Rheumatoid Arthritis: Asia

Su XH, Zhang ML, Zhan WH, Huo CH, Shi QW, Gu YC, Kiyota H. · School of Pharmaceutical Sciences, Hebei Medical University, 361 Zhongshan East Road, Shijiazhuang 050017, Hebei Province, P. R. China. · Chem Biodivers. · Pubmed #19235157 No free full text.

Abstract: The plants of genus Celastrus, distributed in Asia, have been used as natural insecticides and folk medicines to treat fever, chill, joint pain, edema, rheumatoid arthritis, and bacterial infection in China for a long time. This contribution reviews the chemical constituents, isolated from the plants in genus Celastrus in the past few decades, and their biological activities. The compounds listed are sesquiterpenes (beta-agarofurans), diterpenes, triterpenes, alkaloids, and flavonoids.

Yoo SA, Kwok SK, Kim WU. · Division of Rheumatology, Department of Internal Medicine, School of Medicine, Catholic University of Korea, Seoul, South Korea. · Mediators Inflamm. · Pubmed #19223981 links to  free full text

Abstract: Recent experimental and clinical studies have placed new emphasis on the role of angiogenesis in chronic inflammatory disease. Vascular endothelial growth factor (VEGF) and its receptors are the best characterized system in the regulation of rheumatoid arthritis (RA) by angiogenesis. Furthermore, in addition to its angiogenic role, VEGF can act as a direct proinflammatory mediator during the pathogenesis of RA, and protect rheumatoid synoviocytes from apoptosis, which contributes to synovial hyperplasia. Therefore, the developments of synovial inflammation, hyperplasia, and angiogenesis in the joints of RA patients seem to be regulated by a common cue, namely, VEGF. Agents that target VEGF, such as anti-VEGF antibody and aptamer, have yielded promising clinical data in patients with cancer or macular degeneration, and in RA patients, pharmacologic modulations targeting VEGF or its receptor may offer new therapeutic approaches. In this review, the authors integrate current knowledge of VEGF signaling and information on VEGF antagonists gleaned experimentally and place emphasis on the use of synthetic anti-VEGF hexapeptide to prevent VEGF interacting with its receptor.

Basu S, Zhuang H, Torigian DA, Rosenbaum J, Chen W, Alavi A. · Radiation Medicine Center (BARC), Tata Memorial Hospital Annex, Mumbai, India. · Semin Nucl Med. · Pubmed #19187805 No free full text.

Abstract: Molecular imaging with positron emission tomography (PET) and single-photon emission computed tomography (SPECT) is increasingly used to diagnose, characterize, and monitor disease activity in the setting of inflammatory disorders of known and unknown etiology. These disorders include sarcoidosis, atherosclerosis, vasculitis, inflammatory bowel disease (IBD), rheumatoid arthritis (RA), and degenerative joint disease. Gallium-67 ((67)Ga) citrate, labeled leukocytes with technetium-99m ((99m)Tc) or indium-111 ((111)In), and (18)F-fluorodeoxyglucose (FDG) represent the most widely used radiopharmaceutical agents. However, other preparations, such as labeled murine monoclonal antigranulocyte antibodies and labeled human polyclonal nonspecific immunoglobulin G, chemotactic peptides, interleukins, chemokines, and liposomes, have been used to image inflammation. Also, (99m)Tc nanocolloid scintigraphy has been found to be suitable for bone and joint diseases, especially RA. Among the single photon emitting imaging agents, the recommended radiotracer for abdominal inflammation has been (99m)Tc-hexamethylpropylene amine oxime (HMPAO)-labeled leukocytes. During the last several years, FDG-PET imaging has been shown to have great value for the detection of inflammation and has become the centerpiece of such initiatives. This very powerful technique will play an increasingly important role in the management of patients with inflammatory conditions. FDG-PET can provide valuable information in patients with pulmonary and extrapulmonary sarcoidosis, and is a useful tool for testing the efficacy of various treatments. FDG-PET combined with computed tomography holds great promise for assessing atherosclerosis of the large arteries. This modality is very sensitive in detecting large-vessel vasculitis and can be used to monitor the disease course. FDG-PET is also being used to study the inflamed synovial joints both in the experimental and clinical settings, especially for the investigation and management of RA and degenerative joint disease. This technique also has the potential to become the imaging modality of choice in assessing IBD, replacing radiolabeled autologous leukocyte imaging in this setting. Detection of inflammation in the lungs and airways may improve our knowledge about a multitude of disorders that affect these structures. Therefore, functional imaging, led by FDG-PET imaging, is likely to play an increasingly critical role in assessing inflammatory disorders of known and unknown etiologies, and will improve their management immensely in the future.

