S9.1 Espondiloartropatías Español

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Diagnóstico y tratamiento médico actual 2022
2030: Espondiloartropatías seronegativas
Jinoos Yazdany; rebeca l.manno
Las espondiloartropatías seronegativas son la espondilitis anquilosante, la artritis psoriásica, la artritis reactiva, la artritis asociada con la enfermedad
inflamatoria intestinal y la espondiloartropatía indiferenciada. Estos trastornos se caracterizan por un predominio masculino, aparición generalmente
antes de los 40 años, artritis inflamatoria de la columna vertebral y las articulaciones sacroilíacas, oligoartritis asimétrica de las grandes articulaciones
periféricas, entesopatía (inflamación del lugar donde los ligamentos, los tendones y la cápsula articular se insertan en el hueso), inflamación ocular, la
ausencia de autoanticuerpos y una sorprendente asociación con HLAB27 ( eCuadro 201). HLAB27 es positivo hasta en el 90% de los pacientes con
espondilitis anquilosante y en el 75% con artritis reactiva. HLAB27 también ocurre en el 50% de los pacientes con enfermedad intestinal psoriásica e
inflamatoria que tienen sacroileítis. Los pacientes con artritis periférica únicamente en estos dos últimos síndromes no muestran un aumento de HLA
B27.
HLAB27 puede contribuir a la patogenia de las espondiloartropatías de diversas formas. HLAB27 puede plegarse incorrectamente y desencadenar la
producción de citocinas inflamatorias, como IL17 o IL23. HLAB27 también puede presentar péptidos artritogénicos. Los experimentos con ratas
transgénicas demuestran que el propio HLAB27 (y no un gen en desequilibrio de ligamiento con HLAB27) confiere susceptibilidad a estas
enfermedades. Cuando el gen humano HLAB27 se expresa en ratas, los animales desarrollan artritis espinal y periférica, cambios psoriasiformes en
las uñas y la piel e inflamación intestinal. Por lo tanto, HLAB27 es un factor de riesgo importante para las espondiloartropatías. Sin embargo, algunos
pacientes con estos trastornos son HLAB27 negativos y la gran mayoría de los individuos HLAB27 positivos no desarrollan espondiloartropatías.
Infection also appears to play a key role in some of the spondyloarthropathies, especially reactive arthritis, which characteristically develops 1–4 weeks
after bacterial dysentery or a nongonococcal sexually transmitted infection (see below). The interplay of susceptibility genes and environmental
infections is demonstrated by the fact that the risk of developing reactive arthritis is 0.2% in the general population, 2% in the HLAB27 individuals, and
20% in patients with HLAB27 who become infected with Salmonella, Shigella, or enteric organisms. Despite these gains in our understanding of the
importance of HLAB27 and infection, the precise mechanism by which genes and infection cause spondyloarthropathy is not yet known.
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2031: Espondilitis anquilosante
FUNDAMENTOS DEL DIAGNÓSTICO
Lumbalgia crónica y rigidez en adultos jóvenes, peor por la mañana.
Limitación progresiva del movimiento de la espalda y expansión torácica.
Artritis periférica transitoria (50%) o persistente (25%).
Uveítis anterior en 2025%.
Cambios radiográficos de diagnóstico en las articulaciones sacroilíacas.
Pruebas serológicas negativas para factor reumatoide y anticuerpos antiCCP.
La prueba de HLAB27 es más útil cuando existe una probabilidad intermedia de enfermedad.
CONSIDERACIONES GENERALES
La espondilitis anquilosante es una enfermedad inflamatoria crónica de las articulaciones del esqueleto axial, que se manifiesta clínicamente por
dolor y rigidez progresiva de la columna vertebral. La edad de inicio suele ser al final de la adolescencia o principios de los 20 años. La incidencia es
mayor en hombres que en mujeres.
