Ankylosing spondylitis

Introduction to ankylosing spondylitis Ankylosing spondylitis (AS) is a chronic progressive inflammatory disease that mainly affects the spine and can affect the ankle joint and surrounding joints to varying degrees. The disease is also known as Marie-strümpell disease, VonBechterew disease, rheumatoid spondylitis, deformity spondylitis, rheumatoid center type, etc., now known as AS. AS is characterized by inflammation and ossification of the lumbar, cervical and thoracic spinal joints and ligaments, and the ankle joint. The hip joint is often involved and inflammation can occur in other surrounding joints. The disease is generally negative for rheumatoid factor, so it is associated with Reiter syndrome, psoriatic arthritis, enteropathic arthritis and other seronegative spondylosis. basic knowledge The proportion of illness: 0.005% - 0.009% Susceptible people: no specific population Mode of infection: non-infectious Complications: aortic regurgitation atrioventricular block obstruction pericarditis myocarditis pleurisy osteoporosis spinal cord compression prostatitis

Causes of ankylosing spondylitis

Genetic factors (30%):

Genetic factors play an important role in the pathogenesis of AS. According to epidemiological investigation, the positive rate of HLA-B27 in AS patients is as high as 90% to 96%, while the positive rate of HLA-B27 in the general population is only 4% to 9%.

Infection and autoimmunity (30%):

The incidence of AS may be related to infection. Ebrimger et al found that the detection rate of Klebsiella pneumoniae in stools of AS patients was 79%, while that in the control group was <30%. It was found that 60% of AS patients had elevated serum complement, and most cases had IgA type. Wet factor, serum C4 and IgA levels were significantly increased, circulating immune complexes (CIC) in serum, but the nature of the antigen was not determined, the above phenomenon suggests that the immune mechanism is involved in the pathogenesis of this disease.

Other factors (30%):

Trauma, endocrine, metabolic disorders and allergies are also suspected as pathogenic factors. In short, the etiology of the disease is currently unknown. There is no single theory that can fully explain the full performance of AS, and it is likely to be affected by environmental factors based on genetic factors ( Including infections and other effects that cause illness.

(1) Causes of the disease

The etiology of AS has not yet been fully elucidated, and most of them are related to genetics, infection, and immune environment factors.

1. Inheritance: The incidence of AS in HLA-B27-positive patients is about 10% to 20%, while the incidence in the general population is 1~2, which is about 100 times. It is reported that the risk of AS in a group of relatives of AS is higher than that of the average person. 20 to 40 times higher [12], the domestic survey of AS first-degree relatives prevalence rate is 24.2%, 120 times higher than the normal population, HLA-B27 positive healthy, relatives occur AS is much more likely than HLA-B27 positive AS The relatives of the patients are low, all of which indicate that HLA-B27 is an important factor in the pathogenesis of AS.

However, it should be noted that on the one hand, not all HLA-B27-positive patients have spondyloarthropathy. On the other hand, about 5% to 20% of patients with spondyloarthropathy have negative HLA-B27, suggesting that in addition to genetic factors, Other factors affect the onset of AS, so HLA-B27 is an important genetic factor in AS expression, but it is not the only factor affecting the disease. There are several hypotheses that can explain the joints of HLA-B27 and spondyloarthropathy:

1HLA-B27 acts as a receptor site for an infectious agent;

2HLA-B27 is a soil modification of immune response genes, determining the susceptibility to environmental stimuli;

3HLA-B27 can cross-react with foreign antigens to induce tolerance to foreign antigens;

4HLA-B27 enhances neutrophil activity, assisted by monoclonal antibodies, cytotoxic lymphocytes, immunoelectrophoresis and restriction fragment length polymorphism. It has been determined that there are about 7 or 8 HLA-B27 species. Subtype [1], HLA-B27-positive healthy individuals may have genetic differences with spine disease patients. For example, all HLA-B27 individuals have a constant HLA-B27M1 epitope, and antibodies against this antigenic determinant can be associated with HLA. -B27 cross-reaction, most HLA-B27 molecules also have M2 epitopes, HLA-B27M2 negative molecules seem to have stronger association with other HLA-B27 subtypes than AS, especially Asians, and HLA-B27M2 positive subtypes It may be susceptibility to Reiter's syndrome. It has been shown that HLA-B27M1 and M2 antigenic determinants and joint-causing factors, S. cerevisiae, Shigella and Nasrogen can cross-react, and the response is low. It seems that many manifestations are AS, and those with enhanced response develop into reactive arthritis or Reiter syndrome.

