival of the association of anti-TNFα (Infliximab, Etanercept, Adalimumab) plus Methotrexate vs Methotrexate as monotherapy in patients with reumathoid arthritis (RA). METHODS: Review of published controlled randomized clinical studies on the association of anti-TNFα plus Methotrexate vs Methotrexate alone in patients with rheumathoid arthritis (RA). Results in terms of remission and progression of radiologic damage, and clinical response expressed in terms of ACR 50 or ACR 70 were reviewed in the different studies. RESULTS: In patients with RA the association of anti-TNFα plus Methotrexate led to a greater remission of radiologic damage and marked improvement of clinical response expressed as ACR 50 or ACR 70 compared to therapy with Methotrexate only. CONCLUSIONS: In the absence of controlled studies, review of the published studies showed that in RA patients the association of anti-TNFα plus Methotrexate is extremely more efficacious than therapy with Methotrexate only. Choice of the drug depends on the activity of the disease, the necessity of a fast response, the presence of side effects, the schedule of treatment and consequently the direct and indirect costs of the drug, and the easiness on supply and distribution.
15829828 Quantitative assessment of fatty degeneration in rotator cuff muscles determined with comp 2005 May OBJECTIVES: Reliable assessment of fatty degeneration of rotator cuff muscles is desirable to predict the outcome of shoulder surgery. Currently used qualitative assessments are limited by relatively high inter- and intraobserver variability. It was hypothesized that a quantitative measurement of muscle density using computed tomography (CT) was more reliable and reproducible. MATERIALS AND METHODS: Thirty shoulders from patients with rheumatoid arthritis were analyzed using parasagittal multiplanar reconstructions acquired from a 16-slice CT scanner. Three observers visually rated the severity of fatty degeneration and independently outlined the rotator cuff muscles, after which the mean density was calculated. Inter- and intraobserver agreement on both measurements was expressed by the interclass correlation coefficient (ICC) and the standard deviation of the differences (SDD) between the measurements. RESULTS: A strong correlation was found between the quantitative measure and the visual rating (R2 = 0.94; P < 0.0001). The SDD in muscle density did not exceed 2.3 Hounsfield units, and the mean rotator cuff ICC (0.98) was substantially greater than that of the visual rating (0.63). CONCLUSIONS: This study describes a reproducible method to quantify fatty degeneration of the rotator cuff muscles in CT images, with a higher interobserver agreement than the visual score, and may prove a reliable tool to evaluate the quality of the rotator cuff muscles.
17171394 [Computer assisted radiological diagnostics of arthritic joint alterations]. 2006 Dec Computer assisted diagnosis (CAD) schemes are currently used in the field of musculoskeletal diseases to quantitatively assess vertebral fractures, joint space narrowing, andr erosion. Most systems work semi-automatically, i.e. they are operator dependent in the selection of anatomical landmarks. Fully automatic programs are currently under development. Some CAD products have already been successfully used in clinical trials.
17101062 MLN51 and GM-CSF involvement in the proliferation of fibroblast-like synoviocytes in the p 2006 Rheumatoid arthritis (RA) is an inflammatory autoimmune disease of unclear etiology. This study was conducted to identify critical factors involved in the synovial hyperplasia in RA pathology. We applied cDNA microarray analysis to profile the gene expressions of RA fibroblast-like synoviocytes (FLSs) from patients with RA. We found that the MLN51 (metastatic lymph node 51) gene, identified in breast cancer, is remarkably upregulated in the hyperactive RA FLSs. However, growth-retarded RA FLSs passaged in vitro expressed small quantities of MLN51. MLN51 expression was significantly enhanced in the FLSs when the growth-retarded FLSs were treated with granulocyte-macrophage colony-stimulating factor (GM-CSF) or synovial fluid (SF). Anti-GM-CSF neutralizing antibody blocked the MLN51 expression even though the FLSs were cultured in the presence of SF. In contrast, GM-CSF in SFs existed at a significant level in the patients with RA (n = 6), in comparison with the other inflammatory cytokines, IL-1beta and TNF-alpha. Most RA FLSs at passage 10 or more recovered from their growth retardation when cultured in the presence of SF. The SF-mediated growth recovery was markedly impaired by anti-GM-CSF antibody. Growth-retarded RA FLSs recovered their proliferative capacity after treatment with GM-CSF in a dose-dependent manner. However, MLN51 knock-down by siRNA completely blocked the GM-CSF/SF-mediated proliferation of RA FLSs. Taken together, our results imply that MLN51, induced by GM-CSF, is important in the proliferation of RA FLSs in the pathogenesis of RA.
