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2011 Consensus of the Brazilian Society of Rheumatology for diagnosis and early assessment of rheumatoid arthritis

Abstracts

OBJECTIVE: Develop guidelines for management of rheumatoid arthritis (RA) in Brazil, focusing on diagnosis and early assessment of the disease. METHOD: Literature review and expert opinions of RA Committee members of the Brazilian Society of Rheumatology. RESULTS AND CONCLUSIONS: The following ten reccommendations were established: 1) RA diagnosis should be established considering clinical findings and complementary test results; 2) Special attention should be given to the differential diagnosis of arthritis; 3) Rheumatoid factor (RF) is an important diagnostic test, but has limited sensitivity and specificity, mainly in early RA; 4) Anti-CCP (anti-cyclic citrullinated peptide antibody) is a marker with sensitivity similar to that of the RF, but with higher specificity, mainly in the initial phase of disease; 5) Although unspecific, acute-phase reactants should be measured in patients with clinical suspicion of RA; 6) Conventional radiography should be performed for diagnostic and prognostic assessment of the disease. When necessary and available, ultrasound and magnetic resonance may be used; 7) Rheumatoid arthritis classification criteria (ACR/EULAR 2010), although not yet validated, may be used as a guide to aid in diagnosing patients with early RA; 8) One of the combined disease activity indices should be used to assess disease activity; 9) At least one of the functional capacity assessment instruments, such as mHAQ or HAQ-DI, should be regularly used; 10) At the early assessment of the disease, the presence of worse prognostic factors, such as polyarticular involvement, high titers of RF and/or anti-CCP, and early joint erosion, should be investigated.

rheumatoid arthritis; diagnosis; assessment; consensus


OBJETIVO: Elaborar recomendações para o manejo da artrite reumatoide (AR) no Brasil, com enfoque no diagnóstico e na avaliação inicial da doença. MÉTODO: Revisão da literatura e opinião de especialistas membros da Comissão de AR da Sociedade Brasileira de Reumatologia. RESULTADOS E CONCLUSÕES: Foram estabelecidas 10 recomendações: 1) O diagnóstico da AR deve ser estabelecido considerando-se achados clínicos e exames complementares; 2) Deve-se dedicar especial atenção ao diagnóstico diferencial dos casos de artrite; 3) O fator reumatoide (FR) é um teste diagnóstico importante, porém com sensibilidade e especificidade limitadas, sobretudo na AR inicial; 4) O anti-CCP (teste para anticorpos antipeptídeos citrulinados cíclicos) é um marcador com sensibilidade semelhante a do FR, mas com especificidade superior, sobretudo na fase inicial da doença; 5) Embora inespecíficas, provas de atividade inflamatória devem ser solicitadas a pacientes com suspeita clínica de AR; 6) A radiografia convencional deve ser empregada para avaliação de diagnóstico e prognóstico da doença. Quando necessário e disponível, a ultrassonografia e a ressonância magnética podem ser utilizadas; 7) Podem-se utilizar critérios de classificação de AR (ACR/EULAR 2010), embora ainda não validados, como um guia para auxiliar no diagnóstico de pacientes com artrite inicial; 8) Deve-se utilizar um dos índices compostos para avaliação de atividade de doença; 9) Recomenda-se a utilização regular de ao menos um instrumento de avaliação da capacidade funcional; 10) Deve-se verificar, na avaliação inicial da doença, a presença ou não de fatores de pior prognóstico, como o acometimento poliarticular, FR e/ou anti-CCP em títulos elevados e erosão articular precoce.

artrite reumatoide; diagnóstico; avaliação; consenso


ORIGINAL ARTICLE

ICollaborating Professor of Internal Medicine and of the Rheumatology Service of the Medical School of the Universidade de Brasília (FM-UnB); PhD in Medical Sciences by the FM-UnB

IIMaster in Epidemiology; Chief of the Rheumatology Service at BIOCOR Instituto - Belo Horizonte, state of MG

IIIPhD in Medical Sciences by the Universidade Federal do Rio Grande do Sul - UFRGS; Coordinator of the Rheumatoid Arthritis Outpatient Clinic at Rheumatology Service of the Hospital de Clínicas de Porto Alegre

IVPhD in Rheumatology; Chief of the Rheumatology Service at Hospital Universitário of the Universidade Federal de Santa Catarina - HU-UFSC

VRheumatologist; Hospital das Clínicas da Universidade Federal do Paraná - HC-UFPR; former fellow of the Rheumatology Service, General Hospital AKH, Austria

VIAssistant Professor, PhD and Coordinator of the Discipline of Rheumatology at Faculdade de Ciências Médicas (FCM) of the Universidade Estadual de Campinas - Unicamp

VIIAdjunct Professor of Immunology of the Medical School at Universidade Federal do Ceará - UFC

VIIIFull Professor of the Universidade Federal de Goiás - UFG

IXProfessor with habilitation degree (Associated) of the Medical School of Ribeirão Preto at Universidade de São Paulo

XChief-Physician of the Diagnosis and Therapy Section of the Rheumatology Service at Hospital do Servidor Público Estadual de São Paulo - HSPE-FMO

XIRheumatologist; Chief of the Rheumatology Service at Hospital Universitário de Brasília of the UnB

XIIAdjunct Professor of the Discipline of Rheumatology at Faculdade de Ciências Médicas (FCM) of the Universidade do Estado do Rio de Janeiro - UERJ

Correspondence to

ABSTRACT

OBJECTIVE: Develop guidelines for management of rheumatoid arthritis (RA) in Brazil, focusing on diagnosis and early assessment of the disease.

METHOD: Literature review and expert opinions of RA Committee members of the Brazilian Society of Rheumatology.

RESULTS AND CONCLUSIONS: The following ten reccommendations were established: 1) RA diagnosis should be established considering clinical findings and complementary test results; 2) Special attention should be given to the differential diagnosis of arthritis; 3) Rheumatoid factor (RF) is an important diagnostic test, but has limited sensitivity and specificity, mainly in early RA; 4) Anti-CCP (anti-cyclic citrullinated peptide antibody) is a marker with sensitivity similar to that of the RF, but with higher specificity, mainly in the initial phase of disease; 5) Although unspecific, acute-phase reactants should be measured in patients with clinical suspicion of RA; 6) Conventional radiography should be performed for diagnostic and prognostic assessment of the disease. When necessary and available, ultrasound and magnetic resonance may be used; 7) Rheumatoid arthritis classification criteria (ACR/EULAR 2010), although not yet validated, may be used as a guide to aid in diagnosing patients with early RA; 8) One of the combined disease activity indices should be used to assess disease activity; 9) At least one of the functional capacity assessment instruments, such as mHAQ or HAQ-DI, should be regularly used; 10) At the early assessment of the disease, the presence of worse prognostic factors, such as polyarticular involvement, high titers of RF and/or anti-CCP, and early joint erosion, should be investigated.

Keywords: rheumatoid arthritis, diagnosis, assessment, consensus.

INTRODUCTION

Rheumatoid arthritis (RA) is a systemic, chronic and progressive inflammatory disease that affects mainly the synovial membrane of joints, leading to bone and cartilaginous destruction.1

The condition affects 0.5% to 1% of the adult population worldwide, and can occur in all ethnic groups.2 Rheumatoid arthritis predominates in females (two to three times more common) and affects mainly patients in their forth to sixth decades of life, but has been reported at all age groups.3

A Brazilian multicenter study of population samples from Brazilian macroregions (North, Northeast, West-central, and South) has reported RA prevalence of up to 1% in the adult population,4 corresponding to an estimate of 1,300,000 people affected.