2, infection: recent studies suggest that the incidence of AS may be related to infection, the carrier rate of Klebsiella pneumoniae in the active phase of AS and the IgA antibody titer against the bacteria in the serum are higher than the control group, and There was a positive correlation between disease activity and some people who had increased cross-reactivity or common structure during the antigenic residue of Klebsiella and HLA-B27, such as HLA-B27 (host antigen residues 72 to 77) and lungs were Klebsiella (residual Bases 188 to 193) have a homologous oxyacid sequence, and whether other gram-negative bacteria have antibodies that bind to this synthetic peptide sequence, 29% of HLA-B27-positive AS patients, and only 5% of the control group [ 15], Mason et al., 83% of male AS patients with prostatitis, some authors found about 6% ulcerative colitis with AS; other reports also confirmed the incidence of ulcerative ulcers and localized enteritis in AS patients It is much higher than the general population, so it is speculated that AS may be related to infection. Romonus believes that pelvic infection may spread to the ankle joint through the lymphatic route, and then spread to the spine through the spinal venous plexus, but the infection is not found in the lesion ( Bacteria or virus).

(two) pathogenesis

The etiology of AS has not yet been fully elucidated. In recent years, molecular mimicry has comprehensively explained the various aspects of the disease from different perspectives. Epidemiological investigation combined with immunogenetic studies found that HLA-B27 is ankylosing spondylitis. The positive rate in patients is over 90%, which proves that AS is related to heredity. Most scholars believe that it is related to heredity, infection, immunity and environmental factors.

1. Genetics: Genetic factors play an important role in the pathogenesis of AS. According to epidemiological investigation, the positive rate of HLA-B27 in AS patients is as high as 90% to 96%, while the positive rate of HLA-B27 in general population is only 4% to 9%. The incidence of AS in HLA-B27 positive patients is about 10% to 20%, while the incidence rate in the general population is 1% to 2%, which is about 100 times. It is reported that the risk of AS in first-degree relatives of AS patients is higher than that of the average person. 20 to 40 times, the prevalence rate of first-degree relatives of AS patients in China is 24.2%, which is 120 times higher than that of normal people. In HLA-B27-positive healthy people, the incidence of AS in relatives is much lower than that of HLA-B27-positive AS patients. All of these indicate that HLA-B27 is an important factor in the pathogenesis of AS, but it should be noted that on the one hand, not all HLA-B27-positive patients have spondyloarthropathy, on the other hand, about 5% to 20% The detection of HLA-B27 in patients with spondyloarthropathy is negative, suggesting that in addition to genetic factors, there are other factors affecting the pathogenesis of AS. Therefore, HLA-B27 is an important genetic factor in AS expression, but it does not affect the disease. The only factor, there are several hypotheses that explain the relationship between HLA-B27 and spondyloarthropathy:

(1) HLA-B27 acts as a receptor site for an infectious agent.

(2) HLA-B27 is a marker of immune response genes and determines susceptibility to environmental stimuli.

(3) HLA-B27 can cross-react with foreign antigens to induce tolerance to foreign antigens.

(4) HLA-B27 enhances neutrophil activity.

With the help of monoclonal antibodies, cytotoxic lymphocytes, immunoelectrophoresis and restriction fragment length polymorphism, it has been determined that there are about 7 or 8 subtypes of HLA-B27, and HLA-B27 positive healthy people and spinal disease patients may have inheritance. Differences, for example, all HLA-B27 positive individuals have a constant HLA-B27M1 epitope, and antibodies against this epitope can cross-react with HLA-B27, and most HLA-B27 molecules also have M2 epitopes. HLA-B27M2 negative molecules appear to be more strongly associated with AS than other HLA-B27 subtypes, especially in Asians, and HLA-B27M2 positive subtypes may have increased susceptibility to Reiter syndrome. HLA-B27M1 has been shown to M2 two antigenic determinants and arthritis factors such as Klebsiella, Shigella and Yersin can cross-react, the lower response seems to be mostly AS, and the reaction enhancer develops into reactive arthritis or Reiter syndrome.

2. Infection: Recent studies suggest that the incidence of AS may be related to infection. It is found that the carrier rate of Klebsiella pneumoniae in patients with AS during the active phase of AS and the IgA antibody titer against the bacteria in the serum are compared with the control. The group was high and positively correlated with the disease activity. It was suggested that Klebsiella and HLA-B27 may have cross-reactivity or common structure between antigen residues, such as HLA-B27 host antigen (residues 72-77) and pneumonia The common amino acid sequence of R. brevis (residues 188-193) is unclear. It is unclear whether other Gram-negative bacteria have the same sequence. Immunochemical analysis found that about 50% of the serum of HLA-B27-positive Reiter syndrome patients have antibodies. In combination with this synthetic peptide sequence, 29% of HLA-B27-positive AS patients, compared with 5% in the control group, according to statistics, 83% of male AS patients with prostatitis, some scholars found about 6% ulcerative Patients with colitis have AS, and other reports have confirmed that the incidence of ulcerative colitis and localized enteritis in AS patients is much higher than in the general population, so it is speculated that AS may be associated with infection.

