Nature Clinical Practice Rheumatology Journal Impact Factor & Information

Publisher: Nature Publishing Group

Journal description

Nature Clinical Practice Rheumatology provides timely authoritative interpretations of key research developments, translating the latest findings into clinical practice. Content includes editorial and opinion pieces, highlights from the current literature, commentaries on the application of recent research to practical patient care, comprehensive reviews, and in-depth case studies. Content is subject to rigorous peer-review. Coverage includes prevention, diagnosis, and treatment of conditions of the joints, muscle, bones, blood vessels, and connective tissue, including systemic autoimmune disease, inflammatory and degenerative diseases of joints, regional musculoskeletal disorders, osteoporosis and metabolic bone disease, pain management, imaging, immunology, genetics, clinical trials, epidemiology and clinical outcomes.

Current impact factor: 5.85

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2011 Impact Factor 5.846
2010 Impact Factor 7.113
2009 Impact Factor 5.533
2008 Impact Factor 5.677
2007 Impact Factor 3.812
2006 Impact Factor 0.222

Impact factor over time

Impact factor

Additional details

5-year impact 5.25
Cited half-life 4.40
Immediacy index 2.23
Eigenfactor 0.01
Article influence 1.80
Website Nature Clinical Practice Rheumatology website
Other titles Nature clinical practice rheumatology, Rheumatology
ISSN 1745-8382
OCLC 62746469
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Nature Publishing Group

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 6 months embargo
  • Conditions
    • Authors retain copyright
    • Author's pre-print on arXiv or bioRXiv
    • Author's post-print on author's personal website, institutional repository, PubMed Central or funding body's archive
    • Published source must be acknowledged
    • Must link to publisher version with DOI
    • Publisher's version/PDF cannot be used
  • Classification

Publications in this journal

  • Nature Clinical Practice Rheumatology 05/2008; 4(5). DOI:10.1038/ncprheum0793

  • Nature Clinical Practice Rheumatology 10/2007; 3(9):490-1. DOI:10.1038/ncprheum0566

  • Nature Clinical Practice Rheumatology 10/2007; 3(9):492-3. DOI:10.1038/ncprheum0574
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    ABSTRACT: Regional soft-tissue complaints are commonplace, and they usually relate to a disease process, such as strain, inflammation or degeneration of a muscle, tendon or related muscle-tendon unit. The clinical features and investigations of the causative processes of these complaints are characteristic, and outcomes to treatments are usually predictable and satisfactory. Regional pain syndromes are different: these syndromes present with regional pain and tenderness, and other sensory symptoms unaccounted for by a simple musculoskeletal mechanistic explanation. Approved classification criteria for regional pain syndromes are lacking, and these syndromes are poorly understood and frequently misdiagnosed. Regional pain syndromes often occur after injury and overlap extensively with other musculoskeletal pain syndromes, in terms of clinical signs and symptoms. The clinician and patient are often confused about the nature of the problem and routine treatments directed to putative tissue damage will fail. Review of the epidemiology of regional pain syndromes combined with knowledge of other similar pain syndromes has enabled an evolving understanding of the condition. The musculoskeletal and central nervous systems both contribute to regional pain syndromes, through spine-related pain mechanisms and central sensitization, respectively. The patient's emotional state, particularly the effect on pain modulation, links these two systems.
    Nature Clinical Practice Rheumatology 10/2007; 3(9):504-11. DOI:10.1038/ncprheum0598

  • Nature Clinical Practice Rheumatology 10/2007; 3(9):494-5. DOI:10.1038/ncprheum0575
  • Source

    Nature Clinical Practice Rheumatology 10/2007; 3(9):479. DOI:10.1038/ncprheum0576