Rheumatoid arthritis is a chronic disease, with an irreversible joint damage potential, resulting in high costs to affected individuals and society.5-7

The understanding of RA physiopathogeny, its diagnostic methods and therapeutic management have undergone considerable advances in recent years, particularly regarding the initial period of the disease, the so-called early RA (first 12 months of RA symptoms), recognized as a therapeutic "window of opportunity".8-10 Despite these advances, the current diagnostic and prognostic indicators (clinical, laboratory, and radiographic) play a limited role in early RA diagnosis and establishment of individual prognosis.11

The demographic and clinical characteristics of RA vary according to the population affected.12 Most information available originates from Europe and the United States.13,14 Studies conducted in the Brazilian population are scarce.15,16

Rheumatoid arthritis affects patients in their productive years and may provide significant limitation in their functional capacity, in addition to labor capacity loss; thus, the indirect costs related to these factors should be incorporated into pharmacoeconomic analyses.17

In Brazil, as well as in developed countries, RA-related costs are high.18 Such costs have greater repercussion in developing countries, whose financial resources for health are less robust. This emphasizes the need for studies assessing RA costs and allocation of resources for RA diagnosis and treatment adapted to the Brazilian reality.19

METHOD FOR ELABORATING THE CONSENSUS

The present consensus was aimed at elaborating guidelines for RA management, with an emphasis on disease diagnosis, considering peculiar aspects of the Brazilian socioeconomic reality.

The method for elaborating the consensus for the development of guidelines includes literature review and the opinion of experts, who are members of the Rheumatoid Arthritis Committee of the Brazilian Society of Rheumatology (SBR). The bibliographic survey comprised publications existing in the MEDLINE, SciELO, PubMed, and EMBASE databases up to March 2011. The guidelines were written and reassessed by all participants during three meetings held in October 2010, December 2010, and February 2011, in addition to several rounds of questioning and corrections carried out via Internet.

DIAGNOSIS

The diagnosis of RA should be established considering the clinical findings and complementary test results. No isolated test, either laboratory, imaging, or histopathological, confirms the diagnosis.

Arthritis can be part of the course of several diseases, which, thus, should be considered in the differential diagnosis with RA,20,21 as shown in Table 1.

When RA presents in its definite form, with all its typical findings, its recognition is easier. Diagnosing the disease in its early phase, however, may be difficult, because characteristic serological and radiographic alterations are often missing.22

The clinical manifestations of RA can be divided into articular and extra-articular. Because RA is a systemic disease, general symptoms such as fever, asthenia, fatigue, myalgia, and weight loss may precede or accompany the onset of articular manifestations.23

ARTICULAR MANIFESTATIONS

Articular manifestations of RA may be reversible in its early stages. However, when joint destruction has already occurred, the alterations caused by persistent synovitis, bone and cartilage destruction, loss of mobility, and muscle, tendon and ligament changes are irreversible

The basic characteristic of the articular manifestation of RA is synovial inflammation (synovitis), which can affect any of the diarthrodial joints of the body.

The clinical complaint comprises pain, swelling, and reduced range of motion in affected joints. On physical examination, there are joint tenderness, increased joint volume, intra-articular effusion, joint warmth, and, occasionally joint redness. Deep joints, such as hips and shoulders, may not evidence these findings.23

The characteristics of arthritis in RA are as follows:23

a) Polyarticular involvement: usually more than four joints are involved. However, the disease may begin and persist as mono- or oligoarthritis.

b) Arthritis in wrists and hands: the involvement of wrists, metacarpophalangeal (MCP) joints, and proximal interphalangeal (PIP) joints is frequent since disease onset. The distal interphalangeal (DIP) involvement is rare, which is useful in differentiating RA from other conditions, such as osteoarthritis and psoriatic arthritis.

c) Symmetrical arthritis: symmetrical joint involvement is common, although in case of PIP, MCP, and metatarsophalangeal (MTP) joints, symmetry is not necessarily complete.

d) Cumulative or additive arthritis: arthritis usually has a cumulative pattern (progressively involves new joints, but keep the previously affected inflamed).

e) Morning stiffness: prolonged morning stiffness, characterized by joint stiffness and swelling, identified mainly in the morning, is an almost universal finding of synovial inflammation. Unlike the brief stiffness observed in osteoarthritis (usually five to ten minutes), in inflammatory diseases, stiffness lasts more than one hour. This phenomenon is associated with reduction in motion occurring during sleep or rest and not with the time of day. Duration tends to correlate with the degree of inflammation, and is a parameter that should be documented for disease follow-up.24,25

EXTRA-ARTICULAR MANIFESTATIONS

Although articular manifestations are the major characteristics, RA can affect other organs and systems. The most frequent extra-articular manifestations include cutaneous, ocular, pleuropulmonary, cardiac, hematologic, neurological, and osteometabolic findings. They are more common in patients with severe and polyarticular disease, positive serology for rheumatoid factor (RF) or anti-cyclic citrullinated peptide antibody (anti-CCP), and rheumatoid nodules.26,27

Brazilian studies have confirmed the following as early manifestations of RA: polyarticular involvement; persistent synovitis in the hands; prolonged morning stiffness; high number of tender and swollen joints; and fatigue.15,16

LABORATORY TESTS

Acute phase response measurements

The most commonly used laboratory markers for assessing RA activity are the following acute-phase reactants: erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP).28 Erythrocyte sedimentation rate is usually measured using the Westergren method (mm/first hour), and CRP is mainly measured by quantitative method (in mg/dL or mg/L).

Although such tests are often requested during follow-up and might correlate with the periods of disease activity, they are not specific. Erythrocyte sedimentation rate and CRP vary according to age and sex, and ESR can be influenced by several variables, such as hemoglobin levels, pregnancy, hypoalbuminemia, and hypofibrinogenemia.29

In a Brazilian cohort of early RA, more than two thirds of patients assessed had elevated acute-phase reactants (ESR and CRP) at baseline.30

Autoantibodies

Some autoantibodies, such as RF and several anti-citrullinated protein/peptide antibodies (ACPA), including anti-CCP, act as RA potential diagnostic markers.31

Rheumatoid factor

Rheumatoid factor is an autoantibody directed against the Fc portion of IgG.32 It is classically associated with RA, detected in serum of approximately 70% of patients, and correlates statistically with worse prognosis. Higher titers are associated with aggressive disease, presence of rheumatoid nodules, and extra-articular manifestations.31

Individually, the diagnostic value of RF is limited, because 30% to 50% of patients, at disease onset, can be seronegative for this autoantibody.32 In addition to low sensitivity, the test specificity is also limited. RF may be positive in the absence of arthritis, with increased prevalence with aging,33 and may still be present in several other conditions, either rheumatologic or non-rheumatologic.34,35 Thus, a negative RF test does not exclude the diagnosis of RA, and its positivity should be carefully interpreted according to clinical findings.

