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Magnetic resonance imaging (MRI) is the preferred investigation for most spinal diseases and is increasingly requested for people with low back pain (LBP). However, determining the cause of back pain is complicated as it is often multifactorial and anatomical abnormalities are common in the spine and may not necessarily translate into clinical symptoms. Thus, national guidelines discourage the use of MRI in non-specific LBP and recommend reserving it for the investigation of severe or progressive neurological deficits or for those cases in which serious underlying pathology is suspected. It also has an acknowledged role in planning surgical management in cases of radiculopathy and spinal stenosis. This review summarises the indications for MRI in LBP and calls for improved education of patients and health professionals in the limitations of this investigation.

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Magnetic resonance imaging (MRI) is the preferred investigation for most spinal diseases and is increasingly requested for people with low back pain (LBP). However, determining the cause of back pain is complicated as it is often multifactorial and anatomical abnormalities are common in the spine and may not necessarily translate into clinical symptoms. Thus, national guidelines discourage the use of MRI in non-specific LBP and recommend reserving it for the investigation of severe or progressive neurological deficits or for those cases in which serious underlying pathology is suspected. It also has an acknowledged role in planning surgical management in cases of radiculopathy and spinal stenosis. This review summarises the indications for MRI in LBP and calls for improved education of patients and health professionals in the limitations of this investigation.

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Oesophageal dysfunction can occur in a variety of musculoskeletal conditions, most notably the autoimmune connective tissue diseases. However, correlation between oesophageal symptoms and investigations is frequently poor. It is often uncertain whether symptoms are caused by the underlying disease or by its treatment. As the primary disease process may not be responsive to treatment, correctable iatrogenic causes should always be sought.

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A young woman with the HLA phenotype A1, A2, B5, B8, DR3, DR4 developed RA, idiopathic thrombocytopenic purpura (ITP), pernicious anaemia (PA), Hashimoto's thyroiditis (HT), systemic sclerosis (SS), pancreatic exocrine insufficiency (PEI) and coeliac disease (CD) before dying from vasculitic complications. A family study revealed RA, PA and insulin-dependent diabetes mellitus (IDDM) amongst her first degree relatives. Her case emphasizes the clinical and immunogenetic links between the autoimmune diseases.

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Self-induced disease can be difficult to diagnose and costly of time and money to investigate. The key is to think of the possibility. Five patients in whom the evidence for factitious rheumatological illness was strong are discussed and their histories, physical signs and family backgrounds are explored in relationship to factitious disease presenting in other fields. Young immature individuals seem most at risk and the discrepancy between physical signs and understandable pathological mechanisms may suggest the diagnosis. The outlook seems frequently poor.

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Blood polymorphonuclear cells (PMNs) from 40 patients with rheumatoid arthritis (RA) and 40 normal subjects were incubated with confluent cultures of porcine aortic endothelium and their adherence assessed by either a microscopic or radiometric enumeration assay. There was no difference between the number of rheumatoid and control PMNs adhering. The synovial fluid PMNs from patients with RA were less adherent than their paired blood samples when autologous serum was present in the incubation medium and more adherent when serum was absent. Most of the RA sera tested inhibited the adhesion of normal PMNs, an effect that was not due to an increase in PMN aggregation. A similar inhibition was seen with sera obtained from patients with Felty's syndrome. These findings suggest that there is no intrinsic difference between the adhesiveness of rheumatoid PMNs and normal PMNs but that there are soluble factors present in RA serum which inhibit the attachment of normal PMNs to vascular endothelium.

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Rheumatoid sera and plasma inhibited the adherence of normal blood polymorphonuclear cells (PMNs) to cultured porcine endothelium. This inhibition of adhesion was not seen when PMNs were treated with the plasma or serum from normal subjects or patients with other inflammatory arthropathies. The abrogation of PMN adherence was directly related to the levels of circulating immune complexes and was not dependent upon the type of anti-inflammatory therapy that the patients were receiving nor on any of the recorded clinical parameters. A similar inhibition of adhesion was seen with heat induced aggregated human IgG (HAGG) provided that serum was present in the culture medium. In view of these results we propose that circulating immune complexes in RA may have a significant role in controlling the interaction of PMNs with vascular endothelium and in perpetuating the entry of these cells into the synovial fluid of the inflamed joints.

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Disease activity was assessed clinically and erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), orosomucoid, alpha 1-antitrypsin (alpha 1AT) and alpha 2-macroglobulin (alpha 2M) were measured in 65 patients with ankylosing spondylitis (AS). Positive correlations were found between ESR and the acute phase proteins (APP), CRP, orosomucoid and alpha 1AT, but none of these variables correlated with the clinical assessment of activity. No relationship was demonstrated between the protease inhibitor, alpha 2M and clinical activity, ESR or any of the APP. While the treatment of AS remains predominantly symptomatic, routine management of patients should continue to be founded on the clinical assessment of disease activity rather than on laboratory indices of inflammation.

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