关节镜在诊治急性踝关节痛风性关节炎中的应用

目的提高对单纯踝关节起病的急性痛风性关节炎的诊断认识并加强其早期治疗。方法回顾总结1999年以来,关节镜检查发现的14例踝关节急性痛风性关节炎的诊治经过,经过半年以上的随访,进行疗效观察。结果14例病人术前均误诊,分别诊断为化脓性关节炎、类风湿性关节炎、急性滑膜炎、骨性关节炎。全部病例在踝关节镜检查后发现确诊。并一期行关节镜下清理术,术后配合以系统药物治疗,经过随访观察,近、远期均取得满意疗效。结论单纯以踝关节起病的急性痛风性关节炎少见,且容易误诊,随着关节镜技术的不断提高和广泛应用,其诊断率将会获得提高,同时亦为早期治疗急性痛风性关节炎增加了一个新的方法。关节镜下手术仅是急性痛风性关节炎的一种局部治疗方法,它可以防止晚期骨性关节炎的早期发生,但不能代替排酸、抑酸及饮食控制的治疗。     

Causes and management of shoulder arthritis

We recommend that physicians distinguish shoulder arthritis from periarticular disorders. A specific diagnosis should be made in the former, if possible. A number of arthritides have frequent shoulder involvement, and they should be kept in mind. Septic arthritis should always be suspected when there is acute pain and swelling. Joint fluid aspiration should almost always be performed when fluid is present. The diagnosis of gout or CPPD deposition disease usually requires crystal identification from joint fluid for diagnosis. Treatment of shoulder arthritis with oral anti-inflammatory medication is usually indicated; appropriate treatment of the underlying disorder, e.g., rheumatoid arthritis, is necessary. Physical therapy started early, often combined with IA corticosteroids, helps to maintain or improve shoulder motion.     

Diagnosis of rheumatic disease. 1. Radiographs.

Radiographs are a clinician's most valuable tool in differential diagnosis of rheumatic disease and in assessment of its severity. The patterns of joint involvement and the specific bony changes characteristic of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, Reiter's syndrome and psoriatic arthritis, gout, and systemic lupus erythematosus are discussed here.     

磁共振成像在早期风湿病骨关节病的诊断价值

风湿病骨关节病包括一系列以滑膜炎为特点,并导致软骨、骨、关节、肌肉和韧带等损伤的复杂疾病,如类风湿性关节炎(RA)、强直性脊柱炎(AS)、骨关节炎(OA)、系统性红斑狼疮(SLE)、痛风和硬皮病等.这些病变将最终导致关节畸形和功能障碍,早期干预治疗能够延缓病情的进展,因此早期诊断尤为重要.MRI对滑膜、软骨以及肌腱软组...     

国医大师熊继柏辨治顽痹经验举隅

国医大师熊继柏教授临床上善于诊治各种疑难杂症,本文列举熊老诊治顽痹医案-类风湿关节炎案、痛风案、系统性红斑狼疮案、强直性脊柱炎案共4例,通过对上述异病同治案例的分析,展示熊继柏教授的辨证思路,并为临床上治疗顽痹提供参考。     

Purine metabolism enzymes in diagnosis and differential diagnosis of osteoarthritis and gout arthritis

AIM: To characterize purine metabolism in osteoarthritis (OA) and gout arthritis (GA) diagnosis and differential diagnosis of these diseases. MATERIALS AND METHODS: We estimated xanthine oxidase (XA), xanthine dehydrogenase (XDG), 5'-nucleotidase (5'-NT) activity, esoenzymes of XDG and content of uric acid (UA) in the sera of 44 patients with osteoarthritis and 34 patients with gout arthritis. RESULTS: Hyperuricemia was revealed in 25 percent of patients with osteoarthritis, in 64.7 percent of patients with gout arthritis. XO, XDG, 5'NT activity, XO/XDG activities ratio, XDG-2 esoenzymes and content of UA were increased in OA patients compared to healthy controls. XO, XDG activity, XDG-2 esoenzymes and UA content in GA patients were higher than those in OA patients. CONCLUSION: The enzyme difference found may promote differential diagnosis of OA and GA. The enzyme indices essentially depend on clinical specificity of the disease and can be helpful in the assessment of the treatment efficiency.     