16178737 The biology of p38 kinase: a central role in inflammation. 2005 The p38 kinase plays a central role in inflammation, and it has been the subject of extensive efforts in both basic research and drug discovery. This review summarizes the biology of the p38 kinase with a focus on its role in inflammation. The p38 kinase regulates the production of key inflammatory mediators, including TNFalpha, IL-1beta, and COX-2. In addition, p38 also acts downstream of cytokines such as TNFalpha, mediating some of their effects. The potential efficacy of p38 inhibitors may thus be greater than would be expected from the inhibition of the mediators alone. Inhibitors of p38 kinase are currently in development for the treatment of rheumatoid arthritis. The biological processes regulated by p38 kinase suggest a wide variety of additional potential indications.
16547695 Serious liver disease induced by infliximab. 2007 Apr Infliximab, a chimeric monoclonal antibody that binds the tumor necrosis factor alpha (TNFalpha), is used in the treatment of rheumatoid arthritis (RA) and Crohn's disease (CD). Previous cases of significant secondary liver disease associated with infliximab treatment have been reported in patients with RA, CD, and psoriatic arthritis. Two additional patients with RA who developed a serious liver disease associated with infliximab treatment are reported here. A 39-year old RA patient was admitted with cholestatic liver disease after 8 months of treatment with infliximab. She had no history of hepatic diseases, exposure to hepatotoxic or illicit drugs, or alcohol abuse. A liver biopsy showed severe ductal proliferation with collapse and enucleation of the hepatocytes. Despite aggressive treatment with oral prednisolone, she developed hepatic failure. On the 45th day, a liver transplant was performed. The second patient, a 54-year old RA patient, was diagnosed with autoimmune hepatitis after 12 infliximab infusions. She fulfilled autoimmune hepatitis type 1 criteria. A liver biopsy disclosed an altered lobulillar structure with chronic inflammation and the formation of collagen bands. She was treated with prednisolone and azatioprine and a complete recovery was noted 1 month later. These cases should alert rheumatologists to the possibility of new adverse reactions (liver injury) associated with the use of TNFalpha blockers in an autoimmune setting.
16356201 Partial protection against collagen antibody-induced arthritis in PARP-1 deficient mice. 2006 Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear DNA-binding protein that participates in the regulation of DNA repair and maintenance of genomic integrity. In addition, PARP-1 has a role in several models of inflammation disease, where its absence or inactivation confers protection. The aim of this study was to analyze the impact of selective PARP-1 suppression in collagen antibody-induced arthritis. We show that PARP-1 deficiency partially reduces the severity of arthritis, although the incidence of disease was similar in control and deficient mice. Decreased clinical scores were accompanied by partial reduction of histopathological findings. Interestingly, quantitative real-time PCR and ELISA analysis revealed that the absence of PARP-1 down-regulated IL-1beta and monocyte chemotactic protein 1 expression in arthritic joints whereas tumor necrosis factor-alpha transcription was not impaired. Our results provide evidence of the contribution of PARP-1 to the progression of arthritis and identify this protein as a potential therapeutic target for the treatment of rheumatoid arthritis.
