Guidelines for diagnosis and treatment of ankylosing spondylitis
1.Overview
Ankylosing spondylitis (AS) is a chronic inflammatory disease that mainly affects the sacroiliac joints, spinal prominences, paraspinal soft tissues and peripheral joints, and is accompanied by extra-articular manifestations in the town, and in severe cases, spinal deformity and ankylosis can occur. The preliminary survey is about 0.3%. The ratio of men to women is about 2 to 3:1, and the onset of the disease is slow and mild in women. The age of onset is usually from 13 to 31 years old, with a peak of 20 to 30 years old, and it is rare after 40 years old and before 8 years old. The epidemiological investigation revealed that the genetic and environmental factors play an important role in this disease. Genetic and environmental factors play a role in the development of the disease. It has been shown that the development of AS is closely related to human leukocyte antigen (HLA) I B27. and there is a clear tendency for family aggregation. One of the pathological signs and early manifestations of AS is sacroiliac arthritis. The typical manifestation of advanced spinal involvement is “bamboo-like changes”. Synovitis of peripheral joints is histologically indistinguishable from rheumatoid arthritis (RA). Tendinopathy is one of the characteristics of this disease.
2. Clinical manifestations
The onset of the disease is insidious. Patients gradually develop pain and/or morning stiffness in the low back or sacroiliac region and wake up in the middle of the night with pain. It is difficult to turn over and get up in the morning or after sitting for a long time, and the morning stiffness of the lumbar region is clearly silicon when the evidence is given, but it is reduced after activity. Some patients have dull pain in the buttocks or severe pain in the sacroiliac region. Occasionally radiating to the periphery. Coughing, sneezing and sudden twisting of the lumbar pain can be aggravated. In the early stage of the disease, the pain in the hip is mostly intermittent or alternating on one side. After a few months, the pain is mostly bilateral and persistent. In most patients, the disease progresses from the lumbar spine to the thoracic and cervical spine, resulting in pain, restricted movement or spinal deformity in the corresponding areas. 24% and 75% of AS patients develop hip and peripheral joint lesions at the beginning or during the course of the disease, with the knee, ankle and shoulder joints being the majority, and the elbow and small joints of the hand and foot occasionally being involved. Arthritis of the large joints of the lower extremities is one of the features of peripheral arthritis in this disease. Arthritis or arthralgia in the hip and knee, as well as in other joints, occurs early in the course of the disease and causes little or no joint destruction or disability. The hip joint is involved in 38% to 66% of cases, with localized pain, limited motion, flexion contracture, and joint ankylosis, most of which are bilateral, and 94% of hip symptoms begin within the first 5 years after onset. The hip is more likely to develop at a younger age and in peripheral joints. 1/4 of patients develop bullous uveitis during the course of the disease, alternating unilaterally or bilaterally, which can be recurrent or even. Ⅱdin cause visual impairment. The umbilical manifestations of the disease are mild, and a few rhizomatous patients have fever, fatigue, wasting, anemia or other organ involvement. Plantar fasciitis, Achilles tendinitis, and other sites of tendon telangiectasia are common in this disease. Neurologic symptoms arise from compressive spinal neuritis or sciatica, vertebral fractures or incomplete dislocations, and code tail syndrome, the latter of which can cause impotence, nocturnal urinary incontinence, blunted bladder and rectal sensation, and loss of ankle reflexes. Very few patients develop fibrosis of the upper lobe of the lung, sometimes accompanied by cavity formation and mistaken for tuberculosis, which can also be exacerbated by concurrent mycobacterial infections. Aortic atresia and conduction disorders are seen in 3.5% of patients. 10% of patients. as can be complicated by IgA nephropathy and amyloidosis.
3.Diagnostic points
The most common and characteristic early complaints of AS are morning stiffness and pain in the lower back. Since low back pain is an extremely common symptom in the general population, but most of them are mechanical non-inflammatory back pain, while this disease is inflammatory pain. 2009 International As Assessment Study Group (ASAS) experts in inflammatory back pain recommend the following criteria for the diagnosis of inflammatory back pain: at least 4 out of 5: (1) age of onset <40 years; (2) insidious onset; (3) symptoms improve with activity; (4) worsening at rest; (5) nocturnal Pain at night (better after waking up). The diagnosis of AS inflammatory back pain was made when 4 of the above 5 indicators were met. Its sensitivity is 79.6% and specificity is 72.4%.