Brazilian data (incident cohort of early RA) have shown a prevalence of RF in approximately 50% of patients.30

Anti-citrullinated protein/peptide antibodies

Recently, several ACPA have emerged as important diagnostic tools for RA, with sensitivity similar to and specificity greater than that of RF,besides having a possible role in the pathogenesis of disease.36 Their role as possible RA activity markers is controversial.37

Anti-cyclic citrullinated peptide antibodies

Among the antibodies directed against antigens of filaggrin-citrulline system studied, the anti-CCP antibodies have shown the greatest clinical applicability. The test sensitivity is 70%-75%, its specificity is approximately 95%, and it is particularly useful in the subgroup of patients with early arthritis and negative RF.38

Its investigation is valid in assessing undifferentiated arthrites. The anti-CCP antibodies are detected very early in the course of RA and can be used as an indicator of RA progression and prognosis.39-48

Other antibodies

Other autoantibodies have been used in RA investigation. The objective is to develop methods with sensitivity and specificity for earlier RA diagnosis, more reliable activity markers, and prognostic indicators. Some of the autoantibodies used in RA investigation are as follows: mutated citrullinated vimentin antibodies (anti-MCV);49-51 antikeratin antibodies (AKA); anti-perinuclear factor (APF);52 antifilaggrin autoantibodies;53 anti-human citrullinated fibrinogen antibodies (ACF);54 anti-heterogeneous nuclear ribonucleoprotein A2 autoantibody (anti-RA33);52 anti-interleukin 1 antibody (anti-IL1);55 anti-alpha-enolase antibody;56 and anti-advanced glycation end-products antibody.57 These antibodies have, in general, good specificity, but sensitivity lower than that of anti-CCP for diagnosing RA.

The recent criteria for classifying RA,58 jointly established by the American College of Rheumatology (ACR) committee and the 2010 European League Against Rheumatism (EULAR), have defined in the "autoantibodies" item only RF and ACPA. According to these criteria, the RF or ACPA levels have been established as negative, and low- and high-positive. Considering that both RF and anti-CCP are measured in IU, the result is considered negative when the value found is < the upper limit of normal (ULN) for the laboratory and assay; low-positive, when the result is > the ULN, but < three times the ULN; and high-positive when the value found is > three times the ULN.

Genetic assessment

Several genetic markers have been described associated with the occurrence of RA. However, the only well-established genetic alteration associated with RA, with a strong level of evidence, has been the identification of HLA-DRB1 alleles (presence of shared epitope) and of PTPN22 genes.59 The interaction between HLA-DRB1, smoking, and anti-CCP determines a more severe disease profile of worse prognosis. However, although useful for characterizing patients with worse prognosis, the high costs of HLA-DRB1 typifying still limit its use in daily practice.59,60

IMAGING TECHNIQUES

Conventional radiography

Conventional radiography is the most used imaging technique for assessing the structural joint damage in RA. In addition to being useful for diagnosis, it is important when repeated at regular intervals to monitor disease progression.61

The initial radiographic findings include enlarged juxta-articular soft tissues and osteopenia. The most characteristic lesions, such as a reduction in the joint space and bone erosions, appear later.

The presence of bone erosion should be considered a risk factor for development of persistent arthritis when observed in early disease.62 It relates to functional limitation, and, consequently, to worse prognosis.63

Ultrasound

The sensitivity of musculoskeletal ultrasound and magnetic resonance in detecting structural joint damage is greater than that of conventional radiography.64

Ultrasonography, when performed by an expert in musculoskeletal diseases, is useful for the early detection and monitoring of inflammatory activity and signs of joint destruction.65

When compared to magnetic resonance, it is a less expensive exam, and not contraindicated for patients with metallic implants or claustrophobia. Moreover, it allows a dynamic joint examination, a comparative contralateral assessment, as well as the assessment of other anatomic structures.64-67

The use of power Doppler and color Doppler can complement the exam and aid in characterizing inflammatory activity.68

Magnetic resonance

Magnetic resonance is the most sensitive method to detect early RA alterations. It allows the assessment of structural changes in soft tissues, bones, and cartilages, in addition to erosions, prior to conventional radiographies.69

In addition to RA conventional radiographic findings, magnetic resonance can detect bone edema, which proved to be a predictor of bone erosion.65

In Brazil, factors such as its high cost and method standardization have limited its use in clinical practice.

Table 2 shows the advantages and disadvantages of the imaging techniques used to assess patients with RA.

Other imaging techniques

Other imaging techniques, such as bone scintigraphy and computed tomography, are not currently recommended for RA diagnosis.70-72

NEW CLASSIFICATION CRITERIA OF RA

RA classification has been essentially based on criteria introduced by the ACR in 1987,73 and shown in Table 3, which are not suitable for early RA.74 The ACR classification criteria for RA were developed based on individuals with long-term RA, and were considered the standard for selecting patients for clinical studies. Such criteria have sensitivity of 91%-94% and specificity of 89% for established RA. However, they include characteristics less frequent in RA of recent onset, such as radiographic alterations (erosions) and rheumatoid nodules, being considered suboptimal for identifying individuals with early RA (sensitivity of 40%-90% and specificity of 50%-90%).75

Therefore, it became necessary to establish new criteria for RA classification, especially focusing on the early stage of disease.58

The ACR/EULAR new RA classification criteria can be applied to all patients, as long as they meet the two basic requirements:

1) have at least one joint with definite clinical synovitis at the time of assessment;

2) the criteria may be applied only to those patients for whom the observed synovitis is not better explained by another diagnosis.

The criteria proposed (Table 4) are based on a scoring system of direct sum. The manifestations are divided into four domains: joint involvement, serology, duration of symptoms, and acute-phase reactants. Affected joint count can use imaging techniques (ultrasound and magnetic resonance) in case of doubt. A score > 6 classifies a patient as having RA.58 The criteria can be fulfilled in a prospective or retrospective way, in the presence of adequate recording.

It is worth noting that, if a patient has a history consistent with RA, even in the absence of documentation, and typical radiographic erosions, the patient can be directly classified as having RA, regardless of meeting the criteria.58

The new 2010 criteria are not diagnostic, but classifying. Their function is basically defining homogeneous populations for studies.

The clinical diagnosis is extremely complex and comprises several aspects that can hardly be summarized in the form of a scoring criteria.58 Occasionally, formal criteria can serve as a guide for establishing clinical diagnosis.

Several aspects regarding the new criteria need to be carefully analyzed before they are universally accepted. However, these criteria must be validated in different populations, including Brazilian cohorts of early RA.

DISEASE ACTIVITY ASSESSMENT

Once established the diagnosis of RA, its prognostic factors, and the occurrence of comorbidities, it is important to characterize parameters useful for adequately monitoring disease activity still in the early assessment of RA.

