A proposal for funding and monitoring medical education supervision in expanded clinical settings--a 'meducation' card.

CONTEXT: Entry to practice medical programs (graduate- and undergraduate-entry) in Australia are under considerable pressure to provide clinical training as a result of increased student numbers. At the same time modern medical curricula require the development of active placements in expanded settings to achieve graduate medical practitioners who are clinically able. These dual imperatives require a mechanism to fund and maintain the quality of clinical placements outside the traditional hospital setting. ISSUE: For teaching outside traditional teaching hospitals the Australian government's Practice Incentives Program (PIP) currently provides a student-related payment of AU$100 for each half-day teaching session in a general practice setting. This payment is not linked to the quality of the placement and does not support clinical placements in other settings, for example specialist consulting rooms or allied health practices. SOLUTION: This short communication proposes a 'meducation' card as an efficient funding mechanism to facilitate an expansion of quality clinical placements in expanded settings including specialist and allied health practices. This student meducation card would use current Medicare Australia infrastructure to facilitate the payment of clinical teachers in expanded settings. Meducation payments would only be available to practitioners and practices that maintain quality teaching practices certified by medical or allied health schools.

What's new in rheumatoid arthritis? An evidenced based review.

BACKGROUND: Rheumatoid arthritis (RA) is the most common inflammatory arthritis and has been associated with significant functional impairment and a shortened life expectancy. Fortunately, over the past 10 years, there has been a significant change in its management, which has resulted in improved outcomes for RA patients. OBJECTIVE: To critically appraise the recent evidence which affects the contemporary management of RA. DISCUSSION: The bulk of recent evidence suggests that disease modifying anti-rheumatic drugs (DMARDs) should be commenced early and continued indefinitely in RA patients. Single DMARD therapy may be sufficient in some patients but combinations, particularly those which include methotrexate, improve symptomatic and radiological outcomes. The use of newer therapies, including leflunomide and tumour necrosis factor-alpha blocking drugs, promise to further improve these outcomes.

Common corticosteroid injections. An anatomical and evidence based review.

BACKGROUND: The injection of depot corticosteroid preparations into soft tissues and joints has been used for some time to alleviate pain in a variety of musculoskeletal conditions. However the evidence, supporting the efficacy for these procedures, until recently, has been poor. OBJECTIVES: To review the recent literature on the efficacy and toxicity of commonly used corticosteroid injections in musculoskeletal medicine and to illustrate the key anatomy of the injection sites. DISCUSSION: Injections of corticosteroid into the lateral epicondyle, subacromial bursa, carpal tunnel, knee and plantar fascia all result in short term (weeks to months) alleviation of pain and other symptoms in the studies reviewed. The natural history of these conditions, however, is that the majority of patients improve over longer periods (months to a year) whether or not an injection has been given.

Inflammatory arthritis-like and other MR findings in wrists of asymptomatic subjects.

OBJECTIVE: To describe magnetic resonance (MR) imaging findings in the wrists of asymptomatic subjects that might be confused with pathologic findings. DESIGN: MR examination of the dominant wrist was performed in 30 asymptomatic volunteers aged 22-49 years using pre-contrast and post-contrast sequences in the coronal and axial planes. The bases of the metacarpals, the carpus and the distal radius and ulna were evaluated by two musculoskeletal radiologists for lesions, notches, blood vessels and synovial enhancement. RESULTS: There were 24 bright osseous lesions (erosions, intraosseous ganglia, oedema or cysts) in 14 subjects. Intraosseous blood vessels were seen in all but one wrist examined, most commonly in the capitate and lunate bones. Enhancement was present in 26 of 27 notches identified at the base of the second metacarpal and less commonly in the capitate, hamate and triquetral notches. A small joint effusion was present in 14 subjects. Joint or soft-tissue enhancement was identified in 16 wrists. CONCLUSIONS: Many MR abnormalities and variants may be detected in the wrists of asymptomatic subjects. Many of these could be confused with pathologic findings usually associated with inflammatory arthritis.