3. Others: It has been found that 60% AS patients have elevated serum complement levels. Most cases have IgA rheumatoid factor, serum C4 and IgA levels are significantly increased, and circulating immune complexes are present in the serum, but the antigenic properties are not determined. Phenomenon suggests that the immune mechanism involved in the pathogenesis of the disease, trauma, endocrine, metabolic disorders and allergies are also suspected as pathogenic factors. In short, the cause of the disease is currently unknown, and there is no theory that can fully explain the full performance of AS, it is likely On the basis of genetic factors, it is affected by various factors such as environmental factors (including infection).

4. Pathology: The early histopathological features of this disease are different from those of rheumatoid arthritis. The basic pathological changes are tendon and ligament bone attachment lesions. A certain degree of synovial inflammation can also occur. Joint adhesion, fibrosis and bony rigidity can occur, histological changes are chronic inflammation of the joint capsule, tendon, ligament, accompanied by lymphocytes, plasma cell infiltration, these inflammatory cells are clustered around the small synovial blood vessels There may also be chronic inflammatory lesions in adjacent bone tissue, but the inflammatory lesions are not related to the pathological process of synovium. The difference between this disease and the pathological changes of rheumatoid arthritis is joint and para-articular tissues, ligaments, intervertebral discs. And the annular fibrous tissue has obvious calcification tendency. The histological changes of the peripheral joint synovitis of this disease are not the same as those of rheumatoid arthritis. The synovial plasma cells are mainly IgG type and IgA type, and the synovial lymph. There are many cells, and macrophages that phagocytose denaturing multinucleated cells are seen. Synovial inflammation rarely has extensive erosion and deformity changes.

Ankle arthritis is a pathological hallmark of ankylosing spondylitis and is often one of its earliest pathological manifestations. Early pathological changes of sacroiliitis include the formation of subchondral granulation tissue, histologically visible synovial hyperplasia and lymphoid cells. And plasma cell aggregation, lymphoid follicle formation and plasma cells containing IgG, IgA and IgM, bone erosion and cartilage destruction occur, and then gradually replaced by degenerated fibrocartilage, eventually osteogenic, spinal The initial damage is the formation of granulation tissue at the junction of the intervertebral disc annulus and the vertebral edge. The outer layer of the annulus may eventually be replaced by bone to form a ligament callus. Further development will form a bamboo-like spine seen by X-rays. Other damages of the spine include Diffuse osteoporosis, vertebral destruction near the edge of the disc, vertebral body square and disc hardening, and other pathological changes of the central joint can also be observed in other spondyloarthropathy.

Peripheral joint pathology of ankylosing spondylitis shows synovial hyperplasia, lymphoid infiltration and vasospasm formation, but no rheumatoid arthritis common synovial villus proliferation, fibrogenic deposition and ulcer formation, in ankylosing spondylitis, subchondral granulation Tissue hyperplasia often causes cartilage destruction, and other chronic spondyloarthropathy can also see similar synovial pathology, but the early lesions of Wright syndrome are highlighted by more pronounced polymorphonuclear leukocyte infiltration.

Tendonitis is another pathological hallmark of spondyloarthropathy. It is inflammation that occurs in the ligament or tendon attached to the bone. In ankylosing spondylitis often occurs around the spine and pelvis, which may eventually lead to ossification in other spinal joints. The disease is more common in the periphery than in the calcaneus. The latest research shows that the cartilage destruction of ankylosing spondylitis mainly starts from the subchondral bone, and the inflammation of the tendon and bone joint gradually develops toward the cartilage (from the inside out). ), while rheumatoid arthritis is mainly caused by synovitis, and the destruction of cartilage and subchondral bone gradually (from the outside to the inside).

Ankylosing spondylitis prevention

1. Pay attention to prevent cold and dampness: the cause of this disease is closely related to the invasion of external evils such as wind, cold and dampness. Therefore, it is especially important to prevent the cold, dampness, etc., especially when the body is weak, when the season changes, the climate When the drama changes, it is necessary to increase or decrease clothes in time; summer heat or summer delivery, can not wind and lie, live in wet or rainy season, sunny weather should be often exposed, to tidal moisture, when the weather is fine, open the window, to ventilate Wet, etc., in the daily life, pay attention to shelter from the wind, cold, dehumidification, and cut off the road, is a good strategy to prevent nursed back to health.

2, adhere to regular exercise: adhere to regular exercise can enhance physical fitness, improve the ability of the evil spirits, because "the shackles, closed also", the wind and cold dampness within the stagnation, stagnation of blood, through the active limbs, so that the whole body qi and blood Adjust the balance of yin and yang in the body, and achieve the purpose of strengthening the body and reducing the disease for a long time. However, you should pay attention to choosing the appropriate mode of activity according to your own physical condition during exercise. Do not exercise too much, excessive force, must be gradual, expensive Persistence, if necessary, please consult the doctor or the relevant personnel. In addition, the morning exercise in the cold season should not be too early, from the cold, and is not good for the disease.