17142562 Mechanism of the regulation of organic cation/carnitine transporter 1 (SLC22A4) by rheumat 2007 Mar Recently, it was reported that the organic cation/carnitine transporter 1 (OCTN1, SLC22A4) is associated with chronic inflammatory diseases, such as rheumatoid arthritis (RA) and Crohn's disease. OCTN1 in humans is expressed in synovial tissues of individuals with rheumatoid arthritis. Furthermore octn1 in mice is expressed in inflamed joints with collagen-induced arthritis, a model of human arthritis, but not in the joints of normal mice. OCTN1 should be involved in the inflammatory disease and in the present study, the regulatory mechanism of OCTN1 expression was characterized using the human fibroblast-like synoviocyte cell line MH7A, derived from RA patients. A luciferase-reporter gene assay and gel shift assay demonstrated that RUNX1, which is an essential hematopoietic transcription factor associated with acute myeloid leukemia and is related to RA and Sp1, is involved in the regulation of OCTN1 promoter activity. Inflammatory cytokines such as interleukin-1beta and tumor necrosis factor-alpha increased the expression of OCTN1 mRNA. Furthermore, overexpression of nuclear factor-kappaB (NF-kappaB) activated promoter activity of OCTN1. These results clearly demonstrate that expression of OCTN1 is regulated by various factors, including RUNX1, inflammatory cytokines, and NF-kappaB, all of which are also related to the pathogenesis of RA. Further studies on the physiological substrate(s) of OCTN1 should be done to clarify the roles of OCTN1 in these diseases.
16925507 Once-daily tramadol in rheumatological pain. 2006 Sep New once-daily formulations of tramadol have been recently marketed in various countries. This review focuses on the matrix systems used in sustained-release formulations to control drug delivery, the pharmacokinetics and pharmacodynamic profile and the available clinical trials on once-daily tramadol. Four controlled clinical studies with a limited number of patients have shown that once-daily tramadol is safe and effective for up to 12 weeks in rheumatological pain treatment, with a favourable side effects profile. Once-daily tramadol has established efficacy superior to that of placebo for pain management and functional improvement in patients with osteoarthritis. Two randomised clinical trials demonstrated similar rates of efficacy between immediate-release and once-daily sustained-release formulation, without significant differences in the use of escape medications and the number of nights woken. Once-daily tramadol offers the advantage of a reduced dosing regimen that improves patient compliance.
16380673 Beta-endorphin prevents collagen induced arthritis by neuroimmuno-regulation pathway. 2005 Dec OBJECTIVE: To observe the effects and mechanisms of beta-endorphin (beta-END) preventing collagen induced arthritis (CIA) by neuroimmuno-regulating pathway. METHODS: Female wistar (Ws) rats were used in this study. CIA was induced by Native bovine type II collagen emulsified with complete Freund's adjuvant (CFA). Beta-END was administered i.p. to CIA rats every other day from the 14th day (secondary immunization) to the 35th day after primary immunization. Clinical assessments were performed by two independent, blinded examiners every other day. Pathological and radiological observations were taken on the 35th day after the primary immunization. Tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), regulated upon activation, normal T-cell expressed and secreted (RANTES), inducible NO syntheses (iNOS), matrix metalloproteinase-2 (MMP-2) and MMP-9 mRNA expression of synovium tissues of CIA rats was estimated by quantitative RT-PCR. The frequency of spleen Th1 and Th2 cells were assessed by fluorescence activated cell sorter (FACS) assay. RESULTS: Clinical manifestation of rats with CIA were significantly abrogated or ameliorated by treatment with beta-END. Beta-END treatment in vivo could down-regulate mRNA expression of several pro-inflammatory cytokines, chemokines and MMPs in CIA synovial, and polarize Th1/Th2 balance to Th2. CONCLUSION: Beta-END alleviates CIA through both depressing Th1 responses and down-regulating proinflammatory and other rheumatic factors, suggesting beta-END is a promising anti-inflammatory and anti-rheumatic agent in treating CIA.