Multicentric reticulohistiocytosis: a mimic of gout and rheumatoid arthritis

Multicentric reticulohistiocytosis is a rare cutaneous-articular disease that may mimic more common disorders such as rheumatoid arthritis or tophaceous gout. In one fourth of patients, it is a paraneoplastic process. This brief overview is aimed at physicians who care for patients with polyarthritis, to alert them to distinctive features that differentiate multicentric reticulohistiocytosis from the common arthritides.     

Peripheral arthrocentesis in the work-up of acute low back pain

Involvement of the axial skeleton in acute gouty arthritis has rarely been reported. Without the presence of peripheral tophi or history of gout, this diagnosis is often not considered. A patient is described with acute low back pain and for whom a diagnosis of acute axial gout was suggested after arthrocentesis of an asymptomatic peripheral joint yielded monosodium urate crystals. Treatment with colchicine led to prompt resolution of the gouty flare. Demonstration of urate crystals in this manner may encourage the clinician to attempt a trial therapy for acute gout, or at least to add gout to the differential diagnosis of acute back pain.     

Nutrition and the Rheumatic Diseases

Long-term, dietotherapy is particularly important in the management of the rheumatoid diseases since so little is known of their etiology. The chronic character of these conditions, their capricious onset and exacerbations, and their unpredictable remissions can lead the patient to accept dangerous food fads.

Nutritional norms are given for treating nonarticular rheumatism, osteoarthritis, gout, arthritis due to infections, rheumatoid arthritis, rheumatic fever, systemic lupus erythematosus, progressive systemic sclerosis (scleroderma), and polyarteritis nodosa.     

Inhibition of T cell apoptosis in the rheumatoid synovium.

Synovial T cells in rheumatoid arthritis are highly differentiated and express a phenotype suggesting susceptibility to apoptosis (CD45RB dull, CD45RO bright, Bcl-2 low, Bax high, Fas high). However, no evidence of T cell apoptosis was found in synovial fluid from any of 28 patients studied. In contrast, synovial fluid from 10 patients with crystal arthritis showed substantial levels of T cell apoptosis. The failre of apoptosis was not an intrinsic property of rheumatoid synovial T cells, as they showed rapid spontaneous apoptosis on removal from the joint. Synovial T cells from rheumatoid arthritis and gout patients could be rescued from spontaneous apoptosis in vitro either by IL-2R gamma chain signaling cytokines (which upregulate Bcl-2 and Bcl-XL) or by interaction with synovial fibroblasts (which upregulates Bcl-xL but not Bcl-2). The phenotype of rheumatoid synovial T cells ex vivo (Bcl-2 low, Bcl-xL high) suggested a fibroblast-mediated mechanism in vivo. This was confirmed by in vitro culture of synovial T cells with fibroblasts which maintained the Bcl-xL high Bcl-2 low phenotype. Synovial T cells from gout patients were Bcl-2 low Bcl-xL low and showed clear evidence of apoptosis in vivo. Inhibition experiments suggested that an integrin-ligand interaction incorporating the Arg-Gly-Asp motif is involved in fibroblast-mediated synovial T cell survival. We propose that environmental blockade of cell death resulting from interaction with stromal cells is a major factor in the persistent T cell infiltration of chronically inflamed rheumatoid synovium.     

Occult Mood in Musculoskeletal Diseases

Psychophysiologic musculoskeletal reactions are common. Tightening of muscles secondary to emotional stress certainly can cause or aggravate pain. Many studies suggest a relationship between stress or personality characteristics and rheumatoid arthritis. Certain personality characteristics have been associated with gout, and it has been suggested that emotional factors may affect osteoarthritis.     

Assessment and management of gouty arthritis

Gout is a metabolic disorder of purine metabolism that leads to elevated serum concentrations of uric acid. When this happens, urate crystals may precipitate and accumulate in the joints and bursae. Gout is characterized by recurrent, painful attacks of arthritis, which is the major clinical complication of the disease. Early diagnosis and treatment of gout are important to prevent complications, and with early, sustained therapy, most patients can live without functional disability. If gout becomes chronic, individuals may experience severe limitations of activity. This article discusses the clinical manifestations, diagnosis and treatment of acute and chronic gout.     