3, to maintain a happy spirit: the occurrence of disease in a person's mental state has a close relationship, therefore, the seven emotions can be directly caused by internal injuries, can also be caused by the seven emotions of internal injuries caused by yin and yang disorders, blood loss, resistance weakened, and Easy to invade the evil spirits, therefore, to avoid emotional excitement or sullenness, melancholy, to maintain a good spirit to bring good health, righteous memory, illness and safety.

Ankylosing spondylitis complications Complications aortic valve insufficiency atrioventricular block obstruction myocarditis myocarditis pleurisy osteoporosis spinal cord compression prostatitis

AS can invade multiple systems throughout the body and develop multiple diseases:

1, heart disease: aortic valve lesions are more common, according to autopsy, about 25% of AS cases have aortic root lesions, cardiac involvement can be clinically asymptomatic, can also have obvious performance, clinically different degrees of aortic valve About 1% of patients with insufficiency; about 8% of heart block, can occur alone with aortic regurgitation, severe cases of A-Syst syndrome due to complete atrioventricular block, when the lesion involves the coronary Aortic aneurysm, pericarditis and myocarditis can occur in the arterial orifice. A few patients with AS have a higher age, a longer history, more spondylitis and peripheral joint lesions, and more obvious systemic symptoms. Gould et al examined the cardiac function of 21 patients with AS and found that the cardiac function of patients with AS was significantly lower than that of the control group.

2, eye lesions: long-term room, 25% of patients with conjunctivitis, iritis, uveitis or uveitis, the latter can sometimes be spontaneous anterior chamber hemorrhage, iritis is easy to relapse, the longer the disease occurs The higher the rate, but not related to the severity of spondylitis, common in peripheral joint disease, a few can occur before spondylitis, eye disease is often self-limiting, sometimes with corticosteroid treatment, and some without proper treatment Can cause glaucoma or blindness.

3. Ear lesions: Gamilleri et al reported that 1/2 (29%) of 42 patients with AS developed chronic otitis media, which was 4 times higher than that of normal controls. Moreover, in patients with chronic otitis media, the joints were significantly more extra-articular. AS patients without chronic otitis media.

4, lung lesions: a small number of patients with AS can be accompanied by irregular fibrotic lesions of the lung lobe, manifested as cough, asthma, and even hemoptysis, and may be accompanied by recurrent pneumonia or pleurisy, X-ray examination showed bilateral Diffuse fibrosis of the upper lobe of the lung may have cyst formation and substantial destruction, similar to tuberculosis, which needs to be identified.

5, neurological disease: due to spinal rigidity and osteoporosis, easy to cause cervical dislocation and spinal fracture, and cause spinal cord compression; such as the occurrence of discitis caused by severe pain; AS can invade the horsetail in the late stage, the occurrence of cauda equina syndrome, and Causes radiculopathy of the lower extremities or buttocks; loss of infection in the sacral nerve distribution area, decreased Achilles tendon reflexes, and motor dysfunction such as the bladder and rectum.

6, amyloidosis: AS is rare in the concurrent, there are reports of 35 cases of AS, conventional rectal mucosal biopsy found that 3 cases of amyloid deposition, most have no special clinical manifestations.

7, kidney and prostate lesions: compared with RA, AS rarely occurs renal damage, but there are reports of IgAD nephropathy, AS complicated with chronic prostatitis increased compared with the control group, its significance is unknown.

Ankylosing spondylitis symptoms Common symptoms Continuous low back pain associated with morning stiffness of spinal canal size changes Spinal physiological curvature disappears Back pain, joint contracture, bed rest, paraplegia, fatigue, proteinuria, sciatica

1. Clinical overview: The relationship between HLA-B27 discovered 25 years ago and ankylosing spondylitis and spondyloarthropathy has broadened our understanding of these diseases. These diseases are caused by tendonitis and fingertip inflammation. Or less onset of arthritis, some cases can develop into arthritis and spondylitis, with or without extra-articular manifestations such as acute anterior uveitis or skin mucosal damage, inflammation of the tendon at the beginning of the tendon (Figure 1), occurs In the foot (bottom fasciitis and/or calcaneus periostitis and Achilles tendinitis can cause heel pain), tibial tuberosity and other parts, and often lack of obvious inflammatory bowel disease, psoriasis or Intestinal or genitourinary infection, the tendon end is infiltrated by lymphocytes, plasma cells and polymorphonuclear leukocytes, and the adjacent bone marrow cavity also appears edema and infiltration. The prominent feature of ankylosing spondylitis is that the axial muscle end The high incidence of inflammation and synovitis eventually leads to fibrosis of the ankle and spine and advanced bony rigidity.