3.2. Physical examination: Sacroiliac joint and paravertebral muscle pressure pain is a positive sign in the early stage of the disease. With the progression of the disease, the anterior convexity of the lumbar spine is flattened. The movement of the spine in all directions is limited, the thoracic expansion of Fanli is reduced, and the cervical vertebrae are posteriorly protruded. The following methods are used to check the progression of sacroiliac joint pain or spinal lesions: ① Occipital crush test: In a healthy person in a standing position with the heels pressed against the wall, the posterior occipital area should be close to the wall without gaps. In the case of cervical pseudostraightness and/or thoracic segmental deformity, the gap increases to more than a few centimeters, so that the occipital area cannot be placed against the wall. ②Thoracic extension: The normal value of the difference between the range of thoracic extension during deep inspiration and deep expiration is not less than 2.5 cm when measured at the level of the 4th rib interrogation gap, while the thoracic extension is reduced in those with extensive rib and vertebral involvement. ③Schober test: mark the vertical distance of l0 cm above the midpoint of the posterior superior iliac spine, and then ask the patient to bend over (keeping both knees in an upright position) to measure the maximum forward flexion of the spine. The distance increased by normal movement was more than 5cm, while the distance increased by spinal involvement was <4cm. ④Pelvic compression: the patient was lying on his side, and pressure on the pelvis from the other side could cause sacroiliac joint pain. ⑤Patrick's test (lower extremity "4" test): The patient lies on his back with one knee flexed and the heel placed on the opposite knee that is straight. The examiner presses the flexed knee with one hand (when the hip is in flexion, abduction and external rotation) and presses the contralateral pelvis with the other hand, which is considered positive if it leads to pain in the contralateral sacroiliac joint. Those with knee or hip lesions also cannot complete the "4" test.
The earliest change of AS occurs in sacroiliac joint. x-ray film shows blurred subchondral bone edge, bone erosion, blurred joint space, increased bone density and joint fusion in sacroiliac joint. The degree of sacroiliac arthritis on x-ray is usually classified into 5 grades: Grade 0: normal; Grade I: suspicious; Grade II: mild sacroiliac arthritis; Grade III: moderate sacroiliac arthritis; Grade IV: joint fusion ankylosis. Radiographs of the spine show vertebral osteoporosis and square changes, small joint obscuration, calcification of the paravertebral ligaments, and bone bridge formation. Extensive and severe ossifying bridges in the late stage are called “bamboo-like spine”. Bone erosion of the pubic symphysis, sciatic tuberosity, and tendon attachment points (e.g., heel bone), with reactive sclerosis and villous changes in adjacent bone, may result in new bone formation. For early clinical or suspicious cases. Ding choose CT or magnetic resonance imaging (MRI) examination, because the radiation of CT is larger than ordinary x-ray, should be used only as a diagnosis, should not be repeatedly examined.
3.4. Laboratory tests: in active patients, the town sees an increased erythrocyte sedimentation rate (ESR) and an increased C-reactive protein (CRP). Mild anemia and mildly elevated immunoglobulins. Rheumatoid factor (RF) is mostly negative, but a positive RF does not exclude the diagnosis of As. Although the HLA-B27 positivity rate in patients with As is about 90%, it is not diagnostic specific. HLA-B27-negative patients cannot exclude the possibility of AS as long as the clinical manifestations and imaging examinations meet the diagnostic criteria.
4.Diagnostic criteria
In recent years, the New York criteria for As, which were revised in 1984, are more commonly used. For those who temporarily do not meet the above criteria, reference can be made to the diagnostic criteria regarding spondyloarthropathy (SpA), mainly including Amor, the European Spondyloarthropathy Study Group (ESSG) and the 2009 ASAS recommended classification criteria for mid-axis SpA, the latter two being subdivided as follows.
4.1, the revised AS New York criteria in 1984: ① lower back carbuncle lasting at least 3 months, pain improving with activity but not relieved by rest; ② restricted movement of the lumbar spine in the anterior-posterior and lateral flexion directions; ③ thoracic extension van heel less than the normal value for the same age and sex; ④ bilateral sacroiliac arthritis grade II-IV, or unilateral sacroiliac arthritis grade III-IV. If the patient has ④ and any 1 of ①～③ respectively, the diagnosis of AS can be confirmed.
4.2, ESSG diagnostic criteria: inflammatory spinal pain or asymmetric synovitis mainly in the joints of the lower extremities with any of the following additional l items, namely: ① positive family history; ② psoriasis; ③ inflammatory bowel disease; ④ urethritis, cervicitis or acute diarrhea within 1 month before arthritis; ⑤ alternating bilateral hip pain; ⑥ tendon telangiectasia; ⑦ sacroiliac arthritis. Those who meet the town were included in this category for diagnosis and treatment, and were followed up and observed.