Some validated parameters that correlate with RA activity are as follows: patient visual analogue scale regarding pain; patient and physician visual analogue scale regarding disease activity; number of tender and swollen joints; instruments for assessing functional capacity (such as the Health Assessment Questionnaire - HAQ); acute phase reactants (ESR and/or CRP); fatigue; duration of morning stiffness; radiography of the hands, wrists and feet; quality of life indices, such as, the 36-Item Short Form Health Survey (SF-36).76-81

Through these parameters, combined disease activity indices have been created and validated. The major indices are as follows: Disease Activity Score in 28 joints (DAS28); Simplified Disease Activity Index (SDAI); and the Clinical Disease Activity Index (CDAI). These indices use a more simplified count of 28 joints (PIP, MCP, wrists, elbows, shoulders, and knees, bilaterally) and determine a numerical value for RA activity. Tables 5, 6, and 7 show how to calculate and use such indices.82-91

There is a good correlation between these combined disease activity indices (CDAI, SDAI and DAS28), and any of them can be used in isolation. Patients undergoing remission or low disease activity, according to any of these indices, also have slower radiographic progression, and better functional evolution. Thus, patients should always be kept in clinical remission, or, if this is not possible, at least in a state of low disease activity.83

QUALITY OF LIFE AND DISABILITY

Assessing quality of life and disability in RA is of major importance to better understand the disease course.92

Rheumatoid arthritis, even in its early phase, can cause considerable impact on health-related quality of life (HRQoL).93 HRQoL is a very wide concept, which can be simplified as the impact of health on the individual's functional ability and well-being perceived in the physical, mental, and social life domains.94

Several instruments have been proposed aimed at assessing the quality of life of patients with RA, detecting changes in the health status over time, and at assessing the prognosis, risks and benefits of a certain therapeutic intervention, including generic and specific instruments.95-116 The most used are the HAQ, including the modified (mHAQ) and the disability index (HAQ-DI) versions, in addition to the SF-36.

Studies in a Brazilian cohort of early RA have shown an important impact on quality of life at the time of diagnosis, according to assessment using HAQ and SF-36.117

PROGNOSIS DETERMINATION

A great progress has been made in identifying the clinical and laboratory characteristics associated with greater joint destruction and worse prognosis. These characteristics include female sex; smoking; disease onset at an earlier age; low socioeconomic level; presence of high titers of autoantibodies, such as RF and anti-CCP; persistently high ESR and CRP; large number of swollen joints; presence of extra-articular manifestations; high indices of inflammatory disease activity, such as DAS and its variations, SDAI or CDAI; and presence of early erosions (Table 8).118-128 Another factor associated with worse prognosis is the presence of shared epitope, but its use is limited because it is not commercially available.129,130

Guidelines of the Brazilian Society of Rheumatology for diagnosis and early assessment of rheumatoid arthritis

Based on the previous considerations and on peculiar aspects of the Brazilian socioeconomic reality, the experts of the Rheumatoid Arthritis Committee of the Brazilian Society of Rheumatology have issued the guidelines summarized in Table 9 for diagnosis and early assessment of patients with a possible diagnosis of RA.

CONCLUSIONS

This consensus was elaborated by the Rheumatoid Arthritis Committee of the Brazilian Society of Rheumatology aiming at providing guidelines for diagnosis and early assessment of RA in Brazil. Because of the large dimension of the Brazilian territory and diversity between the Brazilian macroregions, peculiar characteristics regarding the differential diagnosis and access to certain technologies (laboratory or imaging techniques) may exist in different locations.

Rheumatoid arthritis should be diagnosed, mainly in its early phase.

When not diagnosed, and, consequently, not treated adequately, a patient with RA has an increased risk to progress with persistent inflammation and progressive joint destruction. The immediate involvement of rheumatologist in the assessment of a patient with arthritis is required, considering mainly his/her greater experience and acquaintance with the possible differential diagnoses and the investigation approach.

Despite the recent guidelines about RA diagnosis, the topic should be reviewed, considering the aspects of the Brazilian reality.

Thus, the final purpose in establishing guidelines for RA is to support Brazilian rheumatologists, by using evidence obtained in controlled studies, aiming at making the diagnostic approach of RA uniform within the Brazilian socioeconomic context.

Because the knowledge in this area progresses extremely rapidly, guidelines should be regularly and periodically updated.

ACKNOWLEDGEMENTS

The authors thank Dr. José Alexandre Mendonça and other members of the Imaging Committee of the Brazilian Society of Rheumatology for reviewing the text about the imaging techniques for RA diagnosis.