Although all patients with ankylosing spondylitis have different degrees of ankle joint involvement, it is rare to have a complete fusion of the spine in the clinic. The inflammatory low back pain caused by ankle arthritis is occult, difficult to locate, and feels Pain in the deep buttocks, at the beginning of the disease, the pain is often unilateral and intermittent, gradually becoming bilateral and persistent after a few months, and pain in the lower lumbar region, the typical symptom is the time to fix a certain posture Longer or wake up in the morning when the symptoms worsen ("morning stiffness"), while physical activity or hot water bath can improve symptoms, tendonitis, is the main feature of spondyloarthropathy, inflammation originates from the attachment of the affected joint ligament or joint capsule In the bone, near the joint ligament and in the synovial membrane, cartilage and subchondral bone, synovitis of spondyloarthropathy is often associated with clinically undetected tendonitis, at least in some joints, this synovitis is only one A secondary inflammation.

Because of the connection of the thoracic ribs, the spinous process, the humeral condyle, the ischial tuberosity, and the tendonitis of the calcaneus, the tenderness of the bone outside the joint or near the joint is an early feature of this disease. Only a few patients have no or only Very mild low back symptoms, while other patients may simply complain of stiffness in the back, muscle pain and tenderness of the tendons, cold or damp can make the symptoms worse, and this part of the patient is often misdiagnosed as fibromyalgia syndrome, early disease Some patients may also have mild systemic symptoms such as anorexia, fatigue or hypothermia. Especially in young patients, these symptoms are more common. The costal cartilage and ribs, tendonitis of the transverse joints of the ribs can cause chest pain. Because of this chest pain, with coughing or sneezing, it is easy to be misdiagnosed as pleurisy.

The ratio of male to female incidence is 7:1 to 10:1. The onset is mostly males aged 15 to 30 years old. Children and those over 40 years old are rare. Ankylosing spondylitis has always been regarded as the main disease seen in men. The PLA General Hospital 20 In the 1980s, the ratio of male to female was 10.6:1. Now the study suggests that the ratio of male to female is 2:1 to 3:1. There is still a satisfactory explanation for the difference in the prevalence of ankylosing spondylitis between men and women. Pregnancy has no significant effect on this disease, and the role of sex hormones is not yet certain. The clinical features of female ankylosing spondylitis are shown in Table 1.

It is generally believed that the incidence of women is later than that of men. Peking Union Medical College Hospital reported that the average age of onset of women is 26.8 years old, 6 years older than the average age of males. The other characteristic of female ankylosing spondylitis is peripheral arthritis, especially the incidence of knee involvement. Compared with men, 200 cases of Peking Union Medical College Hospital analyzed the incidence of peripheral arthritis, which was slightly higher, 57% to 48%, similar to the report of Shantou University Medical College. In addition, female pubic symphysis was more common than men, but the central axis joint The affected is relatively rare and mild, so it is often misdiagnosed as other rheumatic diseases. In terms of the severity of the disease, it is generally considered that women are milder and have a better prognosis. Pay attention to the differences between female ankylosing spondylitis and men, which not only contributes to clinical diagnosis. And differential diagnosis is also a useful clue to the in-depth study of this disease.

Most patients have insidious onset, early symptoms of upper back, hips and hips with intermittent dull pain, stiffness or sciatica, intermittent pain, and lighter, as the disease progresses, in months or years After that, there may be persistent pain, even more severe pain. Sometimes the pain may occur in the higher part of the back, the shoulder joint and its surroundings, but the symptoms of the lower back may appear soon. The patient often feels the symptoms in the morning and after 1 day of work. Heavier, other times are lighter, the symptoms worsen when the weather is cold and humid, and can be relieved after taking salicylic acid preparation and local hot compress. Some patients first have unexplained iritis, which occurs several years or months later. Typical manifestations of ankylosing spondylitis, this type of onset is more children than adults, and occasionally, heel pain caused by palmar fasciitis or Achilles tendinitis is an early symptom, systemic symptoms are fatigue, discomfort, anorexia, weight Reduced and hypothermia, ankylosing spondylitis is a systemic disease with both joint and extra-articular manifestations.

2, arthritis performance: can involve any joint, but the spinal joint involvement is more.

(1) Most patients with sacroiliac arthritis first have symptoms of ankle joint involvement. Individual patients may also have higher symptoms of spinal arthritis first, manifested as lower back stiffness and pain, often radiating to one or both sides of the hip, occasionally emitting To the thigh, further develop to the dorsal side of the knee joint, and even extend below the knee joint. Due to local inflammation of the ankle joint, the lower extremity straightening and elevation sign is generally negative, directly pressing the diseased joint or straightening the affected side lower limb. It can induce pain. In the early stage of the disease, there may be lower back movement limitation and mild ankle paraspinal tendon. Pressing the pubic symphysis with the fingers, the humeral condyle, the ischial tuberosity can also induce pain, and the ankle joint is symmetric. Sexual, pubic symphysis can also be affected, and the patient can be fixed in a certain position (Figures 2, 3).