Iwakura Y, Nakae S, Saijo S, Ishigame H. · Center for Experimental Medicine, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. · Immunol Rev. · Pubmed #19161416 No free full text.

Abstract: T-helper 17 (Th17) cells are a newly discovered CD4(+) helper T-cell subset that produces interleukin-17A (IL-17A) and IL-17F. IL-17A plays important roles in allergic responses such as delayed-type hypersensitivity, contact hypersensitivity, and allergic airway inflammation. IL-17A promotes inflammation by inducing various proinflammatory cytokines and chemokines, recruiting neutrophils, enhancing antibody production, and activating T cells. IL-17A expression is also augmented in autoimmune diseases such as multiple sclerosis and rheumatoid arthritis. Using mouse models of these diseases, we found that IL-17A plays a central role in their development. IL-6 is required for the development of Th17 cells and tumor necrosis factor functions downstream of IL-17A during the effector phase. IL-1 is important both for developing Th17 cells and eliciting inflammation. Th17 cells, like Th1 and Th2 cells, are involved in host defense against infections, but the contribution of these Th subsets to defense mechanisms differs among pathogens. The roles of IL-17F remain largely unknown. In this review, we introduce how IL-17A/IL-17F are involved in inflammatory immune responses and host defense mechanisms and discuss their relationship with other cytokines in the development of inflammatory and infectious diseases.

Shmerling RH. · Division of Rheumatology, Beth Israel Deaconess Medical Center, 110 Francis St, Ste 4B, Boston MA 02215, USA. · Arch Intern Med. · Pubmed #19139318 No free full text.

This publication has no abstract.

Takano H, Komuro I. · Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, Chiba, Japan. · Circ J. · Pubmed #19129679 links to  free full text

Abstract: Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear receptor superfamily and form heterodimers with retinoid X receptor. Three PPAR isoforms have been isolated and termed alpha, beta (or delta) and gamma. Although PPARgamma is expressed predominantly in adipose tissue and associated with adipocyte differentiation and glucose homeostasis, PPARgamma is also present in a variety of cell types. Synthetic antidiabetic thiazolidinediones (TZDs) are well known as ligands and activators for PPARgamma. After it was reported that activation of PPARgamma suppressed production of pro-inflammatory cytokines in activated macrophages, medical interest in PPARgamma has grown and there has been a huge research effort. PPARgamma is currently known to be implicated in various human chronic diseases such as diabetes mellitus, atherosclerosis, rheumatoid arthritis, inflammatory bowel disease, and Alzheimer's disease. Many studies suggest that TZDs not only ameliorate insulin sensitivity, but also have pleiotropic effects on many tissues and cell types. Although activation of PPARgamma seems to have beneficial effects on cardiovascular diseases, the mechanisms by which PPARgamma ligands prevent their development are not fully understood. Recent data about the actions and its mechanisms of PPARgamma-dependent pathway in cardiovascular diseases are discussed here.