REFERENCES

  • 1
    Lee DM, Weinblatt ME. Rheumatoid arthritis. Lancet 2001; 358:903-11.
  • 2
    Alarcón GS. Epidemiology of rheumatoid arthritis. Rheum Dis Clin North Am 1995; 21:589-604.
  • 3
    Silman AJ, Pearson JE. Epidemiology and genetics of rheumatoid arthritis. Arthritis Res 2002; 4:S265-72.
  • 4
    Marques-Neto JF, Gonçalves ET, Langen LFOB, Cunha MFL, Radominski S, Oliveira SM et al Multicentric study of the prevalence of adult rheumatoid arthritis in Brazilian population samples. Rev Bras Reumatol 1993; 33:169-73.
  • 5
    Emery P. The optimal management of early rheumatoid arthritis: the key to preventing disability. British J Rheumatol 1994; 33:765-8.
  • 6
    Sokka T. Work disability in early rheumatoid arthritis. Clin Exp Rheumatol 2003; 21:S71-4.
  • 7
    Chehata JC, Hassell AB, Clarke SA, Mattey DL, Jones MA, Jones W et al Mortality in rheumatoid arthritis: relationship to single and composite measures of disease activity. Rheumatology 2001; 40:447-52.
  • 8
    van der Horst-Bruinsma IE, Speyer I, Visser H, Breedvelt FC, Hazes GM. Diagnosis and course of early-onset arthritis: results of a special early arthritis clinic compared to routine patient care. Br J Rheumatol 1998; 37:1084-8.
  • 9
    Majithia V, Geraci SA. Rheumatoid arthritis: diagnosis and management. Am J Med 2007; 120:936-9.
  • 10
    Haque UJ, Bathon JM. The role of biological in early rheumatoid arthritis. Best Pract & Res Clin Rheum 2005; 19:179-89.
  • 11
    Cabral D, Katz JN, Weinblatt ME, Ting G, Avorn J, Solomon DH. Development and assessment of indicators of rheumatoid arthritis severity: results of a Delphi panel. Arthritis Rheum 2005; 53:61-6.
  • 12
    Sokka T, Kautiainen H, Pincus T, Verstappen SM, Aggarwal A, Alten R et al. Work disability remains a major problem in rheumatoid arthritis in the 2000s: data from 32 countries in the QUEST-RA study. Arthritis Res Ther 2010; 12(2):R42.
  • 13
    Saag KG, Teng GG, Patkar NM, Anuntiyo J, Finney C, Curtis JR et al. American College of Rheumatology. American College of Rheumatology 2008 recommendations for the use of nonbiologic and biologic disease-modifying antirheumatic drugs in rheumatoid arthritis. Arthritis Rheum 2008; 59(6):762-84.
  • 14
    Smolen JS, Landewé R, Breedveld FC, Dougados M, Emery P, Gaujoux-Viala C et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs. Ann Rheum Dis 2010; 69(6):964-75.
  • 15
    da Mota LM, Laurindo IM, dos Santos Neto LL. Demographic and clinical characteristics of a cohort of patients with early rheumatoid arthritis. Rev Bras Reumatol 2010; 50(3):235-48.
  • 16
    Louzada-Junior P, Souza BDB, Toledo RA, Ciconelli RM. Descriptive analysis of the demographical and clinical characteristics of the patients with rheumatoid arthritis in the State of São Paulo, Brazil. Rev Bras Reumatol 2007; 47(2):84-90.
  • 17
    Schoels M, Wong J, Scott DL, Zink A, Richards P, Landewé R et al. Economic aspects of treatment options in rheumatoid arthritis: a systematic literature review informing the EULAR recommendations for the management of rheumatoid arthritis. Ann Rheum Dis 2010; 69(6):995-1003.
  • 18
    de Azevedo AB, Ferraz MB, Ciconelli RM. Indirect costs of rheumatoid arthritis in Brazil. Value Health 2008; 11(5):869-77.
  • 19
    Chermont GC, Kowalski SC, Ciconelli RM, Ferraz MB. Resource utilization and the cost of rheumatoid arthritis in Brazil. Clin Exp Rheumatol 2008; 26(1):24-31.
  • 20
    Mease PJ. Inflammatory musculoskeletal disease: identification and assessment. J Rheumatol 2011; 38(3):557-61.
  • 21
    Scott DL, Wolfe F, Huizinga TW. Rheumatoid arthritis. Lancet 2010; 376(9746):1094-108.
  • 22
    Dixon WG, Symmons DP. Does early rheumatoid arthritis exist? Best Pract Res Clin Rheumatol 2005; 19:37-53.
  • 23
    Woolf AD. How to assess musculoskeletal conditions. History and physical examination. Best Pract Res Clin Rheumatol 2003; 17(3):381-402.
  • 24
    Hazes JM, Hayton R, Silman AJ. A reevaluation of the symptom of morning stiffness. J Rheumatol 1993; 20(7):1138-42.
  • 25
    Yazici Y, Pincus T, Kautiainen H, Sokka T. Morning stiffness in patients with early rheumatoid arthritis is associated more strongly with functional disability than with joint swelling and erythrocyte sedimentation rate. J Rheumatol 2004; 31:1723-6.
  • 26
    Turesson C, Eberhardt K, Jacobsson LT, Lindqvist E. Incidence and predictors of severe extra-articular disease manifestations in an early rheumatoid arthritis inception cohort. Ann Rheum Dis 2007; 66(11):1543-44.
  • 27
    Goeldner I, Skare TL, de Messias Reason IT, Nisihara RM, Silva MB, da Rosa Utiyama SR. Association of anticyclic citrullinated peptide antibodies with extra-articular manifestations, gender, and tabagism in rheumatoid arthritis patients from southern Brazil. Clin Rheumatol 2011; 22:[epub ahead of print]
  • 28
    Devlin J. The acute phase and function in early rheumatoid arthritis. C-reactive protein levels correlate with functional outcome. J Rheumatol 1997; 24:9-13.
  • 29
    da Mota LM, dos Santos Neto LL, de Carvalho JF. Autoantibodies and other serological markers in rheumatoid arthritis: predictors of disease activity? Clin Rheumatol 2009; 28(10):1127-34.
  • 30
    da Mota LM, dos Santos Neto LL, Burlingame R, Ménard HA, Laurindo IM. Laboratory characteristics of a cohort of patients with early rheumatoid arthritis. Rev Bras Reumatol 2010; 50(4):375-88.
  • 31
    Visser H. Early diagnosis of rheumatoid arthritis. Best Pract & Res Clin Rheum 2005; 19:55-72.
  • 32
    Renaudineau Y, Jamin C, Saraux A, Youinou P. Rheumatoid factor on a daily basis. Autoimmunity 2005; 38:11-6.
  • 33
    Vittecoq O, Pouplin S, Krzanowska K, Jouen-Beades F, Menard JF, Gayet A et al. Rheumatoid factor is the strongest predictor of radiological progression of rheumatoid arthritis in a three-year prospective study in community-recruited patients. Rheumatology 2003; 42(8):939-46.
  • 34
    Visser H, Gelinck LB, Kampfraath AH, Breedveld FC, Hazes JM. Diagnostic and prognostic characteristics of the enzyme linked immunosorbent rheumatoid factor assays in rheumatoid arthritis. Ann Rheum Dis 1996; 55:157-61.
  • 35
    Wolfe F, Cathey MA, Roberts FK. The latex test revised rheumatoid factor testing in 8,287 rheumatic disease patients. Arthritis Rheum 1991; 34:951-60.
  • 36
    Vallbracht I, Rieber J, Oppermann M, Förger F, Siebert U, Helmke K. Diagnostic and clinical value of anti-cyclic citrullinated peptide antibodies compared with rheumatoid factor isotypes in rheumatoid arthritis. Ann Rheum Dis 2004; 63:1079-84.
  • 37
    Greiner A, Plischke H, Kellner H, Gruber R. Association of anti-cyclic citrullinated peptide antibodies, anti-citrullin antibodies, and IgM and IgA rheumatoid factors with serological parameters of disease activity in rheumatoid arthritis. Ann N Y Acad Sci 2005; 1050:295-303.
  • 38