HALLAZGOS CLÍNICOS
A. Síntomas y signos
The onset is usually gradual, with intermittent bouts of back pain that may radiate into the buttocks. The back pain is worse in the morning and
associated with stiffness that lasts hours. Pain and stiffness improve with activity, in contrast to back pain due to mechanical causes, which improves
with rest and worsens with activity. As the disease advances, symptoms progress in a cephalad direction and back motion becomes limited, with the
normal lumbar curve flattened and the thoracic curvature exaggerated. Chest expansion is often limited as a consequence of costovertebral joint
involvement. In advanced cases, the entire spine becomes fused, allowing no motion in any direction. Transient acute arthritis of the peripheral joints
occurs in about 50% of cases, and permanent changes in the peripheral joints—most commonly the hips, shoulders, and knees—are seen in about
25%. Enthesopathy, a hallmark of the spondyloarthropathies, can manifest as swelling of the Achilles tendon at its insertion, plantar fasciitis
(producing heel pain), or dactylitis, which is fusiform “sausage” swelling of a finger or toe.
Anterior uveitis is associated in up to 25% of cases and may be a presenting feature of ankylosing spondylitis (eFigure 20–31). Cardiac involvement,
characterized by atrioventricular conduction defects, aortic regurgitation, or aortic root widening, occurs in 3–5% of patients with longstanding severe
disease. Pulmonary fibrosis of the upper lobes, with progression to cavitation and bronchiectasis mimicking tuberculosis, may rarely occur,
characteristically long after the onset of skeletal symptoms. Radicular symptoms due to cauda equina fibrosis may develop years after onset of the
disease.
eFigure 20–31.
2031: Ankylosing Spondylitis, Jinoos Yazdany; rebeca l.manno Page 1 / 7
Acute iridocyclitis in a patient with ankylosing spondylitis. Note fibrin clot in anterior chamber. (Reproduced, with permission, from Vaughan DG,
Asbury T, RiordanEva P [editors]. General Ophthalmology, 15th ed. Originally published by Appleton & Lange. Copyright © 1999 by The McGrawHill
Companies, Inc.)
characterized by atrioventricular conduction defects, aortic regurgitation, or aortic root widening, occurs in 3–5% of patients with longstanding severe
disease. Pulmonary fibrosis of the upper lobes, with progression to cavitation and bronchiectasis mimicking tuberculosis, may rarely occur,
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characteristically long after the onset of skeletal symptoms. Radicular symptoms due to cauda equina fibrosis may develop years after onset of the
disease.
eFigure 20–31.
Acute iridocyclitis in a patient with ankylosing spondylitis. Note fibrin clot in anterior chamber. (Reproduced, with permission, from Vaughan DG,
Asbury T, RiordanEva P [editors]. General Ophthalmology, 15th ed. Originally published by Appleton & Lange. Copyright © 1999 by The McGrawHill
Companies, Inc.)
B. Laboratory Findings
The ESR is elevated in 85% of cases, but serologic tests for rheumatoid factor and antiCCP antibodies are negative. Anemia of chronic disease may be
present but is often mild. HLAB27 is found in 90% of White patients and 50% of Black patients with ankylosing spondylitis. Because this antigen occurs
in 8% of the healthy White population and 2% of healthy Blacks, it is not a specific diagnostic test but is most useful when there is intermediate
probability of disease.
C. Imaging
The earliest radiographic changes are usually in the sacroiliac joints. In the first 2 years of the disease, sacroiliac changes may be detectable only by
MRI. Indeed, patients who have symptoms and findings of ankylosing spondylitis and sacroiliitis evident by MRI but not by conventional radiographs
are classified as having nonradiographic axial spondyloarthritis. With disease progression, erosion and sclerosis of the sacroiliac joints become
evident on plain radiographs. The sacroiliitis of ankylosing spondylitis is bilateral and symmetric (eFigure 20–32). Inflammation where the annulus
fibrosus attaches to the vertebral bodies initially causes sclerosis (“the shiny corner sign”) (eFigure 20–33) and then characteristic squaring of the
vertebral bodies. The term “bamboo spine” describes the late radiographic appearance of the spinal column in which the vertebral bodies are fused by
vertically oriented, bridging syndesmophytes formed by the ossification of the annulus fibrosus and calcification of the anterior and lateral spinal
ligaments (eFigure 20–34, eFigure 20–35, and eFigure 20–36). Fusion of the posterior facet joints of the spine is also common.
eFigure 20–32.
