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ID PMID Title PublicationDate abstract
14977577 The serum growth hormone to somatostatin ratio is skewed upward in rheumatoid arthritis pa 2004 May 1 Basal serum growth hormone, insulin-like growth factor-1 (IGF-1) and somatostatin concentration were measured by standard radioimmunoassay in patients with a diagnosis of rheumatoid arthritis (RA) according to the criteria of the American College of Rheumatology as well as in a group of age-matched normal subjects. RA patients exhibited significantly elevated (age, 45-55 yrs, p less than 0.05; 55 yrs and older, p less than 0.01) serum growth hormone levels compared to age-matched individuals from the control group. IGF-1 was unchanged. Serum somatostatin levels were reduced in RA patients between 45 and 55 yrs but reached a significant reduction (p less than 0.0001) in RA patients, 55 years and older compared to age-matched individuals from the control group. RA patients treated with prednisone did not exhibit changes in either growth hormone or IGF-1 levels compared to RA patients treated principally with non-steroidal anti-inflammatory drugs and methotrexate. These results indicated that symptomatic RA is associated with elevated serum growth hormone without concomitant changes in IGF-1 compared to individuals from the control group. Reduced somatostatin levels in older RA patients resulted in a skewed upward growth hormone to somatostatin ratio. We conclude that the serum growth hormone to somatostatin ratio may be a useful surrogate marker of disease activity in symptomatic RA.
14682224 [Renal tubular dysfunction in patients with rheumatoid arthritis starting with low dose of 2003 Aug BACKGROUND: The elevation of N-acetyl-beta-D-glucosaminidase (NAG) in urine has been shown to be associated with reversible renal tubular damage. OBJECTIVES: The aim of the study was to examine the effect of first oral low dose methotrexate (MTX) on urinary excretion of NAG comparing with MTX concentration in serum and urine in a cohort of patients with rheumatoid arthritis (RA). METHODS: Urinary NAG to urinary creatinine ratio (NAG index) determined in 43 patients (5 males, 38 females) with RA who started taking the first oral dose of 10 mg of MTX. Urinary NAG index was observed at 24 h and 48 h after the first MTX dose. MTX concentration was measured in blood at 90 minutes and in blood and urine at 24 h after the drug administration. RESULTS: NAG-enzymuria was increased in 72.1% of the patients before administration of MTX therapy (10.8 UI/g creatinine). There was no change in NAG index at 24 and 48 h after first dose of MTX (9.1 and 10.7 UI/g of creatinine). No differences of NAG-enzymuria in non-steroidal anti-inflammatory drug (NSAID)-treated patients and NSAID-free patients before and after MTX administration were revealed. The patients with decreased creatinine clearance had before treatment higher NAG index than those with normal creatinine clearance but there was not any significant increase of NAG activity after first dose of MTX in the patients with decreased creatinine clearance. Continued treatment with MTX resulted in a decrease in NAG activity accompanied by serum C-reactive protein concentration. CONCLUSION: The use of low dose MTX with or without NSAIDs does not influence the renal tubular function in patients with RA.
12563675 The use of disease modifying antirheumatic drugs in women with rheumatoid arthritis of chi 2003 Feb OBJECTIVE: To describe the practices of rheumatologists when prescribing the disease modifying antirheumatic drugs (DMARD) methotrexate (MTX), leflunomide (LF), etanercept (ET), and infliximab (IN) to women of childbearing age with rheumatoid arthritis (RA) and the pregnancy outcomes of patients who become pregnant while taking these medications. METHODS: A questionnaire was mailed to 600 members of the American College of Rheumatology inquiring about their perception of fetal risk, their recommendations regarding the use of birth control in women of childbearing age taking DMARD, and the pregnancy outcomes of women with DMARD exposure. RESULTS: One hundred seventy-five rheumatologists (29%) returned completed surveys. Respondents were more likely to agree that pregnancy is contraindicated in women taking MTX (95%) or LF (92.7%) than for women taking ET (38.6%) or IN (46.5%). Accordingly, most required birth control for women taking MTX (95.7%) and LF (97.3%), and fewer for women taking ET (75.4%) or IN (73.4%). A total of 65 pregnancies exposed to these DMARD were reported (MTX 38, LF 10, ET 14, IN 2, MTX and ET 1). Only 3 congenital malformations, all in the MTX group, were reported among the 52 pregnancies with known outcomes. CONCLUSION: Rheumatologists agree that there is a risk of teratogenicity with MTX and LF and usually require the use of reliable methods of birth control in women taking these medications. There is no consensus about ET and IN; however, physicians still tend to discuss reliable birth control methods with their female patients. We have confirmed there is a risk of congenital malformations with in utero exposure to MTX. No malformations were reported in infants exposed to LF, ET, or IN, but the number of reported pregnancy outcomes was small.