15878906 Enhanced gene transfer to arthritic joints using adeno-associated virus type 5: implicatio 2005 Dec BACKGROUND: Gene therapy of the joint has great potential as a new therapeutic approach for the treatment of rheumatoid arthritis (RA). The vector chosen is of crucial importance for clinical success. OBJECTIVE: To investigate the tropism and transduction efficiency in arthritic joints in vivo, and in synovial cells in vitro, using five different serotypes of recombinant adeno-associated virus (rAAV) encoding beta-galactosidase or green fluorescent protein genes. METHODS: rAAV was injected into the ankle joints of rats with adjuvant arthritis after the onset of disease. Synovial tissue was examined at different time points for beta-galactosidase protein and gene expression by in situ staining and polymerase chain reaction (PCR) analysis, respectively. In addition, the ability of rAAV to transduce primary human fibroblast-like synoviocytes from patients with RA was investigated in vitro. RESULTS: Intra-articular injection of the rAAV5 serotype resulted in the highest synovial transduction, followed by much lower expression using rAAV2. Expression of the transgene was already detectable 7 days after injection and lasted for at least 4 weeks. Only background staining was seen for serotypes 1, 3, and 4. Importantly, there was a minimal humoral immune response to rAAV5 compared with rAAV2. Additionally, it was found that both rAAV2 and rAAV5 can efficiently transduce human fibroblast-like synoviocytes obtained from patients with RA. CONCLUSION: Intra-articular rAAV mediated gene therapy in RA might be improved by using rAAV5 rather than other serotypes.
15934109 Impact of managed care on the use of biologic agents for rheumatoid arthritis. 2005 Jun 15 OBJECTIVE: To compare the use of biologic agents among persons with rheumatoid arthritis (RA) in managed care and fee-for-service settings. METHODS: The present study uses data from the University of California, San Francisco RA Panel Study in which 529 patients with RA from a random sample of northern California rheumatologists were interviewed annually between 1999 and 2002 using a structured survey instrument. Linear and logistic regression were used to compare current utilization, initiation, and cessation of biologic agents and other treatments among patients with RA in managed care and fee-for-service settings, with and without adjustment for differences in demographic and health characteristics. RESULTS: After adjustment, patients with RA in health maintenance organizations (HMOs) were significantly less likely to use biologic agents than those in other managed care settings (difference of -6.6%; 95% confidence interval [95% CI] -11.4%, -1.7%) or than those in fee-for-service settings (difference of -12.5%; 95% CI -19.0%, -5.9%); patients in other managed care settings and fee-for-service did not differ significantly in their use of biologic agents. Patients with RA in HMOs were significantly less likely than those in other managed care settings to initiate the use of biologic agents (difference of -7.3%; 95% CI -11.5%, -3.1%); there were no other differences between patients in HMOs and those in other managed care and fee-for-service settings in rates of initiation or cessation of these agents. Patients with RA in HMOs were less likely to use methotrexate, cyclooxygenase 2 (COX-2) inhibitors, and corticosteroids than those in other managed care settings; they were also less likely to use COX-2 inhibitors than those in fee-for-service settings. CONCLUSION: Patients with RA in HMOs were significantly less likely to use biologic agents than those in other managed care and fee-for-service settings, primarily due to lower rates of initiation.
17075483 [Ileal and right colonic strictures due to prolonged non steroidal anti-inflammatory drug 2006 Oct Ileal and right colonic strictures due to long term NSAID intake are well known but rare. We report the case of a patient with rheumatoid arthritis presenting with one ileal, as well as a right and transverse colonic stricture. The latter two were treated by dilatation under colonoscopy, but due to an associated recurrence, and the necessity of treating the ileal stricture which was inaccessible, a transverse ileocolonic shunt was proposed under local anesthesia. Ileal and colonic strictures due to long term NSAID intake should first be treated, if possible, by discontinuing the drug, then by pneumatic dilatations and finally, if necessary, by surgery usually resection. The advantage of a gastrointestinal shunt is that it can be performed under local anesthesia in patients who are often in poor condition.
16218487 Tumor necrosis factor-alpha, biologic agents and cardiovascular risk. 2005 The increased risk of premature cardiovascular disease (CVD) in rheumatoid arthritis (RA) patients may depend on traditional risk factors but may also be attributable to RA-specific risk factors such as disease-related dyslipidemia, or cytokines such as tumor necrosis factor-alpha (TNF-alpha). TNF-alpha is a proinflammatory cytokine that can produce widespread deleterious effects when expressed in large amounts. It is produced in the heart by both cardiac myocytes and resident macrophages under conditions of cardiac stress, and is thought to be responsible for many of the untoward manifestations of cardiac disease. TNF-alpha may play a role in the triggering and perpetuation of atherosclerosis. Treatment with biologic agents directed against TNF-alpha has significant clinical benefits in inflammatory diseases such as RA and may be able to reduce cardiovascular risk. The disappointing results of the recent studies to antagonize TNF-alpha in CVD may have various explanations. However, the effects of TNF-alpha blockers on incident cases of congestive heart failure (CHF) in RA remains controversial. Due to the lack of evidence of a beneficial effect of anti-TNF-alpha agents in treatment of CHF, they should not be used to treat patients with New York Heart Association (NYHA) class III or IV heart failure.