4.3, 2009 ASAS recommended classification criteria for mid-axis SpA: patients with age of onset <45 years and low back pain I >3 months, plus 1 of the following criteriag ① imaging suggestive of sacroiliac arthritis plus ≥1 of the following SpA features; ② HLA-B27 positive plus ≥2 of the following other SpA features. Imaging suggestive of sacroiliac arthritis refers to: (i) MR! suggestive of active (acute) inflammation of the sacroiliac joint, highly suggestive of sacroiliac arthritis associated with SpA or (ii) definite imaging changes of sacroiliac arthritis (according to the New York criteria revised in 1984). spA features include: (i) inflammatory back pain; (ii) arthritis; (iii) onset and endpoint inflammation (Achilles tendon); (iv) oculocutaneous uveitis; (v) finger (toe) inflammation; (vi) psoriasis; ⑦ Crohn’s disease, ulcerative colitis; ⑧ good response to non-steroidal anti-inflammatory drugs (NSAIDs); ⑨ family history of SpA; ① HLA-B27 positive; ⑩ elevated CRP.
5, Differential diagnosis
5.1. Disc herniation: It is one of the common causes of low back pain. The disease is limited to the spine, without fatigue, wasting, fever and other systemic manifestations, mostly of acute onset, and mostly limited to lumbar pain. It is aggravated by activity and relieved by rest; there is often lateral flexion when standing. On palpation, there were l or 2 tender trigger points in the spinal bony prominence. All laboratory tests were normal. The main difference between it and AS ding is confirmed by CT, MR! or spinal canal angiography. Lumbar x-ray narrowing of the intervertebral space or anterior narrowing and posterior widening or anterior-posterior equal widening; posterior superior or inferior angular chip-like hyperplasia of the vertebral body margin or the presence of free small bone masses; confirmed by CT town.
5.2, diffuse idiopathic bone hypertrophy (DISH) syndrome: the onset is mostly in men over 50 years of age, who also have spinal pain, stiffness, and gradually increasing spinal motion limitation. The clinical presentation and x-ray findings are often similar to those of Asj, however, ligamentous calcification is seen on x-ray in this disease. The cervical and low thoracic vertebrae are often involved, and flowing calcifications and ossifications connecting at least 4 anterolateral vertebral bodies are often seen, while there is no erosion of the sacroiliac and spondylolisthesis joints, no increase in morning stiffness, normal ESR and negative HLA-B27.
5.3, iliac dense osteoarthritis: Most commonly seen in middle-aged and young women, especially those with a history of multiple pregnancies, childbirth, or those engaged in long-term standing occupations. The main manifestation is chronic lumbosacral pain. It is aggravated by exertion and is self-limiting. There is no abnormality in clinical examination other than muscle tension in the lumbar region. The diagnosis mainly relies on anteroposterior radiographs. Typically, there is an obvious osteosclerotic area in the middle and lower 2/3 of the iliac bone along the sacroiliac joint, triangular in shape with the tip upward, uniform in density, without invading the sacroiliac joint surface, without joint stenosis or erosion, with clear boundaries, and normal bone and joint space on the sacral side.
5.4.Other: AS is the prototype of SpA and must be differentiated from other SpA associated with sacroiliac arthritis such as psoriatic arthritis, enteropathic arthritis or Wright syndrome in the diagnosis. In addition, osteoarthritis of the spine, RA and tuberculosis involving the sacroiliac joint or spine need to be further differentiated based on other relevant II per bed features.
6. Treatment goals, protocols and principles
6.1, AS patients treatment goals
(1) Relief of symptoms and signs: eliminate or minimize symptoms such as back pain, morning stiffness and fatigue as much as possible. ② Restoration of function: to restore the patient’s physical function to the maximum extent possible. Such as spinal mobility, social mobility and r working ability. ③Prevent joint damage: To prevent new bone formation, bone destruction, bony ankylosis and spinal deformation in patients with involvement of the hip, shoulder, mid-shaft and peripheral joints. ④Improve the quality of life of patients: including socioeconomic factors, ding work, disease retirement, and retirement. ⑤ Prevent complications of spinal diseases: prevent spinal fractures and flexion contractures, especially in the cervical spine.