12730515 Combined oral cyclosporin and methotrexate therapy in patients with rheumatoid arthritis e 2003 Aug OBJECTIVE: To study the pharmacokinetics of methotrexate (MTX) plus cyclosporin A (CSA) in patients with rheumatoid arthritis (RA). METHODS: On day 1 of the study, patients with RA receiving stable doses of MTX had blood and urine levels of MTX and its metabolite 7-hydroxymethotrexate (7-OH-MTX) measured post oral dosing of the drug. MTX was then discontinued and CSA therapy was started on day 8. On day 20, blood levels of CSA and CSA metabolites were measured post drug dosing. On day 23, MTX therapy was restarted and levels of MTX, CSA and their metabolites were again measured as described above. RESULTS: In the 30 patients, coadministration of CSA and MTX led to a 26% increase in mean peak plasma MTX concentration (P < 0.01), an 18% increase in the mean plasma MTX concentration area under the curve (AUC, P=0.01) and an 80% decrease in plasma 7-OH-MTX AUC (P < 0.01). In 13 patients receiving a 10 mg MTX dose, CSA reduced urinary 7-OH-MTX excretion by 87% (P < 0.01) without altering MTX excretion. MTX did not alter the pharmacokinetics of CSA or its metabolites. CONCLUSION: CSA may block oxidation of MTX to its relatively inactive metabolite, 7-OH-MTX, thereby potentiating MTX efficacy.
12051400 Genotoxicity assessment using micronuclei assay in rheumatoid arthritis patients. 2002 Mar OBJECTIVES: This study investigated whether: (i) rheumatoid arthritis (RA) patients have more micronuclei (MN) than healthy controls; (ii) methotrexate (MTX) treated RA patients have more MN than those not using MTX, and (iii) folic acid supplementation decreases the number of MN in MTX treated patients. METHODS: MN assays were performed in oral mucosa sweeps of 50 consecutive MTX treated RA patients, 30 consecutive RA patients not receiving MTX and 39 healthy controls. MTX treated RA patients were then randomly placed in a cross-over design to receive folic acid supplementation, and MN assays were repeated after 6 weeks. RESULTS: The MTX-RA patients had a mean age of 46 +/- 10 yrs and a mean disease duration of 12 +/- 9 yrs; 80% were women. The MTX dose range was 8.7 +/- 1.5 mg/week and the mean duration of use was 16 +/- 18 months. In the non-MTX RA group, the mean age was 48 +/- 14 yrs, the mean disease duration was 13 +/- 9 yrs, and 87% were women. At baseline, the number of MN were significantly higher in RA patients as compared with controls (3.31 +/- 2.3 vs 0.8 +/- 0.8, p <0.001). No difference in MN numbers was observed between users and non-users of MTX. Folic acid supplementation did not decrease the MN number in the MTX treated RA patients. CONCLUSIONS: Genotoxicity, as assessed by the MN assay, is increased in RA patients. These results suggest that genotoxicity is associated with RA itself and not with MTX use. Folic acid supplementation had no effect on the number of MN.