Sugita T. · Pharmacology Laboratory, Mitsubishi Tanabe Pharma Corporation, 1000 kamoshida-cho, Aoba-ku, Yokohama, Japan. · Yakugaku Zasshi. · Pubmed #19122432 links to  free full text

Abstract: TNFalpha (tumor necrosis factor-alpha) plays a critical role in the pathogenesis of inflammatory diseases including rheumatoid arthritis and Crohn's disease. Infliximab is a monoclonal antibody that recognizes human TNFalpha. Clinical trials have been persuasive that infliximab is effective and far superior to the conventional drug therapy in various inflammatory diseases. Combination of infliximab plus methotrexate is effective in patients with active rheumatoid arthritis who have not responded adequately to traditional disease-modifying anti-rheumatic drugs, and has produced significant improvement in clinical, radiographic, and functional outcomes. Infliximab is also an important treatment option in patients with active Crohn's disease who have not responded to conventional therapy and in those with this disease who have fistulae. Moreover, infliximab treatment has resulted in effective suppression of ankylosing spondylitis, psoriasis and ocular inflammation in patients with refractory uveoretinitis due to Behçet's disease. Thus, biologics targeting TNFalpha have revolutionized the therapy of inflammatory diseases. Here, the current status of clinical application of anti-TNFalpha biologics is reviewed by describing the clinical outcome of infliximab and future prospects of biologics are discussed.

Kumano K. · Pulmonary Medicine and Clinical Immunology, Dokkyo University School of Medicine. · Nihon Rinsho Meneki Gakkai Kaishi. · Pubmed #19122375 links to  free full text

Abstract: Human parvovirus B19 infection causes erythema infectiosum in child, aplastic crisis in patients with chronic hemolytic anemia, chronic pure red cell aplasia in immunocompromised patients and hydrops fetalis. Human parvovirus B19 causes arthritis and acute glomerulonephritis due to immunological mechanism. Other disorders, rheumatoid arthritis, vasculitis and thrombotic microangiopathy, are linked in human parvovirus B19 infection. Parvovirus B19 infection causes choronic rheumatoid-like arthropathy. Autoantibody and low complement were seen in acute human parvovirus infection, and parvovirus B19 infection present clinically lupus like tableau.

DasGupta S, Murumkar PR, Giridhar R, Yadav MR. · Pharmacy Department, Faculty of Tech. and Engg., The M. S. University of Baroda, Vadodara 390 001, Gujarat, India. · Bioorg Med Chem. · Pubmed #19095454 No free full text.

Abstract: Rheumatoid Arthritis (RA) is one of the most common autoimmune inflammatory conditions, affecting approximately 1% of the adult population worldwide. TNF-alpha is a pleitropic, pro-inflammatory cytokine which plays a pivotal role in the origin and progression of RA and other immune mediated disorders. The success of anti-TNF-alpha biological agents proved that inhibition of TNF-alpha could result in effective control of RA. Since the discovery of anti-TNF-alpha biologicals, much efforts have gone into developing an orally bioavailable small size TNF-alpha antagonist. One of the ways to block TNF-alpha in biological fluids is to inhibit TNF-alpha converting enzyme (TACE). This target has been validated in preclinical trials using TACE inhibitors. But, even after more than a decade no single TACE inhibitor has passed the Phase II clinical trials. Very recently, it has been shown that TACE inhibitors could also be used for inhibition of pathogenic EGFR signaling in cancer. Hence, TACE inhibitors could perform a dual role, in curing not only RA but also certain cancerous conditions. Developments in the field have prompted us to review the research work on TACE inhibitors, especially their structure activity relationships and molecular modeling studies.

Mirshafiey A, Mohsenzadegan M. · Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. · Iran J Allergy Asthma Immunol. · Pubmed #19052348 No free full text.

Abstract: Rheumatoid arthritis is a disease associated with painful joints that affects approximately 1% of the population worldwide, and for which no effective cure is available. It is characterized by chronic joint inflammation and variable degrees of bone and cartilage erosion. Oxygen metabolism has an important role in the pathogenesis of rheumatoid arthritis. Reactive oxygen species (ROS) are produced in many normal and abnormal processes in humans, including atheroma, asthma, joint diseases, aging, and cancer. TNF-alpha overproduction is thought to be the main contributor to increased ROS release in patients with RA. Increased ROS production leads to tissue damage associated with inflammation. The prevailing hypothesis that ROS promote inflammation was recently challenged when polymorphisms in Neutrophil cytosolic factor 1(Ncf1), that decrease oxidative burst, were shown to increase disease severity in mouse and rat arthritis models. It has been shown that oxygen radicals might also be important in controlling disease severity and reducing joint inflammation and connective tissue damage. In this review article, our aim is to clarify the role of ROS in immunopathogenesis of Rheumatoid arthritis.

