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Artritis reumatoidea 2011 hesv
- 1. Un poco de BASICO… Dr. Hector Simosa R3 Medicina Interna
- 17. Artritis Reumatoidea Dr. Hector Simosa R3 de Medicina Interna
- 18. Contenido
- 20. Definición
- 21. EPIDEMIOLOGÍA, FACTORES DE RIESGO Y POSIBLES CAUSAS
- 24. Factores del género 4.- Arthritis Rheum 2004 Nov;50(11):3458-67. 5 - N Engl J Med 1993 Aug 12;329(7):466-71. 6 - Arthritis Rheum. 2006 Oct;54(10):3087-94 7 - Rheumatology (Oxford) 2002 Mar;41(3):285-9.
- 30. Figure 1 Schematic illustration of the etiological hypothesis for P. gingivalis and citrullinated α-enolase involvement in RA Lundberg, K. et al. (2010) Periodontitis in RA—the citrullinated enolase connection Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2010.139
- 33. ETIOPATOGENIA
- 65. van Venrooij and Pruijn Arthritis Research & Therapy 2008 10 :117 doi:10.1186/ar2504
- 71. DIAGNÓSTICO, CLÍNICA Y DIAGNÓSTICO DIFERENCIAL
- 105. MANEJO Y TRATAMIENTO
- 106. Pronóstico 70% de erosiones detectables por Rx en manos y pies ocurren en los 2 primeros años En 20 años, sobre el 60% de los pacientes están en CF III o IV Incidencia aumentada de: Infecciones Enfermedad cardiovascular Linfomas Expectativa de vida es menor que controles sanos, especialmente en pacientes con: Enfermedad poliarticular Enfermedad extrarticular Actividad de enfermedad persistente (PCR, VHS elevados) FR (+) y complejos inmunes circulantes Cadena HLA-DR “epitopo compartido”
- 107. Etapificación
- 111. Tto. farmacológico
- 112. FARMEs no biológicos
- 113. FARMEs biológicos
- 126. REMISION CLINICA
Notas del editor
- Destruccion y deformidad articular muchas veces invalidante
- - prevalence is about 1 percent in Caucasians, but varies between 0.1 percent (in rural Africans) and 5 percent (in Pima and Chippewa Indians) - because of the consistently higher rates in females, the prevalence of RA in females over age 65 is up to 5 percent.
- In one study, women with RA were more likely to experience a remission during pregnancy if there were maternal-fetal disparities in HLA class II antigens [7] . Such mismatches may produce blocking antibodies to class II MHC antigens that inhibit activation of T cell clones essential for ongoing synovitis. It is uncertain whether such changes in hormone levels are simply the result of chronic inflammation or if men with abnormal testosterone and estrogenic hormone levels are at an increased risk of developing RA.
- Monozygotic twins have a higher concordance than dizygotic twins for developing RA. In two studies of twins, the concordance for monozygotic twins was 12 to 15 percent versus 3.5 percent for dizygotic twins [11,12] . In addition, the risk ratio of developing RA for a first-degree relative of a rheumatoid patient is more than 1.5 compared with controls [13] . Other data have shown that sibship concordance rates are consistently higher when probands have severe disease, thereby suggesting that RA may develop when several genetic and environmental factors are present in the same individual. From these and similar data, it has been estimated that genetic factors contribute from 53 to 65 percent of the risk of developing RA [14] .
- Among the growing list of genetic risk factors for RA, significant overlap exists with genes identified as risk factors for other autoimmune diseases, including systemic lupus erythematosus, inflammatory bowel disease, multiple sclerosis, and ankylosing spondylitis [15] . Why a given genetic factor can be associated with a variable pattern of organ-system involvement in different disease states is not known. (See "Overview of autoimmunity").
- The firmest link between a genetic susceptibility factor and RA is the association of the disease with an epitope in the third hypervariable region of the HLA-DR ß-chains, known as the "shared epitope". Although this finding has been demonstrated in many cohorts, such as those of northern European heritage, Israeli Jews, Yakima Indians, and Koreans, it does not appear to apply to all populations. Among African-Americans, for example, other genetic risk factors, many still undefined, appear to contribute significantly to disease susceptibility and severity.