(2) Lumbar arthritis: Although the ankle and lumbar joints are involved at the same time, most patients with back pain and motor dysfunction are caused by lumbar joint disease, and diffuse pain begins to appear on the back, and then gradually concentrates on the waist. Sometimes severe lumbar stiffness can occur, and the patient is afraid of bending over, standing up and turning, because these actions can cause severe pain. The spinal rigidity may be caused by paravertebral muscle spasm caused by lumbar osteoarthritis. The joints may have tenderness, the paravertebral muscles are obviously paralyzed, the lumbar spine becomes straight, the movement is limited, and the normal physiological curvature of the waist disappears.

(3) Chest arthritis spondylitis progressive progressive development, thoracic joints can also be involved, at this time the patient has upper back pain, chest pain and thoracic expansion movement restriction, some of these symptoms can appear early in the course of the disease, but Most patients appear only after 6 years of onset. Chest pain usually occurs during inhalation. The limitation of thoracic expansion is mainly due to the rib cage joint, the sternum stem-sternal joint, the joint of the rib and the costal cartilage, and the sternocleidal joint. Due to involvement, limited thoracic expansion can cause dyspnea, especially during exercise. Most patients with lung function have no significant changes. This is due to the increased amplitude of diaphragmatic muscle compensation for thoracic expansion limitation. The sternum stem-sternal joint, the joint between the rib and the costal cartilage, and all the thoracic vertebrae can induce tenderness. As the disease progresses, kyphosis can occur and the thoracic activity is limited.

(4) Cervical arthritis: a small number of patients can only use cervical vertebra arthritis as an early manifestation, and the disease progresses progressively. Serious cervical kyphosis or scoliosis can occur, and the final head can be present, fixed anterior flexion, flexion, When rotating and lateral flexion, it may be partially or completely limited, and the spatial field of view is significantly smaller. The pain caused by cervical lesions may be limited to the neck, or may be radiated to the head along the neck structure, and the neck muscles begin to be severe. Finally, atrophy, root pain can be involved in the head and arms. Because of the rigidity and osteoporosis of the entire spine, it is easy to fracture due to trauma, especially in the neck. Once a neck traumatic fracture occurs, it can cause paraplegia.

(5) Peripheral arthritis: About 1/3 of the patients may have shoulder joints and hip joints, which further aggravates the patient's disabling consequences. Joint pain is often mild, but joint movement is limited, for example. Can not comb the hair or squat difficulty, etc., with the development of the disease, cartilage degeneration can occur, the structure around the joint fibrosis, and finally the formation of joint rigidity, early stage of the disease, joint movement limitation is mainly caused by muscle spasm around the joint, hip contracture Compensatory flexion of the knee joint can cause the patient to have a anterior tibiofibular flexion posture, and a duck step state, due to extensive lesions of the spinal joint, can also cause flat chest and severe hunchback.

In the late stage of ankylosing spondylitis, since the inflammation has basically disappeared, the joint has no pain, and the spine fixation and rigidity are the main manifestations. The cervical vertebrae are fixed forward, the kyphosis is fixed, the thoracic cage is often fixed in the exhaled state, and the lumbar spine is physiologically lost. Hip and knee joints are severely flexed and contracted. When standing, both eyes gaze at the ground, and the center of gravity moves forward. Individual patients can be severely disabled, staying in bed for a long time, and cannot take care of themselves.

3, extra-articular manifestations: ankylosing spondylitis can also appear many extra-articular manifestations, these performances can be primary, but most of the secondary, a small number of patients can also occur in the months before the years of spondylitis, some Extra-articular manifestations can overlap with other diseases, such as aortitis, both ankylosing spondylitis and Reiter syndrome, so ankylosing spondylitis can overlap with Reiter syndrome; heel pain is The common features of psoriatic arthritis, Reiter's syndrome, ankylosing spondylitis, and the high rate of HLA-B27 in these three patients, suggesting that the three diseases can overlap each other.

(1) Heart disease necropsy found that about 1/4 of patients had abnormal aortic root abnormalities, but aortic valve insufficiency caused by inflammation of aorta and aortic valve was more common in long course of disease, with peripheral arthritis and Patients with obvious systemic symptoms (fever and anemia), so only 5% of patients have clinical symptoms. Most patients have no symptoms. Only in the second auscultation area of the left aortic valve of the sternum can be heard weakly. The diastolic sound, clinically aortic regurgitation, cardiac enlargement and conduction abnormalities are more common, occasionally complete atrioventricular block or with the onset of A-Syndrome, aorticitis with the disease Development, angina can occur, congestive heart failure can occur in the later stages of the disease, ankylosing spondylitis in addition to aortic inflammation, but also combined with pericarditis, myocarditis and nodular polyarteritis.