    Raza K, Breese M, Nightingale P, Kumar K, Potter T, Carruthers DM et al. Predictive value of antibodies to cyclic citrullinated peptides in patients with very early inflammatory arthritis. J Rheumatol 2005; 32:231-8.
  • 39
    Klareskog L, Widhe M, Hermansson M, Rönnelid J. Antibodies to citrullinated proteins in arthritis: pathology and promise. Curr Opin Rheumatol 2008; 20:300-5.
  • 40
    van der Linden MP, van der Woude D, Ioan-Facsinay A, Levarht EW, Stoeken-Rijsbergen G, Huizinga TW et al. Value of anti-modified citrullinated vimentin and third-generation anti-cyclic citrullinated peptide compared with second-generation anti-cyclic citrullinated peptide and rheumatoid factor in predicting disease outcome in undifferentiated arthritis and rheumatoid arthritis. Arthritis Rheum 2009; 60:2232-41.
  • 41
    Ioan-Facsinay A, Willemze A, Robinson DB, Peschken CA, Markland J, van der Woude D et al. Marked differences in fi ne specificity and isotype usage of the anti-citrullinated protein antibody in health and disease. Arthritis Rheum 2008; 58:3000-08.
  • 42
    van der Helm-van Mil AHM, Verpoort KN, Breedveld FC, Toes REM, Huizinga TWJ. Antibodies to citrullinated proteins and differences in clinical progression of rheumatoid arthritis. Arthritis Res Ther 2005; 7:R949-58.
  • 43
    Scott DL, Wolf F, Huizinga TWJ. Rheumatoid arthritis. Lancet 2010; 376:1094-108.
  • 44
    Mutlu N, Bicakcigil M, Tasan DA, Kaya A, Yavuz S, Ozden AI. Comparative performance analysis of 4 different anti-citrullinated protein assays in the diagnosis of rheumatoid arthritis. J Rheumatol 2009; 36(3):491-500.
  • 45
    Santiago M, Baron M, Miyachi K, Fritzler MJ, Abu-Hakima M, Leclercq S et al. A comparison of the frequency of antibodies to cyclic citrullinated peptides using a third generation anti-CCP assay (CCP3) in systemic sclerosis, primary biliary cirrhosis and rheumatoid arthritis. Clin Rheumatol 2008; 27:77-83.
  • 46
    Anjos LME, Pereira IA, d`Orsi E, Seaman A, Burlingame RW, Morato EF. A comparative study of IgG second and third generation anti-cyclic citrullinated peptide (CCP) ELISAs and their combinaton with IgA third generation ELISA for the diagnosis of RA. Clin Reumatol 2009; 28:153-8.
  • 47
    Caro-Oleas JL, Fernandez-Suarez A, Reneses-Casteros S, Porrino C, Nunes-Roldan A, Wichmann-Schlipf I. Diagnostic usefulness of a third generation anti-cyclic citrulline antibody test in patients with recent-onset polyarthritis. Clin Chem Lab Med 2007; 45:1396-401.
  • 48
    Lutteri L, Malaise M, Chapelle JP. Comparison of second- and third-generation anti-cyclic citrullinated peptide antibodies assays for detecting rheumatoid arthritis. Clin Chim Acta 2007; 386:76-81.
  • 49
    Besada E, Nikolaisen C, Nossent H. Diagnostic value of antibodies against mutated citrullinated vimentin for rheumatoid arthritis. Clin Exp Rheumatol 2011; 29(1):85-8.
  • 50
    Ursum J, Nielen MMJ, van Schaardenburg D, van der Horst AR, van de Stadt RJ, Dijkmans BA Antibodies to mutated citrullinated vimentin and disease activity score in early arthritis: a cohort study. Arthritis Res Ther 2008; 10:R12.
  • 51
    Mathson L, Mullazei M, Wick MC, Sjöberg O, van Vollenhoven R, Klareskog L et al. Antibodies against citrullinated vimentin in rheumatoid arthritis: higher sensitivity and extended prognostic value concerning future radiographic progression as compared with antibodies against cyclic citrullinated peptides. Arthritis Rheum 2008; 58:36-45.
  • 52
    Cordonnier C, Meyer O, Palazzo E, De Bandt M, Elias A, Nicaise P et al. Diagnostic value of anti-RA33 antibody, antikeratin antibody, antiperinuclear factor and antinuclear antibody in early rheumatoid arthritis: comparison with rheumatoid factor. Br J Rheumatol 1996; 35:620-4.
  • 53
    Vittecoq O, Incaurgarat B, Jouen-Beades F, Legoedec J, Letourneur O, Rolland D et al. Autoantibodies recognizing citrullinated rat filaggrin in na ELISA using citrullinatted and non-citrullinated recombinant proteins as antigens are highly diagnostic for rheumatoid arthritis. Clin Exp Rheumatol 2004; 135:173-80.
  • 54
    Nielen MM, van der Horst AR, van Schaardenburg D, van der Horst-Bruinsma IE, van de Stadt RJ, Aarden L et al. Antibodies to citrullinated human fibrinogen (ACF) have diagnostic and prognostic value in early arthritis. Ann Rheum Dis 2005; 64:1199-204.
  • 55
    Graudal N, Svenson M, Tarp U, Garred P, Jurik A, Bendtzen K. Autoantibodies against interleukin-1 alfa in rheumatoid arthritis: association with long-term radiographic outcome. Ann Rheum Dis 2002; 61:598-602.
  • 56
    Saulot V, Vittecoq O, Charlionet R, Fardellone P, Lange C, Marvin L et al. Presence of autoantibodies to the glycolytic enzyme alphaenolase in sera from patients with early rheumatoid arthritis. Arthritis Rheum 2002; 46:1196-201.
  • 57
    Newkirk MM, Goldbach-Mansky R,Lee J,Hoxworth J,McCoy A,Yarboro C et al. Advanced glycation end-product (AGE)-damaged IgG and IgM autoantivodies to IgG-AGE in patients with early synovitis. Arthritis Res Ther 2003; 5:R82-90.
  • 58
    Aletaha D, Neogi T, Silman AJ, Funovits J, Felson DT, Bingham CO 3rd. 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Ann Rheum Dis 2010; 69(9):1580-8.
  • 59
    Klareskog L, Catrina AI, Paget S. Rheumatoid arthritis. Lancet 2009; 373:659-72
  • 60
    McInnes IB, ODell JR. State-of-the-art: rheumatoid arthritis. Ann Rheum Dis 2010; 69:1898-906.
  • 61
    American College of Rheumatology Subcommittee on Rheumatoid Arthritis: Guidelines for the management of rheumatoid arthritis: 2002 Update. Arthritis Rheum 2002; 46:328-46.
  • 62
    Visser H, le CS, Vos K, Breedveld FC, Hazes JM. How to diagnose rheumatoid arthritis early: a prediction model for persistent (erosive) arthritis. Arthritis Rheum 2002; 46:357-65.
  • 63
    Kaarela K. Prognostic factors and diagnostic criteria in early rheumatoid arthritis. Scand J Rheumatol Suppl 1985; 57:1-54.
  • 64
    Jain M, Samuels J. Musculoskeletal ultrasound in the diagnosis of rheumatic disease. Bulletin of the NYU Hospital for Joint Diseases 2010; 68(3):183-90.
  • 65
    Rahmani M, Chegini H, Najafizadeh SR, Azimi M, Habiblollahi P, Shakiba M. Detection of bone erosion in early rheumatoid arthritis: ultrasonography and conventional radiography versus non-contrast magnetic resonance imaging. Clin Rheumatol 2010; 29:883-91.
  • 66
    Wakefield RJ, D'Agostinho MA, Iagnocco A Filippucci E, Backhaus M, Scheel AK et al. The OMERACT ultrasound group: status of current activities and research direction. J Rheumatol 2007; 34:848-51.
  • 67
    Fernandes EA, Castro Júnior MR, Mistraud SAV, Kubota ES, Fernandes ARC. Ultrasonography in rheumatoid arthritis: applicability and expectations. Rev Bras Reumatol 2008; 48:25-30.
  • 68
    Iagnocco A, Epis O, Delle Sedie A, Meenagh G, Filippucci E, Riente L et al. Ultrasoud imaging for the rheumatologist. XVII. Role of colour doppler and power doppler. Clin Exp Rheumatol 2008; 26:759-62.
  • 69