Avalos I, Rho YH, Chung CP, Stein CM. · Department of Medicine, Division of Rheumatology, Beth Israel Deaconess Medical Center, Boston, MA, USA. · Clin Exp Rheumatol. · Pubmed #19026140 No free full text.

This publication has no abstract.

Yao Y, Wang C, Varshney RR, Wang DA. · Division of BioEngineering, School of Chemical and Biomedical Engineering, Nanyang Technological University, 70 Nanyang Drive, N1.3-B2-13, Singapore, 637457, Singapore. · Pharm Res. · Pubmed #19015958 No free full text.

Abstract: The use of antisense strategies such as ribozymes, oligodeoxynucleotides (ODNs) and small interfering RNA (siRNA) in gene therapy, in conjunction with the use of stem cells and tissue engineering, has opened up possibilities in curing degenerative diseases and injuries to non-regenerating organs and tissues. With their unique ability to down-regulate or silence gene expression, antisense oligonucleotides are uniquely suited in turning down the production of pathogenic or undesirable proteins and cytokines. Here, we review the antisense strategies and their applications in regenerative medicine with a focus on their efficacies in promoting cell viability, regulating cell functionalities as well as shaping an optimal microenvironment for therapeutic purposes.

Venkateshan SP, Sidhu S, Malhotra S, Pandhi P. · Department of Pharmacology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. · Pharmacology. · Pubmed #18957873 No free full text.

Abstract: Rheumatoid arthritis (RA) is a chronic multisystem disease. A characteristic feature of RA is persistent inflammatory synovitis, usually involving the peripheral joints in a symmetric distribution. The prevalence of RA is approximately 0.8% of the population (range: 0.3-2.1%); women are affected approximately 3 times more often than men. The current therapeutic approach is to start a disease-modifying agent early in the illness to prevent eventual joint damage. Older disease-modifying anti-rheumatic drugs include methotrexate, sulphasalazine and hydroxychloroquine. Newer ones such as leflunomide and cyclosporin are also used. A recent advance in the management of rheumatoid arthritis is the use of biological agents, which block certain key molecules involved in the pathogenesis of the illness. They include tumour-necrosis-factor-alpha-blocking agents such as infliximab, etanercept and adalimumab, the anti-CD-20 agent, rituximab, and CTLA-4 Ig abatacept. The present study was planned with the aim of evaluating the efficacy of such newer biological therapies in refractory RA at various time points. Databases including Medline, Embase and the Cochrane Library were searched for all relevant studies up to January 2007. A total of 26 studies were included in present meta-analysis. The method of DerSimonian and Laird [Control Clin Trials 1986;7:177-188] was used to calculated a pooled odds ratio (OR) for the American College of Rheumatology (ACR) criteria 20, 50 and 70, at 24, 54 and 96 weeks. The overall pooled OR were found to be significantly more than the placebo at all 3 time points for all 3 criteria (ACR 20, 50 70). In conclusion, biologicals as a group are highly effective in the treatment of RA. Biologicals were efficacious both in treatment naïve and methotrexate-refractory patients.

Hsiao SC, Ichinohasama R, Lin SH, Liao YL, Chang ST, Cho CY, Chuang SS. · Department of Hemato-Oncology, St. Martin de Porres Hospital, Chia-Yi, Taiwan. · Pathol Res Pract. · Pubmed #18951733 No free full text.