慢性肾脏病合并风湿病的治疗

风湿病可以累及多个器官和系统,其中肾脏是最常受累的器官之一。常见风湿病包括系统性红斑狼疮、 类风湿关节炎、系统性硬化症、抗中性粒细胞胞浆抗体(ANCA)相关血管炎、原发性干燥综合征以及痛风均可以合并 慢性肾脏病。本文就慢性肾脏病合并上述风湿病的治疗进展作一综述。     

Uric acid, a neglected molecule--the value of imaging

Imaging plays a key role in two longterm effects of hyperuricemia: those on the urinary tract and on the skeletal system. This overview concentrates on the diagnosis of urinary stones and of musculoskeletal gout. Urinary stones are negative on radiography, i.e., they cannot be differentiated from the surrounding tissues, and even at intravenous urography only non specific filling defects are shown that may be hard to differentiate from blood clots and papillary necrosis whereas computed tomography without a contrast agent is highly sensitive in detecting all types of stones whether negative or positive at radiography. Gout of the musculoskeletal system usually manifests as an acute gouty arthritis after a long-standing asymptomatic hyperuricemia. An intercritical phase may follow before new acute attacks and--in up to 50%--chronic gout develop. During acute gouty arthritis imaging is non-specific. The distribution pattern, the relation of soft tissue changes and osteolytic paraarticular changes, calcifications and the lack of osteoporosis are a typical, nearly pathognomonic constellation of chronic tophaceous gout. In selected cases CT or MRI may add critical local information.     

Rheumatic diseases. 2. Therapeutic considerations.

In the management of rheumatic diseases, the use of corticosteroids should be reserved for active arthritis. Phenylbutazone (Butazolidin) is probably the drug of choice for acute gout and is also effective in ankylosing spondylitis, Reiter's syndrome, and psoriatic arthritis. Indomethacin (Indocin) also is useful in these conditions. Ibuprofen (Motrin) is only slightly more efficacious than aspirin. Aspirin is still the preferred treatment for rheumatoid arthritis and should be tried before ibuprofen. Osteoarthritis of the cervical or lumbar spine calls for a full program of physical therapy. Experimental procedures for total replacement of joints other than hip and knee show promise.     

Diagnosis and management of rheumatoid arthritis

Rheumatoid arthritis is a chronic inflammatory disease characterized by uncontrolled proliferation of synovial tissue and a wide array of multisystem comorbidities. Prevalence is estimated to be 0.8 percent worldwide, with women twice as likely to develop the disease as men. Untreated, 20 to 30 percent of persons with rheumatoid arthritis become permanently work-disabled within two to three years of diagnosis. Genetic and environmental factors play a role in pathogenesis. Although laboratory testing and imaging studies can help confirm the diagnosis and track disease progress, rheumatoid arthritis primarily is a clinical diagnosis and no single laboratory test is diagnostic. Complications of rheumatoid arthritis may begin to develop within months of presentation; therefore, early referral to or consultation with a rheumatologist for initiation of treatment with disease-modifying antirheumatic drugs is recommended. Several promising new disease-modifying drugs recently have become available, including leflunomide, tumor necrosis factor inhibitors, and anakinra. Nonsteroidal anti-inflammatory drugs, corticosteroids, and nonpharmacologic modalities also are useful. Patients who do not respond well to a single disease-modifying drug may be candidates for combination therapy. Rheumatoid arthritis is a lifelong disease, although patients can go into remission. Physicians must be aware of common comorbidities. Progression of rheumatoid arthritis is monitored according to American College of Rheumatology criteria based on changes in specific symptoms and laboratory findings. Predictors of poor outcomes in early stages of rheumatoid arthritis include low functional score early in the disease, lower socioeconomic status, early involvement of many joints, high erythrocyte sedimentation rate or C-reactive protein level at disease onset, positive rheumatoid factor, and early radiologic changes.     

