Case management study: polyarthritis with fever.

In most cases, a thorough initial evaluation will reveal the cause of fever and polyarthritis. However, in some patients the initial diagnosis may be unclear and, as time passes, the characteristic clinical patterns emerge. Recurrent attacks are suggestive of other conditions such as crystal-induced arthritis, Lyme disease, and Mediterranean fever. In rheumatoid arthritis and Reiter's syndrome, the fever resolves and the articular findings predominate with the passage of time. Similarly, Still's disease is initially diagnosed on the basis of clinical criteria, and later confirmed by the evolution of chronic polyarthritis. Diagnostic approaches for the evaluation of patients presenting with acute arthritis have been published and are readily available (2,8,9). The most reliable way to establish the diagnosis for a rheumatic disease is thoughtful and thorough evaluation by an experienced clinician (3,10). Certain discriminating features and confirmatory tests can aid in the diagnosis of polyarthritis with fever (Tables 2 and 3).

Mechanisms of joint destruction, pain and disability in osteoarthritis.

Osteoarthritis is characterised by progressive erosion of articular cartilage, and bony overgrowth at the joint margins. Cartilage integrity requires a balance between synthesis and degradation of matrix components, and the latter is augmented in osteoarthritis through the action of chondrocyte-derived metalloproteinases. Synthesis rates also increase but fail to keep pace with the losses. Synovial inflammation, a mild and inconstant feature of osteoarthritis, is more likely to be a consequence of cartilage breakdown than a cause, and its contribution to pain is uncertain. The origins of pain and disability are complex; pathological changes in the joint capsule and periarticular ligaments are a likely source, but nocturnal pain may be related to raised pressure in subchondral bone. In addition to structural damage in the joint, psychosocial factors, muscle weakness, and comorbidities may contribute.

Leukocytosis in rheumatoid arthritis.

To determine the prevalence and clinical significance of leukocytosis in rheumatoid arthritis (RA), records of 98 consecutive outpatients with this disease were reviewed. Leukocytosis, defined as 2 or more white blood cell counts (WBC) greater than 10,000/mm, was found in 27%. Among patients currently receiving steroid therapy (mean dose prednisone 7 mg daily), the prevalence was 40%; in all others, the prevalence was 7.5%. The WBC elevation was primarily caused by an increase in neutrophils. Patients with leukocytosis tended to have more active arthritis, but there were no differences in extra-articular manifestations or drug therapy except for the use of corticosteroids.A review of the literature confirms the contributions of both disease activity and steroid therapy to WBC elevation. There is little published information on the effect of chronic, low dose corticosteroids on WBC counts, but our study suggests that this is an important factor in leukocytosis in RA.Newly detected leukocytosis in RA should alert the physician to the possibility of occult infection. In the absence of suggestive signs and symptoms, an infectious cause is seldom found, but, despite the few infections found in this series, continuing vigilance is recommended.

Treatment of adhesive capsulitis (frozen shoulder) with arthrographic capsular distension and rupture.

Sixteen patients with adhesive capsulitis of the shoulder were treated in an open trial of capsular distension with intraarticular injection of 30mL of fluid containing 8mL of 1% lidocaine, 2mL of corticosteroid, and 20mL of radiocontrast material. A capsular tear during arthrography occurred in all cases. Rupture usually occurred at the subscapular bursa or the subacromial bursa. Rupture at the distal bicipital sheath occurred in two patients and was not associated with pain relief. Thirteen patients experienced immediate pain relief and increased shoulder mobility. This improvement was maintained over a follow-up interval of 6 months. Disruption of the constricted capsule by hydraulic distension seems to be the mechanism for achieving symptomatic relief in adhesive capsulitis.

Pharmacologic treatment of osteoarthritis.

Current pharmacotherapy for osteoarthritis (OA) is aimed at relief of pain and functional disability. Although an inflammatory component may be found in some cases, there is little evidence that anti-inflammatory drugs commonly used in the treatment of OA provide more relief than simple analgesics. A growing body of knowledge about the pathophysiology of OA now offers opportunities to develop interventions aimed at retarding the progressive degeneration of articular cartilage. This is a function of an imbalance between cartilage matrix synthesis and breakdown. New and experimental treatments include oral, parenteral, and intra-articular agents, some of which are chemicals and others biological products. Their modes of action have generally not been established in humans, but may be inferred from in vitro culture systems and animal models. These mechanisms include inhibition of synovial cell-derived cytokines and chondrocyte-derived degradative enzymes, inactivation of superoxide free radicals, stimulation of matrix synthesis, and enhancement of synovial fluid lubrication. Many of these treatments have been shown to provide short- or long-term symptomatic improvement in clinical trials. Protection of cartilage or promotion of repair has been demonstrated in animal studies, but not convincingly in human OA studies.