(2) Pulmonary lesions: Because the diaphragmatic muscles can compensate for respiratory function, although the thoracic expansion is limited during inhalation, there are few breathing difficulties, and some patients may also have cough and cough after several years of joint symptoms. Symptoms of dyspnea and hemoptysis, the lungs showed a slight flaky dense shadow on the upper lungs, some patients may have fibrosis, some patients have cavities, and there are Aspergillus parasitic, sputum culture can produce Aspergillus, May be associated with the formation of mycosis, the thoracic expansion of the advanced patients is limited, and the lung capacity is significantly reduced.

(3) Patients with iritis about 1/4 may have recurrent iritis, and the longer the course of the disease, the more likely it is. The iritis is non-granulomatous anterior uveitis, usually unilateral, ocular lesions and spine. The severity of inflammation and the activity of the disease are more common in those with peripheral arthritis or previous history of urinary tract infection. If left untreated, it can cause glaucoma or blindness. Individual eye symptoms can occur before joint symptoms appear.

(4) Neurological diseases: The lesions of the nervous system of ankylosing spondylitis are mostly due to spinal rigidity and severe osteoporosis. Even mild trauma can easily lead to spinal cord compression caused by spinal fracture and cervical dislocation, resulting in different degrees of paraplegia. Root pain or sensory loss, as well as dyskinesia, especially cervical fractures, is the highest complication of mortality; occurs in the lumbar vertebrae, can compress the cauda equina, can become a chronic progressive cauda equina syndrome, due to spinal intervertebral disc aneurysm The ossification of the ligamentum flavum and the posterior longitudinal ligament can cause spinal stenosis. However, some literatures indicate that spinal angiography does not show spinal stenosis or oppressive operation, but the lumbosacral arachnoid diverticulum can be seen. The cause may be chronic. Arachnoiditis, some patients with initial symptoms of lower extremity pain and misdiagnosed as sciatica and disc herniation.

(5) urinary system lesions: mainly manifested as renal amyloidosis and lgA nephropathy, the incidence is similar to rheumatoid arthritis, proteinuria can occur, a small number of patients can die from uremia, the incidence of prostatitis is more common The crowd is high.

(6) systemic symptoms: systemic symptoms are generally mild, a few people have low fever, fatigue and weight loss, individual patients may have anemia, a few acute cases may also have high fever, limbs and joints are more severe, and soon can be bedridden At this time, both erythrocyte sedimentation rate and C-reactive protein can be elevated.

(7) Ear lesions: According to the literature, about 29% of patients with ankylosing spondylitis develop chronic otitis media, which is 4 times that of normal people. Patients with ankylosing spondylitis complicated with chronic otitis media are more likely to have other extra-articular lesions. Patient.

4, special signs

(1) Tests that reflect inflammation and injury of the ankle joint: if the "4" word test is positive, the ankle joint separation test is positive or the ankle joint compression test is positive.

(2) Signs of restricted spinal activity: if the Schober test is positive, the lateral curvature is limited, and the pillow wall test is positive.

The ability to touch the ground with a finger when fully extending the knee cannot be used to assess the mobility of the spine, as good hip function can compensate for the apparent limitation of lumbar motion, and the Schober test (Figure 4) can more accurately reflect The degree of lumbar anterior flexion is limited, and with the development of the disease, lumbar lordosis will gradually lose.

Direct compression of the inflamed ankle often causes pain. It can also cause ankle pain through the following examinations: compression of the humeral wing on both sides of the patient in the supine position; maximum flexion of the hip joint while maximizing the hip on the other side Joints (Gaenslen test, Figure 5); maximal flexion, abduction and external rotation of the hip joint (4-word test or Patrick test); compression of the pelvis when the patient is in the lateral position; or direct compression of the tibia in the prone position, some patients It can be without any of the above signs. On the one hand, because the ankle joint is surrounded by strong and strong ligaments, the degree of movement is very small. On the other hand, in the late stage of the disease, the inflammation has been replaced by fiber or bony rigidity.

(3) The difference between deep inhalation and deep end-tidal in the fourth rib cage is less than 2.5cm.

Examination of ankylosing spondylitis

Blood routine and blood sedimentation routine can be generally normal. Some patients may have positive cell hypochromic anemia and leukocytosis. Most patients have increased erythrocyte sedimentation rate in early or active phase, and erythrocyte sedimentation rate is normal in the later stage. ESR is helpful for clinical and X. The line shows suspicious patients for diagnosis, and urine routine can occur when the kidney develops amyloidosis.

1, blood biochemical examination white blood cell count is normal or elevated, the proportion of lymphocytes is slightly increased, a small number of patients have mild anemia (positive cells hypochromic), erythrocyte sedimentation rate can increase, but the disease activity is not significant, and C reaction Protein is more meaningful, serum albumin is reduced, 1 and gamma globulin are increased, serum immunoglobulin IgG, IgA and IgM can be increased, serum complement C3 and C4 are often increased, and about 50% of patients have elevated alkaline phosphatase, serum Creatine phosphokinase is also often elevated, serum rheumatoid factor is negative, although 90% to 95% of AS patients are LHA-B27 positive, but generally do not rely on LHA-B27 to diagnose AS, LHA-B27 is not routinely examined, the diagnosis depends mainly on Clinical presentation and radiographic evidence.