Abstract: Methotrexate-associated lymphoproliferative disorder (MTX-LPD) is a lymphoid proliferation or lymphoma in a patient immunosuppressed with MTX, which is usually administered for treating autoimmune diseases. The majority of MTX-LPD cases develop in patients with rheumatoid arthritis and occasionally with psoriasis who had been treated with MTX. Here, we report on a 50-year-old Taiwanese male with severe psoriasis, who received high doses of MTX. The patient developed EBV-positive MTX-LPD at nodal and extranodal sites. The diffuse and polymorphic lymphoid infiltrate consisted predominantly of immunoblasts and plasmablasts expressing B-cell markers, CD138, Epstein-Barr virus (EBV)-LMP1, and EBNA2, and these were monotypic for kappa light chain. The tumor cells were also positive for EBV by in situ hybridization. These findings indicated a type III latency infection of EBV. The patient died of progressive disease after 19 months. A review of the previously reported cases shows that MTX-LPD, in association with psoriasis, occurs in middle-aged males. The tumors are diffuse large B-cell lymphomas with immunoblastic morphology, and frequently show plasmacytic differentiation.

Goel A, Dange N. · Department of Neurosurgery, Seth Gordhandas Sunderdas Medical College and King Edward VII Memorial Hospital, Parel, Mumbai, India. · J Neurosurg Spine. · Pubmed #18928224 No free full text.

Abstract: The authors report the case of a 35-year-old man who had polyarthritic affliction with rheumatoid disease. He presented with complaints of quadriparesis that had progressed over the course of 2 years. Investigations revealed telltale evidence of rheumatoid disease of the craniovertebral junction with retroodontoid pannus, basilar invagination, and "fixed" atlantoaxial dislocation. The patient underwent lateral mass reconstruction with distraction of the facets and impaction of a spiked metal spacer and bone graft within the joint. Investigations done in the immediate postoperative phase showed complete disappearance of retroodontoid pannus in addition to reduction of basilar invagination and atlantoaxial dislocation. He had remarkable and sustained relief from symptoms. The authors also review the pathogenesis and treatment of retroodontoid pannus.

Kumana CR. · Department of Medicine, Queen Mary Hospital, Pokfulam Road, Hong Kong. · Hong Kong Med J. · Pubmed #18840910 links to  free full text

Abstract: Horizons in Medicine is a series produced annually by the Royal College of Physicians. Volume 19 is based on their Advanced Medicine Conference held in 2007 and offers updates on a wide range of topics in clinical medicine. This 'review of reviews' covers developments described in a selection of chapters. The chapters summarised include: Contemporary management of acute myocardial infarction; Imported infectious disease emergencies; New therapies in the management of type 2 diabetes; Stress and adrenal insufficiency; Making sense of a 'funny thyroid function test'; Myeloproliferative disorders: management and molecular pathogenesis; Drug allergies; Osteoporosis; Rheumatoid arthritis; Understanding migraine from bench to bedside.

Yuasa H, Inoue K, Hayashi Y. · Department of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-dori, Mizuho-ku, Nagoya 467-8603, Japan. · J Pharm Sci. · Pubmed #18823045 No free full text.

Abstract: Proton-coupled folate transporter (PCFT) has recently been identified as the molecular entity of the carrier-mediated intestinal folate transport system. PCFT has been demonstrated to be most abundantly expressed in the upper small intestine, localizing at the brush border membrane of epithelial cells, transport folate and its analogs more efficiently at lower (acidic) pH by a H(+)-coupled cotransport mechanism, and have a high affinity for folate with a Michaelis constant (K(m)) of a few microM at pH 5.5 and somewhat lower affinities for reduced folates and methotrexate (MTX). A loss of PCFT function due to a homozygous mutation in its gene has been indicated to be responsible for hereditary folate malabsorption. Thus, PCFT has all the characteristics of the brush border H(+)-coupled cotransporter for folate and analogs, which has long been suggested to be present in the intestine. Furthermore, sulfasalazine was found to be a potent inhibitor of PCFT, suggesting that it is a risk factor that would cause malabsorption of folate and also MTX, when coadministered in the treatment of rheumatoid arthritis. Understanding the molecular and functional characteristics of PCFT should be important and helpful in exploring therapeutic strategies for folate malabsorption and in optimizing therapies using antifolate drugs.

