Authors introduced some classes of drugs for treating rheumatic arthritis. Basic drug group includes biological agents, anti TNF drugs such as Entanercept- Enbrel; Infliximab; Adalimumab- Humira. In non-steroidal anti-inflammatory drugs (NSAIDs) group, there are Meloxixam - Mobic; Nimesulide- B- Nalgesine; Nise, Celecoxib- Celebrex; Rofecoxib- Vioxx; Valdecoxib-Bextra; Parecoxib- Dynastat; Etoricoxib-arcoxia. Group of slow released antirheumatic drugs included diacetylrÐine or diacerhÐine (ART 50). A new therapy that gave rapid and long lasting pain relieve, more viscosity of articular fluid is administration of sodium hyaluronate (Hyalgan, Ostenil, Hyruan) intra-articular injection
Antirheumatic Agents ; Drugs, Investigational ; Pharmaceutical Preparations

BACKGROUND: Leflunomide, a novel immunoregulatory drug, has been shown to be effective in rheumatoid arthritis (RA) as monotherapy and as combination therapy with methotrexate (MTX). The aims of this study were to investigate the efficacy and safety of combination therapy with leflunomide and MTX in active RA patients and to identify the patients with a better response to this combination. METHODS: The patients received a maintenance dose of 20 mg of leflunomide with or without a loading dose. Parameters for disease activity in RA were measured at baseline and at 12 and 24 weeks after initiation of leflunomide. At 24 weeks, the baseline data from the patients classified as leflunomide responders were compared with data from nonresponders and analyzed to determine the potential predisposing factors for treatment response. RESULTS: A total of 103 patients with RA were included and 93 (90.3%) patients received leflunomide for 24 weeks. At 24 weeks, 67 (65.1%) patients were DAS28 responders; 14 (13.6%) were good responders and 53 (51.5%) moderate responders. At 12 weeks, significant improvements were noticeable in the individual efficacy measures of diseases activity. There were also significant improvements between 12 and 24 weeks in swollen joint count, tender joint count, HAQ disability index, and patients' and physicians' global assessments of diseases activity; but no further improvements in ESR or CRP could be seen after the first 12 weeks. When comparing the baseline data from responders with the nonresponders, patients on a higher MTX dose and patients with a higher disease activity at baseline responded better to leflunomide. However, age, sex, disease duration of RA, functional status, loading dosage of leflunomide, and previous number of DMARDs used did not affect the patients' response to leflunomide. CONCLUSION: Combination therapy with leflunomide and MTX is effective and safe across a wide range of patients, especially those with a high disease activity in spite of treatment with other traditional DMARDs.
Antirheumatic Agents ; Arthritis, Rheumatoid* ; Causality* ; Humans ; Joints ; Methotrexate*

The paradigm for the management of rheumatoid arthritis (RA) has shifted in the past two decades. The appreciation of increased mortality in patients with RA and the poor outcomes with conventional therapy led to the concept of the early aggressive treatment to suppress ongoing inflammation and prevent joint injury. RA results from acute and chronic inflammation in the synovium associated with proliferative and destructive processes in the joint. Affected areas may either heal without structural defects, or be irreversibly damaged if inflammation is severe and does not remit. Therefore, measures aimed at identifying early active disease and ameliorating inflammation are essential and may be highly effective in modifying disease outcome. The goal of treatment is to achieve and maintain a state of remission or, at the least, a state of low disease activity, in order to prevent joint damage and disability. This requires the initiation of treatment early in the disease process, as well as vigilant monitoring throughout the course of disease, with prompt readjustment of therapy, for flares of activity and for medication toxicity. This aggressive approach has been made possible by the increasing number of effective non-biologic and biologic disease-modifying anti-rheumatic drugs (DMARDs). Recent trends and guidelines for the management of RA are presented here.
Antirheumatic Agents ; Arthritis, Rheumatoid ; Humans ; Inflammation ; Joints ; Synovial Membrane