6.2. Treatment options and principles
There is no radical cure for AS. However, patients can achieve symptom control and improve prognosis if they are diagnosed and treated reasonably in a timely manner. Comprehensive treatment such as non-drug, drug and surgery should be used to relieve pain and stiffness, control or reduce inflammation, maintain good posture, prevent deformation of the spine or joints, and correct deformed joints if necessary, in order to improve and enhance patients’ quality of life.
6.2.1. Non-pharmacological treatment
①Education of patients and their families about the disease is an indispensable part of the overall treatment plan, which helps patients to actively participate in treatment and cooperate with physicians. The long-term plan should also include the patient’s psychosocial and rehabilitation needs. ② Advise patients to be reasonably and consistently physically active to obtain and maintain the best position of the spinal joints, strengthen the paravertebral muscles and increase lung capacity; swimming is one of the good and effective adjuncts to treatment. ③Standing should try to maintain a posture with chest up, abdomen in and eyes flat in front. The sitting position should also keep the chest upright. One should sleep on a hard bed and take more supine positions to avoid positions that promote flexion deformity. Pillows should be short and should be discontinued once J: thoracic or cervical spine involvement occurs. ④ Give necessary physical therapy to painful or inflamed joints or soft tissues. ⑤ Advise smokers to quit smoking; patient smoking is one of the risk factors for poor functional prognosis.
6.2.2. Drug therapy
6.2.2.1, NSAIDs: They can rapidly improve patients’ low back pain and morning stiffness, reduce joint swelling and pain and increase range of motion, and are preferred for symptomatic treatment of patients with early or late AS. There is a wide variety of them. The more common adverse reactions to NSAIDs are gastrointestinal discomfort and a few can cause ulcers; other less common are cardiovascular disease such as hypertension, which can be accompanied by headache, dizziness, liver and kidney damage, hematocrit, edema and allergic reactions. Physicians should select one NSAIDs drug for each patient’s specific case. Concomitant use of ≥2 NSAIDs will not only increase the efficacy, but also increase the adverse drug reactions. It may even have serious consequences. Regardless of the type of AIDs used, not only to achieve symptomatic improvement, but also to delay or control progression of the disease, it is usually recommended to continue using the appropriate drug at the appropriate therapeutic dose for a longer period of time. To assess whether a particular NSAIDs is effective, the same dose should be used consistently and regularly for at least 2 weeks. Adverse drug reactions should be monitored and adjusted promptly during the course of drug administration.
6.2.2.2 Biological agents: Anti-tumor necrosis factor (TNF)-a antagonists include etanercept, infliximab and adalimumab, whose treatment of AS has been evaluated in several randomized double-blind placebo-controlled trials with an overall efficiency of 50%-75%. Patients with unsatisfactory or intolerable results with one TNF-Q antibody may be better treated with another agent. Patients who are not satisfied with the efficacy of one TNF-Q flicker or cannot tolerate it may have better efficacy with another agent. However, its long-term efficacy and effect on axial joint x-ray lesions in AS are yet to be studied further. Studies suggest that the initial good response appears to be sustained for at least 2 years of efficacy. The use of TNF–ct antagonists may also reduce the frequency of recurrence of uveitis. Although it is recommended that TNF-et antagonists be used in patients with As who are “diagnostically definite” according to classification criteria, some studies suggest that in patients who lack radiological changes and meet the “probable” or SpA criteria of the AS classification criteria, they may be used in the following situations The most significant adverse reactions to TNF-Ot antagonists are infusion or point-of-injection reactions, ranging from nausea, headache, pruritus, and dizziness to hypotension, dyspnea, and chest pain. The most significant adverse reactions to TNF-Ot antagonists are infusion or point-of-injection reactions, ranging from nausea, headache, pruritus, dizziness to hypotension, dyspnea and chest pain. Other adverse reactions were an increased chance of infection, including common respiratory infections and opportunistic infections (e.g., tuberculosis), but the difference was not statistically significant compared with placebo. Pre-treatment screening for TB significantly reduces the incidence of TB associated with TNF-a antagonist therapy and is now routine. Exacerbations of demyelinating disease, lupus-like syndrome, and congestive heart failure have also been reported, but the incidence is low. Routine blood and urine tests, liver function, and renal function should be reviewed regularly during drug administration.