    Dohn UM, Ejbjerg BJ, Hasselquist M, Narvestad E, Møller J, Thomsen HS et al. Detection of bone erosions in rheumatoid arthritis wrist joints with magnetic resonance imaging, computed tomography and radiography. Arthritis Res Ther 2008;10(1):R25.
  • 70
    Brown AK, Wakefield RJ, Conaghan PG, Karim Z, OConnor PJ, Emery P, New approaches to imaging early infl ammatory arthritis. Clin Exp Rheumatol 2004; 22:S18-25.
  • 71
    Kubota K, Ito K, Morooka M, Mitsumoto T, Kurihara K, Yamashita H et al. Whole -body FDG-PET/CT on rheumatoid arthritis of large joints. Ann Nucl Med 2009; 23(9):783-91.
  • 72
    Basu S, Zhuang H, Torigian DA, Rosenbaum J, Chen W, Alayi A. Functional imaging of inflammatory diseases using nuclear medicine techniques. Semin Nucl Med 2009; 29:124-45.
  • 73
    Arnett FC, Edworthy SM, Bloch DA, McShane DJ, Fries JF, Cooper NS et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 1988; 31:315-24.
  • 74
    Saraux A, Berthelot JM, Chales G, Le Henaff C, Thorel JB, Hoang S et al. Ability of the American College of Rheumatology 1987 criteria to predict rheumatoid arthritis in patients with early arthritis and classification of these patients two years later. Arthritis Rheum 2001; 44:2485-91.
  • 75
    Banal F, Dougados M, Combescure C, Gossec L. Sensitivity and specificity of the American College of Rheumatology 1987 criteria for the diagnosis of rheumatoid arthritis according to disease duration: a systematic literature review and meta-analysis. Ann Rheum Dis 2009; 68:1184-91.
  • 76
    Scott DL, Panayi GS, van Riel PL, Smolen J, van de Putte LB. Disease activity in rheumatoid arthritis: preliminary report of the Consensus Study Group of the European Workshop for Rheumatology Research. Clin Exp Rheumatol 1992; 10:521-5.
  • 77
    Felson DT, Anderson JJ, Boers M, Bombardier C, Chernoff M, Fried B et al The American College of Rheumatology preliminary core set of disease activity measures for rheumatoid arthritis clinical trials. The Committee on Outcome Measures in Rheumatoid Arthritis Clinical Trials. Arthritis Rheum 1993; 36:729-40.
  • 78
    Boers M, Tugwell P, Felson DT, van Riel PL, Kirwan JR, Edmonds JP et al. World Health Organization and International League of Associations for Rheumatology core endpoints for symptom modifying antirheumatic drugs in rheumatoid arthritis clinical trials. J Rheumatol Suppl 1994; 41:86-9.
  • 79
    Tugwell P, Bombardier C. A methodologic framework for developing and selecting endpoints in clinical trials. J Rheumatol 1982; 9:758-62.
  • 80
    van der Heijde DM, vant Hof MA, van Riel PL, van Leeuwen MA, van Rijswijk MH, van de Putte LB. Validity of single variables and composite indices for measuring disease activity in rheumatoid arthritis. Ann Rheum Dis 1992; 51:177-81.
  • 81
    Goldsmith CH, Boers M, Bombardier C, Tugwell P. Criteria for clinically important changes in outcomes: development, scoring and evaluation of rheumatoid arthritis patient and trial profiles. OMERACT Committee. J Rheumatol 1993; 20:561-5.
  • 82
    Aletaha D, Nell VP, Stamm T, Uffmann M, Pflugbeil S, Machold K et al Acute phase reactants add little to composite disease activity indices for rheumatoid arthritis: validation of a clinical activity score. Arthritis Res Ther 2005; 7:R796-806.
  • 83
    Aletaha D, Smolen JS.The Simplified Disease Activity Index (SDAI) and the Clinical Disease Activity Index (CDAI): a review of their usefulness and validity in rheumatoid arthritis. Clin Exp Rheumatol 2005; 23(Suppl. 39):S100-8.
  • 84
    Schulz KF, Grimes DA. Multiplicity in randomized trials I: endpoints and treatments. Lancet 2005; 365:1591-5.
  • 85
    van der Heijde DM, van t Hof M, van Riel PL, van de Putte LB. Development of a disease activity score based on judgment in clinical practice by rheumatologists. J Rheumatol 1993; 20:579-81.
  • 86
    Ritchie DM, Boyle JA, McInnes JM, Jasani MK, Dalakos TG, Grieveson P et al. Clinical studies with an articular index for the assessment of joint tenderness in patients with rheumatoid arthritis. Q J Med 1968; 37:393-406.
  • 87
    Smolen JS, Breedveld FC, Schiff MH, Kalden JR, Emery P, Eberl G et al. A simplified disease activity index for rheumatoid arthritis for use in clinical practice. Rheumatology 2003; 42:244-57.
  • 88
    Siegel JN, Zhen BG. Use of the American College of Rheumatology N (ACR-N) index of improvement in rheumatoid arthritis: argument in favor. Arthritis Rheum 2005; 52:1637-41.
  • 89
    van Gestel AM, Prevoo ML, van t Hof MA, van Rijswijk MH, van de Putte LB, van Riel PL. Development and validation of the European League Against Rheumatism response criteria for rheumatoid arthritis. Comparison with the preliminary American College of Rheumatology and the World Health Organization/International League Against Rheumatism Criteria. Arthritis Rheum 1996; 39:34-40.
  • 90
    van Gestel AM, Haagsma CJ, van Riel PL. Validation of rheumatoid arthritis improvement criteria that include simplified joint counts. Arthritis Rheum 1998; 41:1845-50.
  • 91
    Aletaha D, Funovits J, Wards MM, Smolen JS, Kvien TK. Perception of improvement in patients with rheumatoid arthritis varies with disease activity levels at baseline. Arthritis Rheum 2009; 61(3):313-20.
  • 92
    Brandão L, Ferraz MB, Zerbini CAF. Evaluation of quality of life in rheumatoid arthritis. Rev Bras Reumatol 1997; 37:275-81.
  • 93
    Kosinski M, Kujawski SC, Martin R, Wanke LA, Buatti MC, Ware JR JE et al. Health-related quality of life in early rheumatoid arthritis: impact of disease and treatment response. Am J Manag Care 2002; 8:231-40.
  • 94
    Ward MM. Outcome measurement: health status and quality of life. Curr Opin Rheumatol 2004; 16:96-101.
  • 95
    Walker JG, Littlejohn GO. Measuring quality of life in rheumatic conditions. Clin Rheumatol 2007; 26:671-3.
  • 96
    Chambers LW, MacDonald LA, Turgwell P, Buchanan WW, Kraag G. The McMaster Health Index Questionnaire as a measure of quality of life for patients with rheumatoid disease. J Rheumatol 1982; 9:780-4.
  • 97
    Brook RH, Ware Jr JE, Davies-Avery A, Stewart AL, Donald CA, Rogers WH et al. Overview of adult health status measures fielded in Rand's Health Insurance Study. Med Care 1979; 17:1-131.
  • 98
    Gilson BS, Gilson JS, Bergner M, Bobbit RA, Kressel S, Pollard WE et al. The Sickness Impact Profile: development of an outcome measure of health care. AJPH 1975; 65:1302-10.
  • 99
    Bergner M, Babbitt RA, Pollard WE. The sickness impact profile: validation of a health status measure. Med Care 1976; 14:57-67.
  • 100
    Jenkinson C, Fitzpatrick R, Argyle M. The Nottingham Health Profile: an analysis of its sensitivity in differentiating illness groups. Soc Sci Med 1988; 17: 1411-14.
  • 101
    Ware JE, Sherbourne CD: The MOS 36-Item Short-Form Health Survey (SF-36). Conceptual framework and item selection. Med Care 1992; 30:473-83.
  • 102
    Steinbrocker O, Traeger CH, Batterman RC. Therapeutic criteria in rheumatoid arthritis. JAMA 1949;140:659-62