Fusion of bilateral sacroiliac joints in a patient with ankylosing spondylitis. (Used, with permission, from Nicole Richman, MD.)
ligaments (eFigure 20–34, eFigure 20–35, and eFigure 20–36). Fusion of the posterior facet joints of the spine is also common.
eFigure 20–32.
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Fusion of bilateral sacroiliac joints in a patient with ankylosing spondylitis. (Used, with permission, from Nicole Richman, MD.)
eFigure 20–33.
Radiograph of the lumbar spine of a different patient, demonstrating shiny corners (Romanus lesions) (arrows). (Used, with permission, from Imboden
JB et al. Current Diagnosis & Treatment: Rheumatology, 3e. McGrawHill, 2013.)
eFigure 20–34.
Kidney, ureter, bladder (KUB) view showing bamboo spine and fusion of both sacroiliac joints. (Used, with permission, from Richard P. Usatine, MD, in
Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw Hill, 2019.)
eFigure 20–34.
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Kidney, ureter, bladder (KUB) view showing bamboo spine and fusion of both sacroiliac joints. (Used, with permission, from Richard P. Usatine, MD, in
Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw Hill, 2019.)
eFigure 20–35.
Anterior spinal ligament calcifications and fusion of the lumbar spine in a patient with ankylosing spondylitis. (Used, with permission, from Nicole
Richman, MD.
eFigure 20–36.
Anterior spinal ligament calcifications and fusion of the cervical spine in a patient with ankylosing spondylitis. (Used, with permission, from Nicole
Richman, MD.)
eFigure 20–36.
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Anterior spinal ligament calcifications and fusion of the cervical spine in a patient with ankylosing spondylitis. (Used, with permission, from Nicole
Richman, MD.)
Additional radiographic findings include periosteal new bone formation on the iliac crest, ischial tuberosities and calcanei, and alterations of the pubic
symphysis and sternomanubrial joint similar to those of the sacroiliac joints. Radiologic changes in peripheral joints, when present, tend to be
asymmetric and lack the demineralization and erosions seen in rheumatoid arthritis.
DIFFERENTIAL DIAGNOSIS
Low back pain due to mechanical causes, disk disease, and degenerative arthritis is very common. Onset of back pain prior to age 30 and an
“inflammatory” quality of the back pain (ie, profound morning stiffness and pain that improve with activity) should raise the possibility of ankylosing
spondylitis. In contrast to ankylosing spondylitis, rheumatoid arthritis predominantly affects multiple, small, peripheral joints of the hands and feet.
Rheumatoid arthritis spares the sacroiliac joints and only affects the cervical component of the spine. Bilateral sacroiliitis indistinguishable from
ankylosing spondylitis is seen with the spondylitis associated with inflammatory bowel disease. Sacroiliitis associated with reactive arthritis and
psoriasis, on the other hand, is often asymmetric or even unilateral. Osteitis condensans ilii (sclerosis on the iliac side of the sacroiliac joint) is an
asymptomatic, postpartum radiographic finding that is occasionally mistaken for sacroiliitis. Diffuse idiopathic skeletal hyperostosis (DISH) causes
exuberant osteophytes (“enthesophytes”) of the spine (eFigure 20–37) that may be difficult to distinguish from the syndesmophytes of ankylosing
spondylitis. The enthesophytes of DISH are thicker and more anterior than the syndesmophytes of ankylosing spondylitis, and sacroiliac joints are
normal in DISH.
eFigure 20–37.