Mori M, Naruto T, Imagawa T, Murata T, Takei S, Tomiita M, Itoh Y, Fujikawa S, Yokota S. · Department of Pediatrics, Yokohama City University School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, Kanagawa, 236-0004, Japan. · Mod Rheumatol. · Pubmed #18815725 links to  free full text

Abstract: Methotrexate (MTX), the primary treatment for the articular-type juvenile idiopathic arthritis (JIA), is effective and brings about radiological improvement. Patient compliance is good, and it is recognized that its known side effects, namely, disruption of liver function and induction of pulmonary lesions, are unlikely to be severe at the low MTX doses that are administered. In Japan, MTX was granted approval in 1999 by the then Ministry of Health and Welfare specifically for treating rheumatoid arthritis in adult patients, allowing it be generally used in medical institutions for patients having National Health Insurance. However, in the pediatric field, its use outside the indications has so far been unavoidable, and has been left to the discretion of the physician. Finally, at the present conference, expansion of the indications of MTX for JIA was approved in Japan. It is noteworthy that this expansion of indications was achieved without requiring clinical trials on children sponsored by the pharmaceutical company: it was achieved rather by collecting necessary information through ongoing efforts (including collection and analysis of information about approval status in foreign countries, adequate evidence from the literature, implementation of a clinical use survey in Japan, etc.). It also merits attention that the maximum dose (10 mg/m2) was set on the basis of pharmacokinetic data from children, rather than relying on the dosing method and dose for adults.

Chopra P, Kanoje V, Semwal A, Ray A. · Ranbaxy Research Laboratories, Department of Pharmacology, New Drug Discovery Research, Plot No-20, Sector-18, Gurgaon-122001-Haryana, India. · Expert Opin Investig Drugs. · Pubmed #18808304 No free full text.

Abstract: BACKGROUND: Over the past two decades, p38 MAPK (mitogen-activated protein kinase) has been the subject of intense multidisciplinary research. p38 MAPK inhibitors have been shown to be efficacious in several disease models, including rheumatoid arthritis, psoriasis, Crohn's disease, and stroke. Recent studies support a role for p38 MAPK in the development, maintenance, and/or exacerbation of a number of pulmonary diseases, such as asthma, cystic fibrosis, idiopathic pulmonary fibrosis, and chronic obstructive pulmonary disease (COPD). OBJECTIVE: Many previous attempts to develop p38 MAPK inhibitors have failed as a result of unacceptable safety profiles. These toxicities have been varied and are believed to derive from different off-target effects. METHOD: The above concerns can be overcome by delivering the compound locally to minimize whole-body burden, resulting in low exposure to the gastrointestinal, liver, and CNS. This review discusses the role of p38 MAPK in various inflammatory diseases, followed by the toxicity concerns associated with p38 MAPK inhibition. It also highlights the possible beneficial effect of delivering drugs via the inhalation route. CONCLUSION: We present proof-of-principle confirming the therapeutic potential of inhaled p38 inhibitors for asthma and other inflammatory pulmonary diseases.

Sun J, Lin Z, Feng J, Li Y, Shen B. · Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Science and Technology, Tianjin University, Tianjin 30072, PR China. · Eur J Pharmacol. · Pubmed #18793632 No free full text.

Abstract: Since B cell activating factor belonging to tumor necrosis factor (TNF) family (BAFF) has been identified as a critical factor for B cell maturation and survival, convincing evidence indicates that deregulation of BAFF is involved in pathogenesis of B cell related autoimmune diseases. Blockade of BAFF activity significantly improves the symptoms of autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis both in animal models and clinical trials. Therefore, BAFF-targeting therapy is a promising approach to treat B cell related autoimmune diseases.

Chopra A, Abdel-Nasser A. · Centre for Rheumatic Diseases, Hermes Doctor House, 1988 Convent Street, Camp, Pune 411 001, India. · Best Pract Res Clin Rheumatol. · Pubmed #18783739 No free full text.