2, immunological examination of rheumatoid factor positive rate is not high, serum IgA may have a mild-to-moderate increase, and is associated with AS disease activity, accompanied by peripheral joint involvement may have IgG, IgM increased, it has been reported that AS patients can There are serum complement C3, C4 increased, anti-peptidoglycan antibody, anti-Drosophila 93000 antibody, anti-Klebsiella pneumoniae nitrogenase reductase antibody and other antibodies increased, anti-histone 3 subunit antibody is closely related to patient iritis HLA typing examined 90% of patients with HLA-B27 positive.

3. Microbiological examination The detection rate of Klebsiella pneumoniae in patients with AS was higher than that of normal people.

4, HLA-B27 detection HLA-B27 detection has certain help in the diagnosis of ankylosing spondylitis, but most patients can only make a diagnosis by medical history, physical signs and X-ray examination, although the test for some races It is highly sensitive to diagnosis, but for patients with ankylosing spondylitis with low back pain, it is not used as a routine examination, nor as a screening test for diagnosis and exclusion diagnosis. Its clinical use depends largely on The background of the test.

5, X-ray examination of ankylosing spondylitis

(1) ankle joint changes: This is the main basis for the diagnosis of this disease, it can be said that a normal ankle X-ray film can almost rule out the diagnosis of this disease, the early ankle joint X-ray changes than the lumbar spine More characteristic, easier to identify, in general, the ankle joint can be changed in three phases:

1 Early: The edges of the joints are blurred and slightly dense, and the joint gap is widened.

2 mid-term: stenosis of the joint space, osteoporosis and dense hyperplasia of the joint edge, staggered.

3 Late stage: the joint space disappeared, and the trabecular bone passed through, showing a bone fusion.

However, scholars still use the 1966 New York radiological standard to classify ankle arthritis of ankylosing spondylitis into five grades: grade 0 is normal; grade I is suspicious; grade II is mildly abnormal; grade III is markedly abnormal Grade IV is a severe abnormality and the joint is completely stiff.

(2) Spinal changes: the lesion develops to the middle and the late can be seen:

1 The ligament callus (ie, the intervertebral disc fiber ossification) is formed, even with bamboo-like spine fusion (Fig. 6).

2 square vertebrae.

3 general osteoporosis.

4 articular joints are corroded, narrow, and stiff.

5 vertebral ligament ossification, the ligament of the ligamentum flavum, interspinous ligament and intervertebral annulus is the most common (late stage bamboo-like spine).

6 spinal deformity, including: lumbar and cervical lordosis disappeared or kyphosis; thoracic physiologic kyphosis increased, hunchback deformity occurred in the lumbar and lower thoracic segments.

7 intervertebral disc, vertebral arch and vertebral fatigue fracture and atlantoaxial subluxation.

(3) hip and knee joint changes: hip joints are often bilateral, early osteoporosis, closed hole shrinkage, joint capsule expansion; mid-term visible joint space stenosis, joint edge cystic changes or acetabular rim and femoral head marginal bone Hyperplasia (formation of ligament callus); in the late stage, the joint space disappeared, the trabecular bone passed, and the joint was bony.

(4) Changes in tendon attachment points: mostly bilateral, early intimate bone infiltration and surface erosion, late formation of ligament callus (osteoporosis, marginal irregularities).

Primary AS is associated with inflammatory bowel disease, Reiter syndrome, psoriatic arthritis, etc. with spondylitis, X-ray findings are similar, but the latter is asymmetrical ankle arthritis with spinal irregularities The performance of jumping lesions can be identified.

Other X-ray manifestations of the external joints of the spine may also have osteoporosis of the shoulder joint, mild erosion of the lesion, narrowing of the joint space, destruction of the articular surface, and finally bony rigidity, in the ligament, tendon, and bursa attachment. Osteitis and periostitis can occur, most commonly seen in the calcaneus, ischial tuberosity, humeral condyle, etc., similar X-ray changes can occur in other surrounding joints.

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6CTMRI XCTMRICTXXMRICT(ECT)99m-(99mTc-MDP)(SPECT)AS

diagnosis

1

(1)

(2)<40

(3)3

(4)

(5)

X;ReiterAS

2AS

(1)(1963)

3

(2)(1984)

()

42.5cm

34;342123

34

X(X)

Differential diagnosis

1X

2AS;X

3Forestier() AS

4ASX

5ASRARARFHLA-B27

6(Whipple)XAS;;WhippleHLA-B27CrohnIgGASIgG

7Reiter()AS;

8

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