Exuberant osteophytes (sometimes termed "flowing enthesophytes" or "bridging syndesmophytes") at multiple contiguous levels of the lumbar spine
in a patient with diffuse idiopathic skeletal hyperostosis (DISH). These are occasionally difficult to distinguish from the syndesmophytes of ankylosing
spondylitis. (Used, with permission, from Nicole Richman, MD.)
eFigure 20–37.
Exuberant osteophytes (sometimes termed "flowing enthesophytes" or "bridging syndesmophytes") at multiple contiguous levels of the lumbar spine
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in a patient with diffuse idiopathic skeletal hyperostosis (DISH). These are occasionally difficult to distinguish from the syndesmophytes of ankylosing
spondylitis. (Used, with permission, from Nicole Richman, MD.)
TREATMENT
NSAIDs remain firstline treatment of ankylosing spondylitis and may slow radiographic progression of spinal disease. Because individual patients
differ in their response to particular NSAIDs, empiric trials of several different NSAIDs are warranted if the response to any given NSAID is not
satisfactory. TNF inhibitors have established efficacy for NSAIDresistant axial disease; responses are often substantial and durable. Etanercept (50 mg
subcutaneously once a week), adalimumab (40 mg subcutaneously every other week), infliximab (5 mg/kg every other month by intravenous infusion),
golimumab (50 mg subcutaneously once a month), or certolizumab (200 mg subcutaneously every other week) is reasonable for patients whose
symptoms are refractory to NSAIDs. No particular TNF inhibitor is preferred except in patients with concomitant uveitis or inflammatory bowel disease,
for whom monoclonal antibodies to TNF should be used. Secukinumab and ixekizumab inhibit the proinflammatory cytokine IL17A and are also
highly effective and FDA approved for the treatment of ankylosing spondylitis. There is no convincing evidence that methotrexate benefits patients
with ankylosing spondylitis. Inhibitors of IL6 and abatacept are ineffective. The role of rituximab is unclear. Sulfasalazine (1000 mg orally twice daily) is
sometimes useful for peripheral arthritis but lacks effectiveness for spinal and sacroiliac joint disease. Corticosteroids have minimal impact on the
arthritis—particularly the spondylitis—of ankylosing spondylitis and can worsen osteopenia. All patients should be referred to a physical therapist for
instruction in postural exercises and a safe exercise program.
PROGNOSIS
Almost all patients have persistent symptoms over decades; rare individuals experience longterm remissions. The severity of disease varies greatly,
with about 10% of patients having work disability after 10 years. Developing hip disease within the first 2 years of disease onset presages a worse
prognosis. Biologic agents provide symptomatic relief, improve quality of life, and may slow disease progression for many patients with ankylosing
spondylitis.
Deodhar A et al. Ixekizumab for patients with nonradiographic axial spondyloarthritis (COASTX): a randomised, placebocontrolled trial. Lancet.
2020;395:53.
[PubMed: 31813637]
Koo BS et al. Tumour necrosis factor inhibitors slow radiographic progression in patients with ankylosing spondylitis: 18year realworld evidence.
Ann Rheum Dis. 2020;79:1327.
[PubMed: 32660979]
Rosenbaum JT. The eye in spondyloarthritis. Semin Arthritis Rheum. 2019;49:S29.
[PubMed: 31779847]
Tahir H et al. Impact of secukinumab on patientreported outcomes in the treatment of ankylosing spondylitis: current perspectives. Open Access
Rheumatol. 2020;12:277.
[PubMed: 33273869]
Ward MM et al. 2019 update of the American College of Rheumatology/Spondylitis Association of America/Spondyloarthritis Research and Treatment
Network recommendations for the treatment of ankylosing spondylitis and nonradiographic axial spondyloarthritis. Arthritis Rheumatol.