12495361 Benefit-risk assessment of infliximab in the treatment of rheumatoid arthritis. 2003 In the last decade, there have been substantial advances in the treatment of rheumatoid arthritis with the addition of several new disease-modifying agents to the therapeutic armamentarium. Biological agents targeting tumour necrosis factor (TNF) represent one such important addition. Infliximab, a chimeric anti-TNF monoclonal antibody, has shown remarkable promise in alleviating the signs and symptoms of rheumatoid arthritis in addition to retarding radiographic disease progression when used in combination with methotrexate. In its pivotal phase III trial, the addition of infliximab to patients with methotrexate-refractory disease was associated with substantial clinical benefit. Using American College of Rheumatology criteria for improvement, one-half of patients receiving infliximab (3 mg/kg every 8 weeks) plus methotrexate showed at least 20% improvement compared with only 20% of those receiving placebo plus methotrexate (p < 0.001) with over one-half of eventual responders obtaining criteria for improvement by the second week of observation. Although its use has been met with much deserved enthusiasm, recent reports have highlighted several potential serious adverse effects associated with infliximab (and other TNF antagonists), including infusion reactions, congestive heart failure, drug-induced lupus, and CNS demyelination. In addition, recent reports have cited the potential for reactivation of mycobacterial and fungal infection in patients receiving infliximab, mandating appropriate tuberculosis screening prior to drug initiation. Although the frequency of serious drug-related toxicity (requiring discontinuation of the agent) appears to be quite low, these reports underscore the need for caution and close surveillance with the administration of TNF inhibitors, particularly given that strategies aimed at preventing toxicity remain unproven. Despite its potential for toxicity, infliximab remains a valuable alternative for patients with rheumatoid arthritis.
12794815 Etanercept added to background methotrexate therapy in patients with rheumatoid arthritis: 2003 Jun OBJECTIVE: To observe the long-term safety and efficacy of combination therapy with etanercept and methotrexate in patients with rheumatoid arthritis (RA), and to determine whether the addition of etanercept allowed reductions in methotrexate or corticosteroid dosages while maintaining a clinical response. METHODS: Patients with RA who received methotrexate plus etanercept in a previous randomized, placebo-controlled trial were offered the opportunity to enroll in an open-label extension study for further evaluation of treatment with etanercept and methotrexate. RESULTS: Seventy-nine of the 89 patients in the original blinded study enrolled in the extension study, and 65 of these patients continue in the study. Patients have received etanercept therapy for up to 47 months (median 44 months). The types and rate of adverse events noted during the extension trial were similar to those observed in the controlled trial. At the 3-year assessment, 77% of the 57 patients available for evaluation met American College of Rheumatology 20% (ACR20) criteria for improvement in RA, 47% met the ACR50 criteria, and 23% met the ACR70 criteria. Of the 36 patients assessed at 3 years in the extension study, 30 (83%) were able to decrease their dosages of corticosteroids, and 20 (56%) were able to discontinue corticosteroid therapy. At 3 years, the dosage of methotrexate was decreased in 41 of 66 patients (62%), and methotrexate therapy was discontinued in 19 patients (29%). CONCLUSION: In this observational continuation study, the addition of etanercept to background methotrexate provided sustained clinical benefit over a median period of 44 months. With etanercept therapy, there were trends toward dosage reduction or discontinuation of methotrexate and corticosteroids, without apparent worsening of ACR response rates. Compared with the controlled trial, no increases in the rate of adverse events were observed.
12707361 Albumin-based drug delivery as novel therapeutic approach for rheumatoid arthritis. 2003 May 1 We reported recently that albumin is a suitable drug carrier for targeted delivery of methotrexate (MTX) to tumors. Due to pathophysiological conditions in neoplastic tissue, high amounts of albumin accumulate in tumors and are metabolized by malignant cells. MTX, covalently coupled to human serum albumin (MTX-HSA) for cancer treatment, is currently being evaluated in phase II clinical trials. Because synovium of patients with rheumatoid arthritis (RA) shares various features observed also in tumors, albumin-based drug targeting of inflamed joints might be an attractive therapeutic approach. Therefore, the pharmacokinetics of albumin and MTX in a mouse model of arthritis was examined. Additionally, uptake of albumin by synovial fibroblasts of RA patients and the efficacy of MTX and MTX-HSA in arthritic mice were studied. The results show that when compared with MTX, significantly higher amounts of albumin accumulate in inflamed paws, and significantly lower amounts of albumin are found in the liver and the kidneys. The protein is metabolized by human synovial fibroblasts in vitro and in vivo. MTX-HSA was significantly more effective in suppression of the onset of arthritis in mice than was MTX. In conclusion, albumin appears to be a suitable drug carrier in RA, most likely due to effects on synovial fibroblasts, which might increase therapeutic efficacy and reduce side effects of MTX.