  • Nature Clinical Practice Rheumatology 10/2007; 3(9):480-1. DOI:10.1038/ncprheum0564
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    ABSTRACT: Interactions between environmental and genetic factors are proposed to explain why autoimmunity afflicts certain individuals and not others. Genes and genetic loci predisposing to autoimmunity are being identified, but theories as to how the environment contributes to autoimmunity still rely largely on examples such as drug-induced systemic lupus erythematosus (SLE) and epidemiologic evidence of occupational exposure, without clear mechanistic explanations or identification of specific environmental agents. Eukaryotic gene expression requires not only transcription factor activation but also regional modification of chromatin structure into a transcriptionally permissive configuration through epigenetic mechanisms, including DNA methylation and histone modifications. The realization that epigenetic mechanisms can alter gene expression and, therefore, cellular function has led to new insights into how environmental agents might contribute to the development of diseases in genetically predisposed individuals. The observation that some SLE-inducing drugs, such as procainamide and hydralazine, affect T cell DNA methylation and thereby cellular function, and that identical changes in T cell DNA methylation and cellular function are found in patients with SLE, implicates epigenetic mechanisms in the pathogenesis of human SLE, and perhaps other autoimmune diseases. In this Review we discuss how epigenetic mechanisms affect gene expression, how environmental agents can affect epigenetic mechanisms, and how epigenetic changes in gene expression can contribute to autoimmunity. Similar mechanisms might also contribute to the pathogenesis of other poorly understood human diseases.
    Nature Clinical Practice Rheumatology 10/2007; 3(9):521-7. DOI:10.1038/ncprheum0573
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    ABSTRACT: The assessment of systemic inflammation by means of laboratory tests often complements the results of medical examination. Traditionally, the erythrocyte sedimentation rate and leukocytosis with left shift are diagnostic markers for inflammatory and infectious diseases. The levels of acute-phase proteins--especially C-reactive protein--are used to assess both the presence of inflammation and any response to treatment. The determination of C-reactive protein levels may be advised in three types of pathological situation: infection, acute or chronic inflammation, and evaluation of metabolic risk. Procalcitonin is useful as a marker of sepsis and severe infection. The concentration of serum amyloid A predicts the chances of survival of patients with secondary (AA) amyloidosis. Ferritin and its glycosylated form are of interest in the study of specific diseases such as adult-onset Still's disease. Markers of cartilage and bone turnover are complementary to these markers of inflammation. Although cytokine serum levels are transiently crucial to the generation of inflammation, their usefulness in the clinic is still under investigation. Serum concentrations of cytokine inhibitors or soluble cytokine receptors, as well as the clinical response of patients to treatment with cytokine antagonists, might generate important information for monitoring autoinflammatory diseases.
    Nature Clinical Practice Rheumatology 10/2007; 3(9):512-20. DOI:10.1038/ncprheum0572

  • Nature Clinical Practice Rheumatology 10/2007; 3(9):488-9. DOI:10.1038/ncprheum0565
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    ABSTRACT: Ankylosing Spondylitis (AS) is a chronic inflammatory arthritis that predominantly affects the axial skeleton in adolescent patients causing spinal pain and stiffness. There is a marked delay, on average 8 years, between onset of disease symptoms and clinical diagnosis. The distinction between the symptoms of mechanical and inflammatory back pain remains one of the main contributing factors for the delay in diagnosis. Several classification criteria exist to aid the diagnosis of AS, but their accuracy is poor. The Ankylosing Spondylitis Assessment Study group (ASAS) has defined a core set of domains for clinical outcome measurement in AS in order to assess the disease process in individual patients and to identify those with rapidly progressive disease. New therapies, such as the tumor necrosis factor (TNF) inhibitors, have transformed the treatment paradigm in AS, especially for those patients with aggressive disease. Thus, the definition of both patient selection criteria for these agents and the development of clinical methods to assess response to therapy have become a priority. This Review focuses on measuring the degree of disease activity, function and damage in patients with AS in an ambulatory care setting, and the assessment of suitability of various outcome measures for monitoring response to treatment with TNF inhibitors.
    Nature Clinical Practice Rheumatology 10/2007; 3(9):496-503. DOI:10.1038/ncprheum0591