Corticosteroid injections in adhesive capsulitis: investigation of their value and site.

Forty-eight patients with frozen shoulder for less than six months were assigned at random to receive three shoulder injections into the subacromial bursa or glenohumeral joint at weekly intervals. The treatment groups were (1) intra-articular methylprednisolone and lidocaine, (2) intrabursal methylprednisolone and lidocaine, (3) intra-articular lidocaine, (4) intrabursal lidocaine. The same physical therapy program was carried out for all patients. Assessments of pain and range of motion were performed by a physical therapist who was uninformed about the nature of the injection therapy. There was no significant difference in outcome between intrabursal injection and intra-articular injection. Injection of steroid with lidocaine had no advantage over lidocaine alone in restoring shoulder motion, but partial, transient pain relief occurred in two thirds of the steroid-treated patients.

The effect of diltiazem on calcinosis in a patient with the CREST syndrome.

We describe a patient with a 23-year history of progressive calcinosis and features of the CREST syndrome (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasias) who was treated with diltiazem, 240 mg/day, for 5 years. No clinical exacerbation of calcinosis occurred during treatment. Radiographs showed no new lesions, and there was reduction in the size of the existing lesions. Bone scans revealed a progressive decrease in the uptake of the radionuclide by soft tissue foci. We propose that diltiazem may stop the progression of calcinosis by reducing the cellular calcium influx in affected tissues.

History of enteric coated sulfasalazine in rheumatoid arthritis.

Sulfasalazine was synthesized almost 50 years ago specifically to treat rheumatoid arthritis. At that time bacterial infection was believed to be an important factor in pathogenesis. The linkage of sulfapyridine and salicylate with an azobond was viewed as a method of combining antibacterial and antiinflammatory actions while minimizing gastric irritation. Early therapeutic results were encouraging, but the drug was discarded as an antirheumatic agent for 30 years, until its serendipitous rediscovery. Subsequent controlled trials have confirmed its efficacy, which may be related to sulfasalazine itself or to the sulfapyridine moiety.

Rheumatoid arthritis: a pharmacologic overview.

Numerous drugs are available for the treatment of rheumatoid arthritis. The nonsteroidal anti-inflammatory drugs differ in structure and pharmacokinetics, and they rarely act synergistically. The disease-modifying antirheumatic drugs include gold compounds, penicillamine, hydroxychloroquine and sulfasalazine. Useful immunosuppressive and cytotoxic agents include methotrexate, azathioprine and cyclophosphamide. Costicosteroids find their greatest use in short courses.

Diagnosis of diseases of the lumbar spine: correlation of computerized tomography with myelography and clinical findings.

Data from 339 patients referred for evaluation of suspected lumbar disease were studied retrospectively to correlate findings in the routine clinical evaluation with results of computed tomography and myelography. Clinical features from the patients' history that correlated with an abnormal CT and myelogram included age greater than or equal to 40, a history of previous surgery, and absence of a history of injury. Signs from the physical examination that correlated included reduced lumbar motion, a motor or sensory deficit, abnormal reflexes, and reduced capacity for straight leg-raising or walking. Using a clinical score incorporating these variables, we suggest a diagnostic strategy to promote more efficient and selective use of CT scans and myelograms. We project that the use of this diagnostic approach can reduce the number of myelograms ordered in a similar population by more than 50%.

Myopathy in sarcoidosis: clinical and pathologic study of four cases and review of the literature.

The clinical course and muscle biopsy findings of four adults with sarcoidosis who developed a myopathy are described. Three patients had evidence of an inflammatory myopathy and elevated CPK. Two patients had no detectable granulomas at muscle biopsy and may represent a separate autoimmune disorder (polymyositis) concurrent with sarcoidosis. Asymptomatic muscle disease in sarcoidosis probably occurs with a much greater frequency than symptomatic disease. Isolated sarcoid myopathy without prior or concurrent organ involvement has been described, but comprehensive autopsy studies to confirm this are lacking. The origin of symptoms associated with granulomas is obscure and may be mediated through the effects of lymphokines and monokines. Corticosteroids seem to play a useful role in therapy, but treatment over a prolonged period may be necessary. The use of cytotoxic agents is largely untested.