16087382 Where do T cells stand in rheumatoid arthritis? 2005 Dec Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by destruction of cartilage and bone. The destructive lesions result from both immune responses and non-antigen-specific inflammatory processes. Little is known about the primary cause of RA. Although the primacy of T-cell-related events early in the disease remains debated, strong evidence indicates that autoantigen recognition by specific T cells is crucial to the pathophysiology of rheumatoid synovitis. We will discuss evolving concepts about T-cell involvement in RA and the roles for various T cell subsets in the development of joint abnormalities. The hypothesis that RA is a T-cell driven disease was put forward when studies of RA synovium showed numerous T cells carrying activation markers. These T cells were found to participate in the complex network of cell- and mediator-driven events leading to joint destruction. Conceivably, these T cells may be stimulated by an autoantigen (whether specific to the joints or ubiquitous), a highly conserved foreign protein cross-reacting with its human homolog, or a neo-antigen expressed as a result of posttranslational events. For many years, animal models have provided valuable evidence supporting a role for T cells in RA. We will review three murine models of arthritis caused by different mechanisms. In collagen-induced arthritis, the immune response to a joint antigen is mediated by pathogenic Th1 cells that elicit severe inflammatory synovitis. Spontaneous arthritis in K/BxN T-cell-receptor transgenic mice is related to an adaptive immune response against a ubiquitous protein whose end-stage effector mechanisms are heavily dependent on the innate immune system. In the SKG model of autoimmune inflammatory arthritis, a point mutation in the gene encoding a key signal-transduction molecule in T cells causes defective T cell selection in the thymus, which releases polyclonal autoreactive T cells. Studies in these and other animal models have established that a variety of T-cell subsets whose roles vary with cell location and disease stage can contribute to synovitis. Finally, in addition to direct autoimmune attack by effector T cells, arthritis may result from defective homeostatic control of immunity by regulatory T cells.
15628888 Pulmonary adenocarcinomas associated with rheumatoid nodules: a case report and review of 2005 Jan Necrobiotic lung nodules and primary lung carcinoma both occur with some frequency in patients with rheumatoid arthritis; however, few reports exist of a primary lung carcinoma occurring within a rheumatoid nodule. We report a case of a 62-year-old woman with multiple pulmonary nodules discovered incidentally by computed tomography. Although 2 of the lesions were composed solely of necrotizing granulomas, 2 additional lesions contained malignant glands at the periphery of necrobiotic nodules. Immunohistochemical staining supported the diagnosis of both tumors as primary lung carcinomas. Our literature search revealed only 2 other reported cases of adenocarcinoma occurring in association with a rheumatoid nodule; these cases, as well as the association between rheumatoid disease and malignancy, are briefly reviewed.
16617917 Anesthetic implications for patients receiving exogenous corticosteroids. 2006 Apr Opposing views exist about perioperative replacement of corticosteroids and appropriate replacement dosages. Anesthesia providers must be aware of the need for corticosteroid replacement not only in patients who have primary adrenal insufficiency but also in patients who have adrenal insufficiency resulting from long-term corticosteroid therapy. Without adequate knowledge, the anesthesia provider may fail to prepare the patient to withstand the stress of surgery and may open the way for life-threatening hemodynamic abnormalities that accompany inadequate amounts of corticosteroids. The purpose of this article is to review the literature explaining the rationale and the proper perioperative dosing with corticosteroids for patients with long-standing asthma, rheumatoid arthritis, or Crohn disease. The review of literature reflects articles on endogenous hormones, exogenous hormones, diseases that require long-term corticosteroid therapy, the hypothalamus-pituitary-adrenal axis, and corticosteroid replacement therapy.