2019;71:1599.
[PubMed: 31436036]
[PubMed: 31779847]
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Tahir H et al. Impact of secukinumab on patientreported outcomes in the treatment of ankylosing spondylitis: current perspectives. Open Access
Rheumatol. 2020;12:277.
[PubMed: 33273869]
Ward MM et al. 2019 update of the American College of Rheumatology/Spondylitis Association of America/Spondyloarthritis Research and Treatment
Network recommendations for the treatment of ankylosing spondylitis and nonradiographic axial spondyloarthritis. Arthritis Rheumatol.
2019;71:1599.
[PubMed: 31436036]
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2032: Artritis psoriásica
La psoriasis precede a la artritis en el 80% de los casos.
Artritis: generalmente asimétrica, con apariencia de “salchicha” en los dedos de manos y pies (dactilitis); poliartritis que puede parecerse a la
artritis reumatoide.
Compromiso común de la articulación sacroilíaca.
Hallazgos radiográficos: osteólisis; deformidad de lápiz en copa; carencia relativa de osteoporosis; anquilosis ósea; sacroilitis asimétrica y
sindesmofitos atípicos.
Aunque la psoriasis suele preceder a la aparición de la artritis, la artritis puede preceder (hasta 2 años) u ocurrir simultáneamente con la enfermedad
de la piel en aproximadamente el 20% de los casos.
HALLAZGOS CLÍNICOS
A. Síntomas y signos
Los patrones o subconjuntos de afectación articular en la artritis psoriásica incluyen los siguientes:
1. A symmetric polyarthritis that resembles rheumatoid arthritis. Usually, fewer joints are involved than in rheumatoid arthritis.
2. An oligoarthritis that may lead to considerable destruction of the affected joints.
3. A pattern of disease in which the DIP joints are primarily affected. Early, this may be monoarticular, and often the joint involvement is asymmetric.
Pitting of the nails and onycholysis frequently accompany DIP involvement.
4. A severe deforming arthritis (arthritis mutilans) with osteolysis.
5. A spondylitic form in which sacroiliitis and spinal involvement predominate; 50% of these patients are HLAB27 positive.
Arthritis is at least five times more common in patients with severe psoriatic skin disease than in those with only mild skin findings. Occasionally,
however, patients may have a single patch of psoriasis (typically hidden in the scalp, gluteal cleft, or umbilicus) and are unaware of its presence. Thus,
a detailed search for cutaneous lesions is essential in patients with arthritis of new onset. Also, the psoriatic lesions may have cleared when arthritis
appears—in such cases, the history is most useful in diagnosing previously unexplained cases of monoarthritis or oligoarthritis. Nail pitting is
sometimes a clue. “Sausage” swelling, or dactylitis, of one or more digits is a common manifestation of enthesopathy in psoriatic arthritis.
The ESR is elevated in approximately 50% of patients with psoriatic arthritis; normal values do not rule out the diagnosis. Rheumatoid factor and anti
CCP antibodies are not present. Uric acid levels may be high, reflecting the active turnover of skin affected by psoriasis. There is a correlation between
2032: Psoriatic Arthritis, Jinoos Yazdany; rebeca l.manno Page 1 / 3
the extent of psoriatic involvement and the level of uric acid, but gout is no more common than in patients without psoriasis. Desquamation of the skin
may also reduce iron stores.
appears—in such cases, the history is most useful in diagnosing previously unexplained cases of monoarthritis or oligoarthritis. Nail pitting is
sometimes a clue. “Sausage” swelling, or dactylitis, of one or more digits is a common manifestation of enthesopathy in psoriatic arthritis.
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The ESR is elevated in approximately 50% of patients with psoriatic arthritis; normal values do not rule out the diagnosis. Rheumatoid factor and anti
CCP antibodies are not present. Uric acid levels may be high, reflecting the active turnover of skin affected by psoriasis. There is a correlation between
the extent of psoriatic involvement and the level of uric acid, but gout is no more common than in patients without psoriasis. Desquamation of the skin
may also reduce iron stores.