- - The magnitude of the overall effect of smoking was evaluated in a retrospective report utilizing data on over 370,000 women from the Women's Health Cohort Study [21] . Women who smoked at least 25 cigarettes a day for more than 20 years had a relative risk of 1.4 for developing RA compared to those who had never smoked [21] . Multivariate analysis revealed that the duration of use, but not the number of cigarettes smoked per day, was significantly associated with increased risk. A similar association with smoking and RA was noted in monozygotic and dizygotic twins discordant for RA [22] , and in a prospective population-based study of incident RA in women [23] . - Compared with those who had never smoked, patients with a 25 or more pack-year smoking history are more likely to be seropositive, have nodules, or have radiographically apparent erosions [24,25] . - This was suggested in a population-based study in the United States in which women who had stopped smoking more than ten years before entering the study did not share an increased risk of developing RA with their peers who were actively smoking [27] .
- - Superantigens can activate multiple clones of T cells (1 in 10 cells) through a largely MHC-independent process. By comparison, a specific antigen presented in context of the HLA class II cell surface antigens can activate only one in 10,000 T cells. Examples of superantigens are the staphylococcal endotoxins and heat shock proteins (HSPs). HSPs are intracellular proteins induced by environmental insults, including heat, infectious agents, and oxidative injury, and are remarkably conserved across species. The most logical hypothesis implicating HSPs as causative in RA is that these proteins share antigenic determinants with other host proteins, thereby resulting in the development of crossreacting antibodies that could induce an autoimmune response
- Although it is clear that the presence of RF alone does not cause RA, there is no doubt that patients with significant RF titers have a greater likelihood of extraarticular disease than do seronegative patients RF and anti-cyclic citrullinated peptide (anti-CCP) antibodies may be present in the blood prior to the appearance of arthritis [59-62] . Although these autoantibodies may represent clinically silent disease, the development of such autoantibodies can also be viewed as a risk factor for the later development of disease. The sensitivity of a positive anti-CCP assay and a positive RF in the 1.5 years prior to diagnosis has ranged from 18 to 30 percent and the specificity from 99 to 100 percent.
- El primer evento en el desarrollo de AR es probablemente la activación dependiente del complemento de células T. Ésto trae subsecuentemente varios efectos, que incluyen activación y proliferación del sinovio y de células endoteliales, reclutamiento y activación de celulas adicionales proinflamatorias de la médula osea y de la circulacion, secrecion de citokinas y proteasas por macrófagos y células sinoviales “fibroblasto-like”, y produccion de autoanticuerpos. El sinovio en la AR se organiza y se transforma en un tejido invasivo que, si no se controla, puede degradar cartílago y hueso. El sinovio reumatoide (pannus) comparte muchas características con tejidos malignos con capacidad de invasion local, pero a diferencia de ellos, nunca pierde algun grado de respuesta a los factores antiinflamatorios y antiproliferativos.
- B LYMPHOCYTES AND AUTOANTIBODIES — Rheumatoid factors are immunoglobulins (Ig) reactive against epitopes on the Fc portion of IgG. Compared to those with "seronegative" RA, patients with polyarticular symmetrical arthritis who have a persistently positive test for rheumatoid factor (RF) are likely to have more erosions of bones and joints, more extraarticular manifestations, and worse function [172] . (See "Clinical features of rheumatoid arthritis").
- Whether toxic or antiinflammatory, NO is produced by patients with rheumatoid arthritis in greater amounts than in controls Substance P (SP) up Corticotropin-releasing hormone (CRH) up Calcitonin gene related peptide (CGRP) down Phospholipase A2 - COX-2
- 1. RA often begins insidiously with vague constitutional and musculoskeletal symptoms that may last for weeks or months before synovitis becomes apparent.
- 1. RA often begins insidiously with vague constitutional and musculoskeletal symptoms that may last for weeks or months before synovitis becomes apparent.