  • 103
    Katz S, Fors AB, Jackson BA, Jaffe MW. Studies of illness in the aged. The Index of ADL: a standardized measure of biological and psychosocial function. JAMA 1963;185:914-9
  • 104
    Donaldson SW, Wagner CC, Greshan GE. A unified ADL evaluation form. Arch Phys Med Rehabil 1973; 54:175-9.
  • 105
    Lee P, Jasani MK, Buchanan WN. Evaluation of a functional index in rheumatoid arthritis. Scand J Rheumatol 1973; 2:71-77
  • 106
    Convery FR, Minteer MA, Amiel D, Connett KL: Poliarticular disability: a functional assessment. Arch Phys Med Rehabil 1977; 58:494-9.
  • 107
    Jette AM. Functional Status Index: reliability of a chronic disease evaluation instrument. Arch Phys Med Rehabil 1980; 61:395-401.
  • 108
    Fries JF, Spitz PW, Kraines RG, Holman HR. Measurement of patient outcome in arthritis. Arthritis Rheum 1980; 23:137-45.
  • 109
    Meenan RF, Gertman PM, Mason JH. The Arthritis Impact Measures Scales. Arthritis Rheum 1980; 23:146-52.
  • 110
    Bell MJ, Bombardier C, Tugwell P. Measurement of functional status, quality of life and utility in rheumatoid arthritis. Arthritis Rheum 1990; 33:591-601.
  • 111
    Pincus T, Summey JA, Soraci Jr SA, Wallston KA, Hummon NP. Assessment of patient satisfaction in activities of daily living using a modified Stanford Health Assessment Questionnaire. Arthritis Rheum 1983; 26:1346-53.
  • 112
    Tugwell P, Bombardier C, Buchanan WW, Goldsmith CH, Grace E, Hanna B. The MACTAR patient preference disability questionnaires: an individualized functional priority approach for assessment of improvement in physical disability in clinical trials in rheumatoid arthritis. J Rheumatol 1987; 14:446-51.
  • 113
    Huiskes CJAE, Kraaimaat FW, Bijlsma JTW. Development of a selfreport questionnaire to assess the impact of rheumatic diseases on health and lifestyle. J Rehabil Sci 1990; 3:65-70.
  • 114
    Hochberg MC, Chang RW, Dwosh I, Lindsey S, Pincus T, Wolf F. The American College of Rheumatology 1991 revised criteria for the classification for global functional status in rheumatoid arthritis. Arthritis Rheum 1992; 35:498-502.
  • 115
    Meenan RF, Mason JH, Anderson JJ, Guccione AA, Kaziz LE. AIMS-2: The content and properties of revised and expanded Arthritis Impact Measurement Scales Health Status Questionnaire. Arthritis Rheum 1992; 35:1-10.
  • 116
    Mason JH, Anderson JJ, Meenan RF, Haralson KM, Lewis-Stevens D, Kaine JL: The Rapid Assessment of Disease Activity in Rheumatology (RADAR) Questionnaire: validity and sensitivity to change of a patient self-report measure of joint count and clinical status. Arthritis Rheum 1992; 35:56-62.
  • 117
    da Mota LMH, Laurindo IMM, Santos-Neto LL. Prospective evaluation of the quality of life in a cohort of patients with early rheumatoid arthritis. Rev Bras Reumatol 2010; 50(3):249-61.
  • 118
    Bértolo MB, Brenol CV, Schainberg CG, Neubarth F, Lima FAC, Laurindo IM et al. Update on the Brazilian Consensus for the diagnosis and treatment of rheumatoid arthritis. Rev Bras Reumatol 2007; 47:151-9.
  • 119
    van der Heijde DM, van Riel PL, van Leeuwen MA, van't Hof MA, van Rijswijk MH, van de Putte LB. Prognostic factors for radiographic damage and physical disability in early rheumatoid arthritis. A prospective follow-up study of 147 patients. Br J Rheumatol 1992; 31:519-25.
  • 120
    van Gaalen FA, Linn-Rasker SP, van Venrooij WJ, de Jong BA, Breedveld FC, Verweij CL et al. Autoantibodies to cyclic citrullinated peptides predict progression to rheumatoid arthritis in patients with undifferentiated arthritis: a prospective cohort study. Arthritis Rheum 2004; 50:709-15.
  • 121
    Meyer O, Labarre C, Dougados M, Goupille P, Cantagrel A, Dubois A et al. Anticitrullinated protein/peptide antibody assays in early rheumatoid arthritis for predicting five year radiographic damage. Ann Rheum Dis 2003; 62:120-6.
  • 122
    Hider SL, Silman AJ, Thomson W et al Can clinical factors at presentation be used to predict outcome of treatment with methotrexate in patients with early inflammatory polyarthritis? Ann Rheum Dis 2009; 68:57-62
  • 123
    Lindqvist E, Eberhardt K, Bendtzen K, Lunt M, Bunn D, Symmons DP. Prognostic laboratory markers of joint damage in rheumatoid arthritis. Ann Rheum Dis 2005; 64:196-201.
  • 124
    Machold KP, Stamm TA, Nell VP, Pflugbeil S, Aletaha D, Steiner G et al. Very recent onset rheumatoid arthritis: clinical and serological patient characteristics associated with radiographic progression over the first years of disease. Rheumatology (Oxford) 2007; 46:342-9.
  • 125
    Vastesaeger N, Xu S, Aletaha D, St Clair EW, Smolen JS. A pilot risk model for the prediction of rapid radiographic progression in rheumatoid arthritis. Rheumatology (Oxford) 2009; 48:1114-21.
  • 126
    Visser K, Goekoop-Ruiterman YPM, de Vries-Bouwstra JK, Ronday HK, Seys PE, Kerstens PJ et al A matrix risk model for the prediction of rapid radiographic progression in patients with rheumatoid arthritis receiving different dynamic treatment strategies: post hoc analyses from the BeSt study. Ann Rheum Dis 2010; 69:1333-37.
  • 127
    Markatseli TE, Voulgari PV, Alamanos Y, Drosos AA. Prognostic Factors of Radiological Damage in Rheumatoid Arthritis: a 10-year retrospective study. J Rheumatol 2011; 38(1):44-52.
  • 128
    Jacobi CE, Mol GD, Boshuizen HC, Rupp I, Dinant HJ, Van Den Bos GA. Impact of socioeconomic status on the course of rheumatoid arthritis and on related use of health care services. Arthritis Rheum 2003; 49(4):567-73.
  • 129
    Villeneuve E, Nam J, Emery P. 2010 ACR-EULAR classification criteria for rheumatoid arthritis. Rev Bras Reumatol 2010; 50:481-3.
  • 130
    O'Dell JR, Nepom BS, Haire C, Gersuk VH, Gaur L, Moore GF et al. HLA-DRB1 typing in rheumatoid arthritis: predicting response to specific treatments. Ann Rheum Dis 1998; 57:209-13.
  • 131
    Reveille JD, Alarcon GS, Fowler SE, Pillemer SR, Neuner R, Clegg DO et al HLA-DRB1 genes and disease severity in rheumatoid arthritis. The MIRA Trial Group. Minocycline in Rheumatoid Arthritis. Arthritis Rheum 1996; 39:1802-7.
  • 2011 consensus of the Brazilian Society of Rheumatology for diagnosis and early assessment of rheumatoid arthritis

    Licia Maria Henrique da MotaI; Boris Afonso CruzII; Claiton Viegas BrenolIII; Ivanio Alves PereiraIV; Lucila Stange Rezende FronzaV; Manoel Barros BertoloVI; Max Victor Carioca de FreitasVII; Nilzio Antônio da SilvaVIII; Paulo Louzada-JuniorIX; Rina Dalva Neubarth GiorgiX; Rodrigo Aires Corrêa LimaXI; Geraldo da Rocha Castelar PinheiroXII
  • Publication Dates

    • Publication in this collection
      20 May 2011
    • Date of issue
      June 2011

    History

    • Accepted
      14 Mar 2011
    • Received
      12 Mar 2011
    Sociedade Brasileira de Reumatologia Av Brigadeiro Luiz Antonio, 2466 - Cj 93., 01402-000 São Paulo - SP, Tel./Fax: 55 11 3289 7165 - São Paulo - SP - Brazil
    E-mail: sbre@terra.com.br