Laboratory diagnosis of rheumatoid diseases

The diagnosis of most collagen diseases requires particular clinical findings. Rheumatoid factor assays are tests commonly used to detect seropositive rheumatoid arthritis. Latex tests are highly sensitive for rheumatoid factors but relatively nonspecific for rheumatoid arthritis, while sheep cell agglutination tests are moderately insensitive for rheumatoid factors but highly specific for rheumatoid arthritis. These tests are not helpful in following the course of the disease, however, since titers remain stable. Serial observations of elevated C-reactive protein levels or ESR may be more helpful in this regard. Specific antibodies have been identified for some collagen diseases, notably the mixed connective tissue disease syndrome, aiding in differential diagnosis.     

抗RA33抗体在类风湿关节炎鉴别诊断中的意义及一年随访研究

目的:深入了解抗RA33抗体对类风湿关节炎(RA)的诊断价值,并探讨与类风湿因子(RF)的关系。方法:用酶联免疫吸附试验方法测定了124例RA;60例未分化关节炎;68例其他结缔组织病;40例血清阴性脊柱关节病;31例膝骨性关节炎和12例痛风患者血清抗RA33抗体的水平。结果:抗RA33抗体对RA诊断的敏感性37.1%,特异性90.99%;RF对RA诊断的敏感性54.8%,特异性66.4%。124例RA中,RF阳性组抗RA33抗体阳性率32.3%,56例RF阴性组中抗RA33抗体阳性率42.9%,RA33抗体与RF间无相关性(P>0.05);侵蚀性关节病变组50例RA33抗体阳性率为30.0%,无侵蚀组74例RA33抗体阳性率为41.9%,RA33抗体与关节骨侵蚀的相关性比较,(P>0.05)。在60例未分化关节炎中,18例RA33抗体阳性,阳性率为30%;追随12～18个月,18例阳性者中有10例(55.6%)确诊为RA,明显高于RA33抗体阴性组。结论:抗RA33抗体对RA的诊断虽敏感性不高,但有较高的特异性;抗RA33抗体与RF间无相关性,与RA的关节骨侵蚀也无相关性;RA33抗体阳性对预测未分化关节炎...     

Gout: an update

Arthritis caused by gout (i.e., gouty arthritis) accounts for millions of outpatient visits annually, and the prevalence is increasing. Gout is caused by monosodium urate crystal deposition in tissues leading to arthritis, soft tissue masses (i.e., tophi), nephrolithiasis, and urate nephropathy. The biologic precursor to gout is elevated serum uric acid levels (i.e., hyperuricemia). Asymptomatic hyperuricemia is common and usually does not progress to clinical gout. Acute gout most often presents as attacks of pain, erythema, and swelling of one or a few joints in the lower extremities. The diagnosis is confirmed if monosodium urate crystals are present in synovial fluid. First-line therapy for acute gout is nonsteroidal anti-inflammatory drugs or corticosteroids, depending on comorbidities; colchicine is second-line therapy. After the first gout attack, modifiable risk factors (e.g., high-purine diet, alcohol use, obesity, diuretic therapy) should be addressed. Urate-lowering therapy for gout is initiated after multiple attacks or after the development of tophi or urate nephrolithiasis. Allopurinol is the most common therapy for chronic gout. Uricosuric agents are alternative therapies in patients with preserved renal function and no history of nephrolithiasis. During urate-lowering therapy, the dose should be titrated upward until the serum uric acid level is less than 6 mg per dL (355 micromol per L). When initiating urate-lowering therapy, concurrent prophylactic therapy with low-dose colchicine for three to six months may reduce flare-ups.     

Uric acid levels of the serum of healthy persons and patients with various rheumatic diseases

Serum uric acid levels were investigated in a series of 1715 subjects. Of them 596 were patients with inflammatory rheumatic disorders, 162 gout patients, 236 with osteoarthrosis, 79 with systemic lupus erythematosus or diffuse scleroderma and 642 healthy subjects. On analyzing the results, very high uricemia values were found in the gout patients. Increased uricemia values were observed is patients with psoriatic arthritis and diffuse connective tissue disorders (systemic lupus erythematosus and diffuse scleroderma). Hyperuricemia was found in psoriatic arthritis, rheumatoid arthritis and in nosological entities classified under diffuse connective tissue disorders in 5.6 to 10.1% of patients. In the healthy examinees hyperuricemia was recorded in 3.8% of the cases.