6.2.2.3. Salazosulfapyridine: It can improve joint pain, swelling and stiffness in AS, and reduce serum IgA levels and other laboratory activity indicators, and is particularly suitable for improving peripheral arthritis in patients with As. To date, there is a lack of evidence for the therapeutic effect of this product on the mesial joint lesions of AS and the improvement of disease prognosis. The usual recommended dosage is 2.0 g. per day, divided into 2-3 oral doses. Increasing the dose to 3.0 iso, d increases the efficacy but also increases the adverse effects. The product has a slow onset of action, usually 4.6 weeks after dosing. To increase patient tolerability. It is usually started at 0.25g 3 times daily and then increased by 0.25g per week until I.0g twice daily, or the dose and duration of treatment can be adjusted according to the condition or the patient’s response to treatment and maintained for l. 3 years. In order to compensate for the slow onset of action and the weak anti-inflammatory effect of salazosulfapyridine, a fast-acting NSAID is usually used in combination with it. Adverse reactions include gastrointestinal symptoms, rash, hematocrit, headache, dizziness, and reduced spermatozoa and abnormal morphology in men (recoverable with discontinuation). It is contraindicated in persons with sulfonamide hypersensitivity.
6.2.2.4. Glucocorticoids: Oral or intravenous systemic application of corticosteroids is generally not recommended for the treatment of AS because of their adverse effects and inability to arrest the course of AS. Persistent tendinopathy and persistent synovitis may respond well to local corticosteroid therapy. Anterior uveitis can be better controlled by pupil dilation and hormonal spotting. Systemic hormone or immunosuppressive therapy may be required for refractory iritis. Intra-articular glucocorticoid injections are feasible for refractory peripheral arthritis (e.g., knee) effusions that do not respond well to systemic medications, and repeated injections should be given at 3-4 week intervals, usually no more than 2. 3 times a year. Similarly, CT-guided intra-sacroiliac joint glucocorticoid injections are an option for patients with intractable sacroiliac joint pain. Similar to heel pain-like tendon telangiectasia can also be treated with local glucocorticoid injections.
6.2.2.5. Other drugs: Some male patients with refractory AS showed significant improvement in clinical symptoms, ESR and CRP after the application of thalidomide. The initial dose is 50,rig/night, with increments of 50nag every 10. 14d, to 150-200mr,/night maintenance, and 300mr is useful for maintenance outside of Won. Insufficient dosage is not effective, and the symptoms are likely to recur rapidly after discontinuation. The adverse effects of this product include drowsiness, thirst, decreased blood cells, increased liver enzymes, microscopic hematuria and tingling sensation at the fingertips. Therefore, routine blood, urine and liver and kidney functions should be checked regularly during the initial period of use. Regular neurological examination should be done for long-term drug users to detect possible peripheral neuritis in time. For patients lacking efficacy of the above treatments, methotrexate and anti-rheumatic phytomedicines (see RA diagnosis and treatment guidelines) can be used for AS peripheral joint involvement, etc. However, their efficacy on medial joint lesions is uncertain and needs further study.
6.2.3, Surgical treatment
Joint space narrowing, ankylosis and deformity caused by hip joint involvement are the main causes of disability in this disease. Artificial umbrella hip replacement is the best choice. After the replacement, the joint pain of most patients is controlled, the function of some patients is normalized or close to normal, and the life expectancy of the replaced joint is 90% of lO years or more.
7. Course and prognosis
It should be emphasized that the severity of the disease varies greatly in clinical manifestations, with some patients experiencing repeated and continuous progression and others in a relatively stable state over time. Patients with mild AS with only localized involvement can maintain almost full function and employability. However, some patients develop severe limitations in skeletal activity or life-threatening extramusculoskeletal complications. There is usually individual variation in disease activity. Symptoms usually persist for decades. Rarely, a “bum-out” period of disease activity may occur, followed by long-term remission. The risk of developing lymphoma in AS does not appear to be significantly increased. Several indicators have been shown to be informative in determining the prognosis of AS, including: hip osteoarthritis; salami-like fingers or toes; poor efficacy of NSAIDs; elevated ESR (>30mill/1 h); limited lumbar spine mobility; oligoarthritis and age of onset <16 years. Other factors may also be associated with poor prognosis in patients with AS, such as smoking, progressively worsening radiological changes, active lesions (as assessed by the Disease Activity Index), functional impairment (as assessed by self-report), low educational attainment, presence of other SpA-related conditions (e.g., psoriasis, inflammatory bowel disease), male gender, history of uveitis, and a variety of conditions involving kinesthetic flexibility (ability to bend rapidly, repeatedly and twisting and stretching) or occupational activities that involve body vibration (e.g., driving a truck or operating heavy equipment). In addition, the prognosis is poor for delayed diagnosis, untimely and unreasonable treatment, and non-adherence to long-term functional exercise. Long-term follow-up under the supervision of a specialist should be emphasized.