12632419 Specific increase in enzymatic activity of adenosine deaminase 1 in rheumatoid synovial fi 2003 Mar OBJECTIVE: Adenosine deaminase (ADA; EC 3.5.4.4) activity is elevated in the synovial fluid (SF) of patients with rheumatoid arthritis (RA). Since the antiinflammatory effect of methotrexate is reportedly associated with increased levels of extracellular adenosine, the present study was undertaken to clarify the role of 2 ADA isozymes, ADA1 and ADA2, in the pathogenesis of RA. METHODS: The activities of ADA1 and ADA2 were measured in SF from RA and osteoarthritis (OA) patients, in sera from RA patients, and in lysates prepared from mononuclear and polymorphonuclear cells from SF from RA patients, peripheral blood from RA patients, and fibroblast-like synoviocytes (FLS) from RA and OA patients. Also measured were the effects of proinflammatory cytokines on ADA1 activity and ADA messenger RNA (mRNA) expression in RA FLS, as determined using real-time polymerase chain reaction. The adenosine concentration in RA SF was measured by radioimmunoassay. RESULTS: The adenosine concentration in RA SF ranged from 0.027 microM to 0.508 microM (mean +/- SD 0.156 +/- 0.132 microM). At those concentrations, ADA1 would be expected to be functionally dominant due to its higher affinity for adenosine. ADA1 activity in RA SF (mean +/- SD 14.4 +/- 8.5 IU/liter) was significantly higher than that in OA SF (3.0 +/- 1.1 IU/liter) or RA sera (3.0 +/- 0.6 IU/liter); moreover, ADA1 activity in RA FLS lysate was the highest among the cell lysates tested. Proinflammatory cytokines did not affect ADA1 activity or ADA mRNA expression in RA FLS. CONCLUSION: Elevated ADA1 activity is an intrinsic characteristic of RA FLS, which likely contributes to the pathogenesis of RA by neutralizing the antirheumatic properties of endogenous adenosine.
12209029 Blocking the effects of IL-1 in rheumatoid arthritis protects bone and cartilage. 2002 Sep Destruction of articular joints occurs progressively in patients with rheumatoid arthritis (RA). Although the exact aetiology of RA has not been fully elucidated, a large body of evidence supports a role for interleukin-1 (IL-1) in cartilage and bone erosion. In vitro studies suggest that IL-1 can cause cartilage destruction by stimulating the release of matrix metalloproteinases and other degradative products, and it can increase bone resorption by stimulating osteoclast differentiation and activation. In animal models of RA, blocking the effects of IL-1 with either IL-1 receptor antagonist (IL-1Ra; endogenous), anti-IL-1 monoclonal antibodies, or soluble IL-1 type II receptors significantly reduced cartilage destruction and bone erosion. Gene therapy with IL-1Ra was also effective in reducing joint destruction in experimental RA and osteoarthritis (OA) models. In clinical studies, anakinra, a human recombinant IL-1 receptor antagonist (IL-1ra; exogenous), significantly slowed radiographic progression of RA relative to placebo and significantly reduced clinical symptoms when used as monotherapy or in addition to existing methotrexate therapy. These results demonstrate that blocking IL-1 protects bone and cartilage from progressive destruction in RA.