Rheumatoid arthritis (RA) is a chronic progressive disease, affecting an estimated 1% of the population worldwide. Although the optimal care of RA patients requires various modalities, pharmacotherapy remains the cornerstone of treatment for RA. Clinical studies in patients with RA have broadened understanding of its pathogenesis and have fundamentally changed the therapeutic approach to this disease in the last 10 years. It has become clear that early suppression of RA disease activity is important in preventing progressive joint destruction and functional decline. There has been a complete remodeling of the traditional "therapeutic pyramid" by rheumatologists, who now treat RA earlier and more aggressively than ever before, using combinations of classic disease-modifying antirheumatic drugs or new drugs. Although a cure remains elusive, remission is an approachable goal.
Antirheumatic Agents* ; Arthritis, Rheumatoid ; Drug Therapy ; Humans ; Joints

The administration of disease-modifying antirheumatic drugs (DMARDs) in the early period of rheumatoid arthritis (RA) is critical for protecting against joint damage and inducing remission. Physicians need to identify patients at risk of progression to RA at the early stages of arthritis. Musculoskeletal ultrasonography (MSUS) allows the direct visualization of synovitis and bone erosion in the early phase, and may be useful for differentiating early rheumatoid arthritis from other inflammatory arthritis. Power Doppler sonography is a promising tool for assessing the disease activity and monitoring the effects of DMARDs. This article reviews the current status and recent advances in MSUS imaging in RA.
Antirheumatic Agents ; Arthritis ; Arthritis, Rheumatoid ; Humans ; Joints ; Synovitis

The medical treatment of rheumatoid arthritis has been dramatically improved with the advances of newer disease-modifying antirheumatic drugs (DMARDs) and biologic agents during previous decades. To prevent joint damage, it is essential to start DMARD treatment early, especially within the first 3 months after diagnosis. Tight control of disease activity, and the thorough monitoring of the treatment's efficacy and the side effects of medications are also important. Nonsteroidal anti-inflammatory drugs (NSAIDs) are usually used to control pain and swelling of the joints. However, these drugs cannot alter the disease course of rheumatoid arthritis. It is therefore necessary to introduce DMARDs at the beginning of treatment, and, after achieving the effect of DMARDs, NSAIDs should be tapered as soon as possible. The main treatment should be DMARDs, which must be used wisely and appropriately. It is also important to adjust DMARD therapy during the course of treatment according to disease activity. Glucocorticoids have potent anti-inflammatory effects and can control inflammation dramatically. However, because of the diverse and serious side effects of glucocorticoids, the usage of glucocorticoids should be limited to low-dose oral therapy or intra-articular injection, unless otherwise indicated. Along with biologics, there are now various weapons available against rheumatoid arthritis, and it can be treated much more effectively than before.
Anti-Inflammatory Agents, Non-Steroidal ; Antirheumatic Agents ; Arthritis, Rheumatoid ; Biological Agents ; Glucocorticoids ; Inflammation ; Injections, Intra-Articular ; Joints

Felty syndrome (FS) is a rare manifestation in rheumatoid arthritis (RA) characterized by neutropenia and splenomegaly. Treatment for FS is not well established because there has been no randomized controlled study. A few recent reports found rituximab effective in patients with refractory FS. According to those reports, most patients with RA and FS had active arthritis. Here we report a case of a patient with glucocorticoid dependent and disease-modifying anti-rheumatic drugs (DMARDs) refractory FS and quiescent RA who was successfully treated with rituximab.
Antirheumatic Agents ; Arthritis ; Arthritis, Rheumatoid* ; Felty Syndrome* ; Humans ; Neutropenia ; Splenomegaly ; Rituximab