Pharmacological therapies for the treatment of osteoarthritis.

Non-pharmacological interventions are the first-line therapy for osteoarthritis. If non-pharmacological therapy fails, paracetamol (up to 4 g daily) should be added. If paracetamol fails, the patient's risk factors for gastrointestinal and renal disease should be assessed. In patients with gastrointestinal risk factors, a COX-2-specific inhibitor (CSI) would be used in preference to a conventional non-steroidal anti-inflammatory drug (NSAID). In patients with renal risk factors, NSAIDs and CSIs should be used with care. In patients who continue to have problems, other treatments should be considered; these might include intra-articular hyaluronan or depot corticosteroid, analgesia or glucosamine.

Familial CREST syndrome.

The familial occurrence of scleroderma is uncommon particularly the limited (CREST) form. We describe 2 families in which such an association occurred. Family pedigree 1 consists of 2 of 3 sisters with CREST scleroderma. Both affected sisters shared HLA types and C4 allotypes including DR5, found more frequently in patients with scleroderma. The unaffected sister did not share this MHC allele. Family pedigree 2 includes a grandmother and grandson with CREST scleroderma as well as a family member with Raynaud's phenomena alone. We conclude that familial occurrence of scleroderma may be associated with shared class II MHC antigens.

Tumour necrosis factor inhibitors: risks and benefits in patients with rheumatoid arthritis.

Rheumatoid arthritis (RA) is the most common form of inflammatory arthritis and can, if left untreated, result in significant disability and early death. It is also associated with large direct and indirect costs to the individual and to society. Early and aggressive disease modifying anti-rheumatic drug (DMARD) treatment of patients at risk of erosive disease has improved the outcome in the majority, but not all, RA patients. Tumour necrosis factor (TNF) appears to be a key mediator of the inflammatory and destructive process in RA, and consequently inhibitors of TNF action have been tested in randomized controlled trials in patients with RA. The results of these studies have suggested that TNF inhibitors are potent DMARD particularly when combined with methotrexate. They appear well tolerated with the commonest adverse events related to their parenteral route of administration, and the serious but rare side-effects being various infections, notably tuberculosis, multiple sclerosis, and worsening of cardiac failure. Treatment costs are high and range from $15 000 to $25 000 per patient per year. Etanercept, adalimumab and infliximab have recently been subsidised under the Pharmaceutical Benefits Scheme in Australia for patients with severe DMARD-resistant RA. The availability of TNF inhibitors in RA represents a significant advance in the treatment of patients with severe RA.

Early rheumatoid arthritis: can we predict its outcome?

The continuing trend towards more aggressive treatment of rheumatoid arthritis (RA) has seen an increasing interest in the early phase of this chronic inflammatory disease. Optimal benefit from present and emerging therapies is limited by our prognostic abilities during this period. The present review attempts to outline first the many methodological issues encountered in studies of early RA, and second the extent to which each major outcome measure can be explained, both by readily available clinical variables and by HLA-DR genotyping. The evidence supporting the clinical usefulness of genotyping is discussed separately. Based on this information, a clinically appropriate approach to the management of early RA and the identification of patients suitable for experimental therapies is suggested.

Antibodies to synovial antigens in recent-onset rheumatoid arthritis.