12784387 Leflunomide for the treatment of rheumatoid arthritis: a systematic review and metaanalysi 2003 Jun OBJECTIVE: To systematically review the evidence from clinical trials on the efficacy and toxicity of leflunomide for the treatment of active rheumatoid arthritis (RA). METHODS: We searched Medline, Embase, Current Contents, and the Cochrane Controlled Trial Register for human randomized controlled trials (RCT) and controlled clinical trials up to December 2001. We also hand-searched reference lists and conference proceedings and consulted content experts. Relative benefit (RB), and weighted mean differences or standardized mean differences with their 95% confidence interval (95% CI) were calculated. RESULTS: Six RCT totaling 2044 patients with RA were included in this review. Using specific criteria, all trials were considered of high methodological quality. Leflunomide improved the ACR20 response rate roughly 2 times over placebo both at 6 months (RB = 1.93, 95% CI 1.51, 2.47) and at 12 months (RB = 1.99, 95% CI 1.42, 2.77). Other clinical outcomes of disease activity and function and radiological scores were also significantly better for leflunomide patients than those taking placebo. No significant differences for most of the outcomes were observed between leflunomide and sulfasalazine (SSZ) or methotrexate (MTX). Adverse events were more common in the leflunomide group, but withdrawal rates were fewer than for placebo. Overall, withdrawal rates and adverse events in the leflunomide group were not different from SSZ or MTX. CONCLUSION: Leflunomide improves all clinical outcomes and delays radiographic progression at 6 and 12 months of RA treatment compared to placebo. Its efficacy and adverse events at 2 years of treatment are comparable to SSZ and MTX. Longterm efficacy and toxicity remain to be established.
14600805 Disseminated tuberculosis, pulmonary aspergillosis and cutaneous herpes simplex infection 2003 Dec CASE PRESENTATION: Despite chemoprophylaxis with isoniazid a 58-year-old Creole patient with mild rheumatoid arthritis developed disseminated tuberculosis, pulmonary aspergillosis and cutaneous herpes simplex infection during treatment with infliximab and methotrexate. TREATMENT: The patient received antituberculous drugs (ethambutol, isoniazid, pyrazinamide, rifampicin), amphotericin B, flucytosine, and valaciclovir, along with prolonged intensive care treatment and mechanical ventilation. CONCLUSIONS: The present case confirms that isoniazid prophylaxis (300 mg once daily, during 6 months) does not protect against the reactivation and dissemination of latent tuberculosis. It also shows that combined treatment with infliximab and methotrexate may induce severe immunosuppression with prolonged leukocytopenia and depressed cellular immunity, leading to multiple opportunistic infections. Extensive diagnostic testing, early start of antimicrobial therapy and enteral immunonutrition, and further infection prevention with selective decontamination of the digestive tract may have been the key to a good clinical outcome.
15794195 Clinical and radiological disease-course in a Swedish DMARD-treated early RA-inception coh 2004 OBJECTIVES: Disease-modifying anti-rheumatic drugs (DMARDs) decrease clinical signs and symptoms in rheumatoid arthritis (RA). However, radiographic changes sometimes continue to accrue despite effective suppression of clinical symptoms by therapy. The objective of this study was to identify whether successful clinical disease-control in a Swedish early RA-inception cohort of patients led to an attenuation of radiological progression. PATIENTS AND METHODS: We analysed clinical data and radiographs of 95 patients who were on a stable treatment regimen [methotrexate (MTX), sulfasalazine (SSZ), oral gold (AUR)] or who had changed between different DMARDs during the 2-year observation period [multiple therapy failures (mTF)]. Radiographs were quantified using the modified Larsen score and 'X-Ray RheumaCoach' software. RESULTS: Clinical measures improved markedly (p <0.001) from baseline to year 2 under AUR, MTX, and SSZ therapy but not in the mTF group. Similar levels of disease control were seen for each DMARD. During this period, patients treated with AUR had a deltaLarsen score (+ 14.5+/-1.3) similar to mTF patients (+ 15.8+/-1.1) but greater than patients on MTX (+8.6+/-0.8) or SSZ (+9.1+/-0.8). CONCLUSIONS: This study confirms that radiological progression occurs despite a clinically acceptable disease control, but also shows that, given the same degree of clinical disease control, radiological progression can be different for different DMARDs.