Leflunomide is a novel, isoxazol based disease-modifying anti-rheumatic drug (DMARD) for the treatment of rheumatoid arthritis (RA). Its mechanism differs from other DMARDs in that it inhibits de novo pyrimidine synthesis by inhibiting the enzyme dihydroorotate dehydrogenase (DHODH). It is a pro-drug and undergoes rapid conversion to its active form in vivo, A77-1726. A77-1726 inhibits the mitochondrial enzyme DHODH, which plays a key role in the de novo synthesis of pyrimidine ribonucleotide uridine monophosphate (rUMP). Leflunomide prevents clonal expansion of activated lymphocytes by interfering with the cell cycle progression due to inadequate production of rUMP and utilizing mechanisms involving p53. The relative lack of toxicity of A77-1726 on non-lymphoid cells may be due to the ability of these cells to fulfill their ribonucleotide requirements by use of salvage pyrimidine pathway, which makes them less dependent on de novo synthesis. Several phase II clinical trials of patients with RA revealed that leflunomide was effective and well tolerated. Large-scale phase III clinical trials have shown that leflunomide (20mg/day) provided a statistically significant clinical benefit and prevention of radiographic progression in comparison to placebo. The clinical benefits of leflunomide were similar to or greater than methotrexate and sulfasalazine. Now, many multi-national studies are in progress and planning, including combination therapy with other DMARD. In future, those studies will provide us more information about the effectiveness and potential adverse effect of leflunomide.
Antirheumatic Agents ; Arthritis, Rheumatoid ; Cell Cycle ; Humans ; Lymphocytes ; Methotrexate ; Oxidoreductases ; Sulfasalazine ; Uridine Monophosphate

Leflunomide is a novel, isoxazol based disease-modifying anti-rheumatic drug (DMARD) for the treatment of rheumatoid arthritis (RA). Its mechanism differs from other DMARDs in that it inhibits de novo pyrimidine synthesis by inhibiting the enzyme dihydroorotate dehydrogenase (DHODH). It is a pro-drug and undergoes rapid conversion to its active form in vivo, A77-1726. A77-1726 inhibits the mitochondrial enzyme DHODH, which plays a key role in the de novo synthesis of pyrimidine ribonucleotide uridine monophosphate (rUMP). Leflunomide prevents clonal expansion of activated lymphocytes by interfering with the cell cycle progression due to inadequate production of rUMP and utilizing mechanisms involving p53. The relative lack of toxicity of A77-1726 on non-lymphoid cells may be due to the ability of these cells to fulfill their ribonucleotide requirements by use of salvage pyrimidine pathway, which makes them less dependent on de novo synthesis. Several phase II clinical trials of patients with RA revealed that leflunomide was effective and well tolerated. Large-scale phase III clinical trials have shown that leflunomide (20mg/day) provided a statistically significant clinical benefit and prevention of radiographic progression in comparison to placebo. The clinical benefits of leflunomide were similar to or greater than methotrexate and sulfasalazine. Now, many multi-national studies are in progress and planning, including combination therapy with other DMARD. In future, those studies will provide us more information about the effectiveness and potential adverse effect of leflunomide.
Antirheumatic Agents ; Arthritis, Rheumatoid ; Cell Cycle ; Humans ; Lymphocytes ; Methotrexate ; Oxidoreductases ; Sulfasalazine ; Uridine Monophosphate

Rheumatoid arthritis (RA) is a systemic inflammatory autoimmune disorder that mainly affects the diarthrodial joint. Morning stiffness and symmetric swelling of the wrists, PIPs and MCPs constitue the typical history for rheumatoid arthritis. Extra-articular manifestations in RA include constitutional symptoms, distinct organ manifestations and severe multiorgan disease. The presence of rheumatoid factor and the anti-cyclic citrullinated peptide antibody, which is more specific to RA, are helpful in RA diagnosis. Although conventional radiographs remain the initial imaging modality in patients with RA, other imaging modalities such as MRI or ultrasound have demonstrated increased sensitivity to detecting early erosive change. To the present day, there is no single test that confirms RA. Early diagnosis of RA is essential because there is substantial evidence that early therapeutic intervention with non-biologic/biologic disease-modifying antirheumatic drugs leads to a better outcome. Although the 1987 American College of Rheumatology (ACR) classification criteria for RA have been used as the gold standard in clinical studies, these criteria are misleading early in the disease course. The ACR/European League Against Rheumatism (EULAR) is scheduled to release the new classification criteria for RA soon. This review describes clinical manifestations of RA, diagnostic tools, as well as the classification criteria in the diagnosis of RA.
Antirheumatic Agents ; Arthritis, Rheumatoid ; Early Diagnosis ; Humans ; Joints ; Rheumatic Diseases ; Rheumatoid Factor ; Rheumatology ; Wrist