C. Imaging
Radiographic findings are most helpful in distinguishing the disease from other forms of arthritis. There are marginal erosions of bone and irregular
destruction of joint and bone (eFigure 20–38), which, in the phalanx, may give the appearance of a sharpened pencil. Fluffy periosteal new bone may
be marked, especially at the insertion of muscles and ligaments into bone. Such changes will also be seen along the shafts of metacarpals, metatarsals,
and phalanges. Psoriatic spondylitis causes asymmetric sacroiliitis and syndesmophytes. In psoriatic arthritis as in ankylosing spondylitis, MRI is more
sensitive in detecting axial abnormalities than conventional radiographs, especially in the first few years of disease onset. Ultrasonography and MRI are
more sensitive than conventional radiographs in detecting peripheral arthritis, enthesitis, and dactylitis.
eFigure 20–38.
Erosions at the distal (and proximal) interphalangeal joints in a patient with psoriatic arthritis. (Used, with permission, from Nicole Richman, MD.)
TREATMENT
In patients with active psoriatic arthritis, a TNF inhibitor biologic agent is recommended as firstline agent. If TNF inhibitor is contraindicated or not
tolerated, methotrexate (or other oral small molecule agent, such as leflunomide, sulfasalazine, cyclosporine, or apremilast) may be effective.
Patients who do not respond to TNF inhibitors or oral small molecule agents can be treated with ustekinumab, a monoclonal antibody that inhibits IL
12 and IL23, or secukinumab, guselkumab, or ixekizumab, which inhibit IL17. Tofacitanib (Jakstat inhibitor) and abatacept (CTLA4 inhibitor) may be
options with failure of the above therapies. Corticosteroids are less effective in psoriatic arthritis than in other forms of inflammatory arthritis and may
precipitate pustular psoriasis during tapers.
Gossec L et al. EULAR recommendations for the management of psoriatic arthritis with pharmacological therapies: 2019 update. Ann Rheum Dis.
2020;79:700.
[PubMed: 32434812]
Mease PJ et al. Guselkumab in biologicnaive patients with active psoriatic arthritis (DISCOVER2): a doubleblind, randomised, placebocontrolled
phase 3 trial. Lancet. 2020;395:1126.
[PubMed: 32178766]
Singh JA et al. Special article: 2018 American College of Rheumatology/National Psoriasis Foundation guideline for the treatment of psoriatic
arthritis. Arthritis Care Res (Hoboken). 2019;71:2.
[PubMed: 30499259]
2020;79:700.
[PubMed: 32434812] Universidad Peruana de Ciencias Aplicadas
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Mease PJ et al. Guselkumab in biologicnaive patients with active psoriatic arthritis (DISCOVER2): a doubleblind, randomised, placebocontrolled
phase 3 trial. Lancet. 2020;395:1126.
[PubMed: 32178766]
Singh JA et al. Special article: 2018 American College of Rheumatology/National Psoriasis Foundation guideline for the treatment of psoriatic
arthritis. Arthritis Care Res (Hoboken). 2019;71:2.
[PubMed: 30499259]
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2033: Artritis reactiva
Oligoartritis, conjuntivitis, uretritis, queratodermia blenorrágica y úlceras bucales son comunes.
Por lo general, sigue a la disentería o a una infección de transmisión sexual.
HLAB27 positivo en 50 a 80% de los pacientes.
La artritis reactiva es precipitada por infecciones gastrointestinales y genitourinarias antecedentes y se manifiesta como una oligoartritis estéril
asimétrica, típicamente de las extremidades inferiores. Con frecuencia se asocia con entesitis. Las manifestaciones extraarticulares son frecuentes e
incluyen uretritis, conjuntivitis, uveítis ( eFigura 2039 ), exantema (queratodermia blenorrágica) y lesiones mucocutáneas. La artritis reactiva ocurre
más comúnmente en hombres jóvenes y se asocia con HLAB27 en 80% de los pacientes blancos y 50 a 60% de los negros.
eFigura 20–39.