15077061 [Methotrexate for treatment of rheumatoid arthritis]. 2004 Feb 27 Rheumatoid arthritis (RA) is a common chronic inflammatory and destructive arthropathy that cannot be cured and that has substantial personal, social and economic costs. Methotrexate is a well-known folate analogue, and is the most frequently applied drug for the disease to modify antirheumatic therapy in patients with rheumatoid arthritis. Although results of studies have shown the efficacy of such drugs as methotrexate on rheumatoid arthritis, activity measures and their effect on mortality in patients with the disease remain unknown. The current therapeutic approach to rheumatoid arthritis consists of administration of anti-inflammatory, immunomodulating, and immunosuppressive drugs. Immunomodulating drugs, as opposed to non-steroid anti-inflammatory drugs, which only reduce the signs of inflammation, are capable of gradually checking the course of the disease. However, they do not prevent the slow but progressive destruction of joints. The prominent role of proinflammatory cytokines and growth factors in the pathogenesis of RA has been documented. Recent studies have demonstrated the efficacy of anticytokine treatment. Infliximab is a chimeric monoclonal antibody capable of neutralizing human TNF alpha. A number of clinical trials for the treatment of rheumatoid arthritis with infliximab indicated that TNF alpha blockade was effective and well tolerated, with excellent results occurring at 3 and 10 mg/kg in combination with methotrexate. Treatment of RA patients with the combination of infliximab and methotrexate also prevented radiographic evidence of progression of joint damage. If its clinical efficacy is sustainable and its safety confirmed over the long term, infliximab may become an essential agent of choice for the treatment of RA.
12180718 Hyperhomocysteinemia in rheumatoid arthritis: influence of methotrexate treatment and foli 2002 Aug OBJECTIVE: To examine the effect of methotrexate (MTX) and folic acid supplementation on the homocysteine level in patients with rheumatoid arthritis (RA). METHODS: A cross sectional study was performed in 81 patients with RA, comprising a standardized clinical interview, an examination, and a blood specimen test. RESULTS: P-homocysteine tended to be lower in 41 patients receiving MTX, compared with 40 patients not receiving MTX. Of the MTX treated patients, 76% received folic acid supplementation. Multivariate analysis revealed a statistically significant association between P-homocysteine and P-creatinine (p < 0.001), and disease activity/progression measured by the Health Assessment Questionnaire score (p < 0.001). There was a tendency to negative association between P-homocys-teine and folic acid supplementation. CONCLUSION: P-homocysteine in patients with RA receiving MTX and folic acid supplementation did not differ significantly from P-homocysteine in RA patients receiving other types of treatment.
12106498 Molecular action of methotrexate in inflammatory diseases. 2002 Despite the recent introduction of biological response modifiers and potent new small-molecule antirheumatic drugs, the efficacy of methotrexate is nearly unsurpassed in the treatment of inflammatory arthritis. Although methotrexate was first introduced as an antiproliferative agent that inhibits the synthesis of purines and pyrimidines for the therapy of malignancies, it is now clear that many of the anti-inflammatory effects of methotrexate are mediated by adenosine. This nucleoside, acting at one or more of its receptors, is a potent endogenous anti-inflammatory mediator. In confirmation of this mechanism of action, recent studies in both animals and patients suggest that adenosine-receptor antagonists, among which is caffeine, reverse or prevent the anti-inflammatory effects of methotrexate.