Abstract: The epidemiology of rheumatic musculoskeletal (MSK) disorders in the developing world is much less well known than it is in the developed world. We expect ethnicity, traditions, socioeconomics and lifestyles to have an impact, but overall data are sparse. This report focuses on the WHO-ILAR COPCORD (community-oriented programme for control of rheumatic diseases). COPCORD was designed to collect community data on pain and disability in the developing economies. Several countries in Asia-Pacific and Central South America have completed COPCORD surveys. Despite some limitations in methodology, COPCORD provides a fair estimate of the spectrum and extent of rheumatic MSK disorders. We digress from a general overview to highlight the scenario for rheumatoid arthritis, and draw a few parallels with known statistics from the developed world. Overall, the emerging spectrum and severity are not very different, but in the developing countries the burden of disease, worsened by dismal rheumatology services, is likely to be staggering.

Amano H, Furuhata N, Tamura N, Tokano Y, Takasaki Y. · Department of Rheumatology and Internal Medicine, Juntendo University, Tokyo, Japan. · Lupus. · Pubmed #18755866 No free full text.

Abstract: We describe a female Japanese patient with concomitant hypocomplementemic urticarial vasculitis, Jaccoud's arthropathy and valvular heart disease. In 1996, she developed arthritis with swelling of both proximal interphalangeal joints and urticarial vasculitis on both arms that was resolved by administration of glucocorticoid (prednisolone 30 mg/day). Tests for antineutrophil cytoplasmic antibodies, antinuclear antibody and rheumatoid factor gave negative results. The findings of a skin biopsy examination were consistent with 'leukocytoclastic vasculitis'. During 10 years of observation, the patient manifested polyarthritis leading to progressive deformity of the joints of the hands and feet (without loss of cartilage or erosion of bone), persistent urticaria exacerbated by cold and accompanied by hypocomplementemia and progressive cardiac valvular disease with mitral valve regurgitation. There are only three reports described previously documenting five patients with this rare combination of manifestations.

Mehrpoor G, Owlia MB, Soleimani H, Ayatollahi J. · Department of Internal Medicine, Sadoughi Hospital, Shahid Sadoughi University of Medical Sciences, Safaeieh, Yazd, Iran. · Mod Rheumatol. · Pubmed #18754076 No free full text.

Abstract: Adult-onset Still's disease (AOSD) is a rare systemic inflammatory disorder of unknown etiology. It is characterized by fever, skin rash, polyarthralgias or polyarthritis, sore throat, hepatosplenomegaly, lymphadenopathy, leukocytosis, liver enzyme elevation, and high serum level of ferritin. Several kinds of skin lesions have been reported in this condition. The aim of this study was to assess the clinical and laboratory aspects of 28 patients with AOSD in central Iran. According to the diagnostic criteria of AOSD, we identified 28 patients between 2002 and 2007. We intended to describe the clinical characteristics, treatment, and outcome of our patients with AOSD. Of 28 patients with AOSD, 21 (75%) were female, 7 (25%) were male. Fever (100%), sore throat (92%), Arthralgia (92%), dermatographism (92%), typical rash (85%) and arthritis (60%) were the most common findings. The mean values of laboratory findings were as follows; C-reactive protein (CRP) level of 14.4 mg/dl, erythrocyte sedimentation rate (ESR) of 91.5 mm/h, leukocyte count of 15744.4/microl. Abnormal levels of aspartate aminotransferase and alanine aminotransferase were observed in 25 (89%) patients. Twenty patients (71%) had high ferritin values (>500 ng/ml). The clinical characteristics were similar to previous series. A febrile polyarthritis was the most frequent presentation form. Dermatographism was frequently encountered phenomenon in our patients with AOSD. Being that dermatographism is a simple inducible skin reaction, along with its sensitivity in active disease, we suggest more controlled studies to validate accuracy and positive predictive value of it in convenient clinical setting in the diagnosis of AOSD and to consider including it in diagnostic criteria.