- Symmetrical effusions and soft tissue swelling around the metacarpophalangeal joints and proximal interphalangeal joints typically occur, although distal interphalangeal involvement can be seen later in the disease Occasionally, thickening of the flexor tendons can be detected by palpation of the palm; this finding is due to synovitis of the tendon sheaths ("tenosynovitis") (show figure 4). Nodules may form along the palmar tendon sheaths, resulting in the tendon sheath catching (or triggering) and in an inability to fully extend the finger. The nodules may cause tendon rupture, especially of the extensor pollicis longus (extensor of the DIP joint of the thumb). Reduced grip strength can be a surprisingly sensitive indicator of early disease, as well as a useful parameter in the evaluation of disease activity and progression The whole hand may be swollen in very acute RA, with pitting edema over the dorsum giving rise to the "boxing glove" appearance Between 1 and 5 percent of patients present with carpal tunnel syndrome.
- The characteristic joint deformities appear in more established chronic RA (show picture 1). These findings include ulnar deviation or "ulnar drift" (show picture 2) swan neck or Boutonniere deformities of the fingers (show picture 3), or the "bow string" sign (prominence of the tendons in the extensor compartment of the hand) Late changes due to erosive damage lead to volar subluxation and radial drift of the carpus, resulting in increasing prominence of the ulnar styloid and lateral deviation
- Foot involvement is common in early disease, with a pattern which mirrors that occurring in the hand.
- NODULOS DE HEGAR
- Cervical joint destruction in patients with RA may lead to vertebral malalignment (eg, subluxation). Risk factors for development of cervical subluxation include older age at onset of RA, more active synovitis, and rapidly progressive erosive peripheral joint disease [3] . Both atlantoaxial and subaxial (below C1-C2) joints may be involved.
- Spastic quadriparesis which is slowly progressive Sensory findings are also common, including painless sensory loss in the hands or feet. In patients with C1-C2 subluxation, transient episodes of medullary dysfunction (such as respiratory irregularity) associated with vertical penetration of the odontoid process of C2 and probable vertebral artery compression [19] . Movement of the hands in this setting may result in paresthesias in the shoulder or arms
- Loss of occipitocervical lordosis Resistance to passive spine motion Abnormal protrusion of the axial arch felt by the examining finger on the posterior pharyngeal wall In addition, neurologic findings appropriate to the symptoms described above may be seen, including: Increased deep tendon reflexes Extensor plantar responses Muscle weakness, spasticity, or muscle atrophy Gait disorders
- 1) Anterior arch of atlas 2) Posterior arch of atlas 3) Dens 4) Laminae C2 5) Spinous Process C6 6) C7-T1 Intervertebral Foramina 7) Retropharyngeal Space (Normal < 7mm) 8) Retrotracheal Space (Normal <2cm).
- ) Anterior vertebral line 2) Posterior vertebral line 3) Spinolaminal line 4) Interspinous line.
- Lat eral radiograph of the neck with the head in flexion shows an increased distance between the anterior border of the dens and the posterior border of the anterior tubercle of C1 (blue line) from ligamentous laxity caused by rheumatoid arthritis. The &quot;pre-dentate space,&quot; as this is called, should be less than 3 mm in the adult. The red line above should smoothly connect all of the spinolaminar white lines of each vertebral body but clearly is directed posterior to the spinolaminar white line of C1 (green arrow) since C1 is subluxed forward on C2.
- Clase funcional I : Capacidad completa para efectuar las actividades de la vida diaria: autocuidado, avocacionales y vocacionales. Clase funcional II : Puede realizar las actividades de autocuidado y vocacionales pero tiene limitaciones para las actividades avocacionales. Clase funcional III : Tiene dificultades para realizar actividades vocacionales y avocacionales pero puede realizar las actividades de autocuidado. Clase funcional IV : Tiene dificultades para realizar todo tipo de actividades.
- disease-modifying antirheumatic drugs (DMARDs)
- Abatacept: Rituximab: anti-CD20 B-cell depleting monoclonal antibody
- Ácido Acetil Salicílico y derivados: Ácido Acetil Salicílico, Acetil Salicilato de Lisina (INYESPRIN)! vía parenteral, Trifusal como antiagregante plaquetario más que antiinflamatorio o analgésico, Fosfosal, etc.