15468352 Adverse events with disease modifying antirheumatic drugs (DMARD): a cohort study of leflu 2004 Oct OBJECTIVE: To determine and compare the incidence of serious adverse events (AE) during treatment of rheumatoid arthritis (RA) with disease modifying antirheumatic drugs (DMARD), focusing on leflunomide (LEF). METHODS: A retrospective cohort study of a large US insurance claims database was performed. Study groups were patients with RA classified by DMARD exposure as either no-DMARD therapy, single-agent DMARD (monotherapy), or combination-DMARD therapy. Specific DMARD examined were leflunomide (LEF) and methotrexate (MTX), compared to other DMARD (penicillamine, hydroxychloroquine, sulfasalazine, gold, etanercept, infliximab) and no DMARD (nonsteroidal antiinflammatory drugs, COX-2 inhibitors). All AE reported were considered endpoints; primary endpoints included hepatic, dermatologic, hematologic, infectious, respiratory, hypertension, and pancreatitis AE. RESULTS: The 40,594 RA patients of the study period (September 1998 to December 2000) accumulated 83,143 person-years (PY) of followup. Followup for each of the groups was: DMARD-monotherapy, 46,054 PY (55% of total); combination-DMARD, 25,830 PY (14%); and no-DMARD, 11,259 PY (14%). The incidence rate of all AE combined was significantly lower for LEF monotherapy (94 events/1000 PY) than MTX (145 events/1000 PY), other DMARD (143 events/1000 PY), or no DMARD (383 events/1000 PY) (p < 0.001 for all comparisons). The "all-AE" rates during combination therapy with LEF + MTX (43/1000 PY) and LEF + other DMARD (59/1000 PY) were lower than the "all-AE" rate for DMARD + MTX (70/1000 PY; p = 0.002). LEF monotherapy had the lowest rate of hepatic events in the DMARD monotherapy groups. CONCLUSION: The rates of AE in the LEF group, alone and combined with MTX, were generally lower than or comparable to the AE rates seen with MTX and other agents.
15172044 Infliximab treatment of rheumatoid arthritis. 2004 May Infliximab was the first anti-TNF agent used to treat rheumatoid arthritis to provide proof of concept of the role of TNF-alpha in this condition. It has become widely used since, principally as an effective treatment in combination with methotrexate, but also as monotherapy for the treatment of Crohn's disease, ankylosing spondylitis,and psoriatic arthritis. The benefits of infliximab in controlling signs and symptoms, improving quality of life, preventing structural joint damage, and possible healing of bone provide an important option for the treatment of rheumatoid arthritis.
11994686 [Leflunomide in the treatment of rheumatoid arthritis]. 2002 Feb Leflunomide is a new second-line drug for rheumatoid arthritis. This compound with long half-life inhibits proliferation of activated T lymphocytes. Phase III studies have demonstrated a clinical efficacy superior to placebo and identical to comparators (salazopyrine, methotrexate) with a faster onset of response. Improvement of inflammatory paramaters and functional capacity (HAQ) were observed as well as slowing of structural damage evaluated by X-rays. Global tolerance is fair, but possibility of hepatic involvement, although unfrequent, needs a regular survey.
15309279 [Lead poisoning after ingestion of ayurvedic drugs]. 2004 Aug 15 HISTORY AND CLINICAL FINDINGS: A 60-year-old woman suffering from rheumatoid arthritis and taking methotrexate was admitted with recurrent episodes of nausea, vomiting, constipation, loss of appetite, myalgia and backache, sternal chest pain, costal and jaw pain. On examination the epigastrium was tender to palpation and nonrigid. INVESTIGATIONS: Laboratory tests showed normocytic anemia (with a hemoglobin concentration of 8.6 g/dl), elevated blood urea and creatinine levels, hyponatremia, hypochloremia, hemolysis and polychromasia, anisocytosis, poikilocytosis and basophilic stippling of several red cells. On gastroscopy an ulcer was excluded, ultrasound scan of abdomen, X-ray of chest and pelvis showed no abnormalities. The electrocardiogram showed a right bundle branch block and left anterior hemiblock. DIAGNOSIS, TREATMENT, AND COURSE: In the differential diagnosis of anemia with basophilic stippling and abdominal discomfort, lead poisoning was found. Whole-blood lead concentration was markedly raised to 852 micro g/l (normal < 100 micro g/l). Lead poisoning was the result of the use of ayurvedic drugs during a period of 7.5 months prior to admission to the authors' hospital. CONCLUSION: Heavy metal poisoning, especially lead poisoning, should be considered in the differential diagnosis in patients with unspecific clinical symptoms taking traditional Indian remedies.
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