  • Nature Clinical Practice Rheumatology 09/2007; 3(8):428-9. DOI:10.1038/ncprheum0553
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    ABSTRACT: Gout is one of the most common inflammatory arthritides, which is considered to be a true crystal deposition disorder caused by the formation of monosodium urate crystals in and around joints. A number of epidemiological studies from a diverse range of countries suggest that gout has increased in prevalence and incidence in recent years and that the clinical pattern of gout is becoming more complex. In particular, the greatest increase has been observed in primary gout in older men. Robust epidemiological studies have established risk factors for gout including genetic factors, excess alcohol consumption, purine-rich diet, the metabolic syndrome (obesity, hypertension, hyperlipidemia and insulin resistance), use of diuretics and chronic renal failure. Trends in alcohol use, diet, obesity and the metabolic syndrome in the general population might explain changes in the prevalence and incidence of gout in the community. Osteoarthritis, which is thought to predispose patients to monosodium urate crystal deposition in their joints, is becoming more prevalent as a consequence of increased longevity. In hospital settings, widespread diuretic use, increasing prevalence of end-stage renal failure and the success of organ transplant programmes have led to an increase in clinical complexity. Suboptimal management of gout is likely to have contributed to the rise in the prevalence of clinically overt, symptomatic, chronic gout.
    Nature Clinical Practice Rheumatology 09/2007; 3(8):443-9. DOI:10.1038/ncprheum0556

  • Nature Clinical Practice Rheumatology 09/2007; 3(8):432-3. DOI:10.1038/ncprheum0557
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    ABSTRACT: Angiogenesis inhibition, long studied in the treatment of malignancies, has begun to emerge as a potential therapeutic approach in managing inflammatory arthritis, particularly rheumatoid arthritis. The growth of new vessels is required for the development of the rheumatoid pannus, which then leads to extensive synovial inflammation and joint destruction. Vascular endothelial growth factor is the best studied mediator of angiogenesis, and several therapies have been developed that specifically target this molecule. Several other angiogenesis mediators, such as the angiopoietin-TIE system, hypoxia inducible factor and integrin alpha(V)beta(3), as well as naturally occurring inhibitors of angiogenesis, are also being investigated as potential therapeutic targets. Additionally, there are a number of drugs, including paclitaxel, 2-methoxyestradiol and fumagillin analogs, that might have a role in inhibiting angiogenesis and, thus, in treating proliferative synovitis.
    Nature Clinical Practice Rheumatology 09/2007; 3(8):434-42. DOI:10.1038/ncprheum0559

  • Nature Clinical Practice Rheumatology 09/2007; 3(8):421. DOI:10.1038/ncprheum0561

  • Nature Clinical Practice Rheumatology 09/2007; 3(8):422-3. DOI:10.1038/ncprheum0537
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    ABSTRACT: Rheumatologists with clinical expertise should perform clinical investigations of new molecules in an effort to discover therapies that could be of greater benefit or safety than those currently available for patients with chronic rheumatic diseases. Over the past few years, many studies have been conducted outside the United States and Europe because of the dearth of investigative sites in these countries. A clinician, whether in private practice or academia, who has the resources and desire to conduct clinical investigations, should be able to become involved in the process. The task of starting a new investigative unit is daunting, as it involves acquiring studies, hiring staff and obtaining space prior to any cash flow. If done properly, however, clinical investigation can be rewarding--both intellectually and financially.
    Nature Clinical Practice Rheumatology 09/2007; 3(8):459-63. DOI:10.1038/ncprheum0554
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    ABSTRACT: Early aggressive treatment of rheumatoid arthritis is associated with improved disease control, slower radiological progression and improved functional outcomes. Tumor necrosis factor blocking therapy is effective but there remain concerns about long-term risks. Combining disease-modifying antirheumatic drugs (DMARDs) is a widely used therapeutic alternative; however, there is uncertainty surrounding the most effective regimen. A popular combination is methotrexate plus sulfasalazine, but each of these DMARDs can also be used in combination with other DMARDs and in triple therapy regimens. However, wide variations in study size, design, steroid usage and approaches to combination therapy have made it difficult to form firm conclusions regarding their efficacy. Generally, combination therapy is well tolerated and associated with no significant increase in the rate of adverse events compared with monotherapy. Methotrexate-sulfasalazine, methotrexate-chloroquine, methotrexate-cyclosporin, methotrexate-leflunomide, methotrexate-intramuscular-gold and methotrexate-doxycycline are effective combination regimens. Triple DMARD therapy is better than various DMARD monotherapy and dual therapy regimens. Methotrexate and hydroxychloroquine may have synergistic anti-inflammatory properties. Clinical trial evidence to support the use of other methotrexate and sulfasalazine combinations is often weak or lacking. Further investigation is required to determine the most effective regimen and approach to combination therapy.
    Nature Clinical Practice Rheumatology 09/2007; 3(8):450-8; quiz, following 478. DOI:10.1038/ncprheum0562