Lee MS, Shin BC, Ernst E. · Department of Medical Research, Korea Institute of Oriental Medicine, 461-24 Jeonmin-dong, Yuseong-gu, Daejeon 305-811, South Korea. · Rheumatology (Oxford). · Pubmed #18710899 No free full text.

Abstract: The aim of this systematic review is to evaluate the available evidence, from randomized clinical trials (RCTs), of acupuncture for treating patients with RA. Systematic searches were conducted on 17 databases up to April 2008 without the language restriction. All RCTs of acupuncture, with or without electrical stimulation or moxibustion, for patients with RA were considered for inclusion. A total of 236 potentially relevant studies were identified and eight RCTs were included. Four RCTs compared the effects of manual or electro-acupuncture with penetrating or non-penetrating sham acupuncture and failed to show specific effects of acupuncture on pain [n = 88; weighted mean differences (WMD), 10 cm VAS -0.46; 95% CI -1.70, 0.77; P = 0.46; heterogeneity: tau(2) = 0.19; chi(2) = 2.38; P = 0.30; I (2) = 16%] or other outcome measures. One RCT compared manual acupuncture with indomethacin and suggested favourable effects of acupuncture in terms of total response rate. Three RCTs tested acupuncture combined with moxibustion, vs conventional drugs and failed to show that acupuncture plus moxibustion was superior to conventional drugs in terms of response rate (n = 345; RR 1.12; 95% CI 0.99, 1.28; P = 0.08; heterogeneity: tau(2) = 0.00; chi(2) = 1.34; P = 0.51; I(2) = 0%), pain reduction (n = 105; WMD, 10 cm VAS 1.53; 95% CI -0.57, 3.63; P = 0.15; heterogeneity: tau(2) = 1.18; chi(2) = 1.81; P = 0.18; I(2) = 45%) or joint swelling index (n = 105; WMD, 10 cm VAS 0.25; 95% CI -1.31, 1.82; P = 0.75; heterogeneity: tau(2) = 0.18;chi(2) = 1.14; P = 0.28; I(2) = 13%). In conclusion, penetrating or non-penetrating sham-controlled RCTs failed to show specific effects of acupuncture for pain control in patients with RA. More rigorous research seems to be warranted.

Xu M, Liu L, Qi C, Deng B, Cai X. · School of Chinese Medicine, Hong Kong Baptist University, Kowloon Tong, Hong Kong Special Administrative Region, PR China. · Planta Med. · Pubmed #18683125 No free full text.

Abstract: Sinomenine (SIN), an alkaloid isolated from CAULIS SINOMENII, has been used in the treatment of rheumatoid arthritis (RA) clinically. This study aimed to systematically evaluate the efficacy and safety of SIN by a comparison between SIN and non-steroidal anti-inflammatory drugs (NSAIDs). Forty-three electronic databases were systematically searched. The quality of eligible trials was assessed by Jadad's scale. Revman 5.0 software was used for data syntheses and meta-analyses. The results showed that (i) of the 121 potential studies identified, 10 clinical trials involving 1185 patients met the inclusion criteria; (ii) improved patients and rheumatoid factor disappearance patients after SIN treatments were significantly more than those treated by NSAIDs ( P < 0.00001 and P = 0.008); (iii) compared with NSAIDs, SIN was more effective in amelioration of morning stiffness ( P < 0.00001), painful joints ( P = 0.03), and erythrocyte sedimentation rate ( P < 0.00001), but there was no significant difference between the two remedies in the treatment of swollen joints, grip strength, and C-reactive protein ( P > 0.05); and (iv) adverse events occurred less frequently in the digestive system during SIN treatment than during NSAID treatment ( P = 0.0003) but occurred more frequently in the dermatomucosal system with SIN treatment ( P = 0.03), while adverse events of the nervous system were similar for both treatments ( P = 0.31). In conclusion, SIN may be a valuable remedy to treat RA clinically, although current evidence needs to be further verified by more high-quality trials.