Acute iridocyclitis with hypopyon in a patient with reactive arthritis. (Reproduced, with permission, from Vaughan DG, Asbury T, RiordanEva P
[editors]. General Ophthalmology, 15th ed. Originally published by Appleton & Lange. Copyright © 1999 by The McGrawHill Companies, Inc.)
CLINICAL FINDINGS
A. Symptoms and Signs
2033: Reactive Arthritis, Jinoos Yazdany; rebeca l.manno Page 1 / 3
Most cases of reactive arthritis develop within 1–4 weeks after either a gastrointestinal infection (usually with Shigella, Salmonella, Yersinia, or
Campylobacter) or a sexually transmitted infection (with Chlamydia trachomatis or perhaps Ureaplasma urealyticum). Whether the inciting infection is
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CLINICAL FINDINGS
A. Symptoms and Signs
Most cases of reactive arthritis develop within 1–4 weeks after either a gastrointestinal infection (usually with Shigella, Salmonella, Yersinia, or
Campylobacter) or a sexually transmitted infection (with Chlamydia trachomatis or perhaps Ureaplasma urealyticum). Whether the inciting infection is
sexually transmitted or dysenteric does not affect the subsequent manifestations but does influence the gender ratio: The ratio is 1:1 after enteric
infections but 9:1 with male predominance after sexually transmitted infections. Synovial fluid from affected joints is culturenegative. A clinically
indistinguishable syndrome can occur without an apparent antecedent infection, suggesting that subclinical infection can precipitate reactive arthritis
or that there are other, as yet unrecognized, triggers. Although affected joints are sterile, molecular techniques provide evidence that antigens from
putative inciting organisms (and DNA in the case of Chlamydia) are present in synovial tissue, even years after the clinical disease. The pathogenic
significance of these findings remains unclear.
The arthritis is most commonly asymmetric and frequently involves the large weightbearing joints (knee and ankle); sacroiliitis or ankylosing
spondylitis is observed in at least 20% of patients, especially after frequent recurrences. Systemic symptoms including fever and weight loss are
common at the onset of disease. The mucocutaneous lesions may include balanitis (Figure 20–8), stomatitis, and keratoderma blennorrhagicum
(eFigure 20–40), indistinguishable from pustular psoriasis. Involvement of the fingernails in reactive arthritis mimics psoriatic changes. When present,
conjunctivitis is mild and occurs early in the disease course. Anterior uveitis, which can develop at any time in HLAB27–positive patients, is a more
clinically significant ocular complication. Carditis and aortic regurgitation may occur. While most signs of the disease disappear within days or weeks,
the arthritis may persist for several months or become chronic. Recurrences involving any combination of the clinical manifestations are common and
are sometimes followed by permanent sequelae, especially in the joints (eg, articular destruction).
Figure 20–8.
Circinate balanitis due to reactive arthritis. (From Susan Lindsley, Dr. M. F. Rein, Public Health Image Library, CDC.)
eFigure 20–40.
Keratoderma blennorrhagica of the soles due to reactive arthritis. (From Susan Lindsley, Public Health Image Library, CDC.)
eFigure 20–40.
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Keratoderma blennorrhagica of the soles due to reactive arthritis. (From Susan Lindsley, Public Health Image Library, CDC.)
B. Imaging
Radiographic signs of permanent or progressive joint disease may be seen in the sacroiliac and peripheral joints.
DIFFERENTIAL DIAGNOSIS
Gonococcal arthritis can initially mimic reactive arthritis, but the marked improvement after 24–48 hours of antibiotic administration in gonococcal
arthritis and the culture results distinguish the two disorders. Rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis must also be
considered. By causing similar oral, ocular, and joint lesions, Behçet disease may mimic reactive arthritis. The oral lesions of reactive arthritis,
however, are typically painless, in contrast to those of Behçet disease.