OBJECTIVE: To identify synovial antigens that bind to serum antibodies from subjects with recent-onset rheumatoid arthritis (RA) (< 6 months of synovitis). METHODS: Soluble and insoluble fractions of Triton X-100 extracts of RA and normal synovial tissue, and normal spleen and placenta, were immunoblotted with sera from 27 patients with recent-onset RA, 13 autoimmune disease control subjects, and 13 blood bank control donors. Bound immunoglobulin was probed with 125I-labeled protein A. RESULTS: Antibodies in the sera of 20 (74%) patients with recent-onset RA recognized at least 1 of 5 antigens in both a disease- and tissue-specific and nonspecific manner. Anti-La antibodies, usually associated with primary Sjögren's syndrome, were detected in 2 sera. Eight sera had increased reactivity to an IgG heavy and light chain dimer. There was strong binding of 8 sera with a 35-kd doublet and of 3 sera with a 55-kd species in RA and normal synovial lysates (insoluble fractions). Two sera uniquely recognized a 45-kd protein only in the RA synovial lysate (soluble fraction). CONCLUSION: IgG antibodies in the sera of patients with recent-onset RA show positive immunoblots for 3 novel synovial antigens of 35-kd, 55-kd, and 45-kd, as well as for 2 previously characterized antigens (La and IgG). Thus, a variety of synovial antigens appear to be recognized by B cells even early in the clinical course of RA.

Absence of peripheral blood T cell responses to "shared epitope' containing peptides in recent onset rheumatoid arthritis.

OBJECTIVES: To determine if peptides containing the 'shared epitope' sequence, QKRAA, from either endogenous, HLA-DR beta 1 (0401), or exogenous, Escherichia coli dnaJ, sources activate T cells in recent onset rheumatoid arthritis (RA). METHODS: Peripheral blood mononuclear cell (PBMC) proliferative and whole blood cytokine responses to shared epitope containing peptides from DR beta 1 (0401) and E coli dnaJ, to control peptides from DR beta 1 (0402) and hsp40 and to the recall antigen, tetanus toxoid, were tested in 20 untreated, recent onset RA subjects, 20 HLA, age, and sex matched healthy controls and 18 other subjects with inflammatory arthritis. PBMC proliferative responses to a second E coli dnaJ peptide (with the shared epitope at the N-terminus) and two peptides from type II collagen with high affinity for DR4(0401) were tested in a further 16 recent onset RA and 17 control subjects. RESULTS: PBMC proliferation and whole blood interferon gamma or interleukin 10 production in response to the shared epitope containing and control peptides were not different between the disease and control groups. On the other hand, compared with controls, RA subjects had significantly higher proliferation to a collagen II (aa 1307-1319) peptide, but significantly lower proliferation and interferon gamma production to tetanus toxoid. CONCLUSION: Recent onset RA subjects had no demonstrable increase in peripheral blood T cell reactivity to shared epitope containing peptides. However, a proportion had increased T cell reactivity to a peptide of similar length from a candidate RA autoantigen, collagen type II. Their impaired responses to tetanus are in keeping with evidence for general T cell hyporesponsiveness in RA.

HLA-B27 expression and reactive arthritis susceptibility in two patient cohorts infected with Salmonella Typhimurium.

BACKGROUND: Reactive arthritis (ReA) is an inflammatory arthritis triggered by certain gastrointestinal and genitourinary infections. Single source outbreaks of triggering infections provide an opportunity to elucidate host susceptibility factors in this disease. AIM: To determine the role of Major Histocompatibility Complex (MHC) Class I alleles in ReA susceptibility after two large single source outbreaks of Salmonella Typhimurium gastroenteritis. METHODS: A questionnaire screening for features of ReA and a request for HLA class I typing were sent to all patients affected by two single source outbreaks of S. Typhimurium gastroenteritis. Individuals with arthritis of recent onset were interviewed, examined and diagnostic criteria for ReA applied. RESULTS: Nineteen cases of reactive arthritis, 11 female, were diagnosed in the 424 respondents with S. Typhimurium gastroenteritis from both outbreaks. Clinical features of the arthritis were similar to those described after other large single source outbreaks of Salmonella infection. HLA-B27 was expressed by only two of the 19 ReA patients and therefore did not predict susceptibility to this form of arthritis. Caucasians were, however, more likely to develop reactive arthritis than Asians. CONCLUSIONS: In this study, susceptibility to ReA was not increased in HLA-B27 positive individuals or males but was greater in those of Caucasian descent.