TREATMENT
NSAIDs have been the mainstay of therapy. Antibiotics given at the time of a nongonococcal sexually transmitted infection reduce the chance that the
individual will develop this disorder. For chronic reactive arthritis associated with chlamydial infection, a randomized trial demonstrated that 6 months
of rifampin (300 mg orally twice daily) in combination with either doxycycline (100 mg orally twice daily) or azithromycin (500 mg orally daily for 5 days
then twice weekly) was more effective than placebo. Patients who do not respond to NSAIDs may respond to sulfasalazine or methotrexate. For those
patients with recentonset disease that is refractory to NSAIDs and these DMARDs, antiTNF agents, which are effective in the other
spondyloarthropathies, may be effective.
Hayes KM et al. Evolving patterns of reactive arthritis. Clin Rheumatol. 2019;38:2083.
[PubMed: 30919146]
Lucchino B et al. Reactive arthritis: current treatment challenges and future perspectives. Clin Exp Rheumatol. 2019;37:1065.
[PubMed: 31140399]
Zeidler H et al. Chlamydia induced reactive arthritis: disappearing entity or lack of research? Curr Rheumatol Rep. 2019;21:63.
[PubMed: 31741118]
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2034: Espondiloartritis asociada a enfermedad inflamatoria intestinal
Una quinta parte de los pacientes con enfermedad inflamatoria intestinal tienen artritis, que complica la enfermedad de Crohn con algo más de
frecuencia que la colitis ulcerosa. En ambas enfermedades, ocurren dos formas distintas de artritis. La primera es la artritis periférica, por lo general
una oligoartritis asimétrica no deformante de grandes articulaciones, en la que la actividad de la enfermedad articular es paralela a la de la
enfermedad intestinal. La artritis generalmente comienza meses o años después de la enfermedad intestinal, pero ocasionalmente los síntomas
articulares se desarrollan antes y pueden ser lo suficientemente prominentes como para hacer que el paciente pase por alto los síntomas intestinales.
La segunda forma de artritis es una espondilitis que es indistinguible por síntomas o radiografías de la espondilitis anquilosante y sigue un curso
independiente de la enfermedad intestinal. Alrededor del 50% de estos pacientes son HLAB27 positivos.
El control de la inflamación intestinal suele eliminar la artritis periférica. Los NSAID pueden ser efectivos cuando la artritis es leve, pero deben usarse
con precaución ya que pueden exacerbar la enfermedad inflamatoria intestinal. Los inhibidores de TNF son terapias útiles porque son efectivos tanto
para el intestino como para las articulaciones. Los ejercicios de rango de movimiento prescritos para la espondilitis anquilosante pueden ser útiles.
La enfermedad de Whipple debe considerarse en el diagnóstico diferencial de un paciente con síntomas gastrointestinales y articulares. Dos tercios de
los pacientes con enfermedad de Whipple experimentan artralgia o artritis, más a menudo una poliartritis episódica de grandes articulaciones. La
artritis suele preceder a las manifestaciones gastrointestinales por años y, a menudo, se resuelve a medida que se desarrolla la diarrea.
Chimenti MS et al. Use of synthetic and biological DMARDs in patients with enteropathic spondyloarthritis: a combined gastrorheumatological
approach. Clin Exp Rheumatol. 2019; 37:723.
[PubMed: 31172920]
Ribaldone DG et al. Risk factors of suspected spondyloarthritis among inflammatory bowel disease patients. Scand J Gastroenterol. 2019;54:1233.
[PubMed: 31549896]
2034: Inflammatory Bowel Disease–Associated Spondyloarthritis, Jinoos Yazdany; rebeca l.